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A patient with vertebrobasilar transient ischaemic attacks and provokable basilar steal
A patient with vertebrobasil ar transient ischaemic attacks and provokable basi iar steal C.P. Zwanikken*, Ackerstaff*
J.M. van der Windt*, T.J. Bast* *, E.H.J.F.
introduction In the case of an obstructive lesion located proximally in a subclavian artery, reversal of blood flow in the ipsilateral vertebral artery may occur. This stealing of blood to the compromised territory of the subclavian artery could also lead to stealing of blood from the basilar artery1,2. Usually, this is the plausible explanation for the occurrence of TIAs in the vertebrobasilar vascular territory in patients with subclavian steal. Investigation of blood flow velocities and the direction of blood flow in the basilar artery itself has become possible by the development of transcranial Doppler sonography3,4. Recently, some communications have demonstrated reversal of the direction of blood flow in the basilar artery in the patients with subclavian steaP. Basilar steal has also been revealed in patients with innominate artery obstructive disease’. However, the relation between vertebrobasilar TIA’s and basilar steal has yet to be determined. We had the opportunity to investigate a patient with vertebrobasilar TIA’s and basilar steal. Case history A righthanded 65year-old woman visited the outpatient department because of attacks of vertigo of four months duration which occurred
Boezeman*,
and R.G.A.
Summary In a 65year-old woman with vertebrobasilar transient ischaemic attacks (TIAs) and subclavian steal, a steal phenomenon in the basilar artery could be demonstrated by transcranial Doppler sonography after provocation with ~stischaemic hyperaemia of the arm on the affected side. It was not possible to provoke symptoms or signs at the time. The significance of finding a steal phenomenon in the basilar artery even in a patient with a history of vertebrobasilar TIAs is discussed. Key words: vertebrobasilar transient ischaemic attack, subclavian steal, basilar steal.
several times a day. These attacks lasted between one and five minutes. Attacks of long duration were accompanied by nausea without vomiting and sometimes by diplopia. During an attack walking became clumsy. Though there were no clear provoking causes, attacks were more likely to occur during domestic activities. Sometimes sudden rising caused some vertigo. The patient had not noted palpitations during the attacks. Complaints of the left arm during labour were denied. The patient had had a myocardial infarct 12 years previously. There was no history of hypertension.
* Department of Clinical Neurophysiology, * * Department of Vascular Surgery, St. Anton& CM Nieuwegein ~Uirecht), The Netherlands
Hospital, Koekoekslaan I, 3435
Address for correspondence and reprint requests: Dr. R. G.A. Ackerstaff, Dept. of Ciinical Neurophysiology, Hospital, Koekoekslaan I, 3435 CM Nieuwegein, Utrecht, The Netherlands.
St. Anton&
Accepted 18.9.89 Chin Neurol Neurosurg 1990. Vol. 92-4
369
Figure 1. On intravenous digital subtraction angiography the basilar artery is barely seen with good filling of the internal carotid and vertebral arteries.
On examination the blood pressure on the right side was 155/80 mm Hg, on the left side 105/75 mm Hg. A systolic bruit was heard over the right carotid artery. The extra-ocular movements were full. Tandem gait was normal for the age of the patient. The rest of the neurologic examination showed no abnormalities. Ultrasonic duplex scannings revealed a haemodynamically significant stenosis in both the right internal and external carotid arteries. The right subclavian artery showed a stenosis with a diameter reduction of about 50% proximally to the origin of the vertebral artery. In this vertebral artery the pattern and direction of blood flow were normal. On the left side, the carotid arteries showed no significant obstructive lesions, while the subclavian artery had a tight stenosis at the site of its origin from the aorta. In the left vertebral artery, alternating flow predominantly directed towards the arm was found. Intravenous digital subtraction angiography showed incomplete filling of the basilar artery (Figure 1). An obstructive lesion with a stenosis of 80%~90% was confirmed proximally in the left subclavian artery. The intracranial circulation was investigated by transcranial Doppler ultrasonography3,‘*“. The circle of Willis proved to be functionally intact. Flow velocities and flow direction in the anterior and middle cerebral arteries were nor370
Figure 2. Suboccipital insonation at a depth of 70 up to 85 mm. From 70 to 80 mm signals are obtained from both vertebral arteries, one of them showing reversed flow (RV = right vertebral artery, LV = left vertebral artery). At a depth of 85 mm the basilar artery (BA) is insonated showing an intermediate flow pattern at rest. Flow direction is indicated by the symbol at top right of each panel (<=I flow away from the probe, >=[ flow towards the probe in the positive range of the scale, vice versa in the negative range of the scale).
mal. In both posterior Cerebral arteries (Pl-segment) blood flow was in the antero-posterior direction. By s&occipital insonation, the basilar artery was located at a depth of 85 mm (Figure 2). Despite a slight steal phenomenon, normal flow direction predominated in this ar-
Figure 3. Suboccipital insonation at a depth of 85 mm. After compression of the left brachial artery (bar) the predominantly cephalad flow in the basilar artery reverses on decompression of the artery (arrow). Note inversed way of presentation of the signal as indicated by the symbol at top right.
tery. Mean blood flow velocity was strikingly low. Investigation of the basilar artery by transcranial Doppler ultrasonography was repeatedly carried out after provoking subclavian steal on the left side. In order to provoke subclavian steal, a blood pressure cuff around the left arm was kept inflated above systolic pressure for several minutes and then suddenly released. During inflation of the cuff the patient was asked to clench intermittently the left fist2,5. Each time flow in the basilar artery totally reversed for several minutes on release of the cuff (Figure 3). In order to evaluate the impact of reversal of blood flow in the basilar artery on brain stem function, neurological examination was repeated after provoking basilar steal in the way described. However, no signs or symptoms of vertebrobasilar ischaemia were found at that moment. Notably, ocular movements remained full without diplopia and tandem gait did not change. A brain stem auditory evoked response (BAER) before and after reversal of basilar blood flow did not display any abnormalities. Discussion In this patient with a history of vertebrobasilar TIAs and subclavian steal on the left side there was an intermediate steal phenomenon in the basilar artery as evidenced by suboccipital transcranial Doppler sonography. Repeatedly, the direction of blood flow in the basilar artery
could totally be reversed by lowering the peripheral resistance in the vascular territory of the left subclavian artery. This was carried out by provoking postischaemic hyperaemia of the left arm with a blood pressure cuff inflated above systolic pressure while clenching intermittently the left fist as described by other authors2*5. Subclavian steal can also be increased by lowering peripheral resistance with exercise of the arm”. However, inducing postischaemic hyperaemia has the advantage that the patient can keep the head perfectly motionless while being examined by transcranial Doppler sonography. This provocation reversed blood flow in the basilar artery only for several minutes. The striking point is that this basilar steal did not provoke any subjective symptoms or signs of vertebrobasilar ischaemia. The absence of signs and symptoms of vertebrobasilar ischaemia after provoking subclavian steal was reported by Bornstein et a?. None of their patients had symptoms after provoking postischaemic hyperaemia. However, these authors did not have at their disposal transcranial Doppler sonography. The absence of signs and symptoms despite basilar steal is reported by other authors. Klingelhofer et al. described a neurologically asymptomatic patient with a complete subclavian steal and reversed blood flow in the basilar artery as evidenced by transcranial Doppler sonography6. Their patient did not have signs or symptoms after the postischaemic hyperaemia test although the reversal 371
of blood flow in the basilar artery increased. In a study on 14 patients with innominate artery obstructive disease, Rautenberg et ul. demonstrated various forms of steal in the basilar artery in five patients after provoking postischaemic hyperaemia of the right arm’. Four of them already had abnormal blood flow patterns at rest. Though a clear correlation existed between the possibility of provoking steal in the basal cerebral arteries and the patient being neurologically symptomatic, no mention was made of signs or symptoms at the time of the provocation of steal. Factor et al. reported on the BAER findings in eight patients early after vertebrobasilar TIAs12. All of them showed abnormal responses. In an attempt to show at least some functional alterations in the brain stem because of basilar steal we measured the BAER before and immediately after inducing postischaemic hyperaemia. There were no abnormalities. In a patient with vertebrobasilar TIA’s, a subclavian steal syndrome and reversible blood flow in the basilar artery, one would expect a relation between the disturbances of the posterior circulation and the neurological deficit. In our patient, however, explanation for the absence of signs and symptoms of vertebrobasilar ischaemia and reversal of blood flow in the basilar artery is not clear. One might wonder whether the way we used of provoking steal in the basilar artery was sufficient to cause vertebrobasilar ischaemia. Another explanation for the absence of signs and symptoms despite reversal of blood flow might be that pressure in the basilar artery is independent on the dircction of blood flow and in our case was sufficient to adequately perfuse the arteries of the brain stem. This assumption is supported by the fact that in our patient the circle of Willis proved to be functionally intact. In conclusion, in a patient with a history of vertebrobasilar TIAs we demonstrated the occurrence of basilar steal after augmenting sub-
372
clavian steal with postischaemic hyperaemia 01 the affected arm. Clinical signs or symptoms, however, could not be provoked. Both the mechanism of vertebrobasilar TIA’s and the significance of the finding of reversed blood flow in the basilar artery in patients with subclavian or innominate steal syndromes remain to be elucidated. References FIELDS ws, LEMAK NA. Joint study of extracranial arterial occlusion. VII. Subclavian steal - a review of 168 cases. JAMA 1972; 222:1139-43. BORNSTEIN NM, NORRIS JW. Subclavian steal: a harmless haemodynamic phenomenon? Lancet 1986; 2:303-5. ARNOLDS
BJ, VON REUTERN
G-M.
TranscranialDoppler
sonography. Examination technique and normal reference values. Ultrasound Med Biol 1986; 12: 115-23. BUDINGEN HJ,STAUDACHER rh. Die Identifiierung der Arteria basilaris mit der transkraniellen Doppler-Sonographie. Ultraschall 1987; 8:95-101. HENNERICI, M, KLEMM c, RAUTENBERG w. The subclavian steal phenomenon: a common vascular disorder with rare neurologic deficits. Neurology 1988; 38:66973. KLINGELHOFER
J, CONRAD
B, BENECKE
R, FRANK
B.
Transcranial Doppler ultrasonography of carotid-basilar collateral circulation in subclavian steal. Stroke 1988; 19:1036-42. RAUTENBERG w, HENNERICI M. Pulsed Doppler assessment of innominate artery obstructive diseases. Stroke 1988; 19:1514-20. ACKERSTAFF RCA. Ultrasonic duplex scanning in atherosclerotic disease of the vertebrobasilar arterial system. A non-invasive technique compared with contrast arteriography. Thesis, Elinkwijk B.V., Utrecht (1985). GROLIMUND
P, SEILER RW, AASLID R, HUBER
P, ZUR-
Evaluation of cerebrovascular disease by combined extracranial and transcranial Doppler sonography. Experience in 1,039 patients. Stroke 1987; 18:1018-24. DANA DEWITT L, WECHSLER LR. Transcranial Doppler. Stroke 1988; 19:915-21. BRUEGG
GROSVELD
H.
WJHM,
LAWSON
IA, EIKELBOOM
BC, V.D.
Clinicalandhaemodynamic significance of innominate artery lesions evaluated by ultrasonography and digital angiography. Stroke 1988; 19:958-62. FACTOR SA, DENTINGER MP. Early brain-stem auditory evoked responses in vertebrobasilar transient ischemic attacks. Arch Neurol 1987; 44:544-7. WINDTJM,ACKERSTAFFRGA.
J.M. van der Windt*, T.J. Bast* *, E.H.J.F.
introduction In the case of an obstructive lesion located proximally in a subclavian artery, reversal of blood flow in the ipsilateral vertebral artery may occur. This stealing of blood to the compromised territory of the subclavian artery could also lead to stealing of blood from the basilar artery1,2. Usually, this is the plausible explanation for the occurrence of TIAs in the vertebrobasilar vascular territory in patients with subclavian steal. Investigation of blood flow velocities and the direction of blood flow in the basilar artery itself has become possible by the development of transcranial Doppler sonography3,4. Recently, some communications have demonstrated reversal of the direction of blood flow in the basilar artery in the patients with subclavian steaP. Basilar steal has also been revealed in patients with innominate artery obstructive disease’. However, the relation between vertebrobasilar TIA’s and basilar steal has yet to be determined. We had the opportunity to investigate a patient with vertebrobasilar TIA’s and basilar steal. Case history A righthanded 65year-old woman visited the outpatient department because of attacks of vertigo of four months duration which occurred
Boezeman*,
and R.G.A.
Summary In a 65year-old woman with vertebrobasilar transient ischaemic attacks (TIAs) and subclavian steal, a steal phenomenon in the basilar artery could be demonstrated by transcranial Doppler sonography after provocation with ~stischaemic hyperaemia of the arm on the affected side. It was not possible to provoke symptoms or signs at the time. The significance of finding a steal phenomenon in the basilar artery even in a patient with a history of vertebrobasilar TIAs is discussed. Key words: vertebrobasilar transient ischaemic attack, subclavian steal, basilar steal.
several times a day. These attacks lasted between one and five minutes. Attacks of long duration were accompanied by nausea without vomiting and sometimes by diplopia. During an attack walking became clumsy. Though there were no clear provoking causes, attacks were more likely to occur during domestic activities. Sometimes sudden rising caused some vertigo. The patient had not noted palpitations during the attacks. Complaints of the left arm during labour were denied. The patient had had a myocardial infarct 12 years previously. There was no history of hypertension.
* Department of Clinical Neurophysiology, * * Department of Vascular Surgery, St. Anton& CM Nieuwegein ~Uirecht), The Netherlands
Hospital, Koekoekslaan I, 3435
Address for correspondence and reprint requests: Dr. R. G.A. Ackerstaff, Dept. of Ciinical Neurophysiology, Hospital, Koekoekslaan I, 3435 CM Nieuwegein, Utrecht, The Netherlands.
St. Anton&
Accepted 18.9.89 Chin Neurol Neurosurg 1990. Vol. 92-4
369
Figure 1. On intravenous digital subtraction angiography the basilar artery is barely seen with good filling of the internal carotid and vertebral arteries.
On examination the blood pressure on the right side was 155/80 mm Hg, on the left side 105/75 mm Hg. A systolic bruit was heard over the right carotid artery. The extra-ocular movements were full. Tandem gait was normal for the age of the patient. The rest of the neurologic examination showed no abnormalities. Ultrasonic duplex scannings revealed a haemodynamically significant stenosis in both the right internal and external carotid arteries. The right subclavian artery showed a stenosis with a diameter reduction of about 50% proximally to the origin of the vertebral artery. In this vertebral artery the pattern and direction of blood flow were normal. On the left side, the carotid arteries showed no significant obstructive lesions, while the subclavian artery had a tight stenosis at the site of its origin from the aorta. In the left vertebral artery, alternating flow predominantly directed towards the arm was found. Intravenous digital subtraction angiography showed incomplete filling of the basilar artery (Figure 1). An obstructive lesion with a stenosis of 80%~90% was confirmed proximally in the left subclavian artery. The intracranial circulation was investigated by transcranial Doppler ultrasonography3,‘*“. The circle of Willis proved to be functionally intact. Flow velocities and flow direction in the anterior and middle cerebral arteries were nor370
Figure 2. Suboccipital insonation at a depth of 70 up to 85 mm. From 70 to 80 mm signals are obtained from both vertebral arteries, one of them showing reversed flow (RV = right vertebral artery, LV = left vertebral artery). At a depth of 85 mm the basilar artery (BA) is insonated showing an intermediate flow pattern at rest. Flow direction is indicated by the symbol at top right of each panel (<=I flow away from the probe, >=[ flow towards the probe in the positive range of the scale, vice versa in the negative range of the scale).
mal. In both posterior Cerebral arteries (Pl-segment) blood flow was in the antero-posterior direction. By s&occipital insonation, the basilar artery was located at a depth of 85 mm (Figure 2). Despite a slight steal phenomenon, normal flow direction predominated in this ar-
Figure 3. Suboccipital insonation at a depth of 85 mm. After compression of the left brachial artery (bar) the predominantly cephalad flow in the basilar artery reverses on decompression of the artery (arrow). Note inversed way of presentation of the signal as indicated by the symbol at top right.
tery. Mean blood flow velocity was strikingly low. Investigation of the basilar artery by transcranial Doppler ultrasonography was repeatedly carried out after provoking subclavian steal on the left side. In order to provoke subclavian steal, a blood pressure cuff around the left arm was kept inflated above systolic pressure for several minutes and then suddenly released. During inflation of the cuff the patient was asked to clench intermittently the left fist2,5. Each time flow in the basilar artery totally reversed for several minutes on release of the cuff (Figure 3). In order to evaluate the impact of reversal of blood flow in the basilar artery on brain stem function, neurological examination was repeated after provoking basilar steal in the way described. However, no signs or symptoms of vertebrobasilar ischaemia were found at that moment. Notably, ocular movements remained full without diplopia and tandem gait did not change. A brain stem auditory evoked response (BAER) before and after reversal of basilar blood flow did not display any abnormalities. Discussion In this patient with a history of vertebrobasilar TIAs and subclavian steal on the left side there was an intermediate steal phenomenon in the basilar artery as evidenced by suboccipital transcranial Doppler sonography. Repeatedly, the direction of blood flow in the basilar artery
could totally be reversed by lowering the peripheral resistance in the vascular territory of the left subclavian artery. This was carried out by provoking postischaemic hyperaemia of the left arm with a blood pressure cuff inflated above systolic pressure while clenching intermittently the left fist as described by other authors2*5. Subclavian steal can also be increased by lowering peripheral resistance with exercise of the arm”. However, inducing postischaemic hyperaemia has the advantage that the patient can keep the head perfectly motionless while being examined by transcranial Doppler sonography. This provocation reversed blood flow in the basilar artery only for several minutes. The striking point is that this basilar steal did not provoke any subjective symptoms or signs of vertebrobasilar ischaemia. The absence of signs and symptoms of vertebrobasilar ischaemia after provoking subclavian steal was reported by Bornstein et a?. None of their patients had symptoms after provoking postischaemic hyperaemia. However, these authors did not have at their disposal transcranial Doppler sonography. The absence of signs and symptoms despite basilar steal is reported by other authors. Klingelhofer et al. described a neurologically asymptomatic patient with a complete subclavian steal and reversed blood flow in the basilar artery as evidenced by transcranial Doppler sonography6. Their patient did not have signs or symptoms after the postischaemic hyperaemia test although the reversal 371
of blood flow in the basilar artery increased. In a study on 14 patients with innominate artery obstructive disease, Rautenberg et ul. demonstrated various forms of steal in the basilar artery in five patients after provoking postischaemic hyperaemia of the right arm’. Four of them already had abnormal blood flow patterns at rest. Though a clear correlation existed between the possibility of provoking steal in the basal cerebral arteries and the patient being neurologically symptomatic, no mention was made of signs or symptoms at the time of the provocation of steal. Factor et al. reported on the BAER findings in eight patients early after vertebrobasilar TIAs12. All of them showed abnormal responses. In an attempt to show at least some functional alterations in the brain stem because of basilar steal we measured the BAER before and immediately after inducing postischaemic hyperaemia. There were no abnormalities. In a patient with vertebrobasilar TIA’s, a subclavian steal syndrome and reversible blood flow in the basilar artery, one would expect a relation between the disturbances of the posterior circulation and the neurological deficit. In our patient, however, explanation for the absence of signs and symptoms of vertebrobasilar ischaemia and reversal of blood flow in the basilar artery is not clear. One might wonder whether the way we used of provoking steal in the basilar artery was sufficient to cause vertebrobasilar ischaemia. Another explanation for the absence of signs and symptoms despite reversal of blood flow might be that pressure in the basilar artery is independent on the dircction of blood flow and in our case was sufficient to adequately perfuse the arteries of the brain stem. This assumption is supported by the fact that in our patient the circle of Willis proved to be functionally intact. In conclusion, in a patient with a history of vertebrobasilar TIAs we demonstrated the occurrence of basilar steal after augmenting sub-
372
clavian steal with postischaemic hyperaemia 01 the affected arm. Clinical signs or symptoms, however, could not be provoked. Both the mechanism of vertebrobasilar TIA’s and the significance of the finding of reversed blood flow in the basilar artery in patients with subclavian or innominate steal syndromes remain to be elucidated. References FIELDS ws, LEMAK NA. Joint study of extracranial arterial occlusion. VII. Subclavian steal - a review of 168 cases. JAMA 1972; 222:1139-43. BORNSTEIN NM, NORRIS JW. Subclavian steal: a harmless haemodynamic phenomenon? Lancet 1986; 2:303-5. ARNOLDS
BJ, VON REUTERN
G-M.
TranscranialDoppler
sonography. Examination technique and normal reference values. Ultrasound Med Biol 1986; 12: 115-23. BUDINGEN HJ,STAUDACHER rh. Die Identifiierung der Arteria basilaris mit der transkraniellen Doppler-Sonographie. Ultraschall 1987; 8:95-101. HENNERICI, M, KLEMM c, RAUTENBERG w. The subclavian steal phenomenon: a common vascular disorder with rare neurologic deficits. Neurology 1988; 38:66973. KLINGELHOFER
J, CONRAD
B, BENECKE
R, FRANK
B.
Transcranial Doppler ultrasonography of carotid-basilar collateral circulation in subclavian steal. Stroke 1988; 19:1036-42. RAUTENBERG w, HENNERICI M. Pulsed Doppler assessment of innominate artery obstructive diseases. Stroke 1988; 19:1514-20. ACKERSTAFF RCA. Ultrasonic duplex scanning in atherosclerotic disease of the vertebrobasilar arterial system. A non-invasive technique compared with contrast arteriography. Thesis, Elinkwijk B.V., Utrecht (1985). GROLIMUND
P, SEILER RW, AASLID R, HUBER
P, ZUR-
Evaluation of cerebrovascular disease by combined extracranial and transcranial Doppler sonography. Experience in 1,039 patients. Stroke 1987; 18:1018-24. DANA DEWITT L, WECHSLER LR. Transcranial Doppler. Stroke 1988; 19:915-21. BRUEGG
GROSVELD
H.
WJHM,
LAWSON
IA, EIKELBOOM
BC, V.D.
Clinicalandhaemodynamic significance of innominate artery lesions evaluated by ultrasonography and digital angiography. Stroke 1988; 19:958-62. FACTOR SA, DENTINGER MP. Early brain-stem auditory evoked responses in vertebrobasilar transient ischemic attacks. Arch Neurol 1987; 44:544-7. WINDTJM,ACKERSTAFFRGA.