Cases reported "Hemiplegia"

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1/18. Moyamoya syndrome in a patient with congenital human immunodeficiency virus infection.

    A 10-year-old boy with congenital human immunodeficiency virus (hiv) infection developed recurrent episodes of left hemiparesis at age 7 years. The progression of his disease was followed by computed tomography, magnetic resonance imaging, magnetic resonance angiography, and cerebral angiography. The series of images showed progressive stenosis of both carotid arteries at the suprasellar origin with involvement of his anterior and middle cerebral arteries, while prominent collateral vessels developed from his external carotid supply through ophthalmic and middle meningeal arteries. The pattern of cerebrovascular disease is consistent with moyamoya syndrome. We suggest that further studies on the pathophysiology of cerebrovascular disease in patients with hiv could be helpful in understanding the cause of moyamoya disease as well. Also, with the various advances in treatment of hiv, neurovascular complications could be seen more frequently as the long-term survival in these patients improves.
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2/18. Multiple vasculogenic disabilities : a challenge in rehabilitation.

    A 37 year old male presented with left hemiplegia, left below knee amputation, right partial foot amputation and claudication pain. The limitations in the rehabilitation management in such a high-risk patient are multiplied. The appreciable benefits from supervised rehabilitation and judicious goal setting can help in improving the functional status and retard the disease progression in such patients. This study highlights that coexisting cerebrovascular, coronary and peripheral vascular diseases can pose a real challenge and can result in multiple disabilities.
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3/18. Hypercytokinemia in hemiconvulsions-hemiplegia syndrome associated with dual infection with varicella zoster and Epstein-Barr viruses.

    Hemiconvulsions-hemiplegia (HH) syndrome is an acquired condition in which hemiplegia develops after a preceding febrile unilateral status epilepticus in a previously healthy child. Although viral encephalitis or vascular diseases may be the underlying etiology, the pathogenesis remains unknown in the majority of cases. We measured both plasma and cerebrospinal fluid cytokine levels in a girl with HH syndrome, and found elevated plasma concentrations of soluble interleukin-2 receptor and tumor necrosis factor-alpha, and a slightly increased plasma level of interleukin-6. Furthermore, she had a high serum concentration of soluble e-selectin, which is a marker of inflammatory endothelial activation. These findings suggest that proinflammatory cytokine-induced cerebrovascular endothelial injury could play a role in the pathogenesis of HH syndrome.
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4/18. Hemiparesis in hiv infection. rehabilitation approach.

    persons with acquired immunodeficiency syndrome (AIDS) and human immunodeficiency virus (hiv) infection demonstrate a wide array of central nervous system impairments and may be at a significantly increased risk for cerebrovascular disease. Cerebrovascular disease can be the first manifestation of hiv infection and may be associated with a treatable etiology. Anticipating more referrals for hiv-related physical disability, we detail the rehabilitation management of three persons with hiv infection and hemiparesis. Onset of hemiparesis ranged from just before to 24 months after an AIDS-defining illness. No specific underlying etiology was identified in two of three patients, consistent with previous observations. rehabilitation interventions included lower and upper extremity orthoses, assistive devices to aid gait and activities of daily living, therapeutic exercise and use of antispasticity medication. All patients made at least mild, temporary gains in functional status. survival ranged from 3 to >6 months from initial contact with rehabilitation services. Neurologic and nonneurologic considerations in the rehabilitation of persons with hiv infection are discussed. We conclude that selected individuals with hiv infection and hemiparesis can benefit from rehabilitation intervention. hiv infection should be considered in any young adult presenting with stroke.
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5/18. Acute infantile hemiplegia in a patient with propionic acidaemia.

    A 10-month-old girl with mild developmental delay became hemiplegic after seizures. Cranial CT scan and magnetic resonance imaging (MRI) revealed no lesions related to vascular diseases, but brain atrophy on the right side was remarkable. Digital subtraction angiography showed slightly decreased visualization of peripheral branches of the right medial cerebral artery. Propionic acidaemia was diagnosed on the basis of high plasma levels of propionic acid and its metabolites and the elevated urinary excretion of these acids. With therapy, the levels of these acids fell, and her left hemiplegia disappeared 3 months later.
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6/18. risk factors and clinical manifestations of pathologically verified lacunar infarctions.

    review of 2,859 autopsy reports disclosed lacunar infarctions in 169 patients (6%). review of the charts of 167 of these patients revealed hypertension in 64%, diabetes in 34%, smoking in 46%, and no known risk factor for cerebrovascular disease in 18%. As many as 81% of the patients with lacunes were asymptomatic. Symptomatic lacunes presented most commonly as pure motor hemiparesis (31%), aphasia plus right hemiparesis (20%), or sensorimotor dysfunction (11%); none presented as pure sensory stroke. These results suggest that the spectrum of lacunar infarction is more heterogeneous than previously thought. Most lacunes are asymptomatic, and the majority of symptomatic patients do not present with "classical" lacunar syndromes.
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7/18. Reversible cerebral segmental vasoconstriction.

    vasoconstriction is not recognized as a cause of cerebrovascular disease except in the vasospasm seen following subarachnoid hemorrhage and possibly in migraine. However, we found four patients to have transient, fully reversible vasoconstriction and dilatation prominently involving arteries around the circle of Willis. All four patients were evaluated for severe headaches and fluctuating or recurring motor or sensory deficits. No cause for the clinical syndromes and angiographic abnormalities was found. Similar patients are reported in the literature under various nosologies. This newly recognized clinical-angiographic syndrome should be differentiated from other known causes of vessel constriction and dilatation; the precipitants of reversible vasoconstriction may then be better defined.
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8/18. Hypoglycemic hemiplegia: two cases and a clinical review.

    Hypoglycemic hemiplegia mimics cerebrovascular disease. Two patients are reported who experienced multiple attacks of transient hemiplegia associated with hypoglycemia and who were initially diagnosed as having transient ischemic attacks. In both, angiography was normal and the attacks resolved with reduction of insulin dose. Recognition of hypoglycemia as the cause of transient hemiplegia is important, often obviating the need for cerebrovascular evaluation.
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9/18. Focal neurologic signs associated with hyperkalemia.

    A patient with end-stage renal disease had a flaccid hemiparesis in conjunction with severe hyperkalemia. The hemiparesis resolved with treatment of the hyperkalemia. The patient was later found to have extracranial vascular disease, and we propose that a severe metabolic abnormality associated with an area of relative cerebral ischemia caused the reversible neurologic deficit.
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10/18. Winiwarter-Buerger disease ('thromboangiitis obliterans') with cerebral involvement.

    A patient with clinical and radiological manifestations o Winiwarter-Buerger disease ("thromboangiitis obliterans") in the extremities had three cerebrovascular events during a five-year follow-up. Changes of infarction were confirmed by computed tomographic brain scan and arteriography, but no clinical or laboratory evidence of vasculitis nor a source of recurrent emboli could be found. He had no atherosclerotic risk factors except being a heavy smoker. Cerebrovascular involvement in Buerger's disease is infrequent, but clinical and pathological demonstration has occasionally been found. The existence of Buerger's disease has been questioned, but there appears to be a distinct syndrome of vascular disease that is not atherosclerotic or vasculitic. stroke maybe a component of this syndrome and may be a complication preventable by cessation of smoking.
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