Introduction. Diagnosis of vertebrobasilar insufficiency is often diffi- cult; the pathophysiological mechanisms of transient is- chaemic attacks in the ...
Neuroradiology (1998) 40: 164±166 Ó Springer-Verlag 1998
K. Nakamura Y. Saku R. Torigoe S. Ibayashi M. Fujishima
Received: 1 November 1996 Accepted: 7 March 1997
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K. Nakamura ( ) × S. Ibayashi × M. Fujishima Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-82, Japan Tel. +81-92-6 42-52 56; Fax: +81-92-6 42-52 71 K. Nakamura × Y. Saku Department of Cerebrovascular Disease, Institute of Neuroscience, St. Mary's Hospital, Kurume, Japan R. Torigoe Department of Neurosurgery, Institute of Neuroscience, St. Mary's Hospital, Kurume, Japan
D IA G N O S T I C NE UR OR A DI O LO G Y
Sonographic detection of haemodynamic changes in a case of vertebrobasilar insufficiency
Abstract We present a diagnostically challenging case of vertebrobasilar insufficiency caused by head rotation. The patient was a 58year-old man complaining of dizziness and faintness with head rotation to the left. Vertebral arteriography with the head turned to the left revealed mechanical compression of the right vertebral artery at the occipitoatlantal joints and an occluded left vertebral artery. Duplex sonography demonstrated disappearance of the end-diastolic flow signal in the right vertebral artery on head rotation, paralleling the appearance of symptoms. Decompression of the vertebral artery by transversectomy of the atlas and hemilaminectomy of the axis completely
Introduction Diagnosis of vertebrobasilar insufficiency is often difficult; the pathophysiological mechanisms of transient ischaemic attacks in the vertebrobasilar arterial system are more complex than those in the carotid system [1±4], and symptoms of vertebrobasilar insufficiency are often provoked only by certain conditions such as assuming the upright posture or turning the head. Should mechanical compression of the vertebral artery (VA) be the aetiology, decompression of the artery relieves the symptoms in most cases. However, vascular compression has rarely been objectively demonstrated as the cause of symptoms such as dizziness or faintness provoked by head movement [5±10], which makes the clinician hesitate to perform angiography. This can cause delay in detecting surgically correctable lesions. Duplex
relieved the symptoms and the Doppler flow signal pattern of the vertebral artery returned to normal: End-diastolic flow in the right vertebral artery did not disappear even when the head was rotated to the left. Key words Vertebrobasilar insufficiency × Compression, arterial × Ultrasonography × Surgical decompression
sonography, a noninvasive technique, can be useful for investigating the cerebral circulation [11, 12]. We describe a case of vertebrobasilar insufficiency caused by head rotation, in which we attempted to detect haemodynamic changes during the symptoms by use of duplex sonography.
Case report A 58-year-old man first experienced dizziness and faintness when he turned his head to the left 5 years before admission. These symptoms gradually increased in severity. They cleared rapidly when he returned his head to the neutral position. He had a history of hypertension and gout. His blood pressure was 140/88 mm Hg, and his heart rate was 72 beats/min and regular. There was no significant orthostatic hypotension or any bruit in his neck or subclavian regions. Neuro-
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Fig. 1 A±F Right vertebral angiography and Doppler sonographic waveforms. A, D head in neutral position B, E head rotated to left C, F head rotated to the left following surgery. Angiography shows stenosis at the occipitoatlantal level (arrow) when the head is rotated to the left. Mild stenosis is also demonstrated at the atlantoaxial joint level (arrowhead). Postoperatively, the degree of stenosis is reduced. Preoperatively, during rotation of the head, the Doppler signal is detected only in the systolic phase. Postoperatively, it is also detected in the diastolic phase, even when the head is rotated to the left.
logical examination was negative, but again, forced turning of his head to the left caused dizziness and faintness. Plain films of the cervical spine were normal and there was no malalignment during rotation of the head. Otological investigations were normal. MRI showed small infarcts in the right cerebellar hemisphere and left thalamus. Duplex sonography with the head in the neutral position demonstrated flow in the right vertebral artery throughout the systolic and diastolic phases. When the head was rotated 80 ±90 to the left, however, the end-diastolic flow signal disappeared, paralleling the appearance of symptoms. Carotid arteriography showed no abnormality. Both posterior communicating arteries were small. The left VA ended in the posterior inferior cerebellar artery and the intracranial portion of the vertebrobasilar system filled via the right VA. In the neutral position, no stenosis of the right VA was seen. However, when the patient's head was turned to the left, we showed compression of the right VA at the level of the occipitoatlantal joint and delayed circulation in the vertebrobasilar system, paralleling the appearance of symptoms. These findings suggested that the symptoms were caused by compression of the VA and surgical decompression was performed. The right transverse process of the atlas, which compressed the VA from below, was removed and a hemilaminectomy of the axis was performed. Postoperative vertebral angiography demonstrated reduced compression of the right VA on head rotation, and the patient's symptoms disappeared postoperatively. On sonography, end-diastolic flow did not disappear in the right VA even when the patient rotated his head to the left (Fig. 1).
Discussion In general, unilateral occlusion of the VA does not produce vertebrobasilar ischaemia, because the blood flow is preserved via the opposite vertebral artery and/or the circle of Willis. However, when the vertebrobasilar system is served by only one VA, its occlusion can cause vertebrobasilar ischaemia with vertigo, dizziness or diplopia. In our case, the left VA ended in the posterior inferior cerebellar artery and both posterior communicating arteries were small; the vertebrobasilar system was served by only the right VA and occlusion of the latter was directly linked to ischaemia. The fact that the symptoms were completely relieved by surgical decompression of the VA suggests a close relationship between the symptoms and compression of the VA. It is possible that injury to the intima during rotation of the head leads to the formation of thrombus in the VA and embolism to more distal portions of the basilar arterial tree [13]. However, the rapid clearance of the symptoms makes embolic stroke most unlikely. It is well recognized that during rotation of the head, the VA can be compressed at the transverse foramen of C6, within the transverse foramina from C5 to C2, at the atlantoaxial joint and at the occipitoatlantal level [4, 5, 14]. In our case, the VA was compressed at the occipitoatlantal joint level. Cerebral angiography is essential to detect the site of compression [15], it is however, invasive and inappropriate for screening. Sakai et al. [16] reported that measurement of regional cerebral blood flow using single-photon emission computed tomography is useful for assessing cerebral haemodynamics during attacks of vertebrobasilar insufficiency precipitated by turning the head. This technique, however, is too expensive for use in screening.
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It has been reported that measurement of the VA blood flow velocity by use of duplex sonography may help to localise occlusion of the VA [12]. Occlusion of the VA before the origin of the posterior inferior cerebellar artery was identified by detecting a positive mean velocity and no end-diastolic flow. In our case, the VA was compressed at the occipitoatlantal joint. This condition may be considered as parallel with that produced by occlusion of the VA before the origin of the posterior inferior cerebellar artery, which raises the possibility that haemodynamic changes on head rotation can be detected by sonography. It may be questioned whether the degree of incomplete occlusion of the right VA demonstrated on the angiogram is really related to changes in the Doppler signal. As the Doppler signal
varied with head rotation, the degree of rotation during cerebral angiography may have been insufficient to demonstrate fully the narrowing produced. Flow pattern in the right VA on rotation of the head returned to normal postoperatively, paralleling the symptomatic relief. Brautaset [17] reported the usefulness of transcranial Doppler ultrasonography in detecting bilateral extracranial VA compression, which supports our suggestions. Because insonation of the extracranial VA is not always easy during head movement, especially when a given position can be sustained for only a few seconds, sonography does have limitations. However, it may be helpful in managing patients with vertebrobasilar insufficiency.
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