Cases reported "Paralysis"

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1/14. Drop attacks and vertical vertigo after transtympanic gentamicin: diagnosis and management.

    Drop attacks represent a significant problem during the natural course of Meniere's disease. They are characterized by a sudden fall to the ground without loss of consciousness. diagnosis is clinical and based on the typical description of the patient. Involvement of vertical canal is possible during Meniere's disease and also after gentamicin application. Treatment of drop attacks is still a matter of discussion; most cases have a benign course with spontaneous remission and no treatment is necessary. In severe cases, aggressive treatment (surgical or pharmacological) is necessary. A case of drop attack associated with vertical vertigo is presented. Vestibular tests were performed in order to assess the involvement of inner ear. Caloric test and ice water test reveal no response. vestibular evoked myogenic potentials are present even after high doses of gentamicin. Drop attacks and vertical vertigo can occur after transtympanic gentamicin and can be well managed with high doses of local gentamicin.
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2/14. potassium uptake in muscle during paramyotonic weakness.

    Previous studies have suggested that an abnormal release of potassium from muscle may accompany attacks of paramyotonic weakness. We investigated 3 patients with paramyotonia congenita before and after the induction of forearm muscle weakness by exercise in cold water. Two of these patients had paralysis periodica paramyotonica and the 3rd had paramyotonia congenita. At the time of paramyotonic weakness there was a marked increase in the arterialized-venous concentration difference of potassium across forearm muscle. This indicated a significant uptake of potassium by forearm muscle in all 3 patients. Normal controls showed a slight release of potassium both at rest and after exercise in cold water. These results suggest that (1) the sodium-potassium pump of the muscle fiber is operating efficiently during paramyotonic weakness; and (2) there is a different mechanism responsible for the generalized weakness that occurs in hyperkalemic periodic paralysis.
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3/14. Delayed nonhemorrhagic encephalopathy following mild head trauma. Case report.

    Delayed nonhemorrhagic encephalopathy following mild head trauma is a rare condition with an unknown etiology. The few cases reported in the literature are in young adults, all of them in the era before computerized tomography (CT) became available, and all had a devastating clinical course with multifocal ischemia or necrotic lesions found at autopsy. A case is presented of a young man with this syndrome who survived the acute encephalopathic phase with severe residual neurological deficits. Repeat CT scans during and following the acute phase as well as magnetic resonance imaging showed diffuse multifocal lesions compatible with ischemic changes and demyelination in the "watershed" areas of the brain.
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4/14. Bilateral brachial paralysis from watershed infarction after coronary artery bypass. A report of two cases and review of the predisposing anatomic and physiological mechanisms.

    Bilateral brachial paralysis and bilateral visual field defects developed after coronary artery bypass in two patients. These deficits, caused by cerebral watershed infarctions, probably resulted from global cerebral hypoperfusion during cardiopulmonary bypass, although bypass had been maintained with high perfusion flows (2.0 to 3.0 L/min/m2) and perfusion pressures from 50 to 90 mm Hg. No systemic hypoperfusion or hypotension occurred before or after cardiopulmonary bypass. Cerebral watershed infarctions occur predominantly in the boundary zones between the anterior, middle, and posterior cerebral arteries. In previous reports, watershed infarctions most often occurred as preterminal events in patients after sustained episodes of obvious hypoperfusion. The occurrence of such major neurological deficits in two patients without systemic hypoperfusion suggests that traditionally accepted flows and perfusion pressures do not assure adequate cerebral blood flow during cardiopulmonary bypass.
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5/14. Near-drowning, scuba diving: an unusual late sequela of bulbar polio.

    This case report illustrates an unusual hazard of underwater sports: vagal neuropathology secondary to early poliomyelitis which resulted in residual palato-pharyngeal paresis. Gag and swallowing reflexes appeared to function adequately but in fact were not normal. When stressed, during water aspiration, they were inadequate, resulting in great risk to the underwater enthusiast. A history of early viral myelitis must be considered as a potential hazard in underwater sports.
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6/14. Progressive supranuclear palsy in the course of subclavian steal syndrome.

    A 70-year-old man manifested during four years a progressive clinical picture consisting in palsy of gaze, axial rigidity, disorders of standing and gait, dysarthria, dysphagia. Neuroradiological investigations demonstrated proximal thrombosis of the left subclavian artery with subclavian steal. At necropsy, degenerative changes in several areas of the basal ganglia and brain stem, with presence of globose neurofibrillary tangles, were found, consistently with the pathologic pattern of the Progressive Supranuclear Palsy (PSP). The association of PSP and subclavian steal syndrome has not been previously reported, to our knowledge. We hypothesize that chronic ischemia, due to subclavian steal syndrome, in the vertebral basilar system and its watershed versus carotid system may have favoured the appearance, in these same areas, of the changes of the PSP.
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7/14. Bilateral sixth-nerve palsy. A rare complication of water-soluble contrast myelography.

    The appearance of bilateral sixth-nerve palsy is usually a harbinger of serious intracranial disease or a nonspecific sign of increased intracranial pressure from any cause. Although unilateral sixth-nerve palsy is a well-recognized complication of lumbar puncture, the appearance of bilateral sixth-nerve palsy following water-soluble myelography is not generally recognized. We describe our experience with three patients and emphasize the benign and self-limiting character of these bilateral sixth-nerve palsies.
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8/14. Cerebral edema and neurological function in human beings.

    The assumption that cerebral edema necessarily results in neurological deficits was investigated with the computerized scan. Four cases are cited to demonstrate that normal function can be preserved in spite of marked focal edema. Quantitative analysis of the amount of edema showed a large increase in the local water content, while neural activity was apparently not adversely affected.
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9/14. Anosognosia in parietal lobe syndrome.

    patients with right parietal lesions often deny their paralysis (anosognosia), but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task (e.g., tying shoe laces) vs a unimanual one (e.g., threading a bolt). They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis (or, if such knowledge exists, it is not available for this particular task). Second, I used a "virtual reality box" to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM's left ear canal with cold water, a procedure that is known to shift that patient's spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of the paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also employ a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift." A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor.
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10/14. Postmortem osseous and neuropathologic analysis of the rheumatoid cervical spine.

    methods. Eleven patients with paralysis, secondary to rheumatoid arthritis of the cervical spine were analyzed postmortem. Neurologic classification (Ranawat) included one Class 2, four Class IIIA, and six Class IIIB. Rheumatologic changes included atlantoaxial subluxation, basilar invagination, and subaxial subluxation. During autopsy the entire cervical spine was removed, including the occiput and foramen magnum. The spinal cord and medulla oblongata were removed en toto and examined histologically by a neuropathologist. RESULTS. Nine of the eleven cases revealed abnormal histology of the spinal cord, and in two patients, the spinal cords were normal. Three histologic types of spinal cord compression were identified. In Type 1 (four cases) severe chronic mechanical compression revealed marked mechanical distortion, flattening, and destruction of the cord with secondary wallerian degeneration of the ascending and descending tracts without anoxicischemic neuron changes. In Type 2 (three cases), there was vascular compression showing ischemic damage to the cord with necrosis of the lateral columns in the ischemic watershed regions supplied by anterior and posterior spinal arteries. In Type 3 (two cases), there was mild mechanical compression showing focal gliosis at the site of compression without ascending or descending tract injury. Two of the eleven cases had thrombosis of the vertebral arteries. Of the eleven cases analyzed, two had normal spinal cords. CONCLUSION. This autopsy analysis of rheumatoid cervical spine suggests that paralysis can be due to both mechanical neural compression and/or vascular impairment.
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