Cases reported "Neurologic Manifestations"

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1/8. Acute anticholinergic syndrome due to Jimson seed ingestion. Clinical and laboratory observation in six cases.

    Ten patients presented with acute anticholinergic syndrome secondary to Jimson seed (datura stramonium) ingestion. Six of the 10 patients required hospitalization because of hyperpyrexia and severe neurologic derangement. Electroencephalograms recorded immediately after admission showed [1] slow wave activity, and [2] bizarre rhythmical bursts of high-voltage sharp wave activity; both of which rapidly resolved during the next 24 hours, as did the associated clinical findings of hyperreflexia, bilateral dorsiflexor Babinski responses, and decerebrate posturing. Previously unreported elevation of serum glutamic-oxalacetic transaminase and lactic dehydrogenase and prothrombin time prolongation are documented. The pathogenic mechanism accounting for abberation of these laboratory values remains undefined. All patients showed rapid clinical improvement; follow-up neurologic evaluation and electroencephalograms have been within normal limits. Because of the widespread availability and potential abuse of the Jimson seed, the clinical syndrome associated with its toxicity merits recognition.
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2/8. One-stage decompression and stabilization in the treatment of spinal tumors.

    Nowadays, extradural vertebral neoplasms which compress the spinal cord are being diagnosed earlier and therefore laminectomy for decompression relieves many patients of their neurological deficits before permanent cord damage has set in. In addition, radiotherapy and oncological treatment have prolonged life expectancy as well as the quality of life in these patients. As the indications for surgery have grown, the problem of spinal instability resulting from direct involvement of the supporting structures of the spine or due to the surgical procedure per se, must be considered. Many of these patients would rapidly return to leading their normal activities if not confined to bed rest or uncomfortable orthopedic devices. The Authors present 9 patients with extradural vertebral lesions: 4 plasmacytomas, 3 metastatic carcinomas, 1 malignant lymphoma and 1 aggressive osteoblastoma treated by simultaneous decompression and stabilization of the spine. All patients showed remarkable improvement of neurological symptoms except in one case where massive pulmonary embolism caused death a few hours after surgery. This surgical treatment offers the advantages of performing wider and better decompressive maneuvers and, at the same time, assuring fast mobilization of the patient after surgery who is often in poor general conditions, thus reducing post-operative complications due to delayed physical therapy and bed confinement.
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3/8. Thiazide-induced hyponatremia.

    A 54-year-old woman had seizures and a focal neurologic deficit associated with hyponatremia induced by a thiazide diuretic. Prompt correction of hyponatremia by administration of hypertonic saline solution was followed by resolution of all neurologic defects. Metabolic balance studies and rechallenge with hydrochlorothiazide were undertaken to investigate the mechanism of the thiazide-induced hyponatremia. Abnormal vasopressin secretion was shown by a plasma vasopressin concentration of 0.5 microU/ml with a plasma osmolality of 268 mOsm/kg water after administration of a fluid challenge consisting of 45 ml/kg body weight. Rechallenge with chlorothiazide while on a sodium- and potassium-controlled balanced diet resulted in a decrease in serum sodium concentration (136 to 124 mEq/L) and plasma osmolality (283 to 261 mOsm/kg) within 18 hours. During this period, urine losses of monovalent cation were only 55 mEq and body weight was constant at 48.2 kg. A second challenge while the patient received all fluids and electrolytes intravenously again resulted in decreased serum sodium concentration (134 to 126 mEq/L) after urinary loss of only 69 mEq of cation. Thus this patient's hyponatremia cannot be accounted for solely by changes in external water and electrolyte balance; the rapidity with which changes were produced suggests that osmolar inactivation, probably intracellularly, may contribute to the severe hypotonicity seen in some patients.
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4/8. Treatment of acute intermittent porphyria with large doses of propranolol.

    A patient had an acute attack of intermittent porphyria with severe neurologic manifestations, hypertension, and tachycardia. Treatment with propranolol hydrochloride (Deralin [israel]; Inderal, comparable US product) intravenously administered in a total dose of 284 mg during a period of 18 hours, was followed by clinical remission associated with a decline in urinary excretion of porphyrin precursors.
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5/8. Acute carotid occlusion. Indication for surgery?

    Six patients with acute carotid occlusion causing severe neurological deficits were operated within one to two hours after the first signs of deterioration. In one case the occlusion followed carotid arteriography and in five cases extra-cranial carotid surgery. It was possible to restore the blood flow in all six patients. In three patients the neurological deficits disappeared and in three patients they were unchanged. These cases and others reported in literature indicate that if an acute carotid occlusion is operated within one to two hours it will be possible in many cases to restore cerebral blood flow before the brain has suffered irreversible damage.
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6/8. Developmental process of chronic subdural collections of fluid based on CT scan findings.

    One hundred twenty-four follow-up scans were performed on 24 patients who had had posttraumatic subdural collections of low density. Of the 24 patients, 6 developed chronic subdural hematomas. Six other subdural collections showed a temporary increase in attenuation but eventually resolved. The remaining 12 subdural collections resolved without apparent increase in density. Illustrative cases are presented with computed tomographic scans. The identity of these posttraumatic subdural lesions of low density is discussed. They seem to be posttraumatic subdural hygromas.
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7/8. [Value of the knowledge of the mechanical-traumatic component in the course of delivery under the aspect of electronic birth monitoring]

    Three cases were detailed pointed out. They demonstrate the opinion of the author about the relations between mechanical cerebral pressure on the fetus, fetal CTG, fetal pH and neurological findings during neonatal period. It is possible, that a cerebral damadge resulting from mechanical birth trauma occours without the findings of variable decelerations and Dip II in the fetal CTG or without fetal acidosis. Our conclusions are: terminate the delivery after 2 hours severe Dip I under normal fetal pH or after 12 hours of efficient labour.
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8/8. Wilson's disease: a common liver disorder?

    In two sibships 7 of 24 siblings were homozygous for Wilson's disease. In family A, the largest kindred of this recessively inherited disease thus far reported, the proband presented with chronic active hepatitis, one sibling died of cirrhosis, a second had clinical evidence of chronic liver disease and two others had biochemical and histologic changes in liver biopsy specimens. In family B the proband had cirrhosis and portal hypertension and one sibling had biochemical and histologic evidence of liver disease. All six living patients had low serum concentrations of ceruloplasmin and copper and a high 24-hour urinary excretion of copper, which was greatly increased by administration of D-penicillamine. None showed neurologic abnormalities and only one had Kayser-Fleischer rings (detectable only by slit-lamp examination). Each patient had an erythrocyte sedimentation rate (ESR) of 8 mm/h or less. After 3 and 2 years, respectively, of D-penicillamine therapy the conditions of the two probands had improved. liver function became normal in three siblings, and no abnormalities developed in the remaining one. Thus, since Wilson's disease may present with chronic active hepatitis or cirrhosis with a normal ESR and without ocular or neurologic signs, it may be a more common cause of liver disease in young people than has been appreciated.
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