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)

Two blue cone monochromats and four rod monochromats have been studied by increment threshold measurements applying the Stiles' principle. Some rudimentary colour discrimination was reported by the blue cone monochromats. One patient showed good discrimination between short- and middle-wavelength lights in matching experiments using the Nagel II apparatus. His neutral band in the spectrum was at lambda = 485--495 nm. Dichromatic vision could not be proved in the other patient. The blue cone monochromats also had good responding blue mechanism in the periphery. Indication of cone activity other than blue cones is found in both kinds of monochromats; these cones being probably of the rhodopsin-cone type (pi0 cones). The conclusions are drawn that the inhibitory effect of the pi0 cones upon the rod mechanism may account for the differences shown by our two blue cone monochromats as to visual acuity, nystagmus and photophobia. Likewise, their differences regarding dichromatic vision may be explained by an unequal number of pi0 cones in their retinas rather than by differences in their blue mechanisms.
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PMID:Typical and atypical monochromacy studied by specific quantitative perimetry. 31 35

Chronic intoxication of phenytoin (PHT) is a well known cause of cerebellar atrophy or irreversible cerebellar ataxia. Little attention, on the other hand, is paid for acute PHT intoxication because its clinical signs are believed to be reversible. We here report a patient with acute PHT intoxication, which resulted in irreversible cerebellar ataxia with radiologically definite cerebellar atrophy. A 39-year-old man admitted to our hospital because of cerebellar ataxia and confusional state. He had been treated with PHT for convulsive seizures after receiving craniotomy for left parietal brain abscess 9 years before. The concentration of his serum PHT had been 4 to 7 micrograms/ml because he had frequently omitted taking drug, and the dose of PHT had been increased to 600 mg/day one year before. He had admitted to another hospital 2 months before for left Bell's palsy and had been obliged to take drug regularly. Cerebellar signs and confusion had gradually developed for 7 weeks. On admission to our hospital, he was awake but in severe confusional state with slurred speech and nystagmus. His serum PHT was 86 micrograms/ml, which returned to therapeutic range 2 weeks after the discontinuation of PHT. His consciousness normalized and nystagmus disappeared. However, slurred speech continued and neurological examination revealed postural tremor and severe limb ataxia. During the subsequent 10 months, his cerebellar signs showed minimal improvement. Computed tomographies of his brain on 3rd and 5th month after the onset of his cerebellar dysfunction showed the definite cerebellar atrophy which had not been noted on the CTs 7 months before and 7 weeks after the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebellar atrophy and persistent cerebellar ataxia after acute intoxication of phenytoin]. 156 34

An extraordinary eye movement was seen in a vegetative patient. His eyeballs were exotropic in the primary position and showed dissociated nystagmus which appeared alternately in each eye every few seconds. He also had palatal myoclonus quite asynchronous with the nystagmus. To our knowledge, there has been no such nystagmus documented in the literature. We report the new nystagmus with his EOG and brain MRI.
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PMID:Alternating dissociated nystagmus with palatal myoclonus--a case report. 175 Oct 24

A 64-year-old man with ethanol intoxication, ingested a bottle of Herbiace (100 ml, 32 w/v% of bialaphos, CAS #35597-43-4, Meiji Seika Kaisha, Tokyo, Japan). He had severe metabolic acidosis and was treated with infusions of sodium bicarbonate and furosemide, plus gastric lavage and enema. The metabolic acidosis improved 15 hours after treatment but nystagmus, apnea and convulsions were progressive. Although his sensorium was clear, spontaneous respirations were not observed for 64 hours. The electroencephalographic findings of atypical triphasic waves and slow waves suggest a unique response to bialaphos poisoning. His clinical course indicates that the management of apnea is critically important to recovery from bialaphos poisoning.
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PMID:Bialaphos poisoning with apnea and metabolic acidosis. 200 62

A 73-year-old man complained of pain in his right ear with vesicular lesion for three days. He complained of no weakness of facial musculatures, but muscle test revealed slight weakness in orbital and oral muscles on admission. His hearing acuity of the left ear was intact. Vertigo with spontaneous nystagmus to left was complained. The patient was treated with stellate ganglion block four times a day, prednisolone 80 mg a day p.o. and acyclovir i.v. Mannitol solution 300 ml a day for eight days was given i.v. to reduce edema and to protect facial nerve. On his 3rd hospital day, his paralysis progressed and he could not close his eye or whistle with his mouth. Evoked myogram showed 91% impairment of the nerve. During recovery period there was discrepancy between facial palsy score of clinical signs and degree of nerve impairment by evoked myogram. On his 12th hospital day his facial nerve score improved 9 to 12 (0 complete paralysis, 40 no paralysis) but evoked myogram showed further progress of nerve impairment from 86% to 91% (Evoked wave heights were 14% and 9% of normal site respectively). The discrepancy is probably because facial palsy score reflects also neurapraxia of inflammatory nerve, and stellate ganglion block has no effect on changing course of facial nerve injury.
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PMID:[Early stellate ganglion block failed to prevent progress of facial nerve palsy in a patient with Ramsay-Hunt syndrome--a case report]. 207 6

The propositus (case 1) was a 40 year-old man. He had begun to note unsteady walking at age 26. He was found to have cerebellar ataxia and pyramidal signs in addition to minor features such as progressive external ophthalmoplegia, gaze nystagmus, bulging eyes, intention fasciculation-like movements of facial and lingual muscles, and limb dystonia. These findings were categorized into type II form of the disease. One sister (case 3) aged 37 years, and one brother (case 4) aged 44 years of the propositus had also type II form of the disease. His uncle (case 2) had the same cerebellar and extrapyramidal signs accompanied with peripheral nerve signs such as muscle wasting, weakness, hypo-tonus and decreased deep tendon reflexes, and a diagnosis of type III form of the disease was made. In the T2-weighted magnetic resonance imaging (1.5 T, TR 2000 or 3000 msec, TE 120 msec) of the three patients (case 1, 3 and 4), dorsolateral part of the putamen showed decreased signal intensity. Although hypo-intensity of the putamen is often observed in normal elderly people over 50 years old, it is considered to be abnormal when it exists in relatively young people as in this family members.
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PMID:[A new family of Machado-Joseph disease--an abnormal decrease in signal intensity of the putamen in magnetic resonance imaging]. 224 34

A 56 year-old man presented with vertigo and the right sided weakness. Neurological examination revealed a lethargic man with good orientation to three spheres. His neck was supple. He had anisocoria, the right pupil being larger than the left by 1.5 mm with sluggish light reaction bilaterally. He had exotropia of the right eye in primary gaze. The abduction of both eyes were full with terminal horizontal nystagmus. The adduction of both eyes were quite limited in each eye. He had a limited upward gaze with poor convergence. These were interpreted as the syndrome of the medial longitudinal fasciculus (MLF) bilaterally. He had a depressed gag reflex on the right side with tongue deviation to the right. He had a mild weakness of the right side limb and also had the right sided hemihyperesthesia including his face to pain and temperature. Twenty four hours after the onset, the left brachial angiography revealed a complete occlusion of the rostral portion of the basilar artery without visualization of the posterior cerebral and superior cerebellar arteries bilaterally. CT scans three days after the onset revealed a low density area in the mid pons with extension rostrally up to the mesencephalon. Four days later he became quadriplegic with bilateral horizontal gaze palsy. No more internuclear ophthalmoplegia is noted on both sides. The midline location of the MLF in the pons, and the separate blood supplies by different paramedian branches of the basilar artery, form the anatomical explanation for the frequent unilaterality of vascular and bilaterality of demyelinating lesions. Bilateral MLF syndrome has been considered almost pathognomonic of multiple sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internuclear ophthalmoplegia in association with basilar artery occlusive disease]. 235 Sep 28

A 74-year-old man developed progressive deafness and unsteady gait two years after gastrectomy for a gastric cancer. Neurological examination revealed an alert and intelligent Japanese male in no acute distress. The optic fundi were normal. The pupils and the extraocular muscles were normal, however, horizontal nystagmus was noted in right and left gaze. He showed marked bilateral deafness, and loss of caloric response bilaterally. No muscle atrophy nor weakness was noted. His gait was wide-based and ataxic. Tandem gait was impossible. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Hyperextensibility was noted in the lower extremities. Deep reflexes were normal in the upper limbs, and diminished in the lower extremities. Sensation was intact. He showed the jumbling phenomenon, and the disturbance of the righting reflex in the tilt-table examination. Neuroradiological as well as laboratory studies were unremarkable except for the high titer of CEA in the CSF. Four months after his admission, malignant tumor cells were found in the CSF. It seemed likely that he had completely lost bilateral vestibular and auditory functions caused by meningeal carcinomatosis. His disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, he did not have limb ataxia. The cranial CT scans failed to show cerebellar atrophy. It was our impression that his motor disturbance was in all likelihood caused by the bilateral loss of vestibular functions, i.e., vestibular ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vestibular ataxia caused by meningeal carcinomatosis]. 236 34

Microvascular decompression procedures were carried out to relieve right hemifacial spasm in a 54-year-old man. His facial spasm was satisfactorily cured but he complained of severe vertigo, and slight facial palsy was also shown after the operation. Electronystagmograph disclosed spontaneous horizontal and rotatory nystagmus toward the non-operated (left) side. The postoperative caloric test showed profound dysfunction on the operated side. His hearing was well maintained postoperatively. These findings indicated, in addition to facial nerve injury, that the peripheral portion of the vestibular nerve was selectively damaged by the operative manipulations. It was shown that both the facial and vestibular nerves tended to be injured when the nerve trunk was shifted caudal-to-rostrally due to manipulations in the CP angle. It was stressed that caution should be paid to preserve not only the cochlear but also the vestibular nerve function in cerebellopontine angle manipulations.
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PMID:[Selective injury of the vestibular and facial nerves following microvascular decompression procedures for hemifacial spasm: A case report]. 239 21

A 63-year-old man presented six days after the sudden onset of horizontal double vision. His left eye became divergent two days later. On initial examination he had bilateral internuclear ophthalmoplegia with weakness of adduction and abducting nystagmus. Convergence was weak but there were no other neuro-ophthalmic signs. Constitutional signs included confusion and unsteadiness on his feet. A provisional diagnosis of arteritis was made. His ESR was 92 mm/h and a superficial temporal artery biopsy confirmed the diagnosis of giant cell arteritis. After two weeks or oral prednisolone his eye movements returned to normal. There have been no further relapses. This would appear to be a unique presentation of giant cell arteritis. The causes of internuclear ophthalmoplegia are discussed along with a review of the ocular and neuro-ophthalmic signs of giant cell arteritis.
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PMID:Bilateral internuclear ophthalmoplegia--an unusual initial presenting sign of giant cell arteritis. 276 84


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