Transient global amnesia following spinal anesthesia.
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Biomedical subjects
Publications and source records attributed to L R Caplan.
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The outcomes of infarctions of the cerebellar arteries may range from self-limited neuro-ophthalmic symptoms to sudden death. Identification of the affected territory may assist in clinical management because the vascular syndromes, as well as vascular mechanisms of cerebellar infarcts, are different according to the involved cerebellar arteries. However, it is usually difficult to tell the exact vascular territories using only transaxial imagings. Magnetic resonance imaging is a good tool for obtaining parasagittal and coronal images of the cerebellum, which are better for showing the vascular territories. To illustrate this point we report a 61-year-old woman and bilateral cerebellar infarcts (right posterior inferior cerebellar artery and left superior cerebellar artery who had vertigo, vomiting, headache, intermittent vertical diplopia, and difficulty walking. The clinical value of parasagittal imaging of the cerebellum in this case is discussed.
The average age of patients undergoing cardiac surgery and the number of comorbidities they possess will continue to increase as surgical technology advances. Toxic/metabolic encephalopathy, hemispheric strokes, hypoxic injury, and peripheral nerve lesions all can occur as a result of cardiac surgery. Therefore, an understanding of the neurologic risk, recognizable syndromes, and preventative measures will continue to be important. Careful preoperative assessment, operative risk factor reduction, and careful postoperative assessments and management may reduce the neurologic risk for cardiac surgery.
PURPOSE: The purpose of this work was to determine the efficacy of MR angiography (MRA) in the detection and characterization of occlusive disease in the vertebrobasilar system. METHOD: We retrospectively reviewed the posterior circulation registry of our institution to select 42 consecutive patients with posterior circulation ischemic symptoms who underwent both MRA and angiography. The extracranial vertebral arteries (ECVAs) were examined by two-dimensional time-of-flight MRA above the C6 level, and the intracranial vertebral arteries (ICVAs) and basilar arteries (BAs) were examined by three-dimensional time-of-flight MRA. Sixty-two ECVAs, 63 ICVAs, and 39 BAs were examined by the readers. RESULTS: Occlusive disease was seen on angiography in 22 of the 42 patients. The sensitivity and specificity values for detection of lesions in 12 ECVA, 19 ICVA, and 12 BA abnormalities were as follows: ECVA, 92 and 96% for Reader A and 100 and 90% for Reader B; ICVA, 84 and 93% for Reader A and 74 and 82% for Reader B; and BA, 100 and 88% for Reader A and 100 and 78% for Reader B. For ICVA, the sensitivity of MRA was less than that of angiography because of lesions missed by the readers at the junctional area of the extra-and intracranial MRA. MRA accurately characterized 9 of the 12 (75%) ECVA, 10 of the 19 (43%) ICVA, and 11 of the 12 (92%) BA lesions. CONCLUSION: MRA is an effective method for detection of occlusive lesions in the ECVAs and BAs. Clinically important lesions can be missed by MRA in the ICVA. MRA is more accurate in characterization of occlusive lesions in BAs than in ECVAs or ICVAs.
Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.
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Ten patients with angiographically verified occlusion of the basilar or vertebral artery have been followed for an average of 2.75 years. None has developed further ischemia after the initial stroke, and 4 patients survived without any clinical deficit. In occlusive disease of the posterior circulation, the critical period for deficit acquisition is at the time of occlusion. Extent of the deficit depends on the rapidity of development of adequate collateral circulation, and the presence of distal embolization at the time of occlusion. Some patients survive basilar occlusion without permanent deficit.
A 47-year-old patient had lesser development of her left limbs and face, smaller left vascular structures, and severe occlusive disease of the left internal carotid, left subclavian, left vertebral and left iliac arteries. In 12 examples of occlusion of a carotid artery, 10/11 with unequal vascular luminal size had the occlusion on the smaller side. Of 20 patients with severe asymmetrical carotid stenosis, 13/17 with unequal size had more stenosis on the smaller side. These preliminary observations suggest that a small vessel may be more likely to occlude than its larger counterpart.
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Infarction secondary to cerebral embolism was diagnosed in 127 (23.5%) of 540 patients in the Michael Reese Stroke Registry. Coronary artery disease, atrial fibrillation, valvular heart disease, mitral annulus calcification, and cardiomyopathy were the commonest etiologies. Echocardiography documented a potential embolic source in 7 patients without previously known heart disease, and clarified the cardiac pathology in many of the patients with known heart disease. The left anterior circulation was affected in 48%, right anterior in 37%, and posterior circulation in 15% of patients. CT was abnormal in 71% of the patients, and was approximately equally helpful in all locations. Nineteen percent of emboli presented with a deficit that was other than maximal at onset. Concurrent systemic embolism was unusual (2.3%). Prognosis was somewhat worse than in thrombotic stroke. Grouping of patients according to embolic source (intra-arterial, cardiac, and uncertain source) showed no differences in activity at onset, early course, or in subsequent course of the illness.
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We compared clinical and arteriographic features in 27 white and 24 black patients with symptomatic posterior circulation occlusive disease. The degree of arterial stenosis was measured independently by two examiners at 12 sites within the vertebrobasilar territory. Racial comparisons were made based upon the distribution of extra- and intracranial occlusive lesions and symptomatic sites of the lesions. White patients had significantly more angina pectoris, more lesions of the origin of the left vertebral artery and more high grade lesions of the extracranial vertebral arteries. Black patients had significantly higher mean diastolic blood pressure, more diabetes mellitus, more lesions of the distal basilar artery, more high grade lesions of intracranial branch vessels and more symptomatic intracranial branch disease. Race was found to be the only factor increasing the risk of intracranial posterior circulation occlusive disease. Knowledge of the contribution of race to the distribution of posterior circulation lesions will help guide evaluation and treatment strategies for patients with vertebrobasilar occlusive disease.
Though the syndrome of carotid artery dissection is well known, "spontaneous" vertebral artery dissection is rarely recognized. We now report clinical and radiologic findings in five patients with presumed vertebral dissection, one pathologically confirmed. Mean age was 35.2 years (range 27-41). Two were men; three women. None had hypertension, vascular disease, or trauma. Headache and neck or occipital pain was prominent in all, often preceding other symptoms. Four of five patients had unilateral partial alteral medullary syndromes, in one accompanied by medial medullary signs. One patient had a cerebellar infarct. Angiography in four patients showed severe irregular stenosis of the distal extracranial vertebral artery (three bilaterally). A fifth patient with irregular stenosis above the vertebral origin had verified extensive dissection in the resected segment. No patient developed late ischemia. Repeat angiography in three showed healing. We conclude that spontaneous vertebral artery dissection, though rare, has recognizable clinical and radiologic features.