Cerebral vasocapacitance and TIAs

108

We describe a 63-year-old man with severe bilateral internal carotid artery disease who presented with repeated, brief attacks of left limb shaking precipitated by his standing up. Cerebral blood flow measured by xenon-133 inhalation showed reduced resting flows and a focal perfusion deficit in the right dorsofrontal and upper rolandic regions. Blood flow velocity and pulsatility index of the right middle cerebral artery measured by transcranial Doppler ultrasonography were also reduced. With hypercapnic challenge, both hemispheric tissue perfusion and blood flow velocity showed impaired reactivity. With induced hypotension, the focal perfusion deficit in the right dorsofrontal region was accentuated. Following right internal carotid endartectomy, resting cerebral blood flow and blood flow velocity improved, as did hypercapnic vasoreactivity. These reversible deficits in cerebral blood flow and vasoregulation, which were maximal in the dorsofrontal region, are consistent with low perfusion in the border zone territory or the distal fields and demonstrate that hemodynamic failure is the likely mechanism for limb-shaking transient ischemic attacks from severe carotid artery disease. (Stroke 1990;21:341-347)A ttacks of limb-shaking are an uncommon manifestation of transient cerebral ischemia, L characterized by brief, repetitive jerking movements of the arm or leg, resembling simple partial motor seizures. 1 Since the first recognition of this phenomenon by Fisher, 2 subsequent observations 3 " 5 have firmly established its association with severe carotid occlusive disease. Attacks appear to cease following carotid endarterectomy. 5 Transient focal cerebral ischemia has been the presumed explanation for these attacks, although hemodynamic studies have not been previously reported to support the specific role of perfusion insufficiency in the border zone territory.We describe an unusual patient with limb-shaking transient ischemic attacks (TIAs) whose symptoms occurred repeatedly upon his standing up. Hemodynamic findings from xenon-133 cerebral blood flow Received July 10, 1989; accepted October 3, 1989. (CBF) and transcranial Doppler ultrasonography (TCD) studies obtained during hypercapnia and induced hypotension support the mechanism of distalfield ischemia in the pathogenesis of these attacks. Case ReportA 63-year-old right-handed man with hypertension (treated with o-methyldopa) and diet-controlled diabetes mellitus presented with recurrent, brief, stereotypical attacks of left limb shaking precipitated by his standing up. He described "buckling and jerking" of his left leg, without weakness, which interfered with ambulation; he was unable to grasp objects with his left hand because of clumsiness. Each attack occurred reliably on his standing up from either a supine or a sitting position, with a 5-second latency. Each attack usually lasted no longer than 10 seconds; a few attacks lasted as long as 1-2 minutes. He experienced as many as six attacks daily; during each attack he remained fully alert and was ca...

Section: Discussionsupporting

confidence: 83%

Perfusion insufficiency in limb-shaking transient ischemic attacks.

Tatemichi

Young

Prohovnik

et al. 1990

108

“…17,18,36 -38 Although the anatomic presence of occlusion does not predict distal hemodynamic impairment, several retrospective studies of patients with carotid disease have found an association between 2 angiographic patterns of collateralization and reduced perfusion pressure: ophthalmic artery reconstitution of the internal carotid artery and retrograde pial collateralization. 11,[13][14][15]17,18 Neither these nor other prospectively recorded angiographic findings identified patients with increased OEF in the St Louis Carotid Occlusion Study. 10 Pial collateralization in the St Louis Carotid Occlusion Study was defined as retrograde MCA flow in any cortical vessel.…”

Section: Discussionmentioning

confidence: 95%

Lack of Correlation Between Pattern of Collateralization and Misery Perfusion in Patients With Carotid Occlusion

Derdeyn

Shaibani

Moran

et al. 1999

Background and Purpose-Misery perfusion, identified by increased oxygen extraction fraction (OEF), predicts subsequent stroke in patients with carotid occlusion. The purpose of this investigation was to determine the relationship of angiographic findings to increased OEF in these patients. Methods-Forty-seven patients with carotid occlusion were studied with cerebral angiography and positron emission tomography (PET). The following angiographic data were collected blind to PET results: (1) pial collateralization, defined as retrograde filling of the MCA branches to the level of the insula; (2) presence of border zone shift; (3) presence of delayed venous phase; and (4) measurement of posterior communicating artery size. Patients were divided into 2 groups based on the PET measurement of normal or increased OEF. Results-Seventeen of 47 patients had increased OEF distal to the occluded carotid artery. No significant relationship between increased OEF and any angiographic finding was found. Pial collateralization was present in only 2 patients, both with increased OEF (Pϭ0.105). Border zone shift was equally distributed between the 2 groups (12 of 30 with normal OEF and 6 of 15 with increased OEF). Delayed venous phase was present in 4 patients, 3 of whom had increased OEF (Pϭ0.073). The relationship between the size of the posterior communicating artery and OEF was not significant by linear regression analysis (Pϭ0.242). Conclusions-With the possible but infrequent exceptions of delayed venous phase and pial collateralization, anatomic findings made on routine angiographic studies of patients with carotid occlusion do not correlate with increased OEF.

“…A proportion of patients with a recently symptomatic severe carotid stenosis or occlusion have diminished perfusion of the ipsilateral cerebral hemisphere and cannot increase perfusion in response to raised levels of carbon dioxide. 10 -24 Consistent results have been obtained from studies with transcranial Doppler ultrasound, 10 -13 single-photon emission computed tomography, 14 -16 positron emission tomography, 15,[22][23][24] and other imaging techniques. [17][18][19][20][21] Such patients also have metabolic changes in the affected hemisphere that are consistent with ischemia in the absence of any evidence of cerebral infarction.…”

mentioning

confidence: 78%

Low Risk of Ischemic Stroke in Patients With Reduced Internal Carotid Artery Lumen Diameter Distal to Severe Symptomatic Carotid Stenosis

Rothwell

Warlow

2000

153

on behalf of the European Carotid Surgery Trialists' Collaborative GroupBackground and Purpose-Patients with recently symptomatic severe carotid stenosis have a high risk of ischemic stroke on medical treatment. The main mechanism of stroke appears to be plaque surface thrombus formation and distal embolism. It is unclear to what extent reduction in blood flow across the stenosis, and the consequent reduction in cerebral perfusion pressure, is also important. Angiographic indices of reduced cerebral perfusion may identify patients at a particularly high risk of stroke who require urgent endarterectomy. The most direct angiographic correlate of poststenotic perfusion pressure is the degree of narrowing of the distal internal carotid artery (ICA) lumen. We sought to develop criteria for the definition of poststenotic narrowing of the ICA and to determine the effect of this and other angiographic characteristics likely to be associated with reduced cerebral perfusion on the risk of ipsilateral ischemic stroke in patients with recently symptomatic carotid stenosis. Methods-We studied the carotid angiograms of 3007 patients in the European Carotid Surgery Trial. Poststenotic narrowing of the ICA was defined with use of the ratio of the lumen diameter of the ICA to that of the common carotid artery (CCA). The normal range of the ICA/CCA ratio was defined in 2966 symptomatic or contralateral carotid arteries with 0% to 49% stenosis. Arteries with 70% to 99% symptomatic stenosis and an ICA/CCA ratio below this range were categorized as narrowed. We related the presence of narrowing and other angiographic characteristics to the risk of ipsilateral ischemic stroke on medical treatment. Results-An assessment of the ICA/CCA ratio had good interobserver reproducibility. Poststenotic narrowing of the ICA was defined as an ICA/CCA ratio of Ͻ0.42. The 5-year risk of ipsilateral carotid territory ischemic stroke on medical treatment was 8% in patients with 70% to 99% stenosis and narrowing of the ICA versus 25% in patients without narrowing (log rank test, Pϭ0.02). This difference remained after correction for other clinical and angiographic variables (hazard ratio 0.40, 95% CI 0.17 to 0.94, Pϭ0.03). The other angiographic characteristics did not predict stroke. Conclusions-Poststenotic narrowing of the ICA was associated with a low risk of stroke on medical treatment. This suggests that low flow alone is not usually sufficient to cause ischemic stroke distal to symptomatic carotid stenosis. Poststenotic narrowing may be protective because blood flow distal to the stenosis is insufficient to carry emboli to the brain. (Stroke. 2000;31:622-630.)