Literaturliste - Neurologie, 11. Auflage - Georg Thieme Verlag

Literaturliste Mattle/Mumenthaler Neurologie, 11. Auflage

1 [p 177] Aaslid R, Lindegaard KF. Cerebral hemodynamics. In Aaslid R. (Editor). Transcranial Doppler sonography. Springer, Wien 60-85, 1986

2 [p 178] Aaslid R (Editor). Transcranial Doppler Sonography. Springer, Wien, New York 1986

3 [p 179] Acker W, Aps EJ, Majumdar SK, Shaw GK, Thomson AD. The relationship between brain and liver damage in chronic alcoholic patients. J Neurol Neurosurg Psychiat 45: 984-987, 1982

4 [p 180] Adams CR, Ziegler DK, Lin JT. Mercury intoxication simulating amyotrophic lateral sclerosis. JAMA 250: 642-643, 1983

5 [p 181] Adams HP (Editor). Handbook of cerebrovascular diseases. Marcel Dekker, Inc., New York, 1993

6 [p 182] Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10 172 in Acute Stroke Treatment. Stroke 24: 35-41, 1993

6a [p 183] Adams HP Jr, Bendixen BH, Leira E, Chang KC, Davis PH, Woolson RF, Clarke WR, Hansen MD. Antithrombotic treatment of ischemic stroke among patients with occlusion or severe stenosis of the internal carotid artery: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology 53:122-125, 1999.

7 [p 184] Adams HP Jr, Brott TG, Crowell RM, Furlan AJ, Gomez CR, Grotta J, Helgason CM, Marler JR, Woolson RF, Zivin JA, et al. Guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a special writing group of the stroke council, American Heart Association. Stroke 25: 1901-1914, 1994

1

8 [p 185] Adams HP, Love BB. Medical management of aneurysmal subarachnoid hemorrhage. In Barnett, HJM, JP Mohr, BM Stein, FM Yatsu (Editors). Stroke. Pathophysiology, diagnosis, and management. 2nd edition. Churchill Livingstone. New York, Edinburgh, 1029-1054, 1992

8a [p 186] Adams KK, Jackson CE, Rauch RA, Hart SF, Kleinguenther RS, Barohn RJ. Cervical myelopathy with false localizing sensory levels. Arch. Neurol. 53, 1155-1158, 1996.

9 [p 187] Adams RD, Lyon G. Neurology of hereditary metabolic diseases of children. Hemisphere, New York, 1982

10 [p 188] Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patientes. Arch Neurol Psychiat. 81: 154-172, 1959

11 [p 189] Adams RD, Victor M. Principles of neurology. Fifth edition. McGraw-Hill, Inc., New York, 1993

11a [p 190] Adams RJ, McKie VC, Hsu L, Files B, Vichinsky E, Pegelow C, Abboud M, Gallagher D, Kutlar A, Nichols FT, Bonds DR, Brambilla D. Prevention of a first stroke by tranfusions in children with sickle cell anemia and abnormal results on transcranial Doppler ultrasonography. N.Engl.J.Med. 339, 5-11, 1998.

12 [p 191] Adams R, McKie V, Nichols F, Carl E, Zhang DL, McKie K, Figueroa R, Litaker M, Thompson W, Hess D. The use of transcranial ultrasonography to predict stroke in sickle cell disease. N Engl J Med 326: 605-610, 1992

13 [p 192] Adour KK, Byl FM, Hilsinger RL Jr, Kahn ZM, Sheldon MI. The true nature of Bell’s palsy: analysis of 1000 consecutive patients. Laryngoscope (St. Louis) 88: 787-801, 1978

13a [p 193] Adrogue HJ; Madias NE. Hypernatremia. N Engl J Med 342; 1493-1499, 2000.

2

13b [p 194] Adrogue HJ; Madias NE. Hyponatremia. N Engl J Med 342; 1581-1589, 2000.

14 [p 195] Aggerbeck LP, Mc Mahon JP, Scanu AM. Hypobetalipoproteinemia: clinical and biochemical description of a new kindred with Friedreich’s ataxia. Neurology 24: 1051-1063, 1974

14a [p 196] Agid Y.: Une façon d’examiner un patient parkinsonien. Rev. Neurol. 156, 17-22, 2000.

14b [p 197] Agosti R.: Zervikales Kopfweh - Science oder Fiction? Schweiz. Ärztezeitung 81, 1176-1178, 2000.

14c [p 198] Aguzzi A, Brandner S. The genetics of prions - a contradiction in terms? Lancet 354: 22-25, 1999.

15 [p 199] Ahlskog JE, Muenter MD, Maranganore DM, Matsumoto JY, Lieberman A, Wright KF, Wheeler K. Fluctuating Parkinson’s disease. Treatment with the long-acting Dopamine agonist Cabergoline. Arch Neurol 51: 1236-1241, 1994

16 [p 200] Aiba T, Tanaka R, Koike T, Kameyama S, Takeda N, Komata T. Natural history of intracranial cavernous malformations. J Neurosurg 83: 56-59, 1995.

16a [p 201] Aidi S., El Alaoui Faris M., Mkinssi N, Bourezza M, Jiddane M, Chkili T.: Le syndrome "neck-tongue": un cas par ostéo-arthrite atlöido-axoidienne d’origine tuberculeuse. Rev. Neurol. 153, 694-696 (1997).

17 [p 202] Aikawa H, Suzuki K, Iwasaki Y, Iizuka R. Atypical Alzheimer’s disease with spastic paresis and ataxia. Ann Neurol 17: 297-300, 1985

17a [p 203] Aita J.A.: Neurologic manifestations of dysbarism. In: Handbook of Clinical Neurology, Vol. 12, Vinken P.J., Gruyn G.W. eds. Elsevier Amsterdam (1972).

3

17b [p 204] Aldrich M.S.: The clinical spectrum of narcolepsy and idiopathic hypersomnia. Neurology 46, 393-401 (1996).

17c [p 205] Algra A; van Gijn J. Aspirin at any dose above 30 mg offers only modest protection after cerebral ischaemia. J Neurol Neurosurg Psychiatry 60; 197-199, 1996.

18 [p 206] Al Kawi MZ, Bohlega S, Banna M. MRI findings in neuro-Behçet’s disease. Neurology 41: 405-408, 1991

19 [p 207] Al-Lozi MT, Pestronk A, Yee WC, Flaris N, Cooper J. Rapidly evolving myopathy with myosin-deficient muscle fibers. Ann Neurol 35: 273-279, 1994 Comment in: Ann Neurol. 1994 Mar;35(3):257-9

20 [p 208] el Alaoui-Faris M, Medejel A, Zemmouri K, Yahyaoui M, Chkili T. Le syndrome de sclérose lateral amyotrophique d’origine syphilitique. Rev Neurol 146: 41-44, 1990

21 [p 209] Alexander EL, Ranzenbach MR, Kumar AJ, Kozachuk WE, Rosenbaum AE, Patronas N, Harley JB, Reichlin M. Anti-Ro (SS-A) autoantibodies in central nervous system disease associated with Sjögren’s syndrome (CNS-SS): Clinical, neuroimaging, and angiographic correlates. Neurology 44: 899-908, 1994.

22 [p 210] Alexander EL. Neurologic complications of Sjögren’s syndrome. In Fox R. (Editor). Rheumatic clinics of North America. WB Saunders Company, Philadelphia 18/3: 637-672, 1992

23 [p 211] Alhalabi M, Moore PM. Serial angiography in isolated angiitis of the central nervous system. Neurology 44: 1221-1226, 1994

23a [p 212] Almarcegui C., Lorente S., Romero M.F. et al.: Blink reflex in trigeminal hypoesthesia caused by a pontine demyelinating lesion. J. Neurol. 246, 140-141 (1999).

4

24 [p 213] Amarenco P, Cohen A, Tzourio C, Bertrand B, Hommel M, Besson G, Chauvel C, Touboul PJ, Bousser MG. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 331: 1474-1479, 1994

25 [p 214] Amarenco P. The spectrum of cerebellar infarctions. Neurology 41: 973-979, 1991

26 [p 215] Ameri A, Bousser M-G. Cerebral venous thrombosis. In Barnett, HJM, Hachinski VC (Editors). Cerebral ischemia: treatment and prevention. Neurologic Clinics 10: 87-111, 1992

27 [p 216] Aminoff MJ (Ed.). Neurology and general medicine. The neurological aspects of medical disorders. 2nd edition. Churchill Livingstone, New York, Edinburgh, 1995

28 [p 217] Aminoff MJ (Editor). Electrodiagnosis in Clinical Neurology, 3rd edition. Churchill Livingstone, New York, 1992

28a [p 218] Amlie-Lefond C, Kleinschmidt-DeMasters BK, Mahalingam R, Davis LE, Gilden DH. The vasculopathy of varicella-zoster virus encephalitis. Ann Neurol 37; 784-790, 1995.

28b [p 219] Andreadou E., Yapijakis C., Paraskevas GP, Stavropoulos P, Karadimas C, Zis VP, Davaki P, Karandreas N, Rentzos M, Tsakanikas C, Vassilopoulos D, Papageorgiou C: Hereditary neuropathy with liability to pressure palsies: the same molecular defect can result in diverse clinical presentation. J. Neurol. 243, 225-230 (1996).

28c [p 220] Andrews NJ; Farrington CP; Cousens SN, Smith PG, Ward H, Knight RS, Ironside JW, Will RG.Incidence of variant Creutzfeldt-Jakob disease in the UK [letter]. Lancet 356:481-482, 2000.

29 [p 221] Anetseder M, Hartung E, Klepper S, Reichmann H. Gasoline vapors induce severe rhabdomyolysis. Neurology 44, 2393-2395, 1994

5

30 [p 222] Angelini L, Nardocci N, Rumi V, Zorzi C, Strada L, Savoiardo M. Hallervorden-Spatz disease: clinical and MRI study of 11 cases diagnosed in life. J Neurol 239: 417-425, 1992

31 [p 223] Antiplatelet Trialist’s Collaboration. Collaborative overview of randomized trials of antiplatelet therapy - I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatetet therapy in various categories of patients. Br Med J 308: 81-106, 1994

32 [p 225] Appenzeller O. The autonomic nervous system: an introduction to basic and clinical concepts. 5th editition, Elsevier Amsterdam, New York, 1997

33 [p 226] Aranda B. Les troubles vésico-sphinctériens de la maladie de Parkinson. Rev Neurol 149: 476-480, 1993

34 [p 227] Arbeitsgruppe Lipide der Schweiz. Gesellschaft für Kardiologie und der Schweiz. Stiftung für Kardiologie. Lipide und die Prävention der koronaren Herzkrankheit: Diagnostik und Maßnahmen. Schweiz. Aerztezeitung 73: 1593 -1602, 1992

35 [p 228] Arieff Al. Management of hyponatremia. Br med J 307: 305-308, 1993

35a [p 229] Arita J, Nakae Y, Matsushima H, Maekawa K. Hopkins Syndrome, T2 weighted high intensity of anterior horn on spinal MR imaging. Pediatr. Neurol. 13: 263-265, 1995

36 [p 230] Arnaud O, Pelletier J, Dalecky A, Cherif AA, Azulay JP, Salamon G, Khalil R. Les fistules durales rachidiennes à drainage veineux périmédullaire. Rev Neurol 150: 713-720, 1994

37 [p 231] Arning C. Farbkodierte Duplexsonographie der hirnversorgenden Arterien. Ein Text-Bild-Atlas der methodischen Grundlagen, normalen und pathologischen Befunde. Georg Thieme Verlag, Stuttgart, New York, 1996

37a [p 232] Arsac Ch., Raymond C., Martin-Moutot N. et al.: Immunoassays fail to detect antibodies against neuronal calcium channels in Amyotrophic lateral sclerosis. Ann. Neurol. 40, 695-700 (1996).

6

38 [p 233] Arsura E. Experience with intravenous immunoglobulin in myasthenia gravis. Clin Immunol Immunopathol 53: Suppl. S170-S179, 1989

38a [p 234] Arzimanoglou A.A.: Gilles de la Tourette syndrome. J. Neurol. 245, 761-765 (1998).

38b [p 235] Aschoff J.C., Kailer N.A., Walter K.: Physostigmin in der Behandlung von Kleinhirnataxien. Nervenarzt 67, 311-318 (1996).

39 [p 236] Ashizawa T, Dunne PW, Ward PA, Seltzer WK, Richards CS. Effects of the sex of myotonic dystrophy patients on the unstable triplet repeat in their affected offspring. Neurology 44: 120-122, 1994

40 [p 237] Asplund K. Any progress on progressing stroke? Cerebrovasc Dis 1992; 2: 317-384

41 [p 238] Astrup J, Sjesjö BK, Symon L. Thresholds in cerebral ischemia - the ischemic penumbra. Stroke 12: 723-725, 1981

42 [p 239] Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 273: 1421-1428, 1995

43 [p 240] Atlas SR (Editor). Magnetic resonance imaging of the brain and spine. Second edition. Lippincott-Raven Publishers, Hagerstown, 1995

44 [p 241] Atlas SW. MR angiography in neurologic disease. Radiology 193: 1-16, 1994

44a [p 242] Auer-Grumbach M., Wagner K., Fazekas F, Loscher WN, Strasser-Fuchs S, Hartung HP.: Hereditäre motorisch-sensible Neuropathien (Charcot-Marie-Tooth-Syndrom). Nervenarzt 70, 1052-1061 (1999).

7

45 [p 243] Auger RG, Litchy WJ, Cascino TL, Ahlskog JE. Hemimasticatory spasm: Clinical and electrophysiological observations. Neurology 42: 2263-2266, 1992

46 [p 244] Aupy M, Orgogozo JM, Loiseau P, Aparicio M, Vital C. Atteinte multiple des nerfs craniens révélant une périartérite noueuse. Relation avec le syndrome de Cogan. Rev neurol 136: 59-65, 1980

47 [p 245] Austin EJ, Wilkus RJ, Longstreath WT Jr. Etiology and prognosis of alpha coma. Neurology 33: 773-777, 1988

48 [p 246] Avrahami E, Cohn D-E, Feibel M, Tadmor R. MRI demonstration and CT correlation of the brain in patients with idiopathic intracerebral calcification. J Neurol 241: 381-384, 1994

48a [p 247] Backonja M, Beydoun A, Edwards KR, Schwartz SL, Fonseca V, Hes M, LaMoreaux L, Garofalo E.: Gabapentin for the symptomatic treatment of painful neuropathy in patients with diabetes mellitus: a randomized controlled trial. JAMA 280, 1831-1836 (1998).

48b [p 248] Baird AE, Lövblad K-O, Dashe JF, Connor A, Burzynski C, Schlaug G, Straroselskaya I, Edelman RR, Warach S. Clinical correlations of diffusion and perfusion lesion volumes in acute ischemic stroke. Cerebrovascular Dis 10; 441 448, 2000.

49 [p 249] Baldwin L, Baker RS. Acquired Brown’s syndrome in a patient with an orbital roof fracture. J Clin Neuro Ophthalmol 8: 127-130, 1988

49a [p 250] Balestrino M., Leandri M.: Trigeminal neuralgia in pontine ischaemia. J. Neurol. Neurosurg. Psychiatry 62, 297-298 (1997).

50 [p 251] Ball R. Drug-induced akathisia. A review. J R Soc Med 78: 748-752, 1985

8

51 [p 252] Ballard PA, Tetrud JW, Langston JW. Permanent human parkinsonism due to 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP): Seven cases. Neurology 35: 949-956, 1985

51a [p 253] Balfour HH. Antiviral drugs. N Engl J Med 340; 1255-1268, 1999.

51b [p 254] Balm M., Hammack J. Leptomeningeal carcinomatosis. Arch. Neurol. 53, 626-663 (1996).

52 [p 255] Baloh RW, Honrubia V. H.: Clinical neurophysiology of the vestibular system. 2nd edition. FA Davis Company Philadelphia, 1990.

54 [p 256] Baloh RW, Jacobson K, Honrubia V. Horizontal semicircular canal variant of benign positional vertigo. Neurology 43: 2542-2549, 1993

55 [p 257] Baloh RW, Jacobson K, Honrubia V. Idiopathic bilateral vestibulopathy. Neurology 39: 272-275, 1989

56 [p 258] Baloh RW, Yee RD. Spontaneous vertical nystagmus. Rev Neurol 145: 527-532, 1989

57 [p 259] Baloh RW. Dizziness, hearing loss, and tinnitus. The essentials of neurootology. FA Davis Company, Philadelphia, 1984

57a [p 260] Baloh R.W., Yue Q., Furman J.M, Nelson SF: Familial episodic Ataxia: clinical heterogeneity in four families linked to chromosome 19p. Ann. Neurol. 41, 8-11 (1997).

57b [p 261] Bandmann O., Valente E.M., Holmans P, Surtees RA, Walters JH, Wevers RA, Marsden CD, Wood NW.: Dopa-responsive dystonia: a clinical and molecular genetic study. Ann. Neurol. 44, 649-656 (1998).

9

58 [p 262] Bannister R. Autonomic Failure. A Textbook of Clinical Disorders of the Autonomic Nervous System. Oxford University Press, London 1988

59 [p 263] Barboriak DP, Provenzale JM, Boyko OB. MR diagnosis of Creutzfeldt-Jakob disease: significance of high signal intensity of the basal ganglia. AJR 162: 137-140, 1994

59a [p 264] Barker F.G., Jannetta P.J., Bissonette D.J, Larkins MV, Jho HD: The long-term outcome of microvascular decompression for trigeminal neuralgia. N. Engl. J. Med. 334, 1077-1083 (1996).

59b [p 265] Barker RA; Anderson JR; Meyer P; Dick DJ; Scolding NJ. Microangiopathy of the brain and retina with hearing loss in a 50 year old woman: extending the spectrum of Susac’s syndrome. J Neurol Neurosurg Psychiatry 66; 641-643, 1999.

59c [p 266] Barker RA; Revesz T; Thom M; Marsden CD; Brown P. Review of 23 patients affected by the stiff man syndrome: clinical subdivision into stiff trunk (man) syndrome, stiff limb syndrome, and progressive encephalomyelitis with rigidity. J Neurol Neurosurg Psychiatry 65; 633-640, 1998.

60 [p 267] Barkovich AJ. Pediatric neuroimaging. 2 nd edition. Lippincott-Raven Publishers, Hagerstown, 1995

61 [p 268] Barnett HJM, Eliasziw M, Meldrum HE. Drugs and surgery in the prevention of ischemic stroke. N Engl J Med 332: 238-248, 1995

62 [p 269] Barnett HJM, Mohr JP, Stein BM, Yatsu FM (Editors). Stroke. Pathophysiology, diagnosis, and management. 2nd edition. Churchill Livingstone. New York, Edinburgh, 1992

63 [p 270] Barohn JR, Kissel JT, Warmolts JR, Mendell JR. Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria.Arch Neurol. 46: 878-884, 1989

10

64 [p 271] Barohn RJ, Sahenk Z, Warmolts JR, Mendell JR. The Bruns-Garland Syndrome (Diabetic Amyotrophy) revisited 100 years later. Arch Neurol 48: 1130-1135, 1991

65 [p 272] Baron JC. Positron emission tomography studies in ischemic stroke. In Barnett HJM, Mohr JP, Stein BM, Yatsu FM. Stroke. Pathophysiology, Diagnosis, and Management, Churchill Livingstone, New York, London 111-123, 1992

65a [p 273] Baron J-C. Mapping the ischaemic penumbra with PET: implications for acute stroke treatment. Cerebrovasc Dis 9; 193-201, 1999.

65b [p 274] Baron M.S., Vitek J.L., Bakay R.A.E, Green J, Kaneoke Y, Hashimoto T, Turner RS, Woodard JL, Cole SA, McDonald WM, DeLong MR.: Treatment of advanced parkinson’s disease by posterior GPI Pallidotomy: 1-year results of a pilot study. Ann. Neurol. 40, 355-366 (1996).

66 [p 275] Baron R, Heuser K, Marioth G. Marchiafava-Bignami disease with recovery diagnosed by CT and MRI: demyelination affects several CNS structures. J Neurol 236: 364-366, 1989

66a [p 276] Barone-Kaganas I.: Der medikamenteninduzierte Kopfschmerz und seine Behandlung. Schweiz. Med. Wschr. 129, 446-449 (1999).

67 [p 277] Barton NW, Brady RO, Dambrosia JM, Di Bisceglie AM, Doppelt SH, Hill SC, Mankin HJ, Murray GJ, Parker RI, Argoff CE, et al. Replacement therapy for inherited enzyme deficiency macrophage-targeted glucocerebrosidase for Gaucher’s disease. N Engl J Med 324; 1464-1470, 1991

67a [p 278] Bassetti C.: Diagnose und Therapie der Schlafstörungen aus neurologischer Sicht. Hospitalis 69/11-12, 399-402 (1999).

68 [p 279] Bassetti C, Aldrich MS. Consciousness, delirium and coma. In Albin MS (ed.). Textbook of Neuroanesthesia. McGraw-Hill, Inc., New York, 1997, pp.369-408

11

69 [p 280] Bassetti C, Karbowski K. Prognostischer Wert der Elektroenzephalographie bei nichttraumatischen Komata. Schweiz med Wschr 120; 1425-1434, 1990

70 [p 281] Bassetti C, Mathis J, Hess CW. Multimodal electrophysiological studies including motor evoked potentials in patients with locked-in syndrome: report of six patients. J Neurol Neurosurg Psychiat 57; 1403-1406, 1994

70a [p 282] Bassetti C., Aldrich MS.: Narcolepsy. Neurologic Clinics of North Am. 14, 545-571 (1996). Oder Bassetti C; Bogousslavsky J; Mattle H; Bernasconi A. Medial medullary stroke: report of seven patients and review of the literature. Neurology 48; 882-890, 1997.

70b [p 283] Bassetti C., Aldrich MS.: Idiopathic hypersomniae. A series of 42 patients. Brain 120, 1432-1435 (1997).

70c [p 284] Bassetti C; Aldrich MS. Sleep apnea in acute cerebrovascular diseases: final report on 128 patients. Sleep 22; 217-23, 1999.

70d [p 285] Bassetti C, Gugger M. Hypersomnie - Aetiologie, Klinik, Diagnostik und Therapie der exzessiven Schläfrigkeit. Therapeutische Umschau 57, 421-429, 2000.

70e [p 286] Bassetti C, Aldrich MS. Narcolepsy, idopathic hypersomnia, and periodic Hypersomnias. In Culebras A (Editor). Sleep dosorders and neurological disease. Marcel Dekker, Inc., New York, Basel, 323-354, 2000.

71 [p 287] Batra P, Herrmann C Jr, Mulder D. Mediastinal imaging in myasthenia gravis: correlation of chest radiography, CT, MR, and surgical findings. AJR 148: 515-519, 1987

71a [p 288] Baumert B., Steinauer K., Lütolf U.M. Therapie von ZNS-Metastasen. Therapeutische Umschau 56, 338-341 (1999).

12

72 [p 289] Baumgartner G. Gehirn und Bewußtsein. Schweiz med Wschr 122; 4-10, 1992

73 [p 290] Baumgartner RW, Mattle HP, Aaslid R. Transcranial color-coded duplex sonography, magnetic resonance angiography, and computed tomography angiography: methods, applications, advantages, and limitations. J Clin Ultrasound 23: 89-112, 1995

74 [p 291] Baumgartner RW, Mattle HP, Cerny T. Stroke and cancer. In Bogousslavsky J, Ginsberg M, Caplan LR, van Gjin J (Editors), Cerebrovascular Disease. Pathophysiology, diagnosis, and management. Blackwell Scientific Publications, Boston, 1996

75 [p 292] Baumgartner RW, Schroth G, Mattle HP. Transcranial color-coded Duplex sonography in cerebral arteriovenous malformations, Neuroradiology 38, 734-737 (1996).

76 [p 293] Baumgartner RW, Hauser V, Grob P, Waespe W. Die zerebrotendinöse Xanthomatose. Schweiz med Wschr 121; 858-864, 1991

76a [p 294] Baumgartner RW. Transcranial color-coded duplex sonography. J Neurol 246; 637 647, 1999.

76b [p 295] Baumgartner RW, Mattle HP, Schroth G. Assessment of =50% and so90=46 so90=46

151

913a [p 1602] Strenge H., Speidel H., Albert E., Helbig B.: Psychogene Handdystonie und hereditäre Polyneuropathie mit Neigung zu Druckparesen. Fortschr. Neurol. Psychiat. 64, 20-25 (1996).

913b [p 1603] Strittmatter M., Hamann G., Blaes F., Fischer C, Grauer M, Hoffmann KH, Schimrigk K.: Fehlregulation der hypothalamisch-hypophysär-adrenalen Achse und chronobiologische Auffälligkeiten beim Clusterkopfschmerz. Fortschr. Neurol. Psychiat. 65, 1-7 (1997).

913c [p 1604] Stroink H, Brouwer OF, Arts WF, Geerts AT, Peters AC, van Donselaar CA.: The first unprovoked, untreated seizure in childhood: a hospital based study of the accuracy of the diagnosis, rate of recurrence, and long term outcome after recurrence. Dutch study of epilepsy in childhood. J Neurol Neurosurg Psychiatry 64; 595-600, 1998

914 [p 1605] Strub RL, Black FW. The mental status examination in neurology. 3rd edition. FA Davis Company, Philadelphia, 1993

914a [p 1606] Strupp M; Bruning R; Wu RH, Deimling M, Reiser M, Brandt T. Diffusion-weighted MRI in transient global amnesia: elevated signal intensity in the left mesial temporal lobe in 7 of 10 patients. Ann Neurol 43; 164-170, 1998.

916 [p 1607] Stuart JD. Focal Peripheral Neuropathies. Elsevier, New York: 1987

917 [p 1608] Sturzenegger M, Beer JH, Rihs F. Monitoring combined antithrombotic treatments in patients with prosthetic heart values using transcranial Doppler and coagulation markers. Stroke 26: 63-69, 1995

918 [p 1609] Sturzenegger M, Mattle HP, Rivoir A, Baumgartner RW. Ultrasound findings in carotid artery dissection. Analysis of 43 patients. Neurology 45: 691-698, 1995

919 [p 1610] Sturzenegger M, Stratmann A, Wyss P. Mononeuritis multiplex als Erstmanifestation einer systemischen Granulomatose. Nervenarzt 64: 250-257, 1993

152

920 [p 1611] Sturzenegger M. Headache and neck pain: the warning symptoms of vertebral artery dissection. Headache 34: 187-193, 1994

921 [p 1612] Sturzenegger M. Ptose - klinische Differentialdiagnose. Schweiz med Wschr 119: 1386-1399, 1989

922 [p 1613] Sturzenegger M, Huber P. Cranial nerve palsies in spontaneous carotid artery dissection. J Neurol Neurosurg Psychiat 56: 1191-1199, 1993

924 [p 1614] Sunderland S. Nerves and Nerve Injuries, 2nd ed. Livingstone, Edingburgh, 1978

925 [p 1615] Susac JO. Susac’s syndrome. The triad of microangiopathy of the brain and retina with hearing loss in young women. Neurology 44: 591-593, 1994

926 [p 1616] Swaiman KF (Editor). Pediatric Neurology: Principles and Practice. 2nd edition, Mosby, St. Louis, 1994

927 [p 1617] Swanson JW, Kelly JJ Jr, McConahey WM. Neurologic aspects of thyroid dysfunction. Mayo Clin Proc 56: 504-512, 1981

928 [p 1618] Symon L, Kuyama H, Kendall B. Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60: 238-247, 1984

929 [p 1619] Takamori M, Gutmann L, Crosby TW, Martin JD. Myasthenic syndromes in hypothyroidism. Electrophysiological study of neuromuscular transmission and muscle contraction in two patients. Arch Neurol 26: 326-335, 1972

930 [p 1620] Tanaka H, Endo K, Tsuji S, Nygaard TG, Weeks DE, Nomura Y, Segawa M. The gene for hereditary progressive dystonia with marked diurnal fluctuation maps to chromosome 14 q. Ann

153

Neurol 37: 405-408, 1995

930a [p 1621] Tandberg E., Larsen JP., Karlsen K.: Excessive day-time sleepiness and sleep benefit in Parkinson’s disease: a community based study. Mov. Disord. 14, 922-927 (1999).

930b [p 1622] Targum SD, Abbott JL.: Efficacy of Quetiapine in Parkinson’s patients with psychosis. J. Clin. Psychopharmacol. 20, 54-60 (2000).

930c [p 1623] Tatu L, Moulin T, Martin V, Chavot D, Rousselot JP, Monnier G, Rumbach L.: Astérixis unilatérel et lésions cérébrales focales. Rev. Neurol. 152, 121-127 (1996).

930d [p 1624] Tatu L, Moulin T, Martin V, Monnier G, Rumbach L.: Unilateral pure thalamic asterixis: Clinical, electromyographic, and topographic patterns. Neurology 54, 2339-2342 (2000).

930e [p 1625] Terwindt GM, Ophoff RA, Haan J, Frants RR, Ferrari MD.: Familial hemiplegic migraine: a clinical comparison of families linked and unlinked to chromosome 19. DMG RG. Cephalalgia 16, 153-155 (1996).

931 [p 1626] Tatemichi TK, Desmond DW, Mayeux R, Paik M, Stern Y, Sano M, Remien RH, Williams JB, Mohr JP, Hauser WA, et al. Dementia after stroke: Baseline frequency, risks, and clinical features in a hospitalized cohort. Neurology 42: 1185-1193, 1992

932 [p 1627] Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 2; 81-83, 1974

932a [p 1628] Teunisse R, Cruysberg JR, Hoefnagels WH, Verbeek AL, Zitman FG.: Visual hallucinations in psychologically normal people: Charles Bonnet’s syndrome. Lancet 347, 794-797 (1996)

933 [p 1629] Teuscher AU, Meienberg O. Ischemic oculomotor nerve palsy. Clinical features and vascular risk factors in 23 patients. J Neurol 232: 144-149, 1985

154

933a [p 1630] The Arteriovenous Malformation Study Group. Arteriovenous malformations of the brain in adults. N Engl J Med 340; 1812-1818, 1999.

934 [p 1631] The Canadian cooperative multiple sclerosis study group: The Canadian cooperative trial of cyclophosphamide and plasma exchange in progressive multiple sclerosis. Lancet 337: 441-446, 1991

935 [p 1632] The Cuba Neuropathy Field Investigation Team: Epidemic optic neuropathy in Cuba. Clinical characterization and risk factors. N Engl J Med 333: 1776-1782, 1995

935a [p 1633] The Dutch TIA Trial Study Group. A comparison of two doses of aspirin (30 mg vs. 283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke. N Engl J Med 325; 1261-1266, 1991.

935b [p 1634] The European Ad Hoc Consensus Group: Bogousslavsky J, Brott T, Diener HC imizing intensive care in stroke: An European perspective. Cerebrovascular Diseases 1997; 7: 113-128.

936 [p 1635] The NINDS rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 333: 1581-1587, 1995

936a [p 1636] The Publications Committee for the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. Low molecular weight heparinoid, ORG 10172 (danaparoid), and outcome after acute ischemic stroke: a randomized controlled trial. JAMA 279: 1265-1272, 1998.

936b [p 1637] The Vagus Nerve Stimulation Study Group. A randomized controlled trial of chronic vagus nerve stimulation for treatment of medically intractable seizures. Neurology 45; 224-230, 1995.

937 [p 1638] Theron J, Courtheoux P, Alachkar F, Maiza D. Techniques endovasculaires de revascularisation cérébrale. J Mal Vasc 15: 245-256, 1990

155

937a [p 1639] Theys PA, Peeters E, Robberecht W: Evolution of motor and sensory deficits in amyotrophic lateral sclerosis estimated by neurophysiological techniques. J. Neurol. 246, 438-442 (1999).

937b [p 1640] Thomas PK.: Tropical neuropathies. J. Neurol. 244, 475-482 (1997).

938 [p 1641] §Thompson EJ, Keir G. Laboratory investigation of cerebrospinal fluid proteins. Ann Clin Biochem 27: 425-435, 1990

938a [p 1642] Thompson BM, Corbett JJ, Kline LB, Thompson HS. Pseudo-Horner’s syndrome. Arch Neurol (Chic.) 39: 108-111, 1982

939 [p 1643] Thornton CA, Griggs RC, Moxley RT 3rd. Myotonic dystrophy with no trinucleotid repeat expansion. Ann Neurol 35: 269-272, 1994

940 [p 1644] Threlkeld AB, Miller NR, Golnik KC, Griffin JW, Kuncl RW, Johns DR, Lehar M, Hurko O. Ophthalmic involvement in myo-neuro-gastrointestinal encephalopathy syndrome. Am J Ophthalmol 114: 322-328, 1992

941 [p 1645] Tibbling G, Link H, Ohman S. Principles of albumin and IgG analyses in neurological disorders. I. Establishment of reference values. Scand J Clin Lab Invest 37: 385-390, 1977

942 [p 1646] Tien RD, Gean-Marton AD, Mark AS. Neurosyphilis in HIV carriers: MR findings in six patients. AJR 158: 1325-1328, 1992

942a [p 1647] Tijssen MA, Padberg GW, van Dijk JG: The startle pattern in the minor form of hyperekplexia. Arch. Neurol. 53, 608-613 (1996).

942b [p 1648] Timmerman V, De Jonghe P, Ceuterick C, De Vriendt E, Lofgren A, Nelis E, Warner LE, Lupski JR, Martin JJ, Van Broeckhoven C. Novel missense mutation in the early growth response 2 gene

156

associated with Dejerine-Sottas syndrome phenotype. Neurology 52:1827-1832 (1999)

942c [p 1649] Tison F, Wenning GK, Volonte MA, Poewe WR, Henry P, Quinn NP.: Pain in multiple system atrophy. J. Neurol. 243, 153-156 (1996).

943 [p 1650] Toffel GJ, Biller J, Adams HP Jr. Nontraumatic intracerebral hemorrhage in young adults. Arch Neurol 44: 483-485, 1987

944 [p 1651] Tola MR, Granieri E, Caniatti L, Paolino E, Monetti C, Dovigo L, Scolozzi R, De Bastiani P, Carreras M. Systemic lupus erythematosus presenting with neurological disorders. J Neurol 239: 61-64, 1992

945 [p 1652] Tolosa E, Alom J, Marti M. Drug-induced dyskinesias. In Jankovic J, Tolosa E (eds). Parkinson’s disease and movement disorders. 2 nd ed. Williams & Wilkins, Baltimore, 375-397, 1993

946 [p 1653] Tournier-Lasserve E, Joutel A, Melki J, Weissenbach J, Lathrop GM, Chabriat H, Mas JL, Cabanis EA, Baudrimont M, Maciazek J, et al. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukencephalopathy maps to chromosome 19 q12. Nat Genet 3: 256-259, 1993

946a [p 1654] Touzé E, Blanche P, Zuber M.: A 35-year history of recurrent multiple cranial neuropathy due to primary Sjögren’s syndrome. J. Neurol. 246, 968-969 (1999).

947 [p 1655] Towbin JA, Hejtmancik JF, Brink P, Gelb B, Zhu XM, Chamberlain JS, McCabe ER, Swift M. X-linked dilated cardiomyopathy. Molecular genetic evidence of linkage to Duchenne muscular dystrophy (dystrophin) gene at the Xp21 locus. Circulation 87: 1854-1865, 1993

948 [p 1656] Townsend JJ, Wolinsky JS, Baringer JR, Johnson PC. Acquired toxoplasmosis. A neglected cause of treatable nervous system disease. Arch Neurol 32: 335-343, 1975

949 [p 1657] Toyka KV, Drachman DB, Griffin DE, Pestronk A, Winkelstein JA, Fishbeck KH, Kao I. Myasthenia gravis: study of humoral immune mechanisms by passive transfer to mice. N Engl J

157

Med 296: 125-131, 1977

949a [p 1658] Trenkwalder C, Stiasny K, Pollmächer T, Wetter T, Schwarz J, Kohnen R, Kazenwadel J, Kruger HP, Ramm S, Kunzel M, et al.: L-Dopa therapy of uremic and idopathic restless legs syndrome: a double-blind, crossover trial. Sleep 18, 681-688 (1995).

949b [p 1659] Trojan DA, Collet JP, Shapiro S, Jubelt B, Miller RG, Agre JC, Munsat TL, Hollander D, Tandan R, Granger C, Robinson A, Finch L, Ducruet T, Cashman NR.: A multicenter, randomized, douple-blinded trial of pyridostigmine in postpolio syndrome. Neurology 53, 1225-1233 (1999).

950 [p 1660] Troost BT, Waller MA. Hearing loss and tinnitus without dizziness or vertigo. In Bradley WG, Daroff RB, Fenichel GM, Marsden CD (Editors). Neurology in Clinical Practice. 2nd ed. Butterworth-Heinemann, Boston, 233-241, 1996

951 [p 1661] Truniger B, Richards P. Wasser-und Elektrolythaushalt. Diagnostik und Therapie. Thieme, Stuttgart 1985

952 [p 1662] Truong DD, Sandroni P, v.d. Noort S, Matsumoto RR. Diphenhydramine is effective in the treatment of idiopathic Dystonia. Arch Neurol 52: 405-407, 1995

953 [p 1663] Tsuchiya K, Yamauchi T, Furui S, Suda Y, Takenaka E. MR imaging vs CT in subacute sclerosing panencephalitis. AJNR 9: 943-946, 1988

954 [p 1664] Tsukamoto T, Mochizuki R, Mochizuki H, Noguchi M, Kayama H, Hiwatashi M, Yamamoto T. Paraneoplastic cerebellar degeneration and limbic encephalitis in a patient with adenocarcinoma of the colon. J Neurol Neurosurg Psychiat 56: 713-716, 1993

955 [p 1665] Tucker T, Ellner JJ. Chronic meningitis. In Tyler KL, Martin JB (Editor). Infectious diseases of the nervous system. FA Davis Company, Philadelphia, 188-215, 1993

956 [p 1666] Tuhrim S, Dambrosia JM, Price TR, Mohr JP, Wolf PA, Heyman A, Kase CS. Prediction of intracerebral hemorrhage survival. Ann Neurol 24: 258-263, 1988

158

956a [p 1667] Tullberg M, Mansson JE, Fredman P, Lekman A, Blennow K, Ekman R, Rosengren LE, Tisell M, Wikkelso C.: CSF sulfatide distinguishes between normal pressure hydrocephalus and subcortical arteriosclerotic encephalopathy. J. Neurol. Neurosurg. Psychiatry 69, 74-81 (2000).

957 [p 1668] Tunkel AR, Wispewey B, Scheld WM. Bacterial meningitis: recent advances in pathophysiology and treatment. Ann Intern Med 112: 610-623, 1990

957a [p 1669] Turjanski N, Lees AJ, Brooks DJ: Striatal dopaminergic function in restless legs syndrome. 18F-dopa and 11C-raclopride PET studies. Neurology 52, 932-937 (1999).

958 [p 1670] Turken SA, Cafferty M, Silverberg SJ, De La Cruz L, Cimino C, Lange DJ, Lovelace RE, Bilezikian JP. Neuromuscular involvement in mild asymptomatic primary hyperparathyroidism. Am J Med 87: 553-557, 1989

959 [p 1671] Turner D, Fried M, Hoffman M, Paleacu D, Reider I, Yust I. Brainstem abscess and meningitis due to Listeria monocytogenes in an adult with juvenile chronic polyarthritis. Neurology 45: 1020-1021, 1995

960 [p 1672] Tyler KL, Martin JB (Editors). Infectious diseases of the nervous system. FA Davis Company, Philadelphia, 1993

961 [p 1673] Udd B, Partanen J, Halonen P, Falck B, Hakamies L, Heikkila H, Ingo S, Kalimo H, Kaariainen H, Laulumaa V, et al. Tibial muscular dystrophy. Late adult-onset distal myopathy in 66 Finnish patients. Arch Neurol 50: 604-608, 1993

961a [p 1674] Ueda T, Yuh WT, Maley JE, Quets JP, Hahn PY, Magnotta VA.: Outcome of acute ischemic lesions evaluated by diffusion and perfusion MR imaging. Am J Neuroradiol 20: 983-989 (1999).

962 [p 1675] Uhlenbrock D (Editor). Kernspintomographie des Kopfes. Thieme, Stuttgart New York 1990

159

963 [p 1676] Uldry PA, Regli F. Multinévrite des nerfs crâniens et syndrome d’immuno-déficience acquise (SIDA): 5 cas. Rev Neurol (Paris) 144: 586-589, 1988

964 [p 1677] Uldry PA, Regli F. Syndrome pseudo-radiculaire au cours de la sclérose en plaques: quatre cas avec imagerie par résonance magnétique. Rev Neurol 148: 692-695, 1992

964a [p 1678] Ulfberg J, Carter N, Talbäck M, Edling C.: Headache, snoring and sleep apnoea. J. Neurol. 243, 621-625 (1996).

964b [p 1679] US Modafinil in Narcolepsy Multicenter Study Group. Randomized trial of modafinil as a treatment for excessive daytime somnolence of narcolepsy. Neurology 54; 1166-1175, 2000.

965 [p 1680] Vahedi K, Joutel A, van Bogaert P, Ducros A, Maciazeck J, Bach JF, Bousser MG, Tournier-Lasserve E. A gene for hereditary paroxysmal cerebellar ataxia maps to chromosome 19p. Ann Neurol 37: 289-293, 1995

965a [p 1681] Valente EM, Bentivoglio AR, Albanese A.: The genetic basis of movement disorders. Schweiz. Arch. Neurol. und Psychiatr. 149, 157-162 (1998).

966 [p 1682] Valli G, Barbieri S, Cappa S, Pellegrini G, Scarlato G. Syndromes of abnormal muscular activity: overlap between continuous muscle fiber activity and the stiff man syndrome. J Neurol Neurosurg Psychiat 46: 241-247, 1983

967 [p 1683] Van Coster RN, De Vivo DC, Blake D, Lombes A, Barrett R, DiMauro S. Adult Reye’s syndrome: a review with new evidence for a generalized defect in intramitochondrial enzyme processing. Neurology 41; 1815-1821, 1991

967a [p 1684] Van den Berg-Vos RM, Van den Berg LH, Franssen H, Vermeulen M, Witkamp TD, Jansen GH, van Es HW, Kerkhoff H, Wokke JH.: Multifocal inflammatory demyelinating neuropathy. Neurology 54, 26-32 (2000).

160

967b [p 1685] Van der Laan L, ter Laak HJ, Gabreels-Festen A, Gabreels F, Goris RJ.: Complex regional pain syndrome type I (RSD). Neurology 51, 20-25 (1998).

968 [p 1686] Van der Meche FG, Schmitz PI. A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barré syndrome. Dutch Guillain-Barre Study Group. N Engl J Med 326: 1123-1129, 1992

968a [p 1687] Van der Meché FG.: The Guillain-Barré syndrome: pathogenesis and treatment. Rev. Neurol. 152, 355-358 (1996).

968b [p 1688] Van Dijk GW, Notermans NC, Kater L, Kruize AA, Linssen WH, Wokke JH.

968c [p 1689] Van Doorn PA: Treatment of patients with chronic inflammatory demyelinating polyneuropathy. Rev. Neurol. 152, 383-386 (1996).

968d [p 1690] Van Gijn J. White matters: small vessels and slow thinking in old age. Lancet 356; 612-613, 2000.

969 [p 1691] Van Horn G. Wegener’s granulomatosis. (correspondence). Neurology 44: 1189-1190, 1994

970 [p 1692] van der Knaap MS, Valk J. The MR spectrum of peroxisomal disorders. Neuroradiol 33; 30-37, 1991

971 [p 1693] van Gijn J, van Dongen KJ, Vermeulen M, Hijdra A. Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage. Neurology 35: 493-497, 1985

972 [p 1694] van Gijn J. Subarachnoid hemorrhage. Lancet 339: 653-655, 1992

161

972a [p 1695] Van Veelen MLC, Avezaat CJJ, Kros JM, van Putten W, Vecht C.: Supratentorial low grade astrocytoma: prognostic factors, dedifferentiation, and the issue of early versus late surgery. J. Neurol. Neurosurg. Psychiatry 64, 581-587 (1998).

972b [p 1696] van der Linden EF; Venema PL: Acute urineretentie bij vrouwen. Ned Tijdschr Geneeskd 142, 1603-1606 (1998)

973 [p 1697] Vaney C. Schmerzen bei Multipler Sklerose - Klinik und Therapie. Schweiz Med Wschr 120: 1959-1964, 1990

974 [p 1698] Vanneste JAL. Three decades of normal pressure hydrocephalus: Are we wiser now? J Neurol Neurosurg Psychiat 57: 1021-1025, 1994

974a [p 1699] Vanneste JAL.: Diagnosis and management of normal-pressure hydrocephalus. J. Neurol. 247, 5-14 (2000).

974b [p 1700] Veldman BAJ, Wijn AM, Knoers N, Praamstra P, Horstink MW.: Genetic and environmental risk factors in Parkinson’s disease. Clinical Neurology and Neurosurgery 100, 15-26 (1998).

974c [p 1701] Ven v.d. C, Haupt WF., Rosenow F, Gibbels E, Borberg H.: Klinisch rein motorische Variante der Polyneuritis Guillain-Barré. Darstellung von 3 Fällen. Nervenarzt 67, 1020-1022 (1996).

975 [p 1702] Venables GS, Bates DS, Shaw DA. Hypothyroidism with true myotonia. J Neurol Neurosurg Psychiat 41: 1013-1015, 1978

976 [p 1703] Verdru P, Lammens M, Dom R, Van Elsen A, Carton H. Globoid cell leukodystrophy: A family with both late-infantile and adult type. Neurology 41; 1382-1384, 1991

162

976a [p 1704] Metman LV, Del Dotto P, LePoole K, Konitsiotis S, Fang J, Chase TN.: Amantadine for Levodopa-induced dyskinesias. a 1-year follow-up study. Arch. Neurol. 56, 1383-1386 (1999).

976b [p 1705] Verity CM, Nicoll A, Will R, Devereux G, Stellitano L.: Variant Creutzfeldt-Jakob disease in UK children: a national surveillance study. Lancet 356:1224-1227, 2000.

977 [p 1706] Verma A, Bradley WG. High-dose intravenous immunoglobulin therapy in chronic progressive lumbosacral plexopathy. Neurology 44: 248-250, 1994

978 [p 1707] Vernant JC, Maurs L, Gessain A, Barin F, Gout O, Delaporte JM, Sanhadji K, Buisson G, de-The G. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I. A clinical and seroepidemiological study of 25 cases. Ann Neurol 21: 123-130, 1987

979 [p 1708] Victor M, Adams RD, Collins GH. The Wernicke-Korsakow syndrome and other disorders due to alcoholism and malnutrition. 2nd ed. FA Davis Company, Philadelphia, 1989

980 [p 1709] Victor M, Sieb JP. Myopathies due to drugs, toxins, and nutritional deficiency. In Engel AG, Franzini-Armstrong C (Editors). Myology. Basic and Clinical. 2nd ed. McGraw Hill, New York, 1697-1725, 1994

980a [p 1710] Vidailhet M, Bonnet AM, Agid Y.: Critère cliniques de diagnostic des atrophies multi-systématisées. Rev. Neurol. 154, 17-21 (1998).

981 [p 1711] Vighetto A, Charles N, Salzmann M, Confavreux C, Aimard G. Korsakoff’s syndrome as the initial presentation of multiple sclerosis. J Neurol 238: 351-354, 1991

981a [p 1712] Vilming ST, Kloster R.: Post-lumbar puncture headache: clinical features and suggestions for diagnostic criteria. Cephalalgia 17, 778-784 (1997).

981b [p 1713] Vincent A, Drachman DB.: Amyotrophic lateral sclerosis and antibodies to voltage-gated calcium channels - new doubts. Ann. Neurol. 40, 691-693 (1996).

163

982 [p 1714] Vinters HV. Cerebral amyloid angiopathy: A critical review. Stroke 18: 311-324, 1987

982a [p 1715] Volkmann J, Sturm V, Weiss P, Kappler J, Voges J, Koulousakis A, Lehrke R, Hefter H, Freund HJ.: Bilateral high-frequency stimulation of the internal globus pallidus in advanced parkinson’s disease. Ann. Neurol. 44, 953-961 (1998).

982b [p 1716] Vonk P.: Het syndroom van Elsberg: acute urineretentie na een virale infectie. Ned Tijdschr Geneeskd 1993 137, 2603-2605 (1993).

983 [p 1717] Vollertsen RS, McDonald TJ, Younge BR, Banks PM, Stanson AW, Ilstrup DM. Cogan’s syndrome: 18 cases and a review of the literature. Mayo Clin Proc 61; 344-361, 1986

984 [p 1718] Von Mitzlaff HC, Liechti-Gallati S, Rösler KM, Burgunder JM. Die Quadricepsmyopathie als Dystrophin-assoziierte Myopathie. Schweiz Med Wschr 123: 1865-1869, 1993

985 [p 1719] Von Noorden GK, Murray E, Wong SY. Superior oblique paralysis. A review of 270 cases. Arch Opthalmol 104: 1771-1776, 1986

986 [p 1720] von Büdingen HJ, von Reutern G-H. Ultraschalldiagnostik der hirnversorgenden Arterien. 2. Auflage. Thieme, Stuttgart, 1993

987 [p 1721] Vonsattel JP, Myers RH, Hedley-Whyte ET, Ropper AH, Bird ED, Richardson EP Jr. Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study. Ann Neurol 30: 637-649, 1991

987a [p 1722] Vorgerd M, Grehl T, Jäger M, Muller K, Freitag G, Patzold T, Bruns N, Fabian K, Tegenthoff M, Mortier W, Luttmann A, Zange J, Malin JP. Creatine therapy in myophosphorylase deficiency (McArdle Disease). Arch Neurol 57; 956-963, 2000.

164

988 [p 1723] Voskuhl RR, Hinton RC. Sensory impairment in the hands secondary to spondylotic compression of the cervical spinal cord. Arch Neurol 47: 309-311, 1990

988a [p 1724] Vossler DG, Wyler AR, Wilkus RJ, Gardner-Walker G, Vlcek BW.: Cataplexy and monoamine oxidase deficiency in Norrie disease. Neurology 46, 1258-1261 (1996).

989 [p 1725] Vriesendorp Francine J, Mishu B, Balser MJ, Koski CL. Serum antibodies to GM1, GD1 b, peripheral nerve Myelin, and campylobacter jejuni in patients with Guillain-Barré syndrome and controls: Correlation and prognosis. Ann Neurol 34: 130-135, 1993

990 [p 1726] Vroom FQ, Greer M. Mercury vapour intoxication. Brain 95: 305-318, 1972

991 [p 1727] Waddy HM, Fletcher NA, Harding AE et al. A genetic study of idiopathic focal dystonias. Ann Neurol 29: 320-324, 1991

991a [p 1728] Waldvogel D, Mattle HP, Sturzenegger M, Schroth G. Pulsatile tinnitus - a review of 84 patients. J Neurol 245; 137-142, 1998.

992 [p 1729] Wall M, Wray SH. The one-and-a-half syndrome - a unilateral disorder of the pontine tegmentum: a study of 20 cases and review of the literature. Neurology 33: 971-980, 1983

993 [p 1730] Wallace DC, Zheng X, Lott MT, Shoffner JM, Hodge JA, Kelley RI, Epstein CM, Hopkins LC. Familial mitochondrial encephalomyspathy (MERFF): genetic, pathophysiological and biochemical characterization of a mitochondrial DNA disease. Cell 55: 601-610, 1988

993a [p 1731] Walpoth BH., Walpoth-Aslan BN., Mattle HP, Radanov BP, Schroth G, Schaeffler L, Fischer AP, von Segesser L, Althaus U.: Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood waming. N.Engl.J.Med. 337, 1500-1505 (1997).

165

994 [p 1732] Walser H, Emre M, Janzer R. Somatosensory evoked potentials in comatose patients: correlation with outcome and neuropathological findings. J Neurol 233; 34-40, 1986

995 [p 1733] Walser H, Mattle H, Keller HM, Janzer R. Early cortical median nerve somatosensory evoked potentials. Prognostic value in anoxic coma. Arch Neurol 42; 32-38, 1985

995a [p 1734] Walters AS, Hickey K, Maltzmann J, Verrico T, Joseph D, Hening W, Wilson V, Chokroverty S.: A questionnaire study of 138 patients with restless legs syndrome: the "night-walkers" survey. Neurology 46, 92-95 (1996).

995b [p 1735] Walther EU, Hohlfeld R.: Multiple scerosis. Side effects of interferon beta therapy and their management. Neurology 53, 1622-1627 (1999).

996 [p 1736] Walton J, Karpati G, Hilton-Jones D (eds). Disorders of voluntary muscle. 6 th ed. Churchill-Livingstone, Edinburgh, 1994

997 [p 1737] Wang CH, Klein PW, Vitale R et al. Refinement of the spinal muscular atrophy locus by genetic and physical mapping. Amer J Hum Genet 56: 202-209, 1995

998 [p 1738] Warach S, Gaa J, Siewert B, Wielopolski P, Edelman RR. Acute human stroke studied by whole brain echo planar diffusion-weighted magnetic resonance imaging. Ann Neurol 37: 231-241, 1995

999 [p 1739] Warach S, Li W, Ronthal M, Edelman RR. Evaluation of acute cerebral ischemia using dynamic contrast-enhanced MR and MR angiography. Radiology 182: 41-47, 1992

999a [p 1740] Wardlaw JM, del Zoppo G, Yamaguchi T. Thrombolysis for acute ischemic stroke (Cochran Review). In: The Chochran Library, Issue 4, 1999.Oxford: Updated Software.

999b [p 1741] Warlow CP, Dennis MS, van Gijn J et al.: Stroke. A practical guide to management. Blackwell Science, Oxford, 2001.

166

999c [p 1742] Warner JS., Fenichel GM.: Chronic post-traumatic headache often a myth? Neurology 46, 915-916 (1996).

999d [p 1743] Watson CP, Babul N.: Efficacy of oxycodone in neuropathic pain: a randomized trial in postherpetic neuralgia. Neurology 50, 1837-1841 (1998).

999e [p 1744] Watters MR, Stears JC, Osborn AG, Turner GE, Burton BS, Lillehei K, Yuh WT.: Transdural spinal cord herniation: imaging and clinical spectra. Am. J. Neuroradiol. 19, 1337-1344 (1998).

1000 [p 1745] Weber F, Conrad B. Chronic encephalitis and Eales disease. J Neurol 240: 299-301, 1993

1000a [p 1746] Weber J, Remonda L, Mattle HP, Koerner U, Baumgartner RW, Sturzenegger M, Ozdoba C, Koerner F, Schroth G.: Selective intra-arterial fibrinolysis of acute retinal artery occlusion. Stroke 29, 2076-2079 (1998).

1001 [p 1747] Wechsler D. Wechsler adult intelligence scale - revised (WAIS-R). Psychological Corporation. New York, 1981

1002 [p 1748] Weder B, Meienberg O, Wildi E, Meier C. Neurological disorder of vitamin-E deficiency in acquired intestinal malabsorption. Neurology 34: 1561-1565, 1984

1003 [p 1749] Weder B, Mumenthaler M. Neurolues in einer schweizerischen Universitätsklinik. Nervenarzt 54: 633-639, 1983

1003a [p 1750] Weeks RA, Valentine A, Savy L. et al.: Mild tactile disturbance and a Lhermitte penomenon in a middle-aged man. Arch. Neurol. 56: 1515-1516 (1999).

1004 [p 1751] Weidmann P, Ferrari P. Die antihypertensive Therapie in den neunziger Jahren. Schweiz Rundschau Med (Praxis) 1992; 81: 188-198

167

1005 [p 1752] Weil ML, Itabashi HH, Cremer NE, Oshiro LS, Lennette EH, Carnay L. Chronic progressive panencephalitis due to rubella virus simulating subacute sclerosing panencephalitis. N Engl J Med 292: 994-998, 1975

1006 [p 1753] Weilbach FX, Voltz R, Hohlfeld R, Hartung HP. Copolymer-1 in der Therapie der multiplen Sklerose. Nervenarzt 66: 473-477, 1995

1007 [p 1754] Weilbach FX, Toyka KV, Hartung HP Orales, niedrig dosiertes Methotrexat bei chronisch-progredienter multipler Sklerose. Nervenarzt 66: 643-647, 1995

1008 [p 1755] Weiller C, Isensee C, Rijntjes M, Huber W, Muller S, Bier D, Dutschka K, Woods RP, Noth J, Diener HC. Recovery from Wernicke’s aphasia: a positron emission tomographic study. Ann Neurol 37: 723-732, 1995

1009 [p 1756] Weingarten K, Barbut D, Filippi C, Zimmerman RD. Acute hypertensive encephalopathy: findings on spin-echo and gradient-echo MR imaging. AJR 162: 665-670, 1994

1010 [p 1757] Weingarten K, Zimmermann RD, Beker RD, Heier LA, Haimes AB, Deck MDF. Subdural and epidural empyemas: MR imaging. Am J Neuroradiol 10: 81-87, 1987

1011 [p 1758] Weingeist TA, Goldman EJ, Folk JC, Packer AJ, Ossoinig KC. Terson’s syndrome. Clinicopathologic correlations. Ophthalmol 93: 1435-1442, 1986

1012 [p 1759] Weir B. Headaches from aneurysms. Cephalalgia 14: 79-87 (1994)

1013 [p 1760] Welander L. Myopathia distalis tarda hereditaria. Acta med Scand 265: 100 -124, 1951

1014 [p 1761] Wenger JD, Hightower AW, Facklam RR, Gaventa S, Broome CV. Bacterial meningitis in the United States, 1986 - Report of a multistate surveillance study. The Bacterial Meningitis Study

168

Group. J Infect Dis 162: 1316-1323, 1990

1015 [p 1762] Wenning GK, Ben-Shlomo Y, Magalhaes M, Daniel SE, Quinn NP. Clinicopathological study of 35 cases of multiple system atrophy. J Neurol Neurosurg Psychiat 58: 160-166, 1995

1015a [p 1763] Wenning GK, Odin P, Morrish P, Rehncrona S, Widner H, Brundin P, Rothwell JC, Brown R, Gustavii B, Hagell P, Jahanshahi M, Sawle G, Bjorklund A, Brooks DJ, Marsden CD, Quinn NP, Lindvall O.: Short- and long-term survival and function of unilateral intrastriatal dopaminergic grafts in Parkinson’s disease. Ann. Neurol. 42, 95-107 (1997).

1015b [p 1764] Wenning GK, Litvan I, Jankovic J, Granata R, Mangone CA, McKee A, Poewe W, Jellinger K, Ray Chaudhuri K, D’Olhaberriague L, Pearce RK.: Natural history and survival of 14 patients with corticobasal degeneration confirmed at postmortem examination. J. Neurol. Neurosurg. Psychiatry 64, 184-189 (1998).

1016 [p 1765] Werdelin L, Juhler M. The course of transient ischemic attacks. Neurology 38: 677-680, 1988

1017 [p 1766] Werner EG, Olanow C W. Parkinsonism and amiodarone therapy. Ann Neurol 25: 630-632, 1989

1017a [p 1767] Wetter TC, Stiasny K, Winkelmann J, Buhlinger A, Brandenburg U, Penzel T, Medori R, Rubin M, Oertel WH, Trenkwalder C.: A randomized controlled study of pergolide in patients with restless legs syndrome. Neurology 52, 944-950 (1999).

1017b [p 1768] White HD, Simes RJ, Anderson NE, Hankey GJ, Watson JD, Hunt D, Colquhoun DM, Glasziou P, MacMahon S, Kirby AC, West MJ, Tonkin AM. Pravastatin therapy and the risk of stroke. N Engl J Med 343; 317-326, 2000.

1017c [p 1769] White KD, Ince PG, Lusher M, Lindsey J, Cookson M, Bashir R, Shaw PJ, Bushby KM.: Clinical and pathologic findings in hereditary spastic paraparesis with spastin mutation. Neurology 55, 89-94 (2000).

169

1018 [p 1770] Whitehouse PJ (Editor). Dementia. FA Davis Company, Philadelphia. 1993

1019 [p 1771] Whitley RJ, Alford CA, Hirsch MS, Schooley RT, Luby JP, Aoki FY, Hanley D, Nahmias AJ, Soong SJ. Vidarabine versus acyclovir therapy in herpes simplex encephalitis. N Engl J Med 314: 144-149, 1986

1020 [p 1772] Whitley RJ, Cobbs CG, Alford CA Jr, , Soong SJ, Hirsch MS, Connor JD, Corey L, Hanley DF, Levin M, Powell DA. Diseases that mimic herpes simplex encephalitis: diagnosis, presentation, and outcome. NIAD Collaborative Antiviral Study Group. JAMA 262: 234-239, 1989

1021 [p 1773] Whitley RJ, Soong SJ, Linneman C Jr, Liu C, Pazin G, Alford CA. Herpes simplex encephalitis: clinical assessment. JAMA 247: 317-320, 1982

1022 [p 1774] Whurr R, Lorch M, Fontana H, Brookes G, Lees A, Marsden CD. The use of botulinum toxin in the treatment of adductor spasmodic dysphonia. J Neurol Neurosurg Psychiat 56; 526-530, 1993

1023 [p 1775] Widder B. Doppler-und Duplex-Sonographie der hirnversorgenden Arterien. Springer Verlag, Berlin, New York, 1992

1024 [p 1776] Wiesmann. Medizinische Mikrobiologie. 8. Auflage. Thieme, Stuttgart, 1993

1025 [p 1777] Wijdicks EF, Vermeulen M, ten Haaf JA, Hijdra A, Bakker WH, van Gijn J. Volume depletion and natriuresis in patient with a ruptured intracranial aneurysm. Ann Neurol 18: 211-216, 1985

1026 [p 1778] Wijdicks EFM, Parisi JE, Sharbrough FW. The prognostic value of myoclonus in comatose survivors following cardiac resuscitation. Ann Neurol 34: 298, 1993 (Abstrakt).

1027 [p 1779] Wijdicks EFM. Determining brain death in adults. Neurology 45: 1003-1011, 1995

170

1027a [p 1780] Wilder-Smith E, Wilder-Smith A. Komplex-partielle Anfälle als Ursache passagerer Herzrhythmusstörungen. Schweiz. Med. Wschr 125; 2237 2243, 1995.

1028 [p 1781] Willeit J, Deisenhammer F, Ransmayr G, Gerstenbrand F. Orthostatischer Tremor. Dtsch med Wschr 116: 1509-1512, 1991

1028a [p 1782] Willems PJ. Genetic causes of hearing loss. N Engl J Med 342; 1101-1109, 2000.

1028b [p 1783] Will RG, Ironside JW, Zeidler M, Cousens SN, Estibeiro K, Alperovitch A, Poser S, Pocchiari M, Hofman A, Smith PG. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 347: 921-925, 1996.

1028c [p 1784] Wills AJ Brusa L, Wang HC, Brown P, Marsden CD.: Levodopa may improve orthostatic tremor: case report and trial of treatment. J. Neurol. Neurosurg. Psychiatry 66, 681-684 (1999).

1028d [p 1785] Wilmshurst PT., Nightingale S, Walsh KP, Morrison WL.: Effect on migraine of closure of cardiac right-to-left shunts to prevent recurrence of decompression illness or stroke or for haemodynamic reasons. Lancet 356, 1648-1651 (2000)

1028e [p 1786] Wilson HC, Lunn MPT, Schey S, Hughes RA.: Successful treatment of IgM paraproteinaemic neuropathy with fludarabine. J. Neurol. Neurosurg. Psychiatry 66, 575-580 (1999).

1029 [p 1787] Wilson J, Walton JN. Some muscular manifestations of hypothyroidism. J Neurol Neurosurg Psychiat 22: 320-324, 1959

1029a [p 1788] Windecker S, Wahl A, Chatterjee T, Garachemani A, Eberli FR, Seiler C, Meier B. Percutaneous closure of patent foramen ovale in patients with paradoxical embolism. Long-term risk of recurrent thromboembolic events. Circulation 101; 893-898, 2000.

1029b [p 1789] Wingerchuk DM, Hogancamp WF, O’Brien PC, Weinshenker BG.: The clinical course of neuromyelitis optica (Devic’s syndrome). Neurology 53, 1107-1114 (1999).

171

1029c [p 1790] Wirrell EC Benign epilepsy of childhood with centrotemporal spikes. Epilepsia 39, Suppl. 4; S32-41, 1998.

1030 [p 1791] Wishnant JP, Basford JR, Bernstein EF et al. Classification of cerebrovascular diseases III. Special report from the National Institute of Neurological Disorders and Stroke. Stroke 21: 637-676, 1990

1031 [p 1792] Wispelwey B, Dacey RG, Scheld MW. Brain abscess. In Scheld WM, Whitley RJ, Durack DT (eds). Infections of the Central Nervous System, Raven Press, Ltd, New York, 457-468, 1991

1031a [p 1793] Wissel J, Kabus C, Wenzel R, Klepsch S, Schwarz U, Nebe A, Schelosky L, Scholz U, Poewe W.: Botulinum toxin in writer’s cramp: objective response evaluation in 31 patients. J. Neurol. Neurosurg. Psychiatry 61, 172-175 (1996).

1031b [p 1794] Wohlgemuth WA, Rottach KG, Stoehr M.: Intermittent claudication due to ischaemia of the lumbosacral plexus. J. Neurol. Neurosurg. Psychiatry 67, 793-795 (1999). Oder: Wöhrle JC, Spengos K, Steinke W, Goebel HH, Hennerici M.: Alcohol-related acute axonal polyneuropathy polyneuropathy: a differential diagnosis of Guillain-Barre syndrome. Arch. Neurol. 55, 1329-1334 (1998).

1032 [p 1795] Wolf KJ, Fobbe F (Editors). Farbkodierte Duplexsonographie. Grundlagen und klinische Anwendung. Thieme, Stuttgart, 1993

1033 [p 1796] Wolf PA, Belanger AJ, D’Agostino RB. Management of risk factors. In Barnett HJM, Hachinski VC. Cerebral ischemia: treatment and prevention. Neurologic Clinics 10: 177-191, 1992

1033a [p 1797] Wolfe GI, Baker NS, Amato AA, Jackson CE, Nations SP, Saperstein DS, Cha CH, Katz JS, Bryan WW, Barohn RJ.: Chronic cryptogenic sensory polyneuropathy polyneuropathy: clinical and laboratory characteristics. Arch. Neurol. 56, 540-547 (1999).

172

1033b [p 1798] Wolters EC.: Dopaminomimetic psychosis in Parkinson’s disease patients. Diagnosis and treatment. Neurology 52 (Suppl. 3), 10-13 (1999).

1033c [p 1799] Wood DD, Bilbao JM, O’Connors P, Moscarello MA.: Acute multiple sclerosis (Marburg type) is associated with developmentally immature myelin basic protein. Ann. Neurol. 40, 18-24 (1996).

1034 [p 1800] Woodward TE. Rickettsial diseases. In Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL. Harrison’s Principles of Internal Medicine. 13th edition. McGraw-Hill, Inc, New York, 747-757, 1994

1034a [p 1801] Working Group on Periodic Paralysis. Tawil R; McDermott MP; Brown R Jr, Shapiro BC, Ptacek LJ, McManis PG, Dalakas MC, Spector SA, Mendell JR, Hahn AF, Griggs RC. Randomized trials of dichlorphenamide in the periodic paralyses. Ann Neurol 47; 46-53, 2000.

1034b [p 1802] Wörz R., Editor.: Chronischer Schmerz und Psyche. Fischer Verlag Stuttgart, 1990.

1035 [p 1803] Wrobel CJ, Oldfield EH, Di Chiro G, Tarlov EC, Baker RA, Doppman JL. Myelopathy due to intracranial dural arteriovenous fistulas draining intrathecally into spinal medullary veins. Report of three cases. J Neurosurg 69: 934-939, 1988

1036 [p 1804] Wurthmann C, Klieser E. Das Kleine-Levin-Syndrom. Fortschr Neurol Psychiat 59: 190-194, 371-375, 1991

1036a [p 1805] Yamanishi T, Yasuda K, Sakakibara R, Hattori T, Uchiyama T, Minamide M, Ito H: Urinary retention due to herpes virus infections. Neurourol Urodyn 17, 613-619 (1998)

1037 [p 1806] Yaziki H, Pazarli H, Barnes CG, Tuzun Y, Ozyazgan Y, Silman A, Serdaroglu S, Oguz V, Yurdakul S, Lovatt GE, et al. A controlled trial of azathioprine in Behçet’s syndrome. N Engl J Med 322: 281-285, 1990

173

1038 [p 1807] Yeung KB, Thomas PK, King RHM, Waddy H, Will RG, Hughes RA, Gregson NA, Leibowitz S. The clinical spectrum of peripheral neuropathies associated with benign monoclonal IgM, IgG and IgA paraproteinaemia. Comparative clinical, immunological and nerve biopsy findings. J Neurol 238: 383-391, 1991

1039 [p 1808] Yiannikas C, McLeod JG, Walsh JC. Peripheral neuropathy associated with polycythemia vera. Neurology 33: 139-143, 1983

1040 [p 1809] Yonekawa Y, Goto Y, Ogata N. Moyamoya disease: diagnosis, treatment, and recent achievement. In Barnett HJM, Mohr JP, Stein BM, Yatsu FM (Editors). Stroke. Pathophysiology, diagnosis, and management. 2. Auflage. Churchill Livingstone. New York, Edinburgh, 721-747, 1992

1041 [p 1810] Yoshida K, Ikeda S, Kawaguchi K, Yanagisawa N. Adult GM1 gangliosidosis: Immunohistochemical and ultrastructural findings in an autopsy case. Neurology 44; 2376-2382, 1994

1042 [p 1811] Yoshikawa H, Yamada K, Sakuragawa N. MRI in the early stage of Tay-Sachs disease. Neuroradiology 34; 394-395, 1992

1043 [p 1812] Younge BR, Sutula F. Analysis of trochlear nerve palsies. Diagnosis, etiology, treatment. Mayo Clin Proc 52: 11-18, 1977

1044 [p 1813] Younger DS, Chou S, Hays AP, Lange DJ, Emerson R, Brin M, Thompson H Jr, Rowland LP. Primary lateral sclerosis. A clinical diagnosis reemerges. Arch Neurol 45: 1304-1307, 1988

1044a [p 1814] Youssov K, Wegener K, Bolgert F, Pierrot-Deseilligny C.: Diplégie faciale rélévant une séropositivité au VHI. Rev. Neurol. 154, 258 (1998).

1044b [p 1815] Yuki N, Takahashi M, Tagawa Y, Kashiwase K, Tadokoro K, Saito K.: Association of campylobacter jejuni serotype with antiganglioside antibody in Guillain-Barré syndrome and Fisher’s syndrome. Ann. Neurol. 42, 28-33 (1997).

174

1045 [p 1816] Zee PC, Cohen BA, Walczak T, Jubelt B. Peripheral nervous system involvement in multiple sclerosis. Neurology 41: 457-460, 1991

1046 [p 1817] Zeh W. Progressive Paralyse. Verlaufs-und Korrelationsstudien. Thieme, Stuttgart, 1984

1046a [p 1818] Zeller JA, Machetanz J, Kessler C.: Ageusia as an adverse effect of phenytoin treatment. Lancet 351, 1101 (1998).

1046b [p 1819] Zeman AZJ, Kidd D, McLean BN, Kelly MA, Francis DA, Miller DH, Kendall BE, Rudge P, Thompson EJ, McDonald WI.: A study of oligoclonal band negative multiple sclerosis. J. Neurol. Neurosurg. Psychiatry 60, 27-30 (1996).

1047 [p 1820] Zerres K, Rudnik-Schöneborn S. Natural history of proximal spinal muscular atrophy. Clinical analysis of 445 patients and suggestions for a modification of existing classifications. Arch Neurol 52: 518-523, 1995

1047a [p 1821] Zia S, Cody F, O’Boyle D: Joint position sense is impaired by Parkinson’s disease. Ann. Neurol. 47, 218-228 (2000).

1048 [p 1822] Zierz S. Carnitine palmitoyltransferase deficiency, in Engel AG, Franzini-Armstrong C (Editors). Myology. Basic and Clinical. 2nd ed. McGraw Hill, New York, 1577-1586, 1994

1048a [p 1823] Zirh A., Reich SG, Dougherty PM, Lenz FA: Stereotactic thalamotomy in the treatment of essential tremor of the upper extremity: reassessment including a blinded measure of outcome. J. Neurol. Neurosurg. Psychiatry 66, 772-775 (1999).

1049 [p 1824] Zimmerman RD, Weingarten K. Neuroimaging of cerebral abscesses. Neuroimaging Clin N Amer 1: 1-16, 1991

175

1050 [p 1825] Zuger A, Louie E, Holzman RS, Simberkoff MS, Rahal JJ. Cryptococcal disease in patients with the acquired immunodeficiency syndrome. Diagnostic features and outcome of treatment. Ann Intern Med 104: 234-240, 1986

1051 [p 1826] Zuger A, Lowy FD. Tuberculosis of the central nervous system. In Scheid WM, Whitley RJ, Durack DT (eds). Infections of the Central Nervous System, Raven Press, Ltd, New York, 425-456, 1991

1051a [p 1827] Zühlke C., Thies U.: Chorea Huntington. Molekulargenetische Grundlagen, Mutationsnachweis und prädiktive Diagnostik. Nervenarzt 67, 25-35 (1996).

1052 [p 1828] Zülch KJ. The cerebral infarct. Pathology, pathogenesis, and computed tomography. Springer Verlag, Berlin New York, 1985

1053 [p 1829] Zuniga G, Ropper AH, Frank J. Sarcoid peripheral neuropathy. Neurology, 41: 1558-1561, 1991

1054 [p 1830] Zurkirchen MA, Misteli M, Conen D. Reversible neurologische Komplikationen bei chronischem Alkoholabusus. Schweiz med Wschr 124: 1897 -1912, 1994

1055 [p 1831] Zwiebel WJ (Editor). Introduction to vascular ultrasonography. W.B. Saunders Company, Philadelphia, 1986

1056 [p 1832] Zwimpfer TJ, Bernstein M. Spinal cord concussion. J Neurosurg 72: 894-900, 1990

176

Referenz 1 (Neurologie, 11. Auflage) Aaslid R, Lindegaard KF. Cerebral hemodynamics. In Aaslid R. (Editor). Transcranial Doppler sonography. Springer, Wien 60-85, 1986

177

Referenz 2 (Neurologie, 11. Auflage) Aaslid R (Editor). Transcranial Doppler Sonography. Springer, Wien, New York 1986

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Referenz 3 (Neurologie, 11. Auflage) Acker W, Aps EJ, Majumdar SK, Shaw GK, Thomson AD. The relationship between brain and liver damage in chronic alcoholic patients. J Neurol Neurosurg Psychiat 45: 984-987, 1982 CT scan measures of topographical brain changes, liver status as determined by biopsy, and clinical factors were studied in a group of detoxified chronic alcoholic patients. It was found that greater topographical brain changes were associated with greater severity of liver disease.

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Referenz 4 (Neurologie, 11. Auflage) Adams CR, Ziegler DK, Lin JT. Mercury intoxication simulating amyotrophic lateral sclerosis. JAMA 250: 642-643, 1983 A 54-year-old man had a syndrome resembling amyotrophic lateral sclerosis after a brief but intense exposure to elemental mercury. The syndrome resolved as his urinary mercury levels fell. Mercury toxicity must be considered not only in individuals with recent anterior horn-cell dysfunction but also with otherwise unexplained peripheral neuropathy, tremor, ataxia, and a gamut of psychiatric symptoms including confusion and depression.

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Referenz 5 (Neurologie, 11. Auflage) Adams HP (Editor). Handbook of cerebrovascular diseases. Marcel Dekker, Inc., New York, 1993

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Referenz 6 (Neurologie, 11. Auflage) Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10 172 in Acute Stroke Treatment. Stroke 24: 35-41, 1993 Department of Neurology, University of Iowa College of Medicine, Iowa City 52242, USA. [email protected] BACKGROUND AND PURPOSE: The etiology of ischemic stroke affects prognosis, outcome, and management. Trials of therapies for patients with acute stroke should include measurements of responses as influenced by subtype of ischemic stroke. A system for categorization of subtypes of ischemic stroke mainly based on etiology has been developed for the Trial of Org 10172 in Acute Stroke Treatment (TOAST). METHODS: A classification of subtypes was prepared using clinical features and the results of ancillary diagnostic studies. "Possible" and "probable" diagnoses can be made based on the physician’s certainty of diagnosis. The usefulness and interrater agreement of the classification were tested by two neurologists who had not participated in the writing of the criteria. The neurologists independently used the TOAST classification system in their bedside evaluation of 20 patients, first based only on clinical features and then after reviewing the results of diagnostic tests. RESULTS: The TOAST classification denotes five subtypes of ischemic stroke: 1) large-artery atherosclerosis, 2) cardioembolism, 3) small-vessel occlusion, 4) stroke of other determined etiology, and 5) stroke of undetermined etiology. Using this rating system, interphysician agreement was very high. The two physicians disagreed in only one patient. They were both able to reach a specific etiologic diagnosis in 11 patients, whereas the cause of stroke was not determined in nine. CONCLUSIONS: The TOAST stroke subtype classification system is easy to use and has good interobserver agreement. This system should allow investigators to report responses to treatment among important subgroups of patients with ischemic stroke. Clinical trials testing treatments for acute ischemic stroke should include similar methods to diagnose subtypes of stroke.

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Referenz 6a (Neurologie, 11. Auflage) Adams HP Jr, Bendixen BH, Leira E, Chang KC, Davis PH, Woolson RF, Clarke WR, Hansen MD. Antithrombotic treatment of ischemic stroke among patients with occlusion or severe stenosis of the internal carotid artery: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology 53:122-125, 1999. Department of Neurology, University of Iowa College of Medicine, Iowa City 52242, USA. [email protected] OBJECTIVE: To examine the responses to early IV administration of an anticoagulant or placebo started within 24 hours of stroke among persons with an ipsilateral occlusion or severe stenosis of the internal carotid artery (ICA) identified by carotid duplex imaging. BACKGROUND: Patients with ischemic stroke of the cerebral hemisphere secondary to an ipsilateral occlusion or severe stenosis of the ICA generally have a poor prognosis. Early, accurate identification of these patients might permit improved treatment. METHODS: Exploratory analysis of outcomes at 7 days and 3 months was performed among patients enrolled in the Trial of Org 10172 in Acute Stroke Treatment (TOAST) who had an ischemic stroke in the cerebral hemisphere ipsilateral to an occlusion or a stenosis >50% of the ICA identified by carotid duplex imaging. RESULTS: Regardless of treatment, patients with duplex evidence of an occlusion of the ICA had more severe strokes and poorer outcomes at 7 days and 3 months than patients who had a stenosis. Favorable outcomes at 7 days were noted in 64 of 119 patients given danaparoid (53.8%) and 41 of 108 patients treated with placebo (38.0%; p = 0.023). By 3 months, favorable outcomes were noted in 82 patients given danaparoid (68.3%) and 58 patients administered placebo (53.2%; p = 0.021). CONCLUSIONS: Early identification by duplex imaging of an occlusion or severe stenosis of the ICA ipsilateral to a hemispheric ischemic stroke might improve selection of patients who could be treated with emergent anticoagulation. Further testing of this approach is needed.

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Referenz 7 (Neurologie, 11. Auflage) Adams HP Jr, Brott TG, Crowell RM, Furlan AJ, Gomez CR, Grotta J, Helgason CM, Marler JR, Woolson RF, Zivin JA, et al. Guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a special writing group of the stroke council, American Heart Association. Stroke 25: 1901-1914, 1994 Publication Types: * Guideline * Practice guideline

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Referenz 8 (Neurologie, 11. Auflage) Adams HP, Love BB. Medical management of aneurysmal subarachnoid hemorrhage. In Barnett, HJM, JP Mohr, BM Stein, FM Yatsu (Editors). Stroke. Pathophysiology, diagnosis, and management. 2nd edition. Churchill Livingstone. New York, Edinburgh, 1029-1054, 1992

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Referenz 8a (Neurologie, 11. Auflage) Adams KK, Jackson CE, Rauch RA, Hart SF, Kleinguenther RS, Barohn RJ. Cervical myelopathy with false localizing sensory levels. Arch. Neurol. 53, 1155-1158, 1996. Department of Medicine, University of Texas Health Science Center, San Antonio, USA. BACKGROUND: The diagnosis of cervical myelopathy is not always initially recognized. Only a few reports have described the discrepancy between sensory level and the site of cord compression, but none, to our knowledge, have used magnetic resonance imaging (MRI) for localization. OBJECTIVE: To identify a syndrome of compressive cervical myelopathy with false localizing thoracic sensory levels. DESIGN: Case series. SETTING: A university hospital referral center. RESULTS: Four men, aged 24 to 60 years, presented with progressive weakness and hyperreflexia involving the lower extremities and distinct thoracic sensory levels ranging from T-4 to T-10. None of these patients had cervical pain, history of trauma, or upper extremity symptoms. Results of MRI scans of the thoracic spinal cord were unremarkable. Initially, 1 patient was suspected of having transverse myelitis and was treated with high-dose steroids. All 4 patients were eventually found to have cervical spinal cord compression, diagnosed by MRI. Three patients underwent surgery for decompression of the cervical lesion. While all 3 improved in lower extremity strength, 2 had persistent discrete thoracic sensory levels postoperatively. CONCLUSIONS: Failure to diagnose cervical myelopathy because of the presence of a thoracic sensory level can delay appropriate treatment or lead to incorrect therapy. Persistence of a thoracic sensory level following surgery can occur.

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Referenz 9 (Neurologie, 11. Auflage) Adams RD, Lyon G. Neurology of hereditary metabolic diseases of children. Hemisphere, New York, 1982

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Referenz 10 (Neurologie, 11. Auflage) Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patientes. Arch Neurol Psychiat. 81: 154-172, 1959

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Referenz 11 (Neurologie, 11. Auflage) Adams RD, Victor M. Principles of neurology. Fifth edition. McGraw-Hill, Inc., New York, 1993

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Referenz 11a (Neurologie, 11. Auflage) Adams RJ, McKie VC, Hsu L, Files B, Vichinsky E, Pegelow C, Abboud M, Gallagher D, Kutlar A, Nichols FT, Bonds DR, Brambilla D. Prevention of a first stroke by tranfusions in children with sickle cell anemia and abnormal results on transcranial Doppler ultrasonography. N.Engl.J.Med. 339, 5-11, 1998. Department of Neurology, Medical College of Georgia, Augusta 30912-3200, USA. BACKGROUND: Blood transfusions prevent recurrent stroke in children with sickle cell anemia, but the value of transfusions in preventing a first stroke is unknown. We used transcranial Doppler ultrasonography to identify children with sickle cell anemia who were at high risk for stroke and then randomly assigned them to receive standard care or transfusions to prevent a first stroke. METHODS: To enter the study, children with sickle cell anemia and no history of stroke had to have undergone two transcranial Doppler studies that showed that the time-averaged mean blood-flow velocity in the internal carotid or middle cerebral artery was 200 cm per second or higher. The patients were randomly assigned to receive standard care or transfusions to reduce the hemoglobin S concentration to less than 30 percent of the total hemoglobin concentration. The incidence of stroke (cerebral infarction or intracranial hemorrhage) was compared between the two groups. RESULTS: A total of 130 children (mean [+/-SD] age, 8.3+/-3.3 years) were enrolled; 63 were randomly assigned to receive transfusions and 67 to receive standard care. At base line, the transfusion group had a slightly lower mean hemoglobin concentration (7.2 vs. 7.6 g per deciliter, P=0.001) and hematocrit (20.4 vs. 21.7 percent, P=0.002). Ten patients dropped out of the transfusion group, and two patients crossed over from the standard-care group to the transfusion group. There were 10 cerebral infarctions and 1 intracerebral hematoma in the standard-care group, as compared with 1 infarction in the transfusion group -- a 92 percent difference in the risk of stroke (P 900 mg per day) doses of aspirin in patients after a transient ischaemic attack or non-disabling stroke. The purpose of this study was to resolve the issue. Thus a minimeta-analysis was performed on data from 10 randomised trials of aspirin only v control treatment in 6171 patients after a transient ischaemic attack or nondisabling stroke. The data on the trials were listed in an appendix of the report on the second cycle of the Antiplatelet Trialists’ Collaboration. There was virtually no difference in relative risk reduction for low, medium, and high doses of aspirin (13%, 9%, and 14% respectively). This equivalence corresponds with the results of the UK-TIA trial in a direct comparison of 300 and 1200 mg. The Dutch TIA trial showed no difference in efficacy of 30 and 283 mg. It is concluded that aspirin at any dose above 30 mg daily prevents 13% (95% confidence interval 4-21) of vascular events and that there is a need for more efficacious drugs.

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Referenz 18 (Neurologie, 11. Auflage) Al Kawi MZ, Bohlega S, Banna M. MRI findings in neuro-Behçet’s disease. Neurology 41: 405-408, 1991 Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia. We report MRI findings in 6 patients with Behcet’s disease and CNS involvement. There were 3 different stages of imaging appearance: (1) During the acute illness, there were scattered areas of high signal intensity on T2-weighted images with predilection to the central structures of the cerebrum, the cerebral peduncles, and basis pontis. (2) During the recovery phase, most of these findings improved, but some white matter high signal areas persisted in the upper brainstem and peripheral subcortical white matter. Occasionally, findings were suggestive of microhematoma. (3) During the chronic phase, atrophy of posterior fossa structures became evident with decreased signal intensity suggestive of hemosiderin deposits.

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Referenz 19 (Neurologie, 11. Auflage) Al-Lozi MT, Pestronk A, Yee WC, Flaris N, Cooper J. Rapidly evolving myopathy with myosin-deficient muscle fibers. Ann Neurol 35: 273-279, 1994 Comment in: Ann Neurol. 1994 Mar;35(3):257-9 Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110. Five patients with rapidly evolving, severe weakness had an unusual myopathy with virtually complete loss of myosin in 5 to 40% of muscle fibers. Three of the 5 patients began to develop weakness 1 to 2 weeks after lung transplantation. The fourth became weak after a febrile illness. The fifth presented with diabetic ketoacidosis and weakness. All patients had received corticosteroid therapy. In all cases the weakness was progressive and led to severe disability, with respiratory failure in 4 patients. Initial diagnostic testing did not localize an underlying cause for the weakness. Creatine kinase was normal or minimally elevated. Electromyography generally showed mildly myopathic or nondiagnostic changes. However, muscle biopsy revealed numerous small angular fibers with no myosin ATPase staining at any pH. Immunocytochemical staining and ultrastructural studies confirmed a severe loss of myosin in many fibers. This rapidly evolving myopathy with myosin-deficient muscle fibers appears to be different clinically and pathologically from previously described syndromes involving rapidly progressive weakness. Slow recovery over a period of months is the most common outcome.

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Referenz 20 (Neurologie, 11. Auflage) el Alaoui-Faris M, Medejel A, Zemmouri K, Yahyaoui M, Chkili T. Le syndrome de sclérose lateral amyotrophique d’origine syphilitique. Rev Neurol 146: 41-44, 1990 Service de Neurologie, Hopital des specialites Rabat, Maroc. We studied 5 cases of syphilitic lateral amyotrophic sclerosis. The diagnosis was based on the presence of a lymphocytic reaction in the CSF and positive VDRL and TPHA reactions in both blood and CSF. Clinically, the disease affected the arms in 3 cases and produced paraplegia in 2 cases. The gradual extension of amyotrophy over several months, the diffusion of electromyographic abnormalities and the finding of spinal cord atrophy at myelography and CT suggested a subacute ischemic mechanism with meningo-myelic arteritis involving the anterior horns. After treatment with penicillin G in high doses, the outcome was constantly favourable, with improvement of motor deficit in 4 cases and stabilisation in 1 case in a 5 to 13 years’ follow-up.

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Referenz 21 (Neurologie, 11. Auflage) Alexander EL, Ranzenbach MR, Kumar AJ, Kozachuk WE, Rosenbaum AE, Patronas N, Harley JB, Reichlin M. Anti-Ro (SS-A) autoantibodies in central nervous system disease associated with Sjögren’s syndrome (CNS-SS): Clinical, neuroimaging, and angiographic correlates. Neurology 44: 899-908, 1994. Division of Molecular and Clinical Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD 21224. OBJECTIVE: To examine in Sjogren’s syndrome (SS) the interrelationship between the presence of the anti-Ro(SS-A) antibody response and (1) concomitant presence and type (ie, focal or nonfocal) of CNS disease (CNS-SS), (2) cross-sectional brain MRI or CT, and (3) abnormal cerebral angiography. METHODS: Neurologic, neuroimaging, and angiographic features of CNS-SS patients were correlated with the presence of precipitating anti-Ro(SS-A) autoantibodies detected by gel double-immunodiffusion or quantitative ELISA, which detects antibodies directed against the 60-kd peptide. Statistical analyses were performed using Fisher’s exact test (two-tailed) with Haldane’s adjustment and odds ratio with Cornfield 95% confidence intervals. RESULTS: Precipitating antibodies against the Ro(SS-A) antigen, determined by gel double-immunodiffusion, were present in an increased frequency in CNS-SS patients with (1) documented clinical CNS disease, (2) focal clinical CNS manifestations and serious complications, (3) large regions of increased signal intensity, consistent with ischemia/infarcts on brain MRI scans or regions of decreased attenuation consistent with infarcts on CT, and (4) abnormal cerebral angiograms consistent with small-vessel angiitis. Finally, the anti-Ro(SS-A) antibody response in CNS was directed against the 60-kd peptide specificity, determined by ELISA. CONCLUSIONS: Clinical, neuroimaging (cerebral CT), and angiographic observation suggest that a subset of anti-Ro(SS-A) antibody-positive, in contrast with -negative, CNS-SS patients have more serious and extensive CNS disease, some with frank cerebral angiopathy. Anti-Ro(SS-A) antibodies are postulated to play a role in mediating or potentiating vascular injury in CNS-SS.

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Referenz 22 (Neurologie, 11. Auflage) Alexander EL. Neurologic complications of Sjögren’s syndrome. In Fox R. (Editor). Rheumatic clinics of North America. WB Saunders Company, Philadelphia 18/3: 637-672, 1992

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Referenz 23 (Neurologie, 11. Auflage) Alhalabi M, Moore PM. Serial angiography in isolated angiitis of the central nervous system. Neurology 44: 1221-1226, 1994 Comment in: * Neurology. 1995 Jul;45(7):1422-3 Wayne State University School of Medicine, Detroit, MI. Isolated angiitis of the CNS is a disease of unknown etiology characterized by signs and symptoms of diffuse ischemia or recurrent strokes and histologic evidence of vascular inflammation. Angiography frequently suggests the diagnosis, but angiographic changes over time have not been delineated. This study investigates the evolution of radiographic findings in CNS vasculitis by serial angiography in 19 patients. Abnormal angiographic findings include segmental arterial narrowings and dilatations, vascular occlusions, collateral formation, and prolonged circulation time. Smooth narrowings of the affected vessels occurring in multiple vascular distributions are the most frequent abnormality. Single stenotic areas in multiple vessels are more frequent than multiple stenotic areas along a single vessel segment. Vascular occlusions, the least diagnostic feature, affect small arteries in some patients. Serial studies demonstrate progression of angiographic changes prior to therapy and improvement or stabilization in patients with a clinical response to therapy. Correlation of clinical and angiographic features is consistent with the hypothesis that segmental narrowing initially results from reversible inflammation and vasospasm. The later irreversible angiographic features appear secondary to scarring. A limitation of angiography is demonstrated in this study by the apparently normal angiograms in two patients with biopsy-confirmed small-vessel vasculitis. Four patients with abnormal angiograms and histologic evidence of disease had normal MRIs.

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Referenz 23a (Neurologie, 11. Auflage) Almarcegui C., Lorente S., Romero M.F. et al.: Blink reflex in trigeminal hypoesthesia caused by a pontine demyelinating lesion. J. Neurol. 246, 140-141 (1999). No abstract available.

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Referenz 24 (Neurologie, 11. Auflage) Amarenco P, Cohen A, Tzourio C, Bertrand B, Hommel M, Besson G, Chauvel C, Touboul PJ, Bousser MG. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 331: 1474-1479, 1994 Service de Neurologie, Hopital Saint-Antoine, Universite Pierre et Marie Curie, Paris. BACKGROUND. Atherosclerotic disease of the aortic arch has been suspected to be a potential source of cerebral emboli. We conducted a study to quantify the risk of ischemic stroke associated with atherosclerotic disease of the aortic arch. METHODS. Using transesophageal echocardiography, we performed a prospective case-control study of the frequency and thickness of atherosclerotic plaques in the ascending aorta and proximal arch in 250 consecutive patients admitted to the hospital with ischemic stroke and 250 consecutive controls, all over the age of 60 years. RESULTS. Atherosclerotic plaques > or = mm in thickness were found in 14.4 percent of the patients but in only 2 percent of the controls. After adjustment for atherosclerotic risk factors, the odds ratio for ischemic stroke among patients with such plaques was 9.1 (95 percent confidence interval, 3.3 to 25.2; P < 0.001). Among the 78 patients who had brain infarcts with no obvious cause, 28.2 percent had plaques > or = 4 mm in thickness, as compared with 8.1 percent of the 172 patients who had infarcts whose possible or likely causes were known (odds ratio, 4.7; 95 percent confidence interval, 2.2 to 10.1; P < 0.001). Plaques of > or = 4 mm in the aortic arch were not associated with the presence of atrial fibrillation or stenosis of the extracranial internal carotid artery. In contrast, plaques that were 1 to 3.9 mm thick were frequently associated with carotid stenosis of > or = 70 percent. CONCLUSIONS. These results indicate a strong, independent association between atherosclerotic disease of the aortic arch and the risk of ischemic stroke. The association was particularly strong with thick plaques. Atherosclerotic disease of the aortic arch should be regarded as a risk factor for ischemic stroke and as a possible source of cerebral emboli.

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Referenz 25 (Neurologie, 11. Auflage) Amarenco P. The spectrum of cerebellar infarctions. Neurology 41: 973-979, 1991 Review. No abstract available

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Referenz 26 (Neurologie, 11. Auflage) Ameri A, Bousser M-G. Cerebral venous thrombosis. In Barnett, HJM, Hachinski VC (Editors). Cerebral ischemia: treatment and prevention. Neurologic Clinics 10: 87-111, 1992

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Referenz 27 (Neurologie, 11. Auflage) Aminoff MJ (Ed.). Neurology and general medicine. The neurological aspects of medical disorders. 2nd edition. Churchill Livingstone, New York, Edinburgh, 1995

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Referenz 28 (Neurologie, 11. Auflage) Aminoff MJ (Editor). Electrodiagnosis in Clinical Neurology, 3rd edition. Churchill Livingstone, New York, 1992

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Referenz 28a (Neurologie, 11. Auflage) Amlie-Lefond C, Kleinschmidt-DeMasters BK, Mahalingam R, Davis LE, Gilden DH. The vasculopathy of varicella-zoster virus encephalitis. Ann Neurol 37; 784-790, 1995. Department of Neurology, University of Colorado Health Sciences Center, Denver 80262, USA. Varicella-zoster virus (VZV) encephalitis has become more prevalent in the era of acquired immunodeficiency syndrome and other immunosuppressive diseases and poses diagnostic and therapeutic challenges for clinicians, radiologists, and pathologists. Six cases studied at our institutions shed light on the patterns and pathogenesis of the disease. VZV encephalitis is predominantly a vasculopathy, involving small and large vessels, that generates seizures, mental changes, and focal deficits. Brain imaging reveals large and small ischemic or hemorrhagic infarcts, often both, of cortex and subcortical gray and white matter. Deep-seated white matter lesions often predominate and are ischemic and/or demyelinative, depending on the size of blood vessels involved and the amount of additional demyelination caused by infection of oligodendrocytes. The demyelinative lesions are smaller and less coalescent than those seen in progressive multifocal leukoencephalopathy

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Referenz 28b (Neurologie, 11. Auflage) Andreadou E., Yapijakis C., Paraskevas GP, Stavropoulos P, Karadimas C, Zis VP, Davaki P, Karandreas N, Rentzos M, Tsakanikas C, Vassilopoulos D, Papageorgiou C: Hereditary neuropathy with liability to pressure palsies: the same molecular defect can result in diverse clinical presentation. J. Neurol. 243, 225-230 (1996). Department of Neurology, University of Athens, Greece. Hereditary neuropathy with liability to pressure palsies (HNPP) is a peripheral nerve disorder characterized by autosomal dominant inheritance, recurrent pressure palsies, reduced motor and sensory conduction velocities and sausage-like swellings (tomacula) of myelin sheaths in nerve biopsy. Two young adult patients are reported as index cases of two families in which HNPP was diagnosed. The first patient presented with recurrent pressure palsies, whereas the second suffered from fasciculations and myokymias in his right hand, with difficulty in writing, and upper and lower limb paraesthesias of 3 years’ duration. Electrodiagnostic studies revealed slowing of conduction primarily in common sites of compression in both patients. Sural nerve biopsy revealed the characteristic tomaculous swellings in both patients. DNA analysis showed that both patients have a deletion in chromosome 17p11.2 which is found in the majority of HNPP cases. In light of the common molecular defect, the different clinical symptomatology of the two patients is discussed.

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Referenz 28c (Neurologie, 11. Auflage) Andrews NJ; Farrington CP; Cousens SN, Smith PG, Ward H, Knight RS, Ironside JW, Will RG.Incidence of variant Creutzfeldt-Jakob disease in the UK [letter]. Lancet 356:481-482, 2000. The number of deaths from variant CJD (vCJD) in the UK increased in the last quarter of 1998, although numbers were lower in subsequent quarters. We analysed the numbers of definite and probable (living and dead) vCJD cases since 1994 to assess trends in incidence. We estimated that the number of onsets increased by 23% per year for 1994-2000 (p=0.004), and that deaths increased by 33% for 1995-2000 (p=0.005). The absolute number of cases in the UK is still low, but such an increase should be a matter of concern.

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Referenz 29 (Neurologie, 11. Auflage) Anetseder M, Hartung E, Klepper S, Reichmann H. Gasoline vapors induce severe rhabdomyolysis. Neurology 44, 2393-2395, 1994 Department of Anesthesiology, University Wuerzburg, Germany. A young patient developed rhabdomyolysis after accidentally inhaling gasoline vapors. Although there had been no preexistent myopathy, the caffeine and halothane contracture test classified the patient as being malignant hyperthermia-susceptible (MHS). Abnormal contractures also occurred after exposure of muscle bundles to benzine (at 0.01%); in four control tests, benzine-induced contractures (at 0.1%) could be elicited in MHS, but not in normal, muscles. The complex composition of benzine seems to contain potentially hazardous agents that trigger MH.

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Referenz 30 (Neurologie, 11. Auflage) Angelini L, Nardocci N, Rumi V, Zorzi C, Strada L, Savoiardo M. Hallervorden-Spatz disease: clinical and MRI study of 11 cases diagnosed in life. J Neurol 239: 417-425, 1992 Department of Child Neurology, Istituto Nazionale Neurologico C. Besta, Milan, Italy. The diagnosis of Hallervorden-Spatz disease (HSD) has usually been made post mortem, although the recent description of characteristic abnormalities in the globus pallidus has suggested the possibility of an in vivo diagnosis. We present the clinical histories, neurological features and MRI findings of 11 patients, diagnosed as having HSD. Generalized dystonia with predominance of oromandibular involvement, behavioural changes followed by dementia and retinal degeneration were present in all the patients. MRI pallidal abnormalities consisted of decreased signal intensity in T2-weighted images, compatible with iron deposits, and of a small area of hyperintensity in its internal segment ("eye of the tiger" sign). We propose that the combination of these neurological signs with these MRI findings could be considered as highly suggestive of a diagnosis of HSD in living patients.

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Referenz 31 (Neurologie, 11. Auflage) Antiplatelet Trialist’s Collaboration. Collaborative overview of randomized trials of antiplatelet therapy - I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatetet therapy in various categories of patients. Br Med J 308: 81-106, 1994 OBJECTIVE--To determine the effects of "prolonged" antiplatelet therapy (that is, given for one month or more) on "vascular events" (non-fatal myocardial infarctions, non-fatal strokes, or vascular deaths) in various categories of patients. DESIGN--Overviews of 145 randomised trials of "prolonged" antiplatelet therapy versus control and 29 randomised comparisons between such antiplatelet regimens. SETTING--Randomised trials that could have been available by March 1990. SUBJECTS--Trials of antiplatelet therapy versus control included about 70,000 "high risk" patients (that is, with some vascular disease or other condition implying an increased risk of occlusive vascular disease) and 30,000 "low risk" subjects from the general population. Direct comparisons of different antiplatelet regimens involved about 10,000 high risk patients. RESULTS--In each of four main high risk categories of patients antiplatelet therapy was definitely protective. The percentages of patients suffering a vascular event among those allocated antiplatelet therapy versus appropriately adjusted control percentages (and mean scheduled treatment durations and net absolute benefits) were: (a) among about 20,000 patients with acute myocardial infarction, 10% antiplatelet therapy v 14% control (one month benefit about 40 vascular events avoided per 1000 patients treated (2P < 0.00001)); (b) among about 20,000 patients with a past history of myocardial infarction, 13% antiplatelet therapy v 17% control (two year benefit about 40/1000 (2P < 0.00001)); (c) among about 10,000 patients with a past history of stroke or transient ischaemic attack, 18% antiplatelet therapy v 22% control (three year benefit about 40/1000 (2P < 0.00001)); (d) among about 20,000 patients with some other relevant medical history (unstable angina, stable angina, vascular surgery, angioplasty, atrial fibrillation, valvular disease, peripheral vascular disease, etc), 9% v 14% in 4000 patients with unstable angina (six month benefit about 50/1000 (2P < 0.00001)) and 6% v 8% in 16,000 other high risk patients (one year benefit about 20/1000 (2P < 0.00001)). Reductions in vascular events were about one quarter in each of these four main categories and were separately statistically significant in middle age and old age, in men and women, in hypertensive and normotensive patients, and in diabetic and nondiabetic patients. Taking all high risk patients together showed reductions of about one third in non-fatal myocardial infarction, about one third in non-fatal stroke, and about one third in vascular death (each 2P < 0.00001). There was no evidence that non-vascular deaths were increased, so in each of the four main high risk categories overall mortality was significantly reduced. The most widely tested antiplatelet regimen was "medium dose" (75-325 mg/day) aspirin. Doses throughout this range seemed similarly effective (although in an acute emergency it might be prudent to use an initial dose of 160-325 mg rather than about 75 mg). There was no appreciable evidence that either a higher aspirin dose or any other antiplatelet regimen was more effective than medium dose aspirin in preventing vascular events. The optimal duration of treatment for patients with a past history of myocardial infarction, stroke, or transient ischaemic attack could not be determined directly because most trials lasted only one, two, or three years (average about two years). Nevertheless, there was significant (2P < 0.0001) further benefit between the end of year 1 and the end of year 3, suggesting that longer treatment might well be more effective. Among low risk recipients of "primary prevention" a significant reduction of one third in non-fatal myocardial infarction was, however, accompanied by a non-significant increase in stroke. Furthermore, the absolute reduction in vascular events was much smaller than for high risk patients despite a much longer treatment period (4.4% antiplatelet therapy v 4.8% control; five year Publication Types:

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* Meta-Analysis

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Referenz 32 (Neurologie, 11. Auflage) Appenzeller O. The autonomic nervous system: an introduction to basic and clinical concepts. 5th editition, Elsevier Amsterdam, New York, 1997

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Referenz 33 (Neurologie, 11. Auflage) Aranda B. Les troubles vésico-sphinctériens de la maladie de Parkinson. Rev Neurol 149: 476-480, 1993 Service de Reeducation, Centre Hospitalier, Gonesse, Courbevoie. Urinary bladder disorders often occur, sometimes very early, during the course of Parkinson’s disease. Careful analysis of symptoms including clinical examination, urodynamic studies and radiographic data is essential before choosing a treatment, especially before prostatic surgery. We studied 41 parkinsonian patients. Bladder hyperreflexia occurred in 88% and bladder hyporeflexia in only 12%. In 16 patients, we tested bladder activity after a subcutaneous injection of apomorphine. All patients with hyperreflexia were improved whereas hyporeflexic patients remained unchanged. These findings and data from the literature suggest that in Parkinson’s disease detrusor hyperreflexia is the consequence of dopamine nigrostriatal depletion. The physiopathology of bladder hyporeflexia is less understood. The practical care of parkinsonians with urinary disorders is detailed.

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Referenz 34 (Neurologie, 11. Auflage) Arbeitsgruppe Lipide der Schweiz. Gesellschaft für Kardiologie und der Schweiz. Stiftung für Kardiologie. Lipide und die Prävention der koronaren Herzkrankheit: Diagnostik und Maßnahmen. Schweiz. Aerztezeitung 73: 1593 -1602, 1992

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Referenz 35 (Neurologie, 11. Auflage) Arieff Al. Management of hyponatremia. Br med J 307: 305-308, 1993 Review. No abstract available.

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Referenz 35a (Neurologie, 11. Auflage) Arita J, Nakae Y, Matsushima H, Maekawa K. Hopkins Syndrome, T2 weighted high intensity of anterior horn on spinal MR imaging. Pediatr. Neurol. 13: 263-265, 1995 Department of Pediatrics, Jikei University School of Medicine, Tokyo, Japan. Hopkins syndrome is a poliomyelitis-like illness manifesting flaccid paralysis of an extremity in the recovery stage after an asthmatic attack. A 7-year-old boy who developed acute flaccid paralysis of the left upper extremity 4 days after an asthmatic attack is reported. T2-weighted magnetic resonance imaging of the cervical spine revealed a local high-intensity area in the left anterior horn at the C4 to C6 level. There have been few pathologic or radiologic studies of this syndrome. We suspect that the cause is an anterior horn lesion. Publication Types: * Review * Review of reported cases

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Referenz 36 (Neurologie, 11. Auflage) Arnaud O, Pelletier J, Dalecky A, Cherif AA, Azulay JP, Salamon G, Khalil R. Les fistules durales rachidiennes à drainage veineux périmédullaire. Rev Neurol 150: 713-720, 1994 Service de Neuroradiologie et de Radiologie Vasculaire, CHU Timone, Marseille. Clinical and neuroradiological findings of 8 patients with a spinal dural arteriovenous fistula are reviewed. Disturbance of micturition or defecation and weakness of the legs were always present and the most frequent initial symptom was a progressive spastic paraparesis. Duration of symptoms before diagnosis was 2 years. Lumbar puncture showed elevation of proteins and myelography demonstrated dilated perimedullar posterior veins. In every case, magnetic resonance imaging of the spinal cord (T2weighted images) revealed intramedullary high signal intensity of the conus medullaris and selective angiography confirmed the site of the dural fistula. Each patient was treated with endovascular method consisting in liquid adhesive embolization (0.2 cc of N-butyl cyanoacrylate) with hyperselective catheterism of the dorsospinal artery. Embolization procedure was successful in 6 cases with large improvement of leg weakness and partial regression of disturbed micturition and defecation. The pathophysiological mechanisms explaining the clinical signs are discussed.

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Referenz 37 (Neurologie, 11. Auflage) Arning C. Farbkodierte Duplexsonographie der hirnversorgenden Arterien. Ein Text-Bild-Atlas der methodischen Grundlagen, normalen und pathologischen Befunde. Georg Thieme Verlag, Stuttgart, New York, 1996

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Referenz 37a (Neurologie, 11. Auflage) Arsac Ch., Raymond C., Martin-Moutot N. et al.: Immunoassays fail to detect antibodies against neuronal calcium channels in Amyotrophic lateral sclerosis. Ann. Neurol. 40, 695-700 (1996). INSERM U374, Institut Jean Roche, Faculte de Medecine Secteur Nord, Marseille, France. Recent studies suggested that autoantibodies that bind to voltage-dependent calcium channels and activate calcium entry may play a role in the progressive degeneration of motoneurons in sporadic amyotrophic lateral sclerosis. Immunoassays were performed to assess autoantibody titer in patients with amyotrophic lateral sclerosis or Lambert-Eaton myasthenic syndrome, a disease in which the presence of anti-calcium channel antibodies is well documented. Based on immunoprecipitation assays for antibodies against N-type calcium channels, only 8% (2/25) of amyotrophic lateral sclerosis patients had marginally positive titers, whereas 58% (18/31) of patients with Lambert-Eaton myasthenic syndrome had positive titers. Enzyme-linked immunosorbent assays with purified neuronal N-type calcium channels revealed immunoreactivity in 2 of 25 amyotrophic lateral sclerosis sera and 12 of 31 Lambert-Eaton myasthenic syndrome sera, which is not compatible with suggestions that enzyme-linked immunosorbent assay is a more sensitive technique for the detection of autoantibodies in amyotrophic lateral sclerosis. Furthermore, based on immunoprecipitation assays, amyotrophic lateral sclerosis sera were totally negative for antibodies against L-type calcium channels from skeletal muscle or brain. These data do not support the hypothesis that an autoimmune response against calcium channels plays a primary

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Referenz 38 (Neurologie, 11. Auflage) Arsura E. Experience with intravenous immunoglobulin in myasthenia gravis. Clin Immunol Immunopathol 53: Suppl. S170-S179, 1989 Department of Medicine, St. Vincent’s Hospital and Medical Center, New York, New York 10011. Myasthenia gravis (MG) is an acquired autoimmune disorder of neuromuscular transmission associated with a deficiency of acetylcholine receptor at the neuromuscular junction. Current therapeutic strategies are aimed at increasing the amount of acetylcholine at the neuromuscular junction or at addressing the abnormal immune response. Therapies influencing the immune response include thymectomy, corticosteroids, nonsteroidal immunosuppression, and plasmapheresis. Unfortunately, whether used alone or in combination the toxicities of these agents can be quite significant; thus, an agent with a distinct and more favorable side effect profile might be useful in MG. Intravenous immunoglobulin has such potential.

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Referenz 38a (Neurologie, 11. Auflage) Arzimanoglou A.A.: Gilles de la Tourette syndrome. J. Neurol. 245, 761-765 (1998). Department of Child Neurology and Metabolic Disorders, Hopital Robert Debre, Paris, France. [email protected] The study of childhood movement disorders is still in an early stage. Tics and related disorders are recognized as one of the most common movement disorders. This contribution reviews the main clinical, epidemiological, pathophysiological, and treatment issues on tics and Gilles de la Tourette syndrome. Although these disorders are not life threatening, they may be psychologically or functionally disabling. Early diagnosis and special management permit the alleviation of symptoms. Publication Types: * Review * Review, Tutorial

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Referenz 38b (Neurologie, 11. Auflage) Aschoff J.C., Kailer N.A., Walter K.: Physostigmin in der Behandlung von Kleinhirnataxien. Nervenarzt 67, 311-318 (1996). Neurologische Poliklinik, Universitat, Ulm. Cerebellar ataxias are still a challenging problem for neurologists, and to this day there exists no medical, physiotherapeutic, psychot-erapeutic or surgical therapy which constantly leads to a reduction of ataxic symptoms. In the pathophysiology of cerebellar ataxia a cholinergic defect has often been described. In a double-blind, cross-over study with 14 patients with cerebellar ataxia and an open follow-up, long-term study with 21 patients, the clinical effects of physostigmine capsules in doses up to 10 mg per day were studied. Moreover, a transdermal application (physostigmine patch) was developed, achieving constant physostigmine plasma levels for 24 h. Of 14 patients treated with physostigmine during the double-blind, cross-over study, nine could correctly distinguish between verum and placebo. They all showed small but constant improvements, clearly experienced by the patients. With the physostigmine patch, 12 of 14 patients improved. Thirteen of 14 patients decided to take part in open follow-up studies with physostigmine, and most of them preferred the physostigmine patch as long-term medication. To date, 21 patients with cerebellar ataxia have been treated with physostigmine. As far as we can judge at the end of a treatment period of at least 2 years, the progression of the disease could be stopped in 17 of 21 patients. These patients reported small but constant effects, and none wants to live without the physostigmine patch. Publication Types: * Clinical Trial * Randomized Controlled Trial

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Referenz 39 (Neurologie, 11. Auflage) Ashizawa T, Dunne PW, Ward PA, Seltzer WK, Richards CS. Effects of the sex of myotonic dystrophy patients on the unstable triplet repeat in their affected offspring. Neurology 44: 120-122, 1994 Department of Neurology, Baylor College of Medicine, Houston, TX 77030. The mutation responsible for myotonic dystrophy (DM) is an unstable expansion of the CTG repeat within the myotonin protein kinase gene. To examine whether the parental origin of the expanded repeat influences the repeat size in offspring, we studied 51 father-child and 59 mother-child pairs with DM. Small expansions in fathers resulted in larger size expansions in their offspring, while large paternal expansions resulted in less size change in their offspring. However, there was no correlation between maternal size expansion and size increase in offspring for either congenital or noncongenital DM. These data suggest that the sex of the affected parent influences the unstable expansion of the repeat in DM offspring. While some evidence suggests that DNA methylation status cannot explain this observation, the mechanism for differential maternal/paternal transmission expansion is currently unknown.

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Referenz 40 (Neurologie, 11. Auflage) Asplund K. Any progress on progressing stroke? Cerebrovasc Dis 1992; 2: 317-384

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Referenz 41 (Neurologie, 11. Auflage) Astrup J, Sjesjö BK, Symon L. Thresholds in cerebral ischemia - the ischemic penumbra. Stroke 12: 723-725, 1981 No abstract available.

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Referenz 42 (Neurologie, 11. Auflage) Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 273: 1421-1428, 1995 OBJECTIVE--To determine whether the addition of carotid endarterectomy to aggressive medical management can reduce the incidence of cerebral infarction in patients with asymptomatic carotid artery stenosis. DESIGN--Prospective, randomized, multicenter trial. SETTING--Thirty-nine clinical sites across the United States and Canada. PATIENTS--Between December 1987 and December 1993, a total of 1662 patients with asymptomatic carotid artery stenosis of 60% or greater reduction in diameter were randomized; follow-up data are available on 1659. At baseline, recognized risk factors for stroke were similar between the two treatment groups. INTERVENTION--Daily aspirin administration and medical risk factor management for all patients; carotid endarterectomy for patients randomized to receive surgery. MAIN OUTCOME MEASURES--Initially, transient ischemic attack or cerebral infarction occurring in the distribution of the study artery and any transient ischemic attack, stroke, or death occurring in the perioperative period. In March 1993, the primary outcome measures were changed to cerebral infarction occurring in the distribution of the study artery or any stroke or death occurring in the perioperative period. RESULTS--After a median follow-up of 2.7 years, with 4657 patient-years of observation, the aggregate risk over 5 years for ipsilateral stroke and any perioperative stroke or death was estimated to be 5.1% for surgical patients and 11.0% for patients treated medically (aggregate risk reduction of 53% [95% confidence interval, 22% to 72%]). CONCLUSION--Patients with asymptomatic carotid artery stenosis of 60% or greater reduction in diameter and whose general health makes them good candidates for elective surgery will have a reduced 5-year risk of ipsilateral stroke if carotid endarterectomy performed with less than 3% perioperative morbidity and mortality is added to aggressive management of modifiable risk factors. Publication Types: * Clinical Trial * Multicenter Study * Randomized Controlled Trial

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Referenz 43 (Neurologie, 11. Auflage) Atlas SR (Editor). Magnetic resonance imaging of the brain and spine. Second edition. Lippincott-Raven Publishers, Hagerstown, 1995

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Referenz 44 (Neurologie, 11. Auflage) Atlas SW. MR angiography in neurologic disease. Radiology 193: 1-16, 1994 Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia 19104. Magnetic resonance (MR) angiography has rapidly evolved over the past few years to become a technique that is commonly used in clinical practice as part of the diagnostic work-up of patients with suspected neurologic disease. In this review, the author provides a brief overview of the relevant biophysical principles and some fundamentals of flow imaging by using MR as a baseline for understanding and implementing MR angiography in these patients. A historical perspective is given as a way of emphasizing the need for a healthy degree of skepticism rather than enthusiasm alone when reading MR angiographic literature. The rationale and clinical needs for MR angiography are summarized. The available data from blinded reader studies are summarized for two major clinical entities in which MR angiography is often used in neurologic practice: atherosclerotic disease of the extracranial carotid bifurcation and intracranial aneurysms. Recent refinements and technical innovations are also noted. Publication Types: * Review * Review, tutorial

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Referenz 44a (Neurologie, 11. Auflage) Auer-Grumbach M., Wagner K., Fazekas F, Loscher WN, Strasser-Fuchs S, Hartung HP.: Hereditäre motorisch-sensible Neuropathien (Charcot-Marie-Tooth-Syndrom). Nervenarzt 70, 1052-1061 (1999). Universitatsklinik fur Neurologie, Karl-Franzens-Universitat, Graz. Charcot-Marie-Tooth (CMT) disease is the most common inherited disorder of the peripheral nervous system with an incidence of 40:100,000. Clinically, it is characterized by distal muscle weakness and wasting, primarily of the legs and later of the arms, foot deformity, diminished or absent tendon reflexes, and mild-to-moderate sensory loss. Molecular genetic studies over the past 2 decades have revealed the genetic heterogeneity of this disorder and the identification of different genes or gene loci, respectively. Therefore, a current CMT classification though constantly changing due to ongoing detection of further genetic defects must take into consideration both phenotypic and genotypic criteria. Since certain clinical features appear to be associated with specific genetic subtypes, we provide a detailed description of characteristic phenotypic variants to facilitate differential diagnosis and allow more precise referral to subsequent genetic investigations. Publication Types: * Review * Review, tutorial

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Referenz 45 (Neurologie, 11. Auflage) Auger RG, Litchy WJ, Cascino TL, Ahlskog JE. Hemimasticatory spasm: Clinical and electrophysiological observations. Neurology 42: 2263-2266, 1992 Department of Neurology, Mayo Clinic, Rochester, MN 55905. Hemimasticatory spasm is a rare disorder of the trigeminal nerve that produces involuntary jaw closure due to paroxysmal unilateral contraction of jaw-closing muscles. We report three patients with this disorder. Electrophysiologic studies demonstrated normal blink and masseter reflexes. The masseter inhibitory reflex was absent during periods of spasm. Needle electromyography demonstrated irregular bursts of motor unit potentials that were identical to the pattern observed in hemifacial spasm. The electrophysiologic findings suggest ectopic excitation of the trigeminal motor root or its nucleus, an abnormality that is analogous to ectopic excitation of the facial nerve in hemifacial spasm. One patient improved temporarily with surgery, one improved while on treatment with carbamazepine, and another responded favorably to botulinum toxin injection.

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Referenz 46 (Neurologie, 11. Auflage) Aupy M, Orgogozo JM, Loiseau P, Aparicio M, Vital C. Atteinte multiple des nerfs craniens révélant une périartérite noueuse. Relation avec le syndrome de Cogan. Rev neurol 136: 59-65, 1980 A 43-year-old woman was found to have multiple cranial neuritis affections, present as an isolated disorder over a long period, and characterized by bilateral deafness and associated lesions of the VII and V cranial nerves. On investigation, visual disturbances were discovered which were of a transitory nature and made up a total clinical picture suggesting Cogan’s syndrome. Neuropathological examination revealed the presence of typical periarteritis nodosa lesions in the cranial nerves. The authors suggest, therefore, that certain cases described as Cogan’s syndrome are in fact particular forms of periarteritis nodosa.

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Referenz 47 (Neurologie, 11. Auflage) Austin EJ, Wilkus RJ, Longstreath WT Jr. Etiology and prognosis of alpha coma. Neurology 33: 773-777, 1988 Department of Medicine, University of Washington School of Medicine, Seattle. We reviewed our experience with alpha coma, the finding of predominantly alpha-frequency rhythms in the EEGs of unconscious patients, and identified 50 patients. Cardiac arrest, either inside (n = 25) or outside (n = 24) the hospital, was the cause of unconsciousness in all except one patient who had hyperglycemic, hyperosmolar coma. After out-of-hospital cardiac arrest, the risk of never regaining consciousness or dying during hospitalization did not differ significantly between unconscious patients with (n = 24) and without (n = 69) alpha frequencies in their EEGs. A review of the literature supports our findings that alpha coma most commonly follows cardiac arrest and does not preclude the possibility of neurologic recovery. We conclude that alpha coma is a descriptive term and lacks prognostic significance in itself.

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Referenz 48 (Neurologie, 11. Auflage) Avrahami E, Cohn D-E, Feibel M, Tadmor R. MRI demonstration and CT correlation of the brain in patients with idiopathic intracerebral calcification. J Neurol 241: 381-384, 1994 Radiology Department, Edith Wolfson Medical Center, Holon, Israel. Twenty-two patients aged 36-63 years were diagnosed as having Fahr’s syndrome on the basis of the presence on CT of unexpected extensive calcification of the basal ganglia. Even when associated with calcification of other brain areas, the main diagnostic criterion remained basal ganglia calcification larger than 800 mm2. Normal values of parathormone, serum calcium and phosphorus excluded hypercalcaemia and hypoparathyroidism. Mitochondrial CNS disease was excluded clinically. MRI and repeated CT and neurological examination were performed in all of the patients. The patients were divided into two groups: neurologically asymptomatic (group 1) and neurologically symptomatic (group 2). T2-weighted sequences demonstrated hyperintense areas in all of the patients involving the white and the grey matter of the brain. In group 1 the hyperintense lesions were significantly smaller than in group 2. The neurological symptoms correlated better with the hyperintensities on T2-weighted MR images than with the calcification demonstrated on CT. Hyperintensities in T2-weighted MRI and the areas shown by CT to have calcification had different locations. In 15 patients with dementia, the white matter of the entire centrum semiovale was bilaterally hyperintense. In another 3 patients with hemiparesis, hyperintense areas in the internal capsule, contralateral to the side of hemiparesis, were demonstrated in the T2-weighted sequence. The hyperintense T2 signals may reflect a slowly progressive, metabolic or inflammatory process in the brain which subsequently calcifies and are probably responsible for the neurological deficit observed.

246

Referenz 48a (Neurologie, 11. Auflage) Backonja M, Beydoun A, Edwards KR, Schwartz SL, Fonseca V, Hes M, LaMoreaux L, Garofalo E.: Gabapentin for the symptomatic treatment of painful neuropathy in patients with diabetes mellitus: a randomized controlled trial. JAMA 280, 1831-1836 (1998). Department of Neurology, University of Wisconsin, Madison 53792, USA. [email protected] CONTEXT: Pain is the most disturbing symptom of diabetic peripheral neuropathy. As many as 45% of patients with diabetes mellitus develop peripheral neuropathies. OBJECTIVE: To evaluate the effect of gabapentin monotherapy on pain associated with diabetic peripheral neuropathy. DESIGN: Randomized, double-blind, placebo-controlled, 8-week trial conducted between July 1996 and March 1997. SETTING: Outpatient clinics at 20 sites. PATIENTS: The 165 patients enrolled had a 1- to 5-year history of pain attributed to diabetic neuropathy and a minimum 40-mm pain score on the Short-Form McGill Pain Questionnaire visual analogue scale. INTERVENTION: Gabapentin (titrated from 900 to 3600 mg/d or maximum tolerated dosage) or placebo. MAIN OUTCOME MEASURES: The primary efficacy measure was daily pain severity as measured on an 11-point Likert scale (0, no pain; 10, worst possible pain). Secondary measures included sleep interference scores, the Short-Form McGill Pain Questionnaire scores, Patient Global Impression of Change and Clinical Global Impression of Change, the Short Form-36 Quality of Life Questionnaire scores, and the Profile of Mood States results. RESULTS: Eighty-four patients received gabapentin and 70 (83%) completed the study; 81 received placebo and 65 (80%) completed the study. By intent-to-treat analysis, gabapentin-treated patients’ mean daily pain score at the study end point (baseline, 6.4; end point, 3.9; n = 82) was significantly lower (P/=50% and /=70% carotid stenoses, symptomatic stenoses (peak systolic velocity higher than the corresponding mean value +2 SDs of 104 normal subjects), and occlusions of the middle cerebral or basilar artery previously assessed by ultrasound. The sonographer was not aware of angiographic findings. RESULTS--TCCS would have detected all 31 of >/=50% intracranial stenoses with 1 false-positive and 35 of 38 /=50%//=155/>/=120 cm/s (anterior cerebral artery), >/=220/>/=155 cm/s (middle cerebral artery), >/=145/>/=100 cm/s (posterior cerebral artery), >/=140/>/=100 cm/s (basilar artery), and >/=120/>/=90 cm/s (vertebral artery). CONCLUSIONS--TCCS may reliably assess >/=50% and or = 3) with or without low-dose aspirin (75 mg per day) was significantly more effective (P < 0.001 by the log-rank test) than treatment with low-intensity warfarin (producing an international normalized ratio of < 3) with or without low-dose aspirin or treatment with aspirin alone in preventing further thrombotic events (recurrence rates per patient-year, 0.013, 0.23, and 0.18, respectively). The rate of recurrence of thrombosis was highest (1.30 per patient-year) during the first six months after the cessation of warfarin therapy. Complications involving bleeding occurred in 29 patients during warfarin therapy and were severe in 7 (0.071 and 0.017 occurrence per patient-year, respectively). CONCLUSIONS. The risk of recurrent thrombosis in patients with the antiphospholipid-antibody syndrome is high. Long-term anticoagulation therapy in which the international normalized ratio is maintained at or above 3 is advisable in these patients.

974

Referenz 514a (Neurologie, 11. Auflage) Khanlou H; Eiger G. Long-term remission of refractory stiff-man syndrome after treatment with intravenous immunoglobulin. Mayo Clin Proc 74; 1231-1232, 1999. Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA. The stiff-man syndrome is a rare neuromuscular disorder characterized by progressive rigidity, stiffness, and intermittent spasm of axial and extremity muscles. Its etiology is unknown. Different therapeutic regimens have been used with variable success. We present a case of refractory stiff-man syndrome, in which the symptoms were successfully controlled by the administration of intravenous immunoglobulin (IVIg). This case gives evidence that IVIg can be a safe and an efficient treatment of refractory stiff-man syndrome. The exact indication for and the cost-effectiveness of IVIg in the treatment of this rare entity remain to be determined.

975

Referenz 515 (Neurologie, 11. Auflage) Kieffer SA, Binet EF, Davis DO , Gabrielsen TO, Kido DK, Latchaw RE, Turski PA, Shaw DD. Lumbar myelography with iohexol and metrizamide: a comparative multicenter prospective study. Radiology 151. 665-670, 1984 Diagnostic quality of radiographs and adverse reactions associated with the use of metrizamide and iohexol as contrast agents in lumbar myelography were compared in a prospective randomized double blind study in 350 patients at seven centers. The contrast media were administered in comparable volumes at a concentration of 180 mg I per ml. Overall quality of radiographic visualization was graded good or excellent in 95% of 175 metrizamide studies and in 98% of 175 iohexol studies. Ninety-three patients examined using metrizamide (53%) and 130 patients examined using iohexol (74%) experienced no discomfort during or after myelography. Postmyelographic headache was associated with 38% of metrizamide examinations and 21% of iohexol examinations. Nausea and vomiting were also more common with metrizamide. Five patients examined using metrizamide (3%) experienced transient confusion and disorientation following lumbar myelography. No such reactions were observed following iohexol myelography. Publication Types: * Clinical trial * Randomized controlled trial

976

Referenz 516 (Neurologie, 11. Auflage) Kilpatrick Christine J, Davis SM, Tress BM, Rossiter SC, Hopper JL, Vandendriesen ML. Epileptic seizures in acute stroke. Arch Neurol 47: 157-160, 1990 Department of Neurology, Royal Melbourne Hospital, Victoria, Australia. We evaluated prospectively the incidence of early seizures in 1000 consecutive patients with stroke and transient ischemic attacks to determine whether seizure occurrence correlates with stroke type, pathogenesis, or outcome. Seizures occurred in 44 patients (4.4%; SE, 0.7%), including 10 (15.4%) of 65 (SE, 4.5%) with lobar or extensive hemorrhage, 6 (8.5%) of 71 (SE, 3.3%) with subarachnoid hemorrhage, 24 (6.5%) of 370 (SE, 1.3%) with cortical infarction, and 4 (3.7%) of 109 (SE, 1.8%) with hemispheric transient ischemic attacks. Lacunar infarcts and deep hemorrhages were not associated with seizures. Arteriovenous malformation was a common cause of lobar hemorrhage with early seizures, but in cortical infarcts there was no association between seizure occurrence and pathogenesis. Seizures generally occurred within 48 hours of stroke onset, were usually single, partial, and readily controlled. Seizures were not associated with a higher mortality or worse functional outcome.

977

Referenz 517 (Neurologie, 11. Auflage) Kim RC, Smith HR, Henbest ML, Choi BH. Nonhemorrhagic venous infarction of the spinal cord. Ann Neurol 15: 379-385, 1984 A 71-year-old man experienced gradually progressive leg weakness, urinary retention, and mild loss of sensation in dermatomes T8 through T12 bilaterally. After 5 to 6 weeks of illness, he developed flaccid paraplegia and sensory loss below T8. He died 16 weeks after onset of neurological symptoms. Neuropathologically, there was widespread, subtotal necrosis of the spinal cord, largely of nonhemorrhagic character, from T8 downward. Dorsal and anterior median spinal veins were occluded by a partially organized thrombus. Comparison of this case with 19 previously recorded examples of venous infarction of the spinal cord (8 hemorrhagic, 7 nonhemorrhagic, and 4 embolic) suggests major differences in clinical presentation, rate of progression, and length of survival among the three groups.

978

Referenz 517a (Neurologie, 11. Auflage) Kimber J., Mitchell D., Mathias C.J.: Chronic cough in the Holmes-Adie syndrome: association in five cases with autonomic dysfunction. J. Neurol. Neurosurg. Psychiatry 65, 583-586 (1998). Division of Neuroscience and Psychological Medicine, Imperial College School of Medicine, National Hospital for Neurology and Neurosurgery, London, UK. The Holmes-Adie syndrome consists of unilateral or bilateral tonic pupils with near light dissociation and tendon areflexia. It is associated with autonomic disturbances affecting sudomotor and vasomotor function. Five such patients are reported on who also had a troublesome chronic dry cough, which was of unknown aetiology and was resistant to a range of treatments. The cough may be related to involvement of afferent or efferent pathways in the vagus. Chronic cough may be an accompaniment in the Holmes-Adie syndrome, like other forms of autonomic dysfunction.

979

Referenz 517b (Neurologie, 11. Auflage) Kimber J.R., Watson L, Mathias C.J.: Distinction of idiopathic Parkinson’s disease from multiple-system atrophy by stimulation of growth-hormone release with clonidine. Lancet 349, 1877-1881 (1997). University Department of Clinical Neurology, National Hospital for Neurology and Neurosurgery/Institute of Neurology, London, UK. BACKGROUND: Idiopathic Parkinson’s disease is a common neurodegenerative disease that is difficult to distinguish from other parkinsonian syndromes such as multiple-system atrophy (MSA). In MSA, autonomic dysfunction is common and is associated with either parkinsonian or cerebellar features, or both. Differentiation of idiopathic Parkinson’s disease from MSA is important because prognosis, complications, and response to therapy vary according to disorder. Our aim was to find out whether clonidine/growth hormone (GH) testing distinguishes idiopathic Parkinson’s disease from MSA. METHODS: Clonidine is a centrally active alpha 2-adrenoceptor agonist that raises concentrations of GH in serum in healthy people and those with pure autonomic failure (with peripheral lesions), but not in those with MSA (with a central autonomic deficit). We investigated the effects of clonidine on 14 people with idiopathic Parkinson’s disease (without autonomic deficits). 31 people with MSA of the three different clinical forms (parkinsonian, cerebellar, and mixed), 19 people with pure autonomic failure, and 27 healthy participants. In nine people with parkinsonian MSA (MSA-P), the GH response to levodopa was also assessed. FINDINGS: Clonidine raised serum GH concentrations in patients with idiopathic Parkinson’s disease (median increase 8.98 [IQR 6.6-16.6] mU/L), normal participants (13.2 [7.0-18.6] mU/L), and patients with pure autonomic failure (12.5 [5.6-18.2] mU/L). In those with MSA who had central autonomic failure, GH concentrations were unchanged (MSA-P; 0.41 [-0.30 to 2.09] mU/L and cerebellar MSA [MSA-C] 1.67 [0-4.49] mU/L). The GH response to clonidine in idiopathic Parkinson’s disease was significantly different from that in MSA-P (p < 0.0002). In MSA-P, the dopamine precursor levodopa raised GH concentrations (from mean 2.7 [SE 1.0] mU/L to mean 18.2 [6.0] mU/L, p < 0.05) and GH-releasing hormone (GHRH) concentrations (from mean 20.6 [3.25] ng/L to mean 68.0 [10.6] ng/L, p < 0.05), excluding dysfunction of pituitary somatotrophs or GHRH neurons as a cause for the absent GH response to clonidine in MSA. INTERPRETATION: The GH responses to clonidine clearly differentiated idiopathic Parkinson’s disease from MSA-C and MSA-P. Together with the levodopa studies they indicated a specific alpha 2-adrenoceptor-hypothalamic deficit in MSA. The clonidine-GH test may provide further insight into central neurotransmitter and alpha 2-adrenoceptor-hypothalamic abnormalities in MSA.

980

Referenz 518 (Neurologie, 11. Auflage) Kimura J. Electrodiagnosis in diseases of nerve and muscle. 2nd edition. FA Davis Company, Philadelphia, 1989

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Referenz 518a (Neurologie, 11. Auflage) King MA, Newton MR, Jackson GD, Fitt GJ, Mitchell LA, Silvapulle MJ, Berkovic SF. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. Lancet 352; 1007-1012, 1998. Department of Medicine, University of Melbourne, Victoria, Australia. BACKGROUND: Prognosis and treatment of the first seizure depends on identification of a specific epilepsy syndrome, yet patients with first seizures are generally regarded as a homogeneous group. We studied whether it is possible to diagnose specific epilepsy syndromes promptly by use of standard clinical methods, electroencephalography (EEG) and magnetic resonance imaging (MRI). METHODS: 300 consecutive adults and children presented with unexplained seizures. We systematically collected clinical data from patients and witnesses, and attempted to obtain an EEG within 24 h of the seizure. Where the EEG was negative, a sleep-deprived EEG was done. MRI was done electively. FINDINGS: A generalised or partial epilepsy syndrome was clinically diagnosed in 141 (47%) patients. Subsequent analysis showed that only three of these clinical diagnoses were incorrect. Addition of the EEG data enabled us to diagnose an epilepsy syndrome in 232 (77%) patients. EEG within 24 h was more useful in diagnosis of epileptiform abnormalities than later EEG (51 vs 34%). Neuroimaging showed 38 epileptogenic lesions, including 17 tumours. There were no lesions in patients for whom generalised epilepsy was confirmed by EEG. Our final diagnoses were: generalised epilepsy (23% of patients); partial epilepsy (58%); and unclassified (19%). INTERPRETATION: An epilepsy syndrome can be diagnosed in most first-seizure patients. Ideally, an EEG should be obtained within 24 h of the seizure followed by a sleep deprived EEG if necessary. MRI aids diagnosis and should be done for all patients except for those with idiopathic generalised epilepsies and for children with benign rolandic epilepsy.

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Referenz 519 (Neurologie, 11. Auflage) Klawans HL, Nausieda PA, Goetz CC, Tanner CM, Weiner WJ. Tourette-like symptoms following chronic neuroleptic therapy. Adv Neurol 35: 415-418, 1982 No abstract available.

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Referenz 520 (Neurologie, 11. Auflage) Klawans HL, Tanner CM, Barr A. The reversibility of "permanent" tardive dyskinesia. Clin Neuropharmacol 7: 153-159" 1984 Neuroleptic-induced tardive dyskinesia (TD) that persists for 1 year or more following withdrawal of neuroleptics is usually said to be permanent. Early spontaneous remissions have been well described but most such remissions occurred within the first few months following neuroleptic withdrawal, and no published studies have followed patients for more than 2 years to evaluate permanence of remission. Over the last 12 years, we studied six patients with TD who, on prolonged follow-up, were found to have complete remission of their abnormal movements after a neuroleptic-free period of more than 2 years (2 1/2-5 years). All six patients were 61 years old or younger when their TD was diagnosed and their neuroleptics withdrawn. In five of the patients, remission occurred while the patients were not taking medication for the movements, while one patient had been on long-term, high-dose (2 mg/day) reserpine therapy for more than 3 years. The incidence of late remission of TD is not known and cannot be estimated from these selected patients, but these cases demonstrate that persistence of abnormal movements of TD for 2 or more years following neuroleptic withdrawal does not imply permanence in all patients. We suggest that TD be considered a persistent rather than an invariably permanent disorder.

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Referenz 520a (Neurologie, 11. Auflage) Kleihues P, Cavenee WK (Editors). Pathology and Genetics of Tumours of the Nervous System. Int. Soc. of Neuropathology, 1997

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Referenz 520b (Neurologie, 11. Auflage) Klein C., Vieregge P.: Nichtepileptische paroxysmale Bewegungsstörungen. Nervenarzt 69, 647-659 (1998). Klinik fur Neurologie,f1p4izinischen Universitat zu Lubeck. Non-epileptic paroxysmal dyskinesias present with different forms of extrapyramidal hyperkinesias (dystonia, chorea, athetosis, ballism) in variable combinations and with cerebellar signs, respectively. They may be classified as: 1. paroxysmal dystonias/choreoathetoses (paroxysmal dystonic choreoathetosis = PDC), paroxysmal kinesigenic choreoathetosis = PKC, intermediate form) and 2. paroxysmal ataxias (PA) (PA with myokymia and neuromyotonia, azetazolamide-responsive PA). Nocturnal paroxysmal dystonia is now regarded as one form of nocturnal frontal lobe epilepsy. Research in molecular genetics has substantially contributed to the etiologic understanding of paroxysmal dyskinesias: In different families linkage has been successfully completed for PDC (chromosome 2q) and PA (chromosomes 12p, 19p). PA are now identified as channelopathies with mutations in the potassium channel (PA with myokymia and neuromyotonia) and the calcium channel gene (azetazolamide-responsive PA). Publication Types: * Review * Review, tutorial

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Referenz 521 (Neurologie, 11. Auflage) Klemm E, Tackmann W. Familiäre spastische Spinalanalyse - Klinisches Spektrum und differentialdiagnostische Erwägungen. Fortschr Neurol Psych 59: 176-182, 1991 Neurologische Universitatsklinik Bonn. The familial spastic paraplegia is a rare disorder of the cerebral nervous system characterized by a slowly progressive spasticity of the lower limbs with early or late onset. There are pure and complicated forms. The disease is inherited by an autosomal dominant mode and a recessive one. In this study 6 patients out of 5 families are presented. The clinical variety, genetic aspects, electrophysiological results and differential diagnosis are discussed.

987

Referenz 522 (Neurologie, 11. Auflage) Klockgether T, Döller G, Wüllner U , Petersen D, Dichgans J. Cerebellar encephalitis in adults. J Neurol 240: 17-20, 1993 Neurologische Klinik, Universitat Tubingen, Federal Republic of Germany. We examined 11 adult patients with cerebellar encephalitis (CE) during the acute phase of the disease and at least 12 months later. Five patients were aged between 23 and 31 years, 3 patients between 43 and 44 years and 3 patients between 60 and 64 years. Serological tests gave evidence of Epstein-Barr virus infection in 4 of the 5 young patients. Two patients had serological evidence of varicella-zoster virus reactivation, whereas the serological findings were negative in all other cases. All patients in the younger and middle age groups recovered within 3-30 weeks after onset of CE. If at all, they had only minor cerebellar deficits at the follow-up examination. Magnetic resonance imaging (MRI) examination performed at the follow-up examination was normal in all of them. In contrast, 2 of 3 patients older than 60 years had persistent cerebellar ataxia following CE. In these patients, MRI revealed infratentorial atrophy. Our data show that the clinical spectrum of CE in adults is wider than assumed so far. In addition to typical cases of CE in young male patients with good recovery, CE may also occur in older patients and give rise to persistent cerebellar ataxia.

988

Referenz 523 (Neurologie, 11. Auflage) Klockgether T, Bürk K, Auburger G , Dichgans J. Klassifikation und Diagnostik der degenerativen Ataxien. Nervenarzt 66: 571-581, 1995 Neurologische Universitatsklinik Tubingen. The degenerative ataxias comprise a wide spectrum of neurodegenerative diseases with varying clinical characteristics and heterogeneous neuropathology. Traditionally, classification of these diseases has been based on neuropathological criteria. Recently, however, clinical and genetic classifications have gained wide acceptance. These classifications distinguish between hereditary and non-hereditary ataxias. According to their mode of inheritance, the hereditary ataxias are further subdivided into autosomal-recessive and autosomal-dominant ataxias. The non-hereditary ataxias are divided into symptomatic ataxias with an identified cause and idiopathic ataxia with unknown cause. Diagnostic criteria based on history, clinical presentation and a number of laboratory tests have been defined for each category. More extensive ancillary tests are necessary to identify or exclude symptomatic causes of ataxia. Recent molecular genetic research has led to the identification of a number of gene loci and mutations responsible for certain types of hereditary ataxia. Publication Types: * Review * Review, tutorial

989

Referenz 524 (Neurologie, 11. Auflage) Knapp MJ, Knopman DS, Solomon PR, Pendlebury WW, Davis CS, Gracon SI. A 30-week randomized controlled trial of high-dose tacrine in patients with Alzheimer’s disease. JAMA 271: 985-991, 1994 Clinical Research Department, Parke-Davis Pharmaceutical Research Division of Warner-Lambert Company, Ann Arbor, MI 48106-1047. OBJECTIVE--To evaluate the efficacy and safety of high-dose tacrine hydrochloride over 30 weeks in patients with probable Alzheimer’s disease. DESIGN--A 30-week randomized, double-blind, placebo-controlled, parallel-group trial. SETTING--Outpatients at 33 US centers. PATIENTS--Men and women at least 50 years of age with mild to moderate Alzheimer’s disease and otherwise in good health. INTERVENTIONS--Group 1 received placebo; group 2 received 40 mg/d of tacrine for 6 weeks, then 80 mg/d for 24 weeks; groups 3 and 4 received 40 mg/d of tacrine for 6 weeks, 80 mg/d for 6 weeks, and 120 mg/d for 6 weeks. Group 3 remained on a dosage of 120 mg/d for a total of 18 weeks; after 6 weeks at 120 mg/d, group 4 titrated to 160 mg/d for the last 12 weeks. PRIMARY OUTCOME MEASURES--Clinician Interview-Based Impression (CIBI), Alzheimer’s Disease Assessment Scale--Cognitive subscale (ADAS-Cog), and Final Comprehensive Consensus Assessment (FCCA). RESULTS--A total of 663 patients entered the study; 653 patients were included in an intent-to-treat (ITT) analysis; 263 had evaluable data at 30 weeks. The results of the ITT analysis revealed significant (P < or = .05) dose-response trends and between-group comparisons on CIBI and ADAS-Cog. In evaluable patients, significant dose-response trends were observed for all three primary measures (P < or = .001). Significant differences in favor of 160 mg/d of tacrine vs placebo were observed on the CIBI (P < or = .002) and ADAS-Cog and FCCA (P < or = .001), as well as caregiver-global and quality-of-life assessments (P < or = .05). On the CIBI, 23% and 42% of tacrine-treated patients in the ITT and evaluable-patient populations, respectively, were rated improved compared with 17% and 18% of placebo patients, respectively. The primary reasons for withdrawal of tacrine-treated patients were asymptomatic liver transaminase elevations (28%) and gastrointestinal complaints (16%). These adverse events were reversible on discontinuation of treatment, and many patients were able to restart tacrine. CONCLUSIONS--Tacrine produced statistically significant, dose-related improvements on objective performance-based tests, clinicianand caregiver-rated global evaluations, and measures of quality of life. There was no evidence that the large number of patient withdrawals biased the overall conclusions of the study. Publication Types: * Clinical trial * Multicenter study * Randomized controlled trial

990

Referenz 525 (Neurologie, 11. Auflage) Knochel JP. Central nervous system manifestations of hypophosphatemia and phosphorus depletion. In Arieff AI, Griggs RC (Editors). Metabolic brain dysfunction in systemic disorders. Little, Brown and Company, Boston, 183-204, 1992

991

Referenz 526 (Neurologie, 11. Auflage) Knochel JP. Hypophosphatemia and rhabdomyolysis (Editorial). Am J Med 92: 455-457, 1992 No abstract available.

992

Referenz 526a (Neurologie, 11. Auflage) Koch C., Hansen H.C., Westphal M. , Kucinski T, Zeumer H. Die kongestive Myelopathie durch spinale durale arteriovenöse Fisteln. Nervenarzt 69, 279-286 (1998). Abteilung fur Neuroradiologie, Universitats-Krankenhaus Eppendorf, Hamburg. Congestive myelopathy, formerly referred to as varicosis spinalis or Foix-Alajouanine syndrome, is caused by a spinal dural arteriovenous fistula (SDAVF). So far, the blood supply from the meningeal arteries draining through the fistula into the medullary venous system can only be verified by spinal angiography. Patients predominantly male and over the age of 60 are afflicted. Initially reversible functional disorders caused by the congestion of the spinal cord veins eventually become irreversible, the most common symptom being an increasingly paretic gait disorder, the signs of which generally begin symmetrically and progress from distal to proximal signs. Simultaneously, predominantly transverse sensory dysfunctions develop, as well as bladder and bowel dysfunctions, most often leading to incontinence. MRI typically shows a central medullary signal enhancement with slight swelling of the afflicted region, initially indicative of a reversible congestive edema and later of an irreversible infarction, and extended perimedullar vessels. Thus, if the clinical course and the characteristic MRI findings suggest the possibility of disease related to congestive myelopathy, spinal angiography becomes indispensable. Since ensuing the success of therapy and prognosis depends on rapid determination of the extent of the illness, a speedy diagnostic reaction is mandatory to institute the treatment necessary to prevent paraplegia.

993

Referenz 527 (Neurologie, 11. Auflage) Koch J, Klotz JM, Kahle G , Langohr HD. Einseitige kaudale Hirnnervenlähmungen bei extrakraniellen Karotisdissektionen. Fortschr Neurol Psychiat 62, 46-49, 1994 Klinik fur Neurologie und Neurophysiologie, Stadt. Klinikum Fulda. Focal cerebral ischemic symptoms, Horner’s syndrome and mostly ipsilateral headache are the characteristic clinical triad of extracranial carotid artery dissection. Lower cranial nerve palsies seem to be uncommon and rare. By means of two cases with identical clinical symptoms and of a literature review we make clear, that ipsilateral lower cranial nerve palsies, especially a hypoglossal nerve palsy, are not uncommon. Without focal cerebral ischemic symptoms they can be the only sign of extracranial carotid artery dissection. Computed tomography of the skull base with regard to the high cervical internal carotid artery is as an usually quickly available examination an alternative to magnetic resonance imaging. Publication Types: * Review * Review of reported cases

994

Referenz 528 (Neurologie, 11. Auflage) Koenig E, Thron A, Schrader V Dichgans J. Spinal arteriovenous malformations and fistulae: clinical, neuroradiological and neurophysiological findings. J Neurol 236: 260-266, 1989 Neurologische Klinik, Universitat Tubingen, Federal Republic of Germany. Twenty-six patients with myelographic signs suggestive of a spinal arteriovenous malformation (AVM) were examined neurologically and neurophysiologically. By selective spinal angiography it was possible to differentiate between dural arteriovenous fistulae (dAVF 20 patients) and intradural AVMs (iAVM, 6 patients). Initial complaints were nonspecific and variable, mainly consisting of sensory disorders and muscle weakness. Later, patients suffered involvement of both the upper and lower motor neurons. There was a high percentage of lower motor neuron lesions (95%), especially in dAVF patients, which were mostly of widespread distribution and included several myotomes. Electrophysiological examination regularly revealed lower neuron involvement, frequently with pathological spontaneous activity in several myotomes, pathological sensory-evoked potentials after tibial nerve stimulation, but normal sensory conduction velocities of the sural nerve, indicating sparing of the sensory ganglion. Frequently there was a discrepancy between the localization of the dural fistula or angioma and the spinal level responsible for clinical symptoms. This suggests that it may be the inadequacy of the venous drainage system to cope with the blood volume rather than the AV-shunt that is responsible for the symptoms. An early diagnosis is essential, as removal of the shunt before there has been progression to severe neurological deficits (paraplegia) is the only way to ensure a satisfactory outcome.

995

Referenz 529 (Neurologie, 11. Auflage) Koepp M, Kern A, Schmidt D. Electrocardiographic changes in patients with brain tumors. Arch Neurol 52: 152-155, 1995 Department of Neurology, Universitatsklinikum Rudolf Virchow, Freie Universitat, Berlin, Germany. OBJECTIVE: Electrocardiographic (ECG) abnormalities in patients with cerebral tumors involving the limbic system without known organic heart disease. DESIGN: Retrospective survey. SETTING: A university hospital in Berlin, Germany. PATIENTS: From among 169 consecutive patients with brain tumors, 57 patients were excluded on the basis of preexisting cardiac or other diseases and 27 patients were excluded because neuroimaging revealed multiple lesions or suggestive evidence of raised intracranial pressure. MAIN OUTCOME MEASURES: We compared ECG changes in 85 otherwise healthy patients with limbic and extralimbic brain tumors without evidence of increased intracranial pressure. Tumors were localized by magnetic resonance imaging and, in 15 cases, by computed tomography. Categorization of patients into limbic and extralimbic system groups was specified before routine preoperative ECGs were examined and classified by an independent cardiologist. RESULTS: Electrocardiographic changes were found in 40% of all patients. Abnormal ECG results were associated nearly three times more often with tumors located in the limbic system compared with extralimbic locations (72% vs 27%). Prolonged QTc intervals were significantly more frequent in the limbic system group than in the extralimbic group (mean rates, 113.3% vs 103.6%). CONCLUSIONS: Lesions of limbic structures do exert cardioarrhythmogenic effects and may provide an explanation for ECG abnormalities in patients with cerebral tumors.

996

Referenz 529a (Neurologie, 11. Auflage) Kohler A., Chofflon M., Sztajzel R, Magistris MR.: Cerebrospinal fluid in acute peripheral facial palsy. J. Neurol. 246, 165-169 (1999). Clinique de Neurologie, Hopital Cantonal Universitaire, Geneva, Switzerland. Cerebrospinal fluid (CSF) is rarely analyzed in peripheral facial palsy, and reports in the literature are scarce. We report the CSF findings in 265 patients with acute isolated peripheral facial palsy. The CSF findings were abnormal in 11% of 230 patients with idiopathic peripheral facial palsy, in 60% of 17 patients with Ramsay Hunt syndrome (pleocytosis), in 25% of 8 patients with Lyme disease, in all of 8 patients with HIV infection, and in 2 other patients (sarcoidosis and herpes simplex). We conclude from this large series that the CSF is usually normal in idiopathic peripheral facial palsy. If the CSF is abnormal, a specific cause should be sought.

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Referenz 530 (Neurologie, 11. Auflage) Kokmen E. Dementia - Alzheimer type. Mayo Clin Proc 59: 35-42, 1984 At least half of the patients who present with progressive decline in their memory, cognitive, and intellectual abilities will eventually be diagnosed as having Alzheimer’s disease. The diagnosis is reached by clinical and ancillary evaluation and exclusion of all other causes of dementia. Recently, considerable advances have been made in our understanding of the neurobiologic features of Alzheimer’s disease. Cortical neurons contain paired helical filaments with a very specific electron microscopic appearance. These filaments contain proteins with unusual properties. A severe decline in cholinergic activity in the cortex is related to a marked loss of cholinergic neurons in deep cerebral structures, such as the nucleus basalis of Meynert in the substantia innominata. No specific treatment is available for Alzheimer’s disease. Patients and the relatives who take care of them require substantial help and assistance in coping with the disease.

998

Referenz 530a (Neurologie, 11. Auflage) Kokontis L, Gutmann L. Current treatment of neuromuscular diseases. Arch Neurol 57; 939-943, 2000. No abstract available.

999

Referenz 531 (Neurologie, 11. Auflage) Koller F, Neuhaus K. Internistische Notfallsituationen. Thieme, Stuttgart, 1987

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Referenz 532 (Neurologie, 11. Auflage) Koller WC, Busenbark K, Miner K, Essential Tremor Study Group. The relationsship of essential tremor to other movement disorders: report on 678 patients. Ann. Neurol. 35: 717-723, 1994 Department of Neurology, University of Kansas Medical Center, Kansas City 66160-7314. We examined 678 essential tremor patients in specialty, university, and private practice clinics. The mean age of patients was 65.2 years with a similar number of men and women. Six percent of patients were left-handed. A positive family history of tremor was reported in more than 60% of patients. Alcohol ingestion was reported to decrease tremor in 74% of patients who were cognizant of the effect of alcohol on tremor. Mean age at tremor onset was 45.3 years. An earlier onset of tremor was observed in those patients having a positive family history of tremor. Tremor affected the hands in 90% of patients, head in 50%, voice in 30%, and legs and chin in 15%. Functional disability was common and impairment at work occurred in 18%. Propranolol and primidone were the most frequently used drugs and were effective in 40% of patients. Six and one-tenth percent of essential tremor patients had concomitant Parkinson’s disease, 6.9% had a coexisting dystonia, and 1.8% had myoclonus. It is concluded that the frequency of Parkinson’s disease in essential tremor is more than would be reported in the general population and that other movement disorders are infrequently observed in essential tremor. Publication Types: * Multicenter Study

1001

Referenz 533 (Neurologie, 11. Auflage) Kölmel HW, Paal G, Drings P. Meningosis leucaemica des Erwachsenen. Klinik, Liquorcytologie, Therapie. Nervenarzt 44: 527-536, 1973 No abstract available.

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Referenz 534 (Neurologie, 11. Auflage) Kömpf D, Engelhardt A, Dietrich HJ, Neundorfer B. Die akute cerebelläre Encephalitis im Erwachsenenalter. Nervenarzt 56: 431 -439, 1985 Two cases of rare adult cerebellar encephalitis are reported presenting the distinguishing features of acute onset of cerebellar ataxia, distinct ocular oscillations (opsoclonus, ocular flutter, macro square wave jerks) and generalized myoclonic jerks. The EOG-analysis of the cerebellar oculomotor disorder is emphasized. The course is usually benign ("benign encephalitis") differing from the childhood form only in age of onset. Fatal courses are rare and the histopathologic findings in one case suggest mild encephalitis with diffuse perivascular lesions accentuated in the cerebellum, thus not allowing clear clinicotopodiagnostic correlations.

1003

Referenz 534a (Neurologie, 11. Auflage) Kompoliti K, Goetz CG, Boeve BF Maraganore DM, Ahlskog JE, Marsden CD, Bhatia KP, Greene PE, Przedborski S, Seal EC, Burns RS, Hauser RA, Gauger LL, Factor SA, Molho ES, Riley DE. Clinical presentation and pharmacological therapy in corticobasal degeneration. Arch. Neurol. 55, 957-961 (1998). Rush-Presbyterian-St Luke’s Medical Center, Chicago, Ill 60612, USA. [email protected] BACKGROUND: To date, to our knowledge, there is no systematic presentation of treatment outcome in large series of patients clinically diagnosed as having corticobasal degeneration. OBJECTIVE: To evaluate the clinical presentation and treatment outcome of patients clinically diagnosed as having corticobasal degeneration. SUBJECTS: We gathered case patients seen in 8 major movement disorder clinics during the last 5 years who were diagnosed as having corticobasal ganglionic degeneration. METHODS: Using a chart review method, we recorded the clinical presentation, medications used, response to medications, and adverse effects. RESULTS: A total of 147 case patients were reviewed, 7 were autopsy proven. Parkinsonian features were present in all, other movement disorders in 89%, and higher cortical dysfunction in 93%. The most common parkinsonian sign was rigidity (92%), followed by bradykinesia (80%), gait disorder (80%), and tremor (55%). Other movement disorders were dystonia in 71% and myoclonus in 55%. Higher cortical dysfunction included dyspraxia (82%), alien limb (42%), cortical sensory loss (33%), and dementia (25%). Ninety-two percent of the case patients received dopaminergic drugs, which resulted in a beneficial effect for 24%. Parkinsonian signs were the elements improving the most and levodopa was the most effective drug. Benzodiazepines, primarily clonazepam, were administered to 47 case patients, which resulted in improvement of myoclonus in 23% and dystonia in 9%. The most frequent disabling adverse effects of drug trials in these case patients were somnolence (n = 24), gastrointestinal complaints (n = 23), confusion (n = 16), dizziness (n =12), hallucinations (n = 5), and dry mouth (n = 5). CONCLUSIONS: Pharmacological intervention was largely ineffective in the management of corticobasal degeneration, and new treatments are needed for ameliorating the symptoms of this syndrome. Publication Types: * Clinical Trial * Controlled Clinical Trial * Multicenter Study

1004

Referenz 536 (Neurologie, 11. Auflage) Konstanzer A, Ceballos-Baumann AO, Dressnandt J, Conrad B. Lokale Injektionsbehandlung mit Botulinum-Toxin A bei schwerer Arm- und Beinspastik. Nervenarzt 64, 517-523, 1993 Neurologische Klinik und Poliklinik, Technischen Universitat Munchen. In patients with predominantly focal spasticity, oral antispastic drugs are relatively ineffective or cause unwanted side effects of central origin. Therefore we treated patients disabled by focal spasticity with local injections of Botulinum-Toxin A (Porton Products BOTOX). Efficacy, dosage, side-effects and injection technique were examined. 11 patients (mean age 48 years) with severe focal spasticity of the flexor muscles of the hand and arm (5 patients), the adductor muscles of the legs (5) or the plantar flexors of the foot (1) due to multiple sclerosis, cervical myelopathy or stroke-related hemi-paresis were treated with BOTOX. Rating scales, including Ashford spasticity scale, pain scale and a hygienic rating scale, were used to evaluate the efficacy. 25 to 30 ng (1000-1200 MU Porton) were injected in the flexor group of the hand or arm and 42 to 50 ng (1680-2000 MU Porton) BOTOX in the adductor group of one leg. 10 of the patients showed an improvement of at least one point on the scales for spasticity, pain and hygiene. Effects could be observed after 4-7 days and lasted for 6-13 weeks. There were no unwanted side-effects. We conclude that BOTOX is an alternative to the systemic application of antispastic drugs. Focal spasticity and pain can be successfully reduced and hygienic care is facilitated.

1005

Referenz 537 (Neurologie, 11. Auflage) Kopell HP, Thompson WA. Peripheral Entrapment Neuropathies. rev. ed. Krieger Publishing Co., Melbourne FL USA, 1976

1006

Referenz 538 (Neurologie, 11. Auflage) Kopitnik TA, Samson DS. Management of subarachnoid haemorrhage. J Neurol Neurosurg Psychiat 56: 947-959, 1993 Review. No abstract available.

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Referenz 538a (Neurologie, 11. Auflage) Kori SH, Foley KM, Posner JB. Brachial plexus lesions in patients with cancer: 100 cases. Neurology (Minneap.) 31: 45-50, 1981 In patients with cancer, brachial plexus signs are usually caused by tumor infiltration or injury from radiation therapy (RT). We analyzed 100 cases of brachial plexopathy to determine which clinical criteria helped differentiate tumor from radiation injury. Seventy-eight patients had tumor (34 with previous RT), and 22 had radiation injury. Severe pain occurred in 80% of tumor patients but in only 19% of patients with radiation injury. The lower trunk (C7-8, T1) was involved in 72% of the tumors, and 32% also had epidural tumors. Seventy-eight percent of the radiation injuries affected the upper plexus (C5-6). Horner syndrome was more common in tumor, and lymphedema in radiation injury. The time from RT to onset of plexus symptoms, and the dose of RT, also differed. For symptoms within 1 year of RT, doses exceeding 6000 R were associated with radiation damage, whereas lower doses were associated with infiltration. Therefore, painless upper trunk lesions with lymphedema suggest radiation injury, and painful lower trunk lesions with Horner syndrome imply tumor infiltration.

1008

Referenz 539 (Neurologie, 11. Auflage) Kornhuber J, Weller M. Neuroleptic malignant syndrome. Current Opinion in Neurology 7: 353-357, 1994 Department of Psychiatry, University of Wurzburg, Germany. Neuroleptic malignant syndrome (NMS) was first recognized as a life-threatening complication of dopamine receptor antagonists characterized by extrapyramidal disturbances, hyperthermia, and elevated serum creatine kinase levels. Concepts of NMS have changed because medications other than classic neuroleptic drugs have been implicated as triggering agents and because syndromes identical to NMS have been observed in patients with Parkinson’s disease withdrawn from their medication or suffering akinetic hyperthermic parkinsonian crisis. The neurochemical key features in all these conditions are probably functional dopamine deficiency and ensuing hyperactivity of excitatory amino acid neurotransmission in the basal ganglia and hypothalamus. Recognition of NMS is the most important step in its management; the outcome is good if causative drugs are discontinued or if parkinsonian therapy is readjusted. Supportive care includes management of hyperthermia and fluid replacement. Controversial therapeutic measures include the application of dopamine receptor agonists, excitatory amino acid antagonists, or dantrolene. Psychiatric patients with a history of NMS and psychotic relapse necessitating neuroleptic drugs do not commonly redevelop NMS when reexposed to dopamine receptor antagonists but may be treated most safely with atypical neuroleptic drugs such as clozapine. Publication Types: * Review * Review, Tutorial

1009

Referenz 539a (Neurologie, 11. Auflage) Kothbauer-Margreiter I, Sturzenegger M, Komor J, Baumgartner R, Hess CW. Encephalopathy associated with Hashimoto thyroiditis: diagnosis and treatment. J Neurol 243; 585-593, 1996. Neurologische Klinik, Inselspital, Bern, Switzerland. Six patients with Hashimoto thyroiditis (HT) and associated encephalopathy (HE) are described and compared with 14 well-documented cases retrieved from the literature. HE typically affects patients when they are euthyroid and, in an appropriate clinical situation, antithyroid autoantibodies are the main indicators of HE. Since clinical features of HE are unspecific, other aetiologies such as infectious, metabolic, toxic, vascular, neoplastic, and paraneoplastic causes have to be excluded. Our own six cases and those from the literature show that two types of initial clinical presentation can be differentiated: a vasculitic type with stroke-like episodes and mild cognitive impairment in nine patients, and a diffuse progressive type with dementia, seizures, psychotic episodes or altered consciousness in 11 patients. These types may overlap, particularly in the long-term course without treatment. Response to steroids was usually excellent with complete remission in 80%. Eighteen of the 20 patients were women. Characteristic, though unspecific, findings were abnormal EEG (90%) and CSF (80%). Together with quantitative neuropsychological testing, these proved sensitive for monitoring the efficacy of therapy. Conversely, antithyroid autoantibody titres did not correlate with the severity or type of clinical presentation. The link between HE and HT is not clear. A pathogenetic role for antithyroid autoantibodies in the central nervous system seems unlikely. Publication Types: * Review * Review of Reported Cases

1010

Referenz 540 (Neurologie, 11. Auflage) Koudstaal PJ, Algra A, Pop GA, Kappelle LJ, van Latum JC, van Gijn J. The Dutch TIA Study Group. Risk of cardiac events in atypical transient ischaemic attack or minor stroke. Lancet 340: 630-633, 1992 Department of Neurology, University Hospital Rotterdam Dijkzigt, The Netherlands. Proposed guidelines for the diagnosis of transient ischaemic attack (TIA) involve interpretation of symptoms, so it can be very difficult to distinguish a TIA from other disorders, such as migraine, epilepsy, syncope, or neurosis. Atypical cerebral and visual events may be classified as TIA. To see whether TIA or stroke patients with atypical cerebral or visual symptoms are at high or low risk of cardiac complications, we prospectively followed 572 patients (entered into the Dutch multicentre TIA trial) with a diagnosis of TIA or minor ischaemic stroke, but whose symptoms did not fully accord with internationally accepted criteria. We compared their outcome with that of 2555 other TIA or stroke patients in the trial, who had unequivocal symptoms; all patients were treated with aspirin. During mean follow-up of 2.6 years the risk of a major vascular event did not differ between the groups (14.5% in patients with atypical symptoms vs 15.1% of patients with typical attacks). Patients with atypical attacks had a lower risk of stroke (5.6% vs 9.4%, hazard ratio 0.6, 95% confidence interval 0.4-0.9) and a higher risk of a major cardiac event (8.4% vs 5.9%, 1.4, 1.0-2.0) than did patients with typical attacks. These differences could not be explained by differences in cardiac risk factors, and were independent of minor discrepancies in baseline characteristics between the groups. A heavy or tired feeling in one or two limbs was the only atypical symptom associated with cerebral rather than cardiac events (ratio cardiac/cerebral events 0.8). For all other atypical symptoms cardiac events were about twice as common as cerebral events (range 1.3-2.5). Our findings suggest that TIA or minor stroke patients with atypical symptoms may have symptomatic heart disease, especially cardiac arrhythmia. Publication Types: * Clinical Trial * Multicenter Study * Randomized Controlled Trial

1011

Referenz 540a (Neurologie, 11. Auflage) Krauss JK, Toups EG, Jankovic J, Grossman RG.: Symptomatic and functional outcome of surgical treatment of cervical dystonia. J. Neurol. Neurosurg. Psychiatry 63, 642-648 (1997). Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA. OBJECTIVES: Previous studies of surgical treatment for cervical dystonia have reported highly variable rates of postoperative symptomatic benefit and morbidity. Little is known about functional improvement and long term results. This study evaluates the symptomatic and functional outcome of surgical treatment of cervical dystonia in a consecutive series of 46 patients. METHODS: The most affected muscles were selected for denervation after clinical examination and confirmation by four channel EMG studies. Surgical treatment, aiming at selective elimination of pathological activity while preserving normal motor function and avoiding side effects, was achieved by using a broad scope of techniques including intradural denervation, extradural denervation, and myotomy. Rather than carrying out standard operations, the treatment was tailored to the needs of the patient according to the individual pattern of dystonic activity. Long term benefit was assessed with a global outcome score, and a modified Toronto western spasmodic torticollis rating scale (TWSTRS) in those 34 patients who were available for a recent follow up evaluation. RESULTS: The 46 patients underwent a total of 70 procedures with intradural approaches in 33 instances, extradural approaches in 21, and muscle sections (singly or combined) in 22 instances. Transient mild postoperative side effects occurred in 10% of the procedures. The mean duration of long term follow up was 6.5 years. The global outcome was rated as excellent in nine patients (21%), as marked in 12 (27%), as moderate in nine (21%), as mild in nine (21%), and as no improvement in five (11%). A persistent side effect consisting of mild difficulty with balance was noted in one case. There were highly significant changes of the preoperative and postoperative mean values for almost all TWSTRS subscores for severity of cervical dystonia, functional disability, and pain. Patients with excellent outcome underwent a higher number of surgical procedures on average than those patients who achieved no benefit. CONCLUSIONS: Surgical treatment tailored to the specific pattern of dystonic activity in the individual patient is a valuable alternative in the long term management of cervical dystonia. Publication Types: * Clinical Trial

1012

Referenz 540b (Neurologie, 11. Auflage) Kremenchutzky M., Cottrell D., Rice G, Hader W, Baskerville J, Koopman W, Ebers GC: The natural history of multiple sclerosis: a geographically based study. 7. Progessive-relapsing ind relapsing-progressive multiple sclerosis: a reevaluation. Brain 122, 1941-1950 (1999). Department of Clinical Neurological Sciences, University of Western Ontario, London, Canada. Classifications of multiple sclerosis subtypes have been largely based on clinical phenomenology. Nevertheless, definitions of relapse, remission and progression have been imprecise. Recently an international consensus group, as part of a reclassification of disease subtypes, recommended dropping the term ’relapsing-progressive’ (RP) and retaining the term ’progressive-relapsing’ (PR) multiple sclerosis. The term ’RP’ multiple sclerosis had been applied when the early course combined both relapses and progression and was believed to identify some patients with a worse than average outcome. The PR group consisted of patients with primary progressive disease who later in their course developed relapses. Since the terminology has been largely arbitrary, we have evaluated the validity of the terms ’RP’ and ’PR’ multiple sclerosis in the context of long-term outcome within a large population-based cohort of progressive multiple sclerosis patients seen at the London Multiple Sclerosis Clinic (Canada) between 1972 and 1984. Mean follow-up of the entire cohort was 25 years. Designation of RP multiple sclerosis did identify a more rapidly progressive subgroup. To realign these natural history data with consensus recommendations, these patients were reassigned to secondary progressive (SP) or to primary progressive (PP) multiple sclerosis, with progression defined as at least 1 year of progressive deterioration. PP multiple sclerosis patients with relapses after a year were designated as having PR multiple sclerosis. Relapses in primary progressive multiple sclerosis occurred in 27.8% of patients at some point even two to three decades after onset. In general these relapses were mild and remitting, but served to blur the distinction between progressive and relapsing-remitting disease. The long-term outcomes of time to Kurtzke disability scores (DSS) of 3, 6, 8 and 10 were compared among the progressive subtypes. Times to these disability end-points and to death were not different between PR and PP multiple sclerosis. Survival curves for progressive patients have been amended to incorporate the reassignment of PR multiple sclerosis patients into the PP group and the RP multiple sclerosis patients into the PP and SP subgroups. The time to reach DDS 3, 6, 8 and 10 for a population-based cohort of primary and secondary progressive patients resulting from the elimination of the categories of RP multiple sclerosis and PR multiple sclerosis has been established. These results provide justification for retaining only PP and SP multiple sclerosis as the subgroups of progressive disease.

1013

Referenz 541 (Neurologie, 11. Auflage) Kretzschmar HA, Kufer P, Riethmüller G, DeArmond S, Prusiner SB, Schiffer D. Prion protein mutation at codon 102 in an Italien family with Gerstmann-Sträussler-Scheinker syndrome. Neurology 42: 809-810, 1992 Institute of Neuropathology, University of Munich, Germany. We present the first family from Italy with the Gerstmann-Straussler-Scheinker syndrome (GSS) and a substitution of leucine for proline at codon 102 of the prion protein gene. This mutation is associated with the ataxic form of GSS in a number of reported families. The clinical presentation of our family includes amyotrophic changes in some affected family members in addition to ataxia.

1014

Referenz 541a (Neurologie, 11. Auflage) Kreyden OP: Die Giftspritze gegen Schwitzen: Botulinumtoxin A in der Behandlung der fokalen Hyperhidrose. Schweiz. Ärztezeitung 80, 2821-2826 (1999).

1015

Referenz 542 (Neurologie, 11. Auflage) Krick JA, Remington JS. Toxoplasmosis in the adult - an overview. N Engl J Med 298: 550-553, 1978 Review. No abstract available.

1016

Referenz 543 (Neurologie, 11. Auflage) Krivit W, Shapiro E, Kennedy W, Lipton M, Lockman L, Smith S, Summers CG, Wenger DA, Tsai MY, Ramsay NK, et al. Effective treatment of late infantile metachromatic leukodystrophy by bone marrow transplantation. N Engl J Med 332; 28-32, 1990 No abstract available.

1017

Referenz 544 (Neurologie, 11. Auflage) Krumholz A, Niedermeyer E. Psychogenic seizures: a clinical study with follow-up data. Neurology (Minneap.) 33: 498-502, 1983 We evaluated the natural history and prognosis of psychogenic or hysterical seizures in patients discharged from the Johns Hopkins Hospital in the 3 years between 1971 and 1974. Follow-up data were obtained 5 years or more after discharge. Among 41 patients with convincing evidence of psychogenic seizures, there were coexisting organic neurologic disorders in 18 (44%). Mental subnormality or retardation was present in 17% and true epileptic seizures in 37%. EEG abnormalities found in 38% of individuals with psychogenic seizures were attributed to these organic neurologic disorders or anticonvulsant drug toxicity. There was significant long-term morbidity in 56% of these individuals because of psychosocial problems rather than misdiagnosis of psychogenic seizures.

1018

Referenz 544a (Neurologie, 11. Auflage) Krupp LB, Coyle PK, Doscher C, Miller A, Cross AH, Jandorf L, Halper J, Johnson B, Morgante L, Grimson R.: Fatigue therapy in multiple sclerosis: results of a double-blind, randomized, parallel trial of amantadine, pemoline, and placebo. Neurology 45, 1956-1961 (1995). Multiple Sclerosis Comprehensive Care Center, State University of New York (SUNY) at Stony Brook, USA. OBJECTIVE: To determine the relative efficacy of amantadine, pemoline, and placebo in treatment of multiple sclerosis (MS)-related fatigue. BACKGROUND: Fatigue is a complication of MS. Both pemoline and amantadine have been used to treat MS fatigue, but their relative efficacy is not known. METHODS: Amantadine, pemoline, and placebo were compared in a randomized, double-blind, placebo-controlled study using a parallel-group design. Ninety-three ambulatory MS patients completed the study. Primary outcome measures were the fatigue severity scale (FSS); the MS-specific fatigue scale (MS-FS); and subjective response determined by verbal self-report. Secondary outcome measures consisted of assessments of sleep, depression, and vitality. Repeated-measures analysis of variance with planned post-hoc contrasts and Fisher’s exact test were used to compare treatment response. RESULTS: Amantadine-treated patients showed a significantly greater reduction in fatigue, as measured by the MS-FS, than did patients treated with placebo (p = 0.04). By verbal report at the end of the study, 79% of patients treated with amantadine versus 52% treated with placebo and 32% treated with pemoline preferred drug therapy compared with no treatment (p = 0.03). No significant differences in any primary outcome measures were noted between pemoline and placebo. Neither amantadine nor pemoline affected sleep or depression relative to placebo. CONCLUSION: Amantadine was significantly better than placebo in treating fatigue in MS patients, whereas pemoline was not. The benefit of amantadine was not due to changes in sleep, depression, or neurologic disability. Publication Types: * Clinical Trial * Randomized Controlled Trial

1019

Referenz 545 (Neurologie, 11. Auflage) Kryger MH, Roth T, Dement WC (Editors). Principles and Practice of Sleep Medicine, 2nd ed. WB Saunders Company, Philadelphia, 1994

1020

Referenz 546 (Neurologie, 11. Auflage) Kubic C, Adams R. Occlusion of the basilar artery: a clinical and pathologic study. Brain 69: 73-121, 1946

1021

Referenz 547 (Neurologie, 11. Auflage) Kudrow L. Cluster headache. Mechanisms and management. Oxford University Press, London 1980

1022

Referenz 547a (Neurologie, 11. Auflage) Kuhl V, Urban PP, Mayet WJ, Hopf HC.: Isolated trochlear nerve palsy and repetitive Raynaud’s Phenomenon of the tongue in primary Sjögren’s syndrome. J. Neurol. 246, 974-975 (1999). No abstract available.

1023

Referenz 547b (Neurologie, 11. Auflage) Kujowa K., Leurgans S., Raman R, Blasucci L, Goetz CG.: Acute orthostatic hypotension when starting dopamin agonists in Parkinson’s disease. Arch. Neurol. 57, 1461-1463 (2000). Department of Neurological Sciences, Rush-Presbyterian-St Luke’s Medical Center, Chicago, IL, USA. [email protected]. OBJECTIVE: To study the frequency and severity of acute orthostatic hypotension (OH) in patients with Parkinson’s disease who are starting dopamine agonist therapy. PATIENTS AND METHODS: In the context of an outpatient clinical practice, 29 consecutive patients with Parkinson’s disease who were starting dopamine agonist therapy were brought into the clinic for their first dose of agonist. After a baseline supine and standing blood pressure assessment, patients were given a test dose of either pergolide mesylate (0.025, 0.05, 0. 125, or 0.25 mg), pramipexole dihydrochloride (0.125 mg), or ropinirole hydrochloride (0.125 or 0.25 mg). At 3 selected times, blood pressure readings were repeated in the supine and standing positions. MAIN OUTCOME MEASURE: Orthostatic hypotension was defined as a drop in either systolic blood pressure of more than 25 mm Hg or diastolic pressure of more than 10 mm Hg. Patients with OH before the administration of the dopamine agonist were excluded. RESULTS: Ten subjects (34%) met the criteria for acute OH. There was no evidence that OH was related to the use of a specific dopamine agonist or the concurrent use of levodopa. Of the patients who met the criteria for OH, only 3 (30%) had symptoms of OH, such as lightheadedness or general malaise. CONCLUSIONS: Acute OH occurs frequently when starting dopamine agonist therapy in Parkinson’s disease, but is frequently not appreciated by patients. Knowledge of acute blood pressure responses may be useful when making decisions regarding agonist titration schedules in clinical practice. Arch Neurol. 2000;57:1461-1463

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Referenz 548 (Neurologie, 11. Auflage) Kurtz G, Kapfhammer HP, Peuker B. Pisa-Syndrom unter Clozapintherapie. Nervenarzt 64: 742-746, 1993 Psychiatrische Klinik und Poliklinik, Universitat Munchen. Neuroleptic therapy frequently induces undesirable extrapyramidal side effects. The Pisa syndrome is a rare extrapyramidal side effect caused by neuroleptic treatment. Twisting and bending to one side of the upper thorax, the neck and the head are its typical symptoms. These symptoms mainly develop in elderly patients with a history of neuroleptic treatment. To our knowledge there have been no reports of Pisa syndrome occurring during therapy with clozapine--an atypical neuroleptic drug with no major extrapyramidal side effects. We report on 4 female patients suffering from a chronic schizophrenic and/or depressive condition and having been on a long-term neuroleptic treatment. These patients developed a dystonia equivalent to the Pisa syndrome during an acute clozapine therapy. All four women had signs of marked brain atrophy, two of them also showing tardive dyskinesia already prior to the treatment with clozapine. The etiology of the Pisa syndrome is discussed with respect to discontinuation of treatment with classic neuroleptics, coinciding with the beginning of the clozapine therapy, clinical phenomenology, history of medication, course of treatment, and results of cranial computer tomography.

1025

Referenz 549 (Neurologie, 11. Auflage) Kurtzke JF. Rating neurologic impairment in multiple sclerosis: An expanded disability status scale (EDSS). Neurology (Minneap.) 33: 1444-1452, 1983 One method of evaluating the degree of neurologic impairment in MS has been the combination of grades (0 = normal to 5 or 6 = maximal impairment) within 8 Functional Systems (FS) and an overall Disability Status Scale (DSS) that had steps from 0 (normal) to 10 (death due to MS). A new Expanded Disability Status Scale (EDSS) is presented, with each of the former steps (1,2,3 . . . 9) now divided into two (1.0, 1.5, 2.0 . . . 9.5). The lower portion is obligatorily defined by Functional System grades. The FS are Pyramidal, Cerebellar, Brain Stem, Sensory, Bowel & Bladder, Visual, Cerebral, and Other; the Sensory and Bowel & Bladder Systems have been revised. Patterns of FS and relations of FS by type and grade to the DSS are demonstrated.

1026

Referenz 549a (Neurologie, 11. Auflage) Kwiecinski H, Ryniewicz B, Ostrzycki A. Treatment of myotonia with antiarrhythmic drugs. Acta Neurol Scand 86; 371-375, 1992. Department of Neurology, Warsaw Medical Academy, Poland. The effects of disopyramide, phenytoin, mexiletine, and tocainide were compared in 30 patients with myotonic disorders. The severity of myotonia was assessed by clinical and electromyographic criteria at the end of each treatment phase lasting four weeks. Mexiletine (MXT) and tocainide (TCD) were found to be the most potent antimyotonic agents. The antimyotonic efficacy of MXT and TCD is explained by their fast-blocking effect on voltage-dependent sodium channels in the muscle membrane. The benefits of myotonia control with pharmacological agents must be weight against the risk of therapy in the individual patient. Because of the risks of hematologic problems, TCD is not recommended by us for the treatment of myotonia. Publication Types: * Clinical Trial * Randomized Controlled Trial

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Referenz 549b (Neurologie, 11. Auflage) Lacomblez L, Bensimon G, Leigh PN, Guillet P, Meininger V.: Dose-ranging study of riluzole in amyotrophic lateral sclerosis. Amyotrophic Lateral Sclerosis/Riluzole Study Group II. Lancet 347, 1425-1431 (1996). Department of Pharmacology, Hopital de la Pitie-Salpetriere, Paris, France. BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a progressive disease with no effective treatment. In an initial study, riluzole decreased mortality and slowed muscle-strength deterioration in ALS patients. We have carried out a double-blind, placebo-controlled, multicentre study to confirm those findings and to assess drug efficacy at different doses. METHODS: 959 patients with clinically probable or definite ALS of less than 5 years’ duration were randomly assigned treatment with placebo or 50 mg, 100 mg, or 200 mg riluzole daily; randomisation was stratified by centre and site of disease onset (bulbar or limb). The primary outcome was survival without a tracheostomy. Secondary outcomes were rates of change in functional measures (muscle strength, functional status, respiratory function, patient’s assessments of fasciculation, cramps, stiffness, and tiredness). The primary analysis was the comparison of the 100 mg dose with placebo by intention-to-treat. Drug-effect on survival was assessed before (log-rank test) and after adjustment for known prognostic factors (Cox’s model). FINDINGS: At the end of the study, after median follow-up of 18 months, 122 (50.4%) placebo-treated patients and 134 (56.8%) of those who received 100 mg/day riluzole were alive without tracheostomy (unadjusted risk 0.79, p = 0.076; adjusted risk 0.65, p = 0.002). In the groups receiving 50 mg and 200 mg riluzole daily, 131 (55.3%) and 141 (57.8%) patients were alive without tracheostomy (relative to placebo 50 mg adjusted risk 0.76, p = 0.04; 200 mg 0.61, p = 0.0004). There was a significant inverse dose response in risk of death. No functional scale discriminated between the treatment groups. The most common adverse reactions were asthenia, dizziness, gastrointestinal disorders, and rises in liver enzyme activities; they were commonest with the 200 mg dose. INTERPRETATION: Overall, efficacy and safety results suggest that the 100 mg dose of riluzole has the best benefit-to-risk ratio. This study confirms that riluzole is well tolerated and lengthens survival of patients with ALS. Publication Types: * Clinical Trial * Multicenter Study * Randomized Controlled Trial

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Referenz 549c (Neurologie, 11. Auflage) Lalu T, Mercier B, Birouk N, Maisonobe T, Catala M, Le Forestier N, Leger JM, Bouche P: Neuropathies motrice pures post-radiques: 6 cas. Rev. Neurol. 154, 40-44 (1998). Service d’explorations fonctionnelles, Hopital de la Salpetriere, Paris. We report clinical and neurophysiological characteristics of six patients (five women and one man) presenting a pure motor bilateral asymmetric proximal and distal weakness in the setting of radiation therapy for Hodgkin’s lymphoma in four cases, carcinoma of the uterus in one, and cancer of the ovary in one. Motor deficit, amyotrophy, cramps, fasciculations and tendinous areflexia were confined to the lower limbs in five patients and to the upper limbs in one. No sensory or sphincter disturbance was noted. The progression of the disease was slow with sometimes secondary stabilization. In some patients, CSF showed a slight increase in protein content with no cell. Blood and MRI medullary examination were normal. Delay between radiation therapy and onset of neurological symptoms range from 6 to 24 years (mean 15). Neurophysiological findings suggest ventral roots proximal conduction blocks. We found an increase F-waves latency, a complete distal palsy contrasting with persistent muscle action potential after distal stimulation, in most of the patients; and an evidence of a conduction block between the erb point and the cervical roots using magnetic stimulation in the patient with upper limbs involvement. Mechanisms and sites of nerve radiation injury remains still unclear. These data could indicate, as it was already reported, a proximal damage involving predominantly the motor roots.

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Referenz 550 (Neurologie, 11. Auflage) Lance JW, Adams RD. The syndrome of intention or action myoclonus as a sequel to hypoxic encephalopathy. Brain 86: 111-135, 1963

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Referenz 551 (Neurologie, 11. Auflage) Lance JW. Mechanism and Management of Headache, 4th ed. Butterworths, London 1982

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Referenz 551a (Neurologie, 11. Auflage) Lane RJM: Recurrent coital amnesia. J. Neurol. Neurosurg. Psychiatry 63, 260 (1997). No abstract available.

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Referenz 552 (Neurologie, 11. Auflage) Landis T, Cummings JL, Benson DF, Palmer EP. Loss of topographic familiarity. An environmental agnosia. Arch Neurol 43, 132-136, 1986 Sixteen patients manifested the syndrome of loss of environmental familiarity. The syndrome is characterized by an inability to recognize familiar surroundings in spite of relatively intact verbal memory, cognition, and perception. In addition to the loss of environmental familiarity, other clinical disturbances, including central achromatopsia, prosopagnosia, palinopsia, visual hallucinations, dressing disturbances, or impaired revisualization, were present in several cases. Radiologic studies revealed that all patients had right medial temporo-occipital lesions; three had additional left-sided lesions. Clinical observations suggest that the syndrome is a class-specific agnosia similar to prosopagnosia.

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Referenz 553 (Neurologie, 11. Auflage) Lang AE. Akathisia and the restless legs syndrome. In Jankovic J, Tolosa E (eds). Parkinson’s disease and movement disorders. 2nd edition. Williams & Wilkins, Baltimore, 399-418, 1993

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Referenz 553a (Neurologie, 11. Auflage) Langhorne P, Duncan P.: Does the organization of postacute stroke care really matter? Stroke 32, 268-274 (2001). Academic Section of Geriatric Medicine, Royal Infirmary, Glasgow, UK. [email protected] BACKGROUND AND PURPOSE: Postacute rehabilitation stroke services represent a large component of stroke care. In the United States and elsewhere, major changes in the organization and funding of these services are limiting patient access to organized inpatient multidisciplinary care. We conducted a systematic review to evaluate the effectiveness of such services. SUMMARY OF REVIEW: We defined our intervention as organized inpatient multidisciplinary rehabilitation commencing at least 1 week after stroke and sought randomized trials that compared this model of care with an alternative. The analysis was stratified by the particular service characteristics. We identified a heterogeneous group of 9 trials (6 of stroke rehabilitation units; 3 of general rehabilitation wards) recruiting 1437 patients. Organized inpatient multidisciplinary rehabilitation was associated with a reduced odds of death (odds ratio, 0.66; 95% CI, 0.49 to 0.88; P: