Management of acute peripheral vestibular disorders.
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Biomedical subjects
Publications and source records attributed to L R Caplan.
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Downbeat nystagmus (DBN) uncommonly occurs as a transient phenomenon, and it rarely occurs in patients with cerebrovascular disease. We observed a patient with intermittent DBN and lightheadedness due to transient obstruction of his dominant vertebral artery when he turned his head to his left side. Surgical removal of an osteophyte at the site of the angiographically demonstrated lesion relieved his symptoms.
OBJECTIVE: To study the clinical features and causes of postoperative brainstem and cerebellar infarcts. METHODS: Two groups were studied. The 10 group 1 patients had cardiac (eight) or aortic (two) surgery. The 12 group 2 patients had noncardiac-nonvascular surgery, including orthopedic (five), gynecologic (four), and general (three). Patients were studied by stroke services at university hospitals in Boston (13), Charlottesville (three), Baltimore (three), and Mainz (three) during 2 consecutive years. RESULTS: Onset of strokes was immediately postoperative (six), during the first 48 postoperative hours (nine), and delayed 3 days or more (seven). Clinical syndromes were altered level of consciousness or cognition (15), vestibulocerebellar (four), and hemiparesis with focal brainstem signs (three). Infarction involved the brainstem (13), cerebellum (13), and posterior cerebral artery hemispheric territory (10). Causes: In group 1, five infarcts were due to cardiogenic embolism and three to embolism from the aorta. One patient had a postoperative pontine lacunar infarct and one developed an infarct in the territory of a known stenotic basilar artery. In group 2, one patient had vertebral artery injury from instrumentation, one had medical complications with severe hemorrhage and hypotension, and 10 most likely had position-related vertebral artery thromboses. CONCLUSIONS: Patients with postoperative brainstem and cerebellar infarcts present with altered consciousness or vestibulocerebellar syndromes. The major cause of brain infarcts after cardiac surgery is embolism from the heart and aorta. The causes of infarction after general surgery are less clear, but neck positioning during or after surgery may play an important role by promoting thrombi in compressed arteries that later embolize intracranially when neck motion becomes free.
Treatment of brain embolism should depend on the nature of the embolic material, if discoverable or predictable, not on whether the source was cardiac or intra-arterial. The middle cerebral artery territory is the most common recipient site for emboli, but many emboli do go to the carotid arteries and the posterior circulation. Cardiac and intra-arterial embolism probably each account for about one in five posterior circulation infarcts. Paradoxical embolism is much more common than formerly appreciated. The carotid arteries are probably the most common sources of intra-arterial emboli to the brain, but emboli also frequently arise from the aorta and the vertebral arteries. Potential embolic materials probably frequently enter the circulation but rarely cause strokes.
Cerebral hemorrhagic infarction visualized on CT, secondary to embolic stroke in an anticoagulated individual, is usually associated with clinically stable or improving neurologic signs; fear of transforming the hemorrhagic infarction into a hematoma, however, usually prompts cessation of anticoagulation until the blood has cleared on CT, despite the recognized risk of recurrent embolism during this non-anticoagulated period. We now report our experience with 12 patients with hemorrhagic infarction who remained anticoagulated. Eleven men and one woman, ages 33 to 77, developed hemorrhagic infarction while on heparin, warfarin, or both, for prevention of recurrent embolism. Patients were either continued on uninterrupted anticoagulation from stroke onset (n = 6), or anticoagulation was withheld for several days and then resumed (n = 4), or it was withheld for 5 and 14 days (n = 2) after stroke onset and then continued uninterrupted despite the CT appearance of hemorrhagic infarction. Eleven patients had a definite cardioembolic source for stroke (atrial fibrillation, seven; ventricular thrombus, two; and ventricular dyskinesia, two). One patient had carotid occlusion with local intra-arterial embolism. Hemorrhagic infarcts varied in size and were located in the middle cerebral artery territory in 11 patients and posterior cerebral artery territory in one. All patients remained clinically stable or improved on anticoagulation. Serial CTs showed fading hemorrhagic areas. When the risk of recurrent embolism is high, anticoagulation may be safely used in some patients with hemorrhagic infarction.
PURPOSE: Occlusion of the common carotid artery (CCA) is generally associated with occlusion of the ipsilateral internal carotid artery (ICA) and external carotid artery (ECA). Occasionally, however, collateral circulation to the ECA may preserve patency of the ICA via retrograde perfusion through the bulb. These patients may suffer ongoing transient ischemic attacks and risk for stroke. Recognition of this pathologic variant may allow for effective surgical intervention. METHODS: We have performed seven operations in six patients with occluded CCAs and patent ECA and ICAs. The occluded CCA was on the left side in each case (p < 0.01). Six of the operations were performed for ischemic symptoms, including amaurosis fugax in five patients, hemispheric TIA in one patient, and profound global ischemia in two patients who had concomitant occlusions of other extracranial vessels. In the five most recent cases the patent ECA and ICA above the occluded CCA were recognized by preoperative duplex scanning, which prompted cerebral angiography. A variety of reconstructive procedures were used, depending on the pathologic anatomy. These procedures included subclavian or axillary artery to carotid artery bypass with carotid endarterectomy (five), carotid endarterectomy with thrombectomy of the proximal CCA (one), and ascending aorta to carotid artery bypass (one). RESULTS: There were no strokes associated with the surgery, although one patient had transient neurologic symptoms and a seizure associated with documented reperfusion edema. Three of the patients had preoperative and postoperative transcranial Doppler studies that documented significant improvement in intracranial hemodynamics. Five of the patients have had continuously patent grafts with relief of symptoms for an average of 40 months (range 3 to 155 months). The remaining patient had graft occlusion after 72 months and underwent repeat operation for amaurosis fugax and global ischemia. His second graft remains patent, and he is symptom free 21 months later. CONCLUSIONS: Recognition of patent distal vessels above a CCA occlusion depends on a high index of suspicion, careful investigation of the carotid bulb with duplex scanning, and delayed arteriographic views of the bulb allowing for late collateral vessel filling. The favorable results in this small series of patients supports an aggressive surgical approach when patients with symptoms are encountered with patent distal vessels above an occluded CCA.
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Depression and neurological disease often coexist but sometimes are difficult to distinguish. By analyzing eight patients, all seen by psychiatrists and the same neurologist, and by reviewing the pertinent literature, we will explore the complex differential features, coexistence, and interaction between depression and neurological disease. Neurological disease may lead to changes in mood and behavior, and these patients may present to psychiatrists with depression. In addition, depression may present with or exaggerate neurological signs and symptoms. Awareness of these interactions can lead to appropriate evaluation and treatment of both these disorders.
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BACKGROUND AND PURPOSE: Our purpose was to describe and further understand the determinants of the time of onset of parenchymatous intracerebral hemorrhage and subarachnoid hemorrhage in patients enrolled in the Stroke Data Bank. METHODS: We analyzed the observed times of onset of intracerebral hemorrhage (n = 237 patients) and subarachnoid hemorrhage (n = 243 patients) compared with expected times of onset if the probability of onset was constant across all time intervals. We also analyzed the role of clinical features (if any) in explaining the findings. RESULTS: For intracerebral hemorrhage, 52.5% of patients reported onset times between 0600 hours and 1400 hours, with peak onset between 1000 and 1200 hours (chi 2 = 62.94, df = 11, p less than 0.001). Patients with subarachnoid hemorrhage were more likely to lack a history of hypertension compared with patients who had intracerebral hemorrhage (chi 2 = 23.3, df = 1, p less than 0.001). Patients with subarachnoid hemorrhage were more likely to have more uniform onset time throughout the day (chi 2 = 12.92, df = 7, p = 0.074). However, subarachnoid hemorrhage patients with a history of hypertension were more likely to have peak onset times in mid-to-late morning compared with patients without such a history (chi 2 = 35.25, df = 10, p less than 0.001). The nonuniformity of onset times for intracerebral hemorrhage persisted even if patients with unknown onset times were treated as through their onset times were randomly distributed between 0000 and 0800 hours. Seasonal periodicity and the relation between initial systolic or diastolic blood pressure and time of onset for either type of hemorrhage were not observed. CONCLUSIONS: Our data suggest that the time of onset for both intracerebral hemorrhage and subarachnoid hemorrhage patients with a history of hypertension is similar to the diurnal variation in blood pressure.
BACKGROUND AND PURPOSE: Ischemic cerebrovascular disease in children and young adults usually affects the anterior circulation. SUMMARY OF REPORT: We describe two cases of cerebellar infarction in the territory of vertebral artery supply, associated with physical exertion, in a young adult and in a child. Review of 31 previous cases of cerebellar infarction occurring in the first 2 decades of life demonstrated a mostly obscure causation; where a likely cause was found, trauma was most frequent. In 12 of the 31 patients, a vertebral artery (usually the left) was occluded. Patients were sometimes predisposed to such occlusions by subluxation between the first and second cervical vertebrae, allowing abnormal neck movements that can cause arterial injury and thromboembolism. Some of these cerebellar infarcts, like those of our patients, have followed physical exertion. CONCLUSIONS: Cerebellar infarction can be life-threatening, but half of the patients, including ours, have had complete or near-complete recovery.
To gain insight into neurologic signs relevant to the diagnosis of cardiogenic embolism, we analyzed data from 1,290 patients with cerebral infarcts in the NINDS Stroke Data Bank. Based solely on the presence of potential cardiac sources of embolism, we divided patients into groups of high (N = 250), medium (N = 167), and low (N = 873) risk of a cardiogenic mechanism for their stroke. Diminished level of consciousness was highly associated with the presence of a cardiac source of embolism. Of the four primarily cortical deficits assessed, three (visual field abnormalities, neglect, and aphasia) showed a highly significant graded relationship to the cardiac risk groups. For the fourth cortical deficit (other nonlanguage cognitive functions), this relationship did not attain statistical significance. Conversely, hemiparesis without sensory or cortical deficits had a strong inverse association to the presence of a cardiac source of embolism. This inverse association was weaker for sensorimotor strokes and nonexistent for pure sensory strokes. Although some neurologic findings had highly significant associations with the presence of a cardiac source of embolism, their predictive value for an embolic source was low.
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We report 10 patients with severe occlusive disease of the vertebral artery (VA) origin in the neck with intra-arterial embolism to the posterior circulation. The VA lesions in seven patients were complete occlusions, and three patients had severe atherostenosis. All patients had strokes in the vertebrobasilar territory. The most frequent recipient sites of intra-arterial embolism were the intracranial VA-posterior inferior cerebellar artery region (8), and the distal basilar artery (BA) and its superior cerebellar and posterior cerebral artery branches (7). Two patients had pontine infarction due to BA embolism. The most common clinical signs were due to cerebellar infarction. Atherosclerotic disease of the VA origin has features in common with disease of the internal carotid artery origin. Both have similar risk factors and demography, and each can cause strokes by intracranial intra-arterial embolism.
The role of cerebral angiography in the diagnosis of cerebrovascular disease is currently being questioned because of the increasing availability of MR angiography. The purpose of this essay is to place the use of cerebral angiography in perspective in light of these new developments. In patients with atherosclerotic cerebrovascular disease, MR angiography can almost entirely supplant cerebral angiography as a screening procedure in the evaluation of the carotid bifurcation. However, detection of "pseudoocclusion" still requires cerebral angiography for accurate diagnosis. Atherosclerotic stenosis or occlusion of the major intracranial vessels at the base of the brain can be detected with MR angiography, but not as accurately as with cerebral angiography. Furthermore, for detection of more distal occlusions, cerebral angiography is still needed. A number of erroneous concepts about the risks and value of cerebral angiography have prevented its optimal use for patients with cerebrovascular disease. These myths can be countered by applying several rules to optimize the use of cerebral angiography. Subarachnoid hemorrhage is best evaluated with CT followed by detailed cerebral angiography, although MR angiography can be used as a screening test for aneurysms 3 mm or larger. Cerebral angiography is still necessary to confirm the diagnosis of cerebrovascular malformations, although MR angiography is a useful screening test. Cerebral angiography is required for the definitive diagnosis of arteritis, arterial dissection, or fibromuscular dysplasia.
Hypertension is the major risk factor for intracerebral hemorrhage (ICH) and is present in about 50% of patients with ICH. Common clinical findings are focal neurologic deficits at onset, gradually progressive deterioration, and the presence of headache, vomiting, and depressed level of consciousness. The clinical syndromes of ICH at common locations are reviewed. CT scanning has dramatically changed our thinking about ICH and allowed better correlation of neurologic findings with lesions at various sites.
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