Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 40-year-old man was admitted after 8 months of speech disturbance and locomotive ataxia. He had no seizures, lightning pains, paresthesia, visual loss, bladder disturbance or rectal incontinence. He had never been neurologically or psychiatrically ill and had no history of syphilis. When the patient was admitted, his general physical examination including blood pressure and dermatologic examination was normal. His consciousness was alert. He was found to have a deterioration of mental status such as inability to concentrate, failing memory, amnesia and circumstantiality. His pupils were anisocoric and Achilles jerks were absent. No rigidity of the neck muscles, paralysis and sensory disturbance were recognized. Romberg's sign was absent. The right pupil was 7.0 mm and the left was 6.0 mm in room illumination. The pupils were nonreactive to bright light and both did not constricted to near stimuli. 0.125% pilocarpine eyedrops produced bilateral pupillary constriction. The results indicated bilateral tonic pupils. Laboratory data revealed white cell count of 12,600/mm3 and normal erythrocyte sedimentation rate of 8 mm/hr. Cerebrospinal fluid (CSF) examination revealed the following: opening pressure, 140 mm of water; cell counts, 76/mm2 (mononuclear cells); total protein, 116 mg/dl; glucose, 57 mg/dl. A serum venereal disease research laboratories (VDRL) test was positive in a 1:32 titer confirmed by positive treponema pallidum hemagglutination (TPHA) test in a 1:40,960 titer and positive fluorescent treponemal antibody-absorption (FTA-ABS) test. Serum TPHA-IgM was positive in a 1:320 titer but TPHA-IgG was negative. CSF examination revealed positive TPHA test (titer of 1:2,560) and positive FTA-ABS test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of early syphilis presenting general paresis-like symptoms and bilateral tonic pupils]. 130 Feb 74

We report a sporadic case of periodic ataxia characterized by recurrent attacks of vertigo and ataxia. A 62-year-old male was known to have nystagmus at the age of 18. He has had recurrent episodes of vertigo and ataxia since the age of 48. During an attack remarkable downbeat nystagmus, limb ataxia predominant in the lower extremities and ataxic gait were present. MRI demonstrated an atrophy of the anterosuperior region of the cerebellar vermis. Vertical nystagmus, dysesthesia of gloves and stocking type and deep sensory disorder persisted during interictal intervals. There is no finding which supports this case to be vascular disorder, congenital anomaly, tumor, infection or demyelinating disease. We thought this case to be periodic ataxia and to belong to vestibulocerebellar ataxia reported by Farmer and his colleagues.
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PMID:[A case of periodic ataxia]. 130 26

We reported a 65-year-old man whose sister was suffering from HTLV-I-associated myelopathy (HAM) and who presented slowly progressive spastic paraparesis, sensory disturbance in the feet, tremors and cerebellar ataxia. He was also positive for serum anti-HTLV-I antibody. He first showed a head tremor at the age of 3 years. He developed a spastic and ataxic gait when aged 15 years, and it became difficult for him to walk at the age of 50 years. Examination at 65 years showed a spastic and ataxic gait and scanning speech. Hyper-reflexia and Bahinski's signs were observed. Sensation in the feet was decreased. The anti-HTLV-I antibody titer in the serum was 1:512 by the PA method, and Western blot analysis revealed bands of P19, P24, P28 and P32. Examination of the cerebrospinal fluid (CSF), including oligoclonal bands, gave normal results. The CSF was negative for anti-HTLV-I antibody. CT and MRI of the head showed cerebellar atrophy. His sister was 60 years old. She had developed a spastic gait at the age of 15 years. Sensory defects and bladder dysfunction developed when aged 35 years. Hyper-reflexia, Babinski's sign and foot clonus were observed. Sensation in the feet was decreased. The urinary residual volume was increased. Ataxia was not observed. The anti-HTLV-I antibody titer in the serum was 1:8,192 by the PA method, and Western blot analysis revealed bands of p24, p28 and p32. Examination of the CSF, including oligoclonal bands, gave only normal results.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spastic paraparesis and sensory disturbance improved by prednisolone therapy]. 139 32

A 60-year-old man developed left hemiparesis and homolateral ataxia with normal sensation and normal somatosensory evoked potentials. A lacunar infarct with gadolinium enhancement in the right dorsolateral part of the thalamus was demonstrated on magnetic resonance imaging. Thalamic lesion is a relatively rare cause of ataxic hemiparesis; most of the reported cases of ataxic hemiparesis caused by thalamic lesion were accompanied by sensory disturbances. This is an interesting case which suggested that the thalamic lesion could be responsible for the ataxic hemiparesis without a sensory disturbance.
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PMID:Ataxic hemiparesis following thalamic lacunar infarction. 145 Apr 97

Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a "cerebellar type" of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia-hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamogeniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.
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PMID:Thalamic ataxia. 151 9

Six patients had isolated hemiataxia and ipsilateral sensory loss, as a manifestation of thalamic infarction in the thalamogeniculate territory. Acute hemiataxia-hypesthesia was not found in 1075 other patients from the Lausanne Stroke Registry who were admitted during the same period. Stroke onset was progressive in five patients and immediately complete in one. Five patients had an objective sensory loss. In two patients this affected light touch, pain and temperature sense, and in another three light touch, pain temperature, position and vibration sense. One patient had a purely subjective sensory disturbance. The sensory deficit cleared or was clearing although the ataxia persisted in all patients. On lesion mapping on CT or MRI, all patients had involvement of the lateral part of the thalamus (ventral posterior nucleus and ventral lateral nucleus). The presumed causes of stroke were cardioembolism in one patient, posterior cerebral artery occlusion in one patient and meningovascular syphilis in one patient, hypertensive small vessel disease in two patients, and undetermined in one patient. Hemiataxia-hypesthesia is a new stroke syndrome involving the perforating branches to the lateral thalamus, but in which small vessel disease may not be the leading cause.
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PMID:Hemiataxia-hypesthesia: a thalamic stroke syndrome. 164 Feb 35

We reported a case of bilateral cerebellar hemorrhagic infarction in the distribution of the bilateral superior cerebellar artery. A 58-year-old man suddenly developed dizziness and transient loss of consciousness. The neurological examination revealed left hearing disturbance, left sensory disturbance involving face, dysarthria and bilateral ataxia. This patient was considered to be classic clinical syndrome of right superior cerebellar artery. CT and MRI revealed hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery. The right posterior cerebral artery was filling through the right posterior communicating artery on the right carotid angiography taken 2 hours after the onset. Bilateral vertebral angiography on the 18th day demonstrated no occlusions in the basilar artery and the bilateral superior cerebellar artery. Hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery, sparing other territories as the present case, is extremely rare. In this case, cerebral embolism (top of the basilar syndrome) was suggested because of existence of atrial fibrillation and sudden onset.
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PMID:[A case of bilateral cerebellar infarction in the distribution of the bilateral superior cerebellar artery]. 181 96

A 75-year-old man was admitted because of chest pain and gait disturbance. He noticed pain in the left anterior chest regardless of exercise 3 months prior to admission. Two months later, the chest became smart with motion, followed by sensory disturbance of the lower extremities. On admission, he was anemic. His lower extremities showed exaggerated deep tendon reflexes with positive Babinski signs and an impairment of superficial and deep sense with sensory ataxia. Muscular weakness, muscular wasting, or urinary disturbance was not found. An X-ray film of his thoracic spine disclosed compression fracture and protein content of his cerebrospinal fluid was increased. Magnetic resonance image (MRI) of the ill spines revealed fusion of the bodies of the fifth and sixth thoracic vertebrae with a low signal intensity on T1-weighted images and a partially high signal intensity on T2-weighted images. The intervertebral disc was destroyed. Although histological or bacteriological confirmation was absent, characteristic MRI findings were compatible with spinal osteomyelitis. After antibacterial chemotherapy, his clinical symptoms improved and he came to be able to walk again.
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PMID:[A case of spinal osteomyelitis detected by MRI]. 181 99

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
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PMID:[A case of epidural lipomatosis presenting spinal ataxia]. 206 Feb 46

Two patients with a marked hypointensity of the globus pallidus on magnetic resonance imaging (MRI), which is known to be diagnostic for Hallervorden-Spatz disease (HSD), are presented. Patient 1 fell ill at about 10 years of age with visual disturbance, spastic paraplegia and mild ataxia, while patient 2 was affected during the second year of life with clinical features compatible with infantile neuroaxonal dystrophy (INAD). The two patients had certain clinical features in common; upper and lower motor neuron involvement, visual disturbance secondary to optic nerve atrophy, and dorsal column dysfunction, the evidence of which was seen from abnormal somatosensory evoked potentials (SEPs) obtained after posterior tibial nerve stimulation. In both patients, electron microscopic examination of the biopsied skin or sural nerve showed dystrophic axons, spheroids, and involvement of the peripheral nerve was indicated. Sharing of these clinical, pathological and MRI characteristics by the two patients supports the view of Seitelberger, who regarded HSD and INAD as constituents of a single disease entity, therefore the two patients were described as belonging to a disease spectrum of "Hallervorden-Spatz-neuroaxonal-dystrophy complex (HS-ND)." Sensory impairment has been a rare clinical feature in "HS-ND" complex, although its existence is not inconceivable considering the usual affection of the dorsal column/lemniscal pathway with spheroids. SEP was considered very useful in disclosing this often unmanifested sensory disturbance in "HS-ND" complex.
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PMID:Somatosensory evoked potentials in Hallervorden-Spatz-neuroaxonal-dystrophy complex with dorsal column involvement. 233 40


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