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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the threshold characteristics of optokinetic nystagmus (OKN), contrast thresholds for involuntary OKN were measured for gratings of different spatial frequency to yield an OKN-contrast sensitivity function (OKN-CSF). The OKN-CSF resembled an inverted U-shaped function with temporal-to-nasal and nasal-to-temporal movement yielding similar functions. In addition, when psychophysical CSFs were determined for separate form and movement thresholds, it was discovered that the OKN-CSF approximated the psychophysical-movement CSF rather than the psychophysical-form CSF.
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PMID:Contrast sensitivity of optokinetic nystagmus. 200 57

The authors present a case report of two female patients, aged 16 and 33. Both patients had the same sudden onset of illness, with diplopia and nystagmus and very severe ataxia. The younger patient had absent tendon reflex, while the older one had the tendon reflex preserved. The younger patient had the triparesis present, both patients had no sphincter disorders. They did not have sensibility disturbances, except that the younger patient had hypesthesia of the soft palate (the motor function was preserved). The first patient was somnolent at the beginning. The clinical course being favourable, the younger patient recovered faster than the older one. Electoencephalogram was normal in both patients. CT of the brain was changed at one moment, locking like inflammatory changes. CSF of the younger patient, done twice, was normal. Serologic findings on viruses were normal. Electromyography in both patients showed, beside good motor velocity, the marked sensory velocity which recovered at the control check-ups. The authors present these two cases and they consider the differential-diagnostic difficulties of Fisher's syndrome compared to "brain stem encephalitis".
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PMID:[The Miller-Fisher syndrome (clinical report)]. 226 12

Two brothers, 31 and 25 years of age, with distal hereditary motor neuropathy (distal HMN) and choroideremia are reported. Their parents were second cousins. During the first decade, their visual acuity gradually diminished with night blindness, accompanied by weakness of the legs. From the third decade, they noticed weakness of the hands. The neurological signs of both cases could be summarized as follows: bilateral pes cavus, Charcot-Marie-Tooth type distal atrophy and weakness of the four limbs, no sensory deficit, hyperreflexia in the upper limbs and knees, absent ankle jerks and plantar reflexes, and severe visual impairment due to choroideremia. In addition to these signs, the younger patient showed nystagmus and limb kinetic ataxia suggesting cerebellar involvement. Muscle biopsies and EMG studies revealed chronic neurogenic changes. MCV's in the median nerves were normal, but the extensor digitorum brevis muscles were totally denervated. SCV's, the amplitude of sensory action potentials and sural nerve biopsies were normal. In both patients, elevated CSF protein without pleocytosis and high level of serum IgA & E were demonstrated. Associations of choroideremia and abnormal laboratory findings as noted in our cases have not been so far reported in distal HMN, but we suppose these disorders may be genetically related.
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PMID:[Two siblings of distal hereditary motor neuropathy with choroideremia]. 226 99

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

Observation of neurosarcoidosis in a thirty-year-old black female characterised predominantly by bilateral facial nerve paralysis gave rise to a review of literature since 1978 and also to a comparison with an early study in 1963. As described 1963 the clinical picture is characterized by increased protein content of the CSF (33.8%), facial nerve paresis (25.5%), pleocytosis (23%), diabetes insipidus (21%), hemiparesis (17.2%), organic psychosis (16.9%), papilloedema (15.5%), ataxia (13%), convulsive seizures (12.5%), optic atrophy (12.5%), loss of hearing (12.2%), nystagmus (8.6%) and numerous other symptoms more rarely found. This corresponds to the symptoms of chronic basal meningitis with an infiltration in the neighbouring structures of brain and less frequently the spinal cord. In only 58.7% of the cases (presumably at the onset of sarcoidosis) was the bronchial tract (or the lungs) affected, in 11.5% the skin or the eyes. Although the clinical picture is clear enough the etiology has yet to be determined. Evidence of a pathogen or a pathogenic agent (analogous to berylliosis) has never been established to date. On the other hand there are some indications of a disturbance in the immune system, perhaps of a particular genetic foundation since sarcoidosis strikes black patients with conspicuous frequency. There exist more cases in one family. Exceeding expected random distribution, many patients have the HLA-Factor B 8 (on the chromosome 6) and DR 3. The Kveim-Test was in 71 cases positive, in 12 cases negative. The possibilities of carrying out studies of CSF - analogous to the studies of bronchial lavage - in the most cases of neurosarcoidosis have not been exhausted as to determine the activity of the T-lymphocytes, the interleucines, the angiotensin-converting enzyme while the Gallium 67 scintigraphy and other methods to determine the non-specific activity of the inflammation. The efficiency of the treatment with corticosteroids (Prednison or Triamcinolonacetonid) depends of the phase of the inflammatory process. 12% of the registered cases died.
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PMID:[Neurosarcoidosis. Comparative analysis of the clinical profile based on 537 cases from the world literature up to 1963 and from 1976-1988]. 240 26

A 36 years-old man was admitted in September 1987. For 5 years he suffered from 4 recurrent episodes of throbbing headache, tinnitus, nausea, diplopia and divergent strabismus to which a facial palsy was recently added. In all episodes, the symptoms disappeared spontaneously and completely. A neuro-ophthalmological examination at admission disclosed an exotropia of the right eye, gaze paralysis to the left, paralysis of adduction of the left eye and preserved right eye abduction which triggered a rhythmic horizontal nystagmus. The upward and downward gazes and the convergence were well preserved. Moreover, there was a left peripheral facial palsy, and Babinski sign at the right side. Auditory evoked potentials were slowed at the mesencephalopontine transition. CT scan showed a low-density area with no contrast enhancement at the left pontine tegmentum and a left anterolateral atrophy of the pons. CSF examination showed increase in protein content and increase in the IgG content. Additional investigation included a dopplerometry of the cervical arteries, a panangiography and a bidimensional echocardiography which were normal. Diagnosis of one-and-a-half syndrome was made, possibly secondary to multiple sclerosis, and immunossuppressive therapy was initiated.
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PMID:[One-and-a-half syndrome: anatomo-clinical considerations apropos of a case]. 261 17

Metronidazole, administered to 5 dogs for periods ranging from 3 to 14 days, was associated with acute development of CNS dysfunction. Metronidazole dosage ranged from 67.3 to 129.0 mg/kg of body weight/d. Clinical signs of toxicosis began with anorexia and intermittent vomiting and progressed rapidly to include pronounced, generalized ataxia and vertical, positional nystagmus. These signs were consistent with lesions of the vestibular nuclei and/or cerebellum. High CSF protein content was detected in 2 of 3 dogs from which CSF was collected. Two dogs were euthanatized because of severe neurologic dysfunction. Three dogs improved slowly and recovered completely over several months. These findings suggest that currently recommended dosages of metronidazole may be too high for some dogs.
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PMID:Central nervous system toxicosis associated with metronidazole treatment of dogs: five cases (1984-1987). 276 64

A twelve-year-old girl with multiple sclerosis and peripheral neuropathy is reported. When nine years old, she was diagnosed as having Devic disease (optic atrophy and transverse myelitis). During the three years after onset of her illness, she suffered from three relapses and remissions of her multiple sclerosis. On the third occasion, neurological examination revealed signs of cerebellar dysfunction including ataxic gait, nystagmus and dysmetria, and absence of all tendon reflexes with muscle weakness especially on the left side. Markedly slowed conduction velocity in her ulnar nerve especially on the left and elevated CSF protein were noted. Biopsied sural nerve showed decreased density of myelinated fibers and a selective loss of large diameter fibers. Electron microscopy disclosed onion-bulb formation, myelin debris within Schwann cell cytoplasm and demyelinated axons. These findings showed demyelination and remyelination of the peripheral nervous system in this patient with multiple sclerosis. We discuss the relation of multiple sclerosis and peripheral neuropathy.
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PMID:A case of childhood multiple sclerosis with peripheral neuropathy. 300 68

A 10-year-old boy had gait and speech disturbances 17 days after the initial symptoms of a fever, headache and cough. Four days later he was admitted to a hospital with mild disturbances of gait, speech, writing, visual acuity, left facial nerve, nystagmus and consciousness. Impairments of cranial nerves (II, III and VII), pyramidal sign and cerebellar sign were noticed. EEG showed generalized slow waves. Auditory brain stem response showed prolongation of the interval between I and V waves and poor differentiation between them. Brain CT could not find any abnormalities. Brain stem encephalitis was diagnosed. Clinical signs and symptoms continued for two weeks when steroid therapy was started and it was effective to improve the disease. He was discharged from the hospital without sequelae. Herpes simplex virus (HSV) type 1 was detected from cells in CSF on admission by fluorescence antibody method. HSV antibody titers in sera changed from 1/8 to 1/64 during three months by complement fixation test. Specific IgG and IgA by enzyme linked immunosorbent assay (ELISA) was high in CSF. Specific antibody in CSF/total antibody in CSF: specific antibody in serum/total antibody in serum for IgG and IgA classes were more than 1. Reports of mild type of HSV brain stem encephalitis seemed to be rare. Our case which was followed for several months carefully would be important to discuss.
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PMID:[A mild form of brain stem encephalitis due to herpes simplex virus]. 301 73

A new patient with Leigh's syndrome (subacute necrotizing encephalomyelopathy due to pyruvate dehydrogenase complex deficiency) is presented. A Turkish boy of consanguinously married healthy parents developed progressive muscle weakness since infancy. At the age of 3 years he was unable to sit, stand or walk. Clinical examination showed general muscle weakness, hypotonia, muscle hypotrophy, bilateral ptosis, partial bilateral external ophthalmoplegia, nystagmus, intention tremor and hypoactive tendon reflexes. The EEG showed diffuse slowing, the cerebral CT scan disclosed mild hydrocephalus e vacuo. Motor nerve conduction velocity was slightly decreased, the EMG revealed signs of neuropathy. In the biopsied muscle only a mild hypotrophy of type 2 fibres was found, no abnormal mitochondria could be detected. The sural nerve was slightly abnormal: loss of large myelinated axons, loss of unmyelinated nerves. CSF protein was elevated to 80 mg/dl, protein electrophoresis revealed the pattern of markedly impaired blood-CSF barrier. Serum lactate and pyruvate were permanently elevated. In the urine the excretion of alanine was raised. The clinical state deteriorated during intercurrent infections; somnolence, vomiting and Cheyne-Stoke's respiration occurred. At the age of 3 1/2 years the child died of pneumonia. In the liver tissue a decreased activity of the pyruvate dehydrogenase complex was found. Neuropathological examination of the brain demonstrated wide-spread changes of Leigh's spongiform encephalopathy. Several enzyme deficiencies have hitherto been associated with Leigh's syndrome: This patients confirms earlier findings that a subgroup of Leigh's syndrome is caused by pyruvate dehydrogenase complex deficiency.
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PMID:[Leigh's subacute necrotizing encephalomyelopathy due to decreased activity of the pyruvate dehydrogenase complex]. 312 26


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