Cases reported "Neurologic Manifestations"

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1/9. neurologic manifestations of intravascular coagulation in patients with cancer. A clinicopathologic analysis of 12 cases.

    Among 1,459 autopsied patients with cancer, 12 had multifocal infarcts of the brain that appeared to be caused by intravascular coagulation. Most of these patients were women with leukemia or lymphoma, and all had a clinical course in which neurologic signs and symptoms were prominent. All had evidence of generalized brain disease (delirium and stupor or coma), and several also had focal brain disease (focal seizures, hemiparesis). All patients had laboratory evidence of coagulation abnormalities, although these were often not severe when neurologic symptoms began. Pathologically, there were multifocal hemorrhagic or ischemic infarcts in the distribution of several cerebral vessels, without a systemic source for cerebral emboli. fibrin thrombi were identified in cerebral vessels and in vessels of several other organs. The clinical findings fit the pathologic picture, and in most instances the correct diagnosis might have been made earlier had it been considered.
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keywords = coma
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2/9. Metastatic cystosarcoma phyllodes. A report of 2 cases presenting with neurological symptoms.

    Two cases of cystosarcoma phyllodes of the breast are presented with central nervous system (CNS) metastases appearing several years after mastectomy for the primary lesion. Unusual features in these cases include the widespread metastases themselves, neurologic symptomatology and CNS involvement, metastases into a uterine leiomyoma and into an area of hepatic adenomatous hyperplasia, and glomus-like structures in one of the primaries with similar structures resembling glomus cells in metastases. The distant metastases were of stromal cells only and frequently surrounded epithelial cells to isolate the indigenous glandular structures. The concept that cytosarcoma is a peculiar stromal neoplasm rather than a tumor of dual neoplastic origin is discussed.
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keywords = coma
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3/9. neurologic manifestations of cogan syndrome.

    cogan syndrome is a multisystem inflammatory vascular disease, characterized by nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Recent reports have directed attention to involvement of other organ systems. Respiratory, cardiovascular, gastrointestinal, and musculoskeletal problems are common, as are laboratory abnormalities and general symptoms such as fever, chills, and weight loss. Prominent neurologic problems in two patients prompted a review of 79 cases of cogan syndrome. More than half had nervous system involvement, including electroencephalographic or spinal fluid abnormality, headache, psychosis, coma, convulsion, neuropathy, and stroke. cogan syndrome should be considered when neurologic deficits are accompanied by eye, ear, and systemic symptoms.
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4/9. hypoglycemia: causes, neurological manifestations, and outcome.

    During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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ranking = 2
keywords = coma
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5/9. Hyperosmolar nonketotic diabetic coma.

    Hyperosmolar nonketotic coma occurs most frequently in the elderly patient with underlying renal impairment. It often has an insidious onset, and may be precipitated by an identifiable illness, medication or procedure. Various neurologic manifestations may occur and obscure the diagnosis. Rapid recognition and appropriate treatment can greatly reduce the high mortality rate.
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ranking = 5
keywords = coma
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6/9. Brain damage in infancy and dietary vitamin B12 deficiency.

    A case of the exclusively breast-fed infant of a vegetarian mother is reported. Neurological deterioration commenced between three and six months of age, and progressed to a comatose premoribund state by the age of nine months. Investigations revealed a mild nutritional vitamin B12 deficiency in the mother, and a very severe nutritional B12 deficiency in the infant, with severe megaloblastic anaemia. Treatment of the infant with vitamin B12 resulted in a rapid clinical and haematological improvement, but neurological recovery was incomplete. Evidence is presented that dietary B12 deficiency was the sole cause of the infant's deterioration, and the literature relating to the condition is reviewed. It is recommended that all strict vegetarians (vegans), especially women in the child-bearing age group, take vitamin B12 supplements.
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keywords = coma
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7/9. neurologic manifestations of legionnaires' disease.

    The neurologic manifestations of legionnaires' disease were reviewed in this paper. Nine (42.9%) of 21 patients seen at this institution had neurologic abnormalities during acute infection, comparable to 52% of patients found in the literature. Abnormal mentation was most common, occurring in all our patients and in 29.6% of patients in the literature. Encephalopathy disproportionate to metabolic disturbances varied from mild confusion to coma, was not associated with increased mortality, and tended to resolve with acute illness although some patients reported persistent memory defects. Rarely did these changes in mentation precede the development of pulmonary infiltrates. headache occurred in two (22.2%) of our patients and in 28.7% of those in the literature. headache, noted in many febrile illnesses, is common but nonspecific in legionnaires' disease. Other neurologic abnormalities including cerebellar dysfunction and focal deficits were relatively infrequent and tended to persist beyond resolution of clinical infection. In some cases these neurologic derangements may have occurred coincidentally with legionnaires' disease. Diagnostic evaluations and autopsies were frequently normal, nonspecific, or revealing of pathology unrelated to infection. Only two patients had evidence of direct invasion of the central nervous system by legionella, and the cause of encephalopathy and neurologic abnormalities in most cases remains unclear. patients with neurologic abnormalities and legionnaires' disease deserve full evaluation to exclude other entities. Only encephalopathy appears to be a characteristic manifestation of legionnaires' disease.
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8/9. Opsoclonus and palatal myoclonus during prolonged post-traumatic coma. A clinico-pathologic study.

    A case of opsoclonus and palatal myoclonus following blunt head injury is described. The syndrome appeared 1 month after the injury and lasted unchanged until death. Postmortem examination showed the presence of widespread lesions of the brain stem affecting the dentato-rubro-olivary system. The main clinical features of the syndrome and their anatomical correlates are discussed.
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ranking = 4
keywords = coma
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9/9. Neurological complications of drug abuse.

    Widespread drug abuse, a comparatively recent medicosocial phenomenon, presents protean clinical patterns and challenging diagnostic problems daily that mimic classical medical syndromes. However, few reports have delineated predominantly neurologic syndromes associated with drug abuse. Five patients were observed illustrating the critical importance of considering drug abuse in the differential diagnosis of neurologic disease, particularly in the young population. It has been found that attention directed to four sources of information will substantiate the diagnosis of drug abuse in the large majority, thus expenditing the prompt initiation of appropriately directed treatment. In addition careful history and neurologic examination, a routine screeen of blood and urine should be run for barbiturates, bromides, alcohol and salicylates. An electroencephalogram is highly recommended as an initial study. It is informative, non-traumatic and inexpensive. Low voltage fast activity is consistent with drug effect and usually rules out other metabolic causes of coma. Other diagnostic principles are enumerated and illustrative cases are cited.
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