Delayed TIAs distal to bilateral occlusion of carotid arteries -- evidence for embolic and hemodynamic mechanisms.

Bogousslavsky, Julien; Régli, F

doi:10.1161/01.str.14.1.58

Cited by 21 publications

(7 citation statements)

References 16 publications

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“…As such cases are uncommon, it might be of value to understand the differ ent mechanisms responsible for the recur rence of transient cerebral ischemia. Bogousslavsky and Regli [11] reported that de layed TIAs in unilateral ICA occlusion seemed to be more often related to hemo dynamic factors, although embolization through homolatcral collateral pathways might also have been responsible. Such a concept is partly in accordance with our find ings, e.g.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Transient Ischemic Episodes after Anticoagulation or Bypass Operation

Tsuda¹,

Kimura²,

Yoneda³

et al. 1986

Eur Neurol

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Three patients who suffered delayed transient ischemic episodes despite adequate anticoagulation or successful extracranial-intracranial (EC-IC) bypass anastomosis were studied. A hemodynamic mechanism was prominent in 1 patient with moderate orthostatic hypotension. After adequate anticoagulation he had further episodes of transient ischemia, which were finally controlled by an EC-IC bypass. Cerebral blood flow studies revealed flow changes with progression of the arterial lesion from stenosis to occlusion. The bypass was patent postoperatively, which suggested that the ischemia in this patient had been hemodynamic in origin. In the other patient the cerebral ischemic symptoms showed a remarkable improvement after the bypass operation. However, ischemia recurred after the operation until anticoagulants were started. Postoperative cerebral ischemia suggested microemboli, whereas preoperatively, it was presumably a hemodynamic phenomenon. In another patient where microembolism was more apparent, anticoagulation controlled the recurrent ischemia after a bypass operation. A hemodynamic as well as an embolic mechanism needs to be considered in a cerebral ischemia which recurs after treatment.

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Section: Discussionmentioning

confidence: 99%

Recurrent Transient Ischemic Episodes after Anticoagulation or Bypass Operation

Tsuda¹,

Kimura²,

Yoneda³

et al. 1986

Eur Neurol

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“…15 " 17 Severe occlusive disease of the extracranial arteries 18 " 20 or increased viscosity from polycythemia 21 are the usual causes of these episodes of TMB, which are often triggered by orthostatic changes in blood pressure.' 6 -18 -" In AVM's, transient or permanent neurological deficits may occur on a hemodynamic basis, from a critical lowering of cerebral blood flow in discrete brain areas, a phenomenon which has been called intracranial "steal."…”

Section: Collateralsmentioning

confidence: 99%

Amaurosis fugax as the presenting manifestation of dural arteriovenous malformation.

Bogousslavsky¹,

Viñuela²,

Barnett³

et al. 1985

Stroke

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SUMMARY A 46-year-old woman under investigation for three episodes of amaurosis fugax in the left eye proved to have a left anterior-middle fossa dural arteriovenous malformation with pial venous drainage. The malformation received its main supply from the left middle meningeal artery, but its anterior part was fed by the recurrent meningeal branch of the left ophthalmic artery. Transient episodic lowering of retinal arterial pressure due to shunting of blood from the ophthalmic artery to the malformation is the most likely explanation for the occurrence of amaurosis fugax, indicating that this symptom occurs in some patients on a hemodynamic basis. Stroke Vol 16, No 5, 1985TRANSIENT ISCHEMIC ATTACKS rarely occur in relation to intracranial arteriovenous malformations (AVM's),' and among them transient monocular blindness (TMB) seems to be exceptional. 2 -3 We report a patient with recurrent episodes of isolated TMB as the presenting manifestation of a dural AVM. Patient ReportThe patient, a 46-year-old white housewife, was admitted to University Hospital on July 17, 1984.In 1979, she noted a continuous left frontal noise, without headache, which spontaneously resolved in a few minutes. One year before admission, she experienced transient monocular blindness in the left eye just after standing up from a chair, with no other associated symptoms. This loss of vision was characterized by a quick (2 seconds) centripetal darkening of vision to complete blindness; the eye maintained completely blind for 1 minute, followed by a progressive reappearance of the vision in the entire visual field within 30 seconds. Eight months later, while bending forward, the patient suffered a similar episode of transient monocular blindness in the left eye of slightly longer duration (5 minutes). Two months later, a similar event recurred while she was sitting in a boat, and lasted at least 15 minutes, but the patient experienced the loss of vision only in the lower half-field of the left eye, in an ascending curtain-like fashion. A few weeks later, she became aware of transient recurrence of the noise in the left forehead. A CT scan and a carotid angiogram were performed revealing two dural AVM's of the From the Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada.•Supported by grants from the Swiss Academy of Medical Sciences and the S1CPA Foundation.Address correspondence to: Dr. F. Vinuela, Department of Diagnostic Radiology, University Hospital, P.O. Box 5339, London, Ontario, Canada N6A-5A5.Received November 19, 1984; revision #1 accepted January 24, 1985. anterior-middle fossa: a larger one in the region of the pterion on the left and a smaller one in the area of the insertion of the falx anteriorly. She was referred to this institution for treatment.On physical examination, the patient was alert and cooperative. Blood pressure ws 120/70 mm.Hg. and cardiac auscultation was normal. No bruits were heard on the supraclavicular fossa, neck, eyes or head. Optic fundi were normal, wi...

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Positional ischemia • Hypertension«Postural stroke • Orthostatic hypotension Transient ischemic attacks have been associated with hypoten sive episodes in only a few published cases [1,2], and even more rarely changes in neurological symptoms and signs have been precip itated by postural changes [3][4][5][6][7][8][9].We present a patient with an ischemic stroke who had a transient increase in focal deficits related to orthostatic hypotension.A 67-year-old right-handed woman had loss of strength of the right arm over 4 days, and difficulty in speaking subsequently during 24 h. Hypertension had been observed 3 years earlier and she was taking enalapril 20 mg daily with good BP control. She also had a 3 years' history of intermittent claudication.

Neurological examination showed a moderate right faciobrachial hemiparesis and a decreased verbal fluency.

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confidence: 99%

“…Caplan and Sergay [3] first described 4 cases with PCI that appeared in acute ischemic stroke patients upon elevation from the supine position. Subsequently, few cases of orthostatic transient ischemic attacks have been reported [4][5][6][7][8][9].Presented in abstract form at the 4th Meeting of the European Neurological Society. …”

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confidence: 99%