Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five hundred seventy-five children from low-income urban neighborhoods who were between 10 and 12 years of age were examined by pediatricians for certain neurological signs. Classroom teachers ranked each child according to types of behavior. Data on neurological signs found in more than 15 children and on types of classroom behavior clinically expected to be related to central nervous system defects were studied statistically. Significant positive associations were found between nystagmus and hyperactivity, mixed dominance and hyperactivity, and mixed dominance and variable day-to-day performance. Errors in moving parts of the body on verbal command were associated with distractibility and underachievement. Head circumference greater than the 90th percentile for age was associated with unvarying behavior and clumsiness; tactile agnosia with unvarying behavior; asymmetry of the eyes with hyperactivity; and asymmetrical position of the child's head with underachievement. A negative association was found between nystagmus and musical ability.
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PMID:Relationships between neurological findings and classroom behavior. 108 39

Bromisoval has been used as a hypnotic for the past several decades, and its abuse was known to cause various neurological as well as psychiatric symptoms. Three patients showed a variety of symptoms which could not be explained neuroanatomically: nystagmus, gait disturbance and hyperreflexia of the limbs in all the cases, dysarthria, double vision, hypotonia, ataxic gait and disturbance of consciousness occasionally and auditory agnosia in one case. For the purpose of determining the diagnosis, an energy dispersive X-ray microanalysis (EDX) was used to detect bromine. Five microliters of specimens were placed on the carbon-coated mesh, and using a TN-2000 analyzer, characteristic X-ray peaks of bromine were detected in the serum, urine and cerebrospinal fluid. The sensitivity to detect bromine in the serum was 30 micrograms/ml.
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PMID:Three cases of chronic bromisoval intoxication: clinical symptoms and application of energy dispersive X-ray analysis (EDX) to detect bromine in serum, urine and cerebrospinal fluid. 362 93

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
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PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

We report a 37-year-old man who presented memory loss, homonymous right hemianopsia, and elevation of anti-herpes simplex antibody titer. He had an auto accident in January 1992 in that the car he was driving slipped down a 3 m slope; his car was severely damaged, however, he himself was not injured. Shortly after this accident, he went out of his house less often than before, and he noted some difficulty in his vision. He changed his glasses twice, but his vision was unchanged. In July of 1992, he had an onset of difficulty in recent memory and disorientation to time. He also noted diplopia, and difficulty in seeing objects in his right visual field. He was admitted to our hospital on August 26 of the same year. General physical examination was unremarkable. On neurologic examination, he was alert but disoriented to time and place; calculation was also impaired. Mini-mental state examination was 18/30. He had no aphasia, apraxia, or agnosia. He showed a tendency to neglect his left side. Optic fundi and visual acuity were normal; right homonymous hemianopsia was present. Ocular movement was moderately restricted to most of the directions; pupils were isocoric and reacted to light promptly. He complained of diplopia in right gaze, and monocular nystagmus was induced in his right eye upon right lateral gaze. Trigeminal nerves appeared intact. Minimum left facial weakness was present. The remaining of the cranial nerves appeared intact. His gait was wide-based and tandem gait was impossible. Muscle strength was normal as was the muscle tone. Finger to nose and heel to knee tests were done normally.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 37-year-old man with memory loss, homonymous hemianopsia, and elevation of anti-herpes simplex virus antibody titer]. 782 5

Anatomic elements of the retrochiasmatic pathway. Synopsis of homonymous pathway. Synopsis of homonymous hemianopia: unilateral forms [quadrant, total], bilateral forms [tunnel field, cerebral blindness], homonymous scotomas, horizontal hemianopsias, checkerboard hemianopsias, sparing of temporal crescent. Additional disorders: hemi-neglect, color agnosia, hemi-achromatopsia, alexia, abnormal optokinetic nystagmus, cog-wheel pursuit movement, hemianopic pupillary defect, statokinetic dissociation [Riddoch phenomenon], hallucinations, illusions, visual agnosia, prosopagnosia.
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PMID:[Vision disorders in retrochiasmatic lesions of the visual pathways]. 865 Jun 20

Cerebral visual impairment is one of the main causes of childhood visual impairment in developed countries. These disorders are often linked with pre- or perinatal hypoxic brain injuries. The patterns of brain injuries depend on the severity and duration of hypoxia and the child's age. In premature children, periventricular leukomalacia affects the optic radiations and the subcortical visual brain. In full-term newborn babies, chronic hypoxia leads to the damage of the visual cortex and acute hypoxia damages the basal ganglia. They recover from cortical blindness in variable ways. Visual dysfunction is characterized by fixation troubles, subnormal acuity (crowding), difficulty with perceiving visual fields, movements, depth, cognitive defects (agnosia of images, objects or faces, visuospatial disorders), ocular motility disorders (tonic gaze deviation, strabismus, nystagmus). Accompanying these cerebral injuries, there are accommodation defects and optic disk abnormalities that vary according to the gestational age at the time of hypoxia.
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PMID:[Cerebral visual impairment in brain-damaged children - four case studies]. 1646 20