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

Head movement-dependent oscillopsia (HMDO) with peripheral vestibular, brainstem and cerebellar lesions is reviewed. The differentiation of this kind of oscillopsia is based mainly on clinical grounds. HMDO with bilateral abolition of caloric responses, and in the absence of disease of the central nervous system, is due to bilateral vestibular disease. HMDO in patients with internuclear ophthalmoplegia and other brainstem signs is probably due to a lesion of VOR pathways in or near the medial longitudinal fasciculus. The occurrence of HMDO with ataxia of gait and cerebellar eye movement disorders (rebound nystagmus, flutter-like oscillations), in the absence of brainstem lesions (medial longitudinal fasciculus), is clinical evidence for HMDO due to a cerebellar lesion. An attempt is made to associate the different kinds of oscillopsia with current knowledge of the vestibulo-ocular reflexes.
 ...
PMID:Clinical and theoretical aspects of head movement dependent oscillopsia (HMDO). A review. 8 58

This report entails a case of acute cerebellitis manifested with ocular flutter and truncal ataxia on a 24-year-old man. He became dizzy and unsteady beginning October 7, 1991. Transient horizontal to-and-fro movement of objects while gazing, and prominent gastrointestinal tract symptoms were also present. A neurological examination showed ocular flutter and truncal ataxia. Cerebrospinal fluid studies showed mild lymphocytic pleocytosis. Computed tomogram and magnetic resonance imaging of the head were normal. Electronystagmography showed typical ocular flutter in various eye positions. The ocular flutter and truncal ataxia subsided gradually and disappeared completely after October 28th.
 ...
PMID:Acute cerebellitis with ocular flutter and truncal ataxia: a case report. 132 77

With reference to previous reports on hypocalcemia in horses special attention is given to the principal symptoms such as anxiety, increased muscular tension, esp. of the musculature of the extremities, in severe cases leading to ataxia, and to a pulse-synchronized respiration (Synchronous Diaphragmatic Flutter). The time of appearance of the symptoms are much more variable than it is the case for hypocalcemic agalactia in cows. Furthermore the condition has been reported in foals as well as in geldings. Thus the triggering factor seems to be somewhat different from that of agalactia. Hypocalcemic horses also develop decreased manganese blood-level. Treatment with Ca-borogluconat in the horse can be as efficient as is the case in agalactia in the cows, but quite often it is necessary to repeat the treatment. This is illustrated by the fact that the relatively high dose (17 mg Ca/kg) administered to the present patient only increased the Calcium blood level to somewhat below normal. The triggering condition, estrus, weaning of the foal, stress, hard (sweat-provoking) work etc., in many cases perhaps a kind of mental stress, must be adequately treated. An all-round and sufficient feed ration in accordance with the working load and eventually with milk production may prove to be much more essential than realized so far for the prevention of hypocalcemia in horses.
 ...
PMID:[Hypocalcemia in the horse. A case report]. 738 45

In this study we compare the results of quantitative oculomotor function testing in patients with Friedreich's ataxia (FA), olivopontocerebellar atrophy (OPCA) and cerebello-olivary atrophy (CA). Common features in all three syndromes included gaze-evoked nystagmus, saccade dysmetria and prolonged saccade reaction times. Patients with FA showed a characteristic combination of frequent saccadic intrusions, especially ocular flutter, relatively preserved optokinetic nystagmus (OKN) and smooth pursuit, and impaired vestibulo-ocular reflex (VOR) responses. In patients with CA saccadic intrusions were infrequent, OKN and smooth pursuit were severely impaired and VOR gain was normal or increased. Results in OPCA were more variable. When present, slowing of saccades or the combined loss of pursuit and vestibular function were characteristic for OPCA. The ability to suppress the VOR with a head fixed target was relatively preserved in FA, normal to moderately impaired in OPCA and always severely impaired in CA. We conclude that oculomotor testing is useful in the differential diagnosis of the progressive ataxia syndromes.
 ...
PMID:Comparison of oculomotor findings in the progressive ataxia syndromes. 814 9

We report on three patients who presented a rare, uniform clinical syndrome consisting of ocular flutter and truncal ataxia. In all patients the symptoms followed an upper respiratory infection and resolved without sequelae within a few weeks. Previous reports have emphasized the apparent relationship of this entity to infectious disease, but the infectious agent remained uncertain. In one patient we could find a significant rise in antibody titres to enterovirus. We are not aware of any other similar documented case.
 ...
PMID:Ocular flutter and truncal ataxia may be associated with enterovirus infection. 917 52

A 53-year-old man presented with progressive ataxia two and a half years prior to admission. Initially he was treated in a local hospital for 4 months with a diagnosis of spinocerebellar degeneration. Subsequently he developed psychomotor excitement with hallucination and was admitted to a mental hospital for 7 months with a diagnosis of Wernicke's encephalopathy. After a year of partial remission, he presented with increasing difficulty in thinking and walking. On admission he developed mental agitation and excitement, ocular flutter and opsoclonus, and prominent cerebellar ataxia. A lymphocytic pleocytosis in the CSF and a high-intensity lesion in the superior cerebellar peduncle of the upper brainstem revealed on a T2-weighted MRI led to a diagnosis of brainstem encephalitis. Treatment with steroid (two series of 3 days of 1,000mg methylprednisolone DIV, followed by 60mg oral prednisolone) brought about a dramatic improvement in mental and ocular symptoms corresponding with the CSF findings. He was left with mild cerebellar ataxia and returned to work on a small dose of steroids. Differential diagnoses including Bickerstaff's encephalitis and pathomechanism were discussed.
 ...
PMID:[Steroid responsive chronic brainstem encephalitis featuring mental symptoms, abnormal eye movement and cerebellar ataxia]. 923 54

After two days of malaise, headache, nausea, and vomiting, a 26-year-old man suddenly developed opsoclonus and stance and gait ataxia, without myoclonus. Having excluded a paraneoplastic etiology, we assumed that the disorder was probably related to a viral infection. Spontaneous resolution occurred in about two months. Opsoclonus became flutter dysmetria and then resolved. Saccadic eye movement recording disclosed the occurrence of hypermetria, increased velocity, and delayed latency, which also resolved. In this patient, the correspondence between clinical and ocular motor abnormality courses suggests a transient cerebellar dysfunction as the possible pathophysiologic mechanism for opsoclonus.
 ...
PMID:Opsoclonus in a patient with cerebellar dysfunction. 1060 72

Celiac disease may be associated with various neurologic manifestations, most commonly cerebellar ataxia. This report describes a 2-year-old male who presented with opsoclonus-myoclonus syndrome including action myoclonus, palpebral flutter, opsoclonus, and ataxia. Given the severity of ataxia, the child was unable to sit or walk independently. Brain magnetic resonance imaging was normal on two occasions (4-week interval). Oligoclonal bands were found in the cerebrospinal fluid. Blood and serum examinations were unremarkable, with no evidence of infectious seroconversion. However autoantibody testing indicated the presence of antigliadin antibodies of immunoglobulin A subtype, anti-endomysial antibodies, and anti-CV2 antibodies that were not, however, detected in the cerebrospinal fluid. Duodenal biopsy documented villous atrophy confirming the diagnosis of celiac disease. This case confirms that initial presentation of celiac disease may be restricted to neurologic features. We suggest that a search for evidence for celiac disease should be included in the evaluation of opsoclonus-myoclonus.
 ...
PMID:Opsoclonus-myoclonus associated with celiac disease. 1663 9

We report an autopsy case of paraneoplastic opsoclonus-myoclonus-ataxia syndrome associated with small cell carcinoma of the lung. Chemotherapy and lung lobectomy resulted in complete tumor remission and disappearance of myoclonus. However, emotional and behavioral disturbances relapsed and remitted associated with exacerbation of truncal ataxia and ocular flutter, which responded favorably to prednisolone. At autopsy, after 2 years and 11 months of illness, there was no recurrence of cancer. Neuropathologically, only the cerebellum was affected, with diffuse loss of Purkinje cells and dentate neurons, suggesting that the paraneoplastic cerebellar involvement may be responsible for the cognitive affective symptoms in our patient.
 ...
PMID:Autopsy case of opsoclonus-myoclonus-ataxia and cerebellar cognitive affective syndrome associated with small cell carcinoma of the lung. 1753 81

We report a case of Fisher syndrome accompanied by ocular flutter. A 19-year-old man presented with diplopia and vertigo, associated with preceding symptoms of common cold. Since symmetric weakness of abduction in both eyes, truncal ataxia, diminution of tendon reflexes, and gaze nystagmus were noted, he was diagnosed as having Fisher syndrome. Ocular flutter also was noticed during horizontal gaze. Serum anti-GQ1b antibody and anti-GM1 antibody were detected. He was followed without therapy and the symptoms resolved. The accompanying ocular flutter may suggest that a central nervous system disorder may also be present in Fisher syndrome.
 ...
PMID:[Case of Fisher syndrome with ocular flutter]. 2059 60


1 2 Next >>