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)

The effect of head position on conjugate horizontal gaze was studied in healthy adults, in patients with multiple sclerosis without eye movement signs, and in patients with downbeat nystagmus indicative of low brain stem lesions. Displacements of gaze from primary position to 30 degrees left and right were recorded using the electro-oculogram, with the head in the primary position, and turned voluntarily to the left and right (in yaw). The quality of eye movements was noted and peak velocities of saccades were measured. The head turning test trebled the incidence of abnormal eye movements found in the multiple sclerosis patients and increased it by tenfold in the patients with downbeat nystagmus. Disorders of eye movement were also found in approximately 20--30% of healthy subjects tested. Weakness of abduction was the most common eye movement defect and appeared to be posterior internuclear ophthalmoplegia. A hypothesis is made which unifies the theoretical explanations of anterior and posterior internuclear ophthalmoplegia. The most likely cause of the disorders of eye movement observed is vertebrobasilar ischaemia induced by stretching and compression of the vertebral arteries during eccentric head posture.
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PMID:Eccentric head positions reveal disorders of conjugate eye movement. 59 79

A case of multiple sclerosis (MS) in a 39 year old Japanese female with high antibody titer to human T-lymphotropic virus type I (HTLV-I) in serum and cerebrospinal fluid (CSF) was reported. At the age of 15, gait and urinary disturbances accompanied by sensory impairment in the lower abdomen and lower extremities developed suddenly. The motor disturbance slowly progressed to tetraparesis over a period of 15 years with several remissions. At the age of 28 the patient suffered from an acute loss of visual acuity, unilateral initially, and became blind by the age of 34. On admission to our department in September, 1987, the patient was alert and had spastic paraparesis, the impairment of all sensory modalities below the level of Th 10 and urinary disturbance. Weakness of facial muscles, nystagmus, deviation of the tongue and dysarthria were also noted. By the PA method, the antibody titer to HTLV-I was measured x512 in the serum and x64 in the CSF. Western blotting analysis of the CSF disclosed the bands to p19, p24 and p28 of HTLV-I gag proteins. The CSF contained a few ATL-like atypical cells and showed mild lymphocytosis, but the total protein was not increased. The computed tomography revealed diffuse low density areas in the cerebral white matter. The magnetic resonance imaging disclosed high intensity signal areas in the cerebral white matter and in the dorsolateral portion of the medulla oblongata on the T2 weighted image. The link of HTLV-I infection to the pathogenesis of human demyelinating diseases was discussed.
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PMID:[A case of multiple sclerosis with high CSF antibody titer to HTLV-I]. 275 51

Central nervous system involvement in systemic lupus erythematosus (SLE) requires immediate treatment. We report a case in a 30-year-old woman. Clinical features associated asthenia, headache, right nystagmus and coma. A mechanical ventilation was started. The neurologic pattern appeared three months after an initial treatment with pulsed doses of glucocorticoid (500 mg per day for 3 days) and one month after an oral cyclophosphamid regimen (50 mg twice a week). The cerebral involvement was evidenced by MRI and comparative analysis of the antinuclear auto antibodies (ANA) and the complement components in cerebral spinal fluid (CSF), pleural fluid and serum. The MRI slices showed a well-defined meningeal focal lesion. CSF-cell count was normal. CSF-proteins were elevated. ANA were positive, total complement (UI/l) was low, C4 component (g/l) was 0.11, undetectable and 0.25 respectively in plasma, CSF fluid and pleural fluid. The ANA specific pattern was anti-Sm2. We affirmed that specific cerebral injury was present because there were clinical and imaging features and a decrease of the C3 and C4 component in the CSF. The treatment associated in travenous pulsed doses of methylprednisolone (1000 mg per days for 3 days) and cyclophosphamid (500 mg per day for three days). Mechanical ventilation was with drawn one day after the end of the pulse therapy. The diminution of the complement component could help improving cerebral involvement of SLE. More clinical studies are required.
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PMID:[Cerebrospinal fluid complement and antinuclear antibodies in lupus meningoencephalitis]. 977 91

This paper presents a case of a perfectly healthy 36-year-old male, who went to the emergency department with a clinical picture of diffuse headache, dizziness, and asthenia with 3 days of evolution, after a long cycling race. He was admitted to the ENT Department with suspected diagnosis of peripheral vertigo. The patient developed hypoesthesia of the face, diplopia, right lateropulsion, and Romberg with preferential rightward fall, and imaging studies demonstrated an extracranial vertebral artery dissection concomitant with PICA territory infarction. This is a rare described case of a vertebral artery dissection concomitant with an infarction of the PICA territory. This case demonstrates the importance of maintaining a high degree of suspicion of stroke in patients with signs/symptoms of nystagmus/vertigo and the relevance of magnetic resonance imaging instead of tomography in the detection of these serious clinic conditions.
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PMID:Threat of a Cycle Proof: Vertebral Artery Dissection Associated with Posterior Inferior Cerebellar Artery Infarction. 3068 55