Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mutant strain of Han-Wistar rat carries an autosomal recessive gene producing spastic paresis which is characterized by ataxia, tremor and hind limb rigidity. Brains of affected rats and unaffected littermate controls were transected at the mesencephalon into rostral and caudal portions (the caudal portion contained the cerebellum and brainstem). Poly(A)+ mRNA was isolated from pooled rostral or caudal portions and injected into Xenopus oocytes. The oocytes were voltage-clamped and exposed to 1 mM L-glutamate, 500 microM kainate, 500 microM quisqualate, 200 microM N-methyl-D-aspartate (NMDA) or 1 mM gamma-aminobutyric acid (GABA). Oocytes injected with mRNA isolated from the caudal portions of the affected rat brains exhibited statistically significant increases in glutamate and kainate peak current responses compared to oocytes injected with mRNA from other brain samples. No differences were noted in the responses of the groups when exposed to quisqualate, NMDA or GABA. Cerebellar and brain stem mRNA were also isolated separately in different groups of mutants and unaffected littermates. Only oocytes injected with cerebellar mRNA from mutants displayed statistically significant increases in responses to glutamate and kainate. In parallel morphological studies changes in the cerebellum of mutants were also observed. These consisted of a loss of Purkinje cells and an asymmetrical disarrangement of the granule cell layer of cerebellar cortex. Taken together, the physiological and morphological results suggest that alterations in glutamate/kainate receptors in the cerebellum are phenotypic manifestations of the Han-Wistar mutation. The results are consistent with the hypothesis that this mutant rat might serve as a model of glutamate/kainate excitotoxicity in the brain.
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PMID:Altered excitatory amino acid function and morphology of the cerebellum of the spastic Han-Wistar rat. 168 5

Brown-Sequard syndrome (BSS) and Brown-Sequard-plus syndrome (BSPS) are characterised by asymmetrical paresis with hypalgesia more marked on the less paretic side. This study examined the clinical features of 38 patients (30 males and 8 females; mean age = 32 years) with traumatic cervical BSS or BSPS who underwent comprehensive inpatient rehabilitation. Twenty two injuries were caused by road traffic accidents, 8 by penetrating injuries, 5 by diving injuries, and 3 by other causes. After an average of 35 days in acute care and 79 days in rehabilitation, 37 patients had increased muscle strength, all 38 patients improved functional abilities, 29 patients walked independently, 34 had spontaneous bladder emptying, 36 were discharged home, and 14 were employed. Statistically significant increases (p less than 0.001) were made in modified Barthel index functional scores between admission and discharge. Patients with BSPS had a better prognosis than did those with 'pure' BSS. Patients with predominant upper limb weakness had more favourable outcomes than did those with predominant lower limb weakness. Few other potentially predictive demographic, injury, or neurological factors were associated with functional outcome. Patients with BSS or BSPS generally have a good prognosis for neurological and functional improvement.
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PMID:Traumatic cervical Brown-Sequard and Brown-Sequard-plus syndromes: the spectrum of presentations and outcomes. 178 82

Clinical and epidemiologic analyses of PPMA in Japan based on the nation-wide case survey were reported, and differences between PPMA and ALS were discussed. The present survey covering the years from 1984 through 1991 cited 42 PPMA cases (30 male:12 female). The absolute incidence of PPMA is estimated 0.12/10(5) of the Japanese population (about 150 cases in total), which indicates 0.5% of the polio survivors. In Japan an actual increase of patients is noticed in these 10 years, which reflects the big epidemic of polio around 1950-60. The antecedent poliomyelitis occurred at the mean age of 2.6, mostly between 1940 and 1960. Residual paralysis was generally absent or only minimal. Late muscular atrophy and weakness were noticed at age from 16 to 63 y (mean:41.5), with the mean latency of 40.1 years after polio. Both polio-affected and unaffected site of the limb were equally involved by PPMA, but the left leg tends to be predominantly involved. Neurological symptoms were summarized as an asymmetrical proximal muscular atrophy and flaccid motor paresis in one or two limbs with decreased tendon reflexes. Fasciculation in 45.2%, myalgia in 28.6%, and hypesthesia in 28.5% were noticed. Electromyography and muscle CT scan showed marked selective neurogenic changes. In most cases symptoms are stable or slowly progressive, with some recovery by rest or rehabilitation and deterioration by over work and/or trauma. On regarding these clinical features, PPMA is essentially different from classical ALS. Long-term hyperfunction of survived neurons with potential fragility by polio infection is suspected to mediate PPMA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-poliomyelitis late progressive muscular atrophy (PPMA)--clinical analyses of Japanese cases]. 181 99

The beta-carbolines harmane, norharmane, tetrahydronorharmane, harmine, harmaline and harmol were administered to sheep to assess their effects on upper motor neurone function. Harmane at a dose rate of 54 mg/kg induced hypomotility, head tremors, pelvic limb paresis, hypermetria and a wide based stance. A range of similar effects were observed with norharmane at the same dose rate. Tetrahydronorharmane at a dose rate of 54 mg/kg induced hypermotility followed by hypomotility, asymmetrical pelvic limb paresis, hypermetria, a wide based stance, and stereotyped eating behaviour. Harmine and harmaline at 6 mg/kg induced mild head and body tremors, and at 18 mg/kg induced hypomotility, intense head and body tremors, pelvic limb paresis, crossing over of limbs, neck extension and head swaying. Harmol was not effective at 54 mg/kg by either the subcutaneous or intraperitoneal routes, but at an intravenous dose of 27 mg/kg it induced hypermotility followed by hypomotility, body tremors, limb paresis, muscle asynergy, a wide based stance and jumping behaviour. Harmane, tetrahydronorharmane, harmaline and harmol were convulsive in some sheep at high dose rates.
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PMID:Upper motor neurone effects in sheep of some beta-carboline alkaloids identified in zygophyllaceous plants. 239 71

Recently a subset of chronic demyelinating inflammatory polyneuropathies with asymmetrical involvement limited to upper limbs, at least at the onset, resembling a multifocal mononeuropathy has been described. Electrodiagnostic testing disclosed multifocal CB outside the common entrapment sites has been described. We report a 55 years old man with a 4 years history of paresis, numbness, fasciculations, myokymia, cramps and mild amyotrophy. Electrophysiological evaluation showed proximal multifocal conduction block and abundant spontaneous activity as fasciculations, myokymia and scarce denervation activity. The importance of taking into account this entity in the differential diagnosis of patients with suspected mononeuritis multiplex or motoneuron disease is emphasized. The nosologic place of this entity is also discussed.
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PMID:[Multifocal polyneuropathy with persistent conduction blockage. A new subset of chronic inflammatory polyneuropathies]. 255 98

Based on statistical analysis of 97 chronic low back patients, a pelvic list model has been proposed explaining the correlation between leg length discrepancies (LLD) and sciatica. This model suggests that asymmetrical pronation patterns (one pedal arch dropping more than the contralateral pedal arch) initiates a forward downward rotation within the sacroiliac joint. Entrapment of the sciatic nerve between the piriformis muscle and sacrospinous ligament occurs. Clinically, paresis is observed: numbness, weakness and eventually paralysis of the affected limb. Based on this work, the authors have comprised a classification dividing LLD into two main categories: functional and anatomical. Functional LLD have been subdivided into two types of lists: static and dynamic. Treatment based on a combination of chiropractic and podiatric therapy is presented with a 6-month follow-up. Analysis of the success in this tandem approach is very promising. Concurrently, a chondromalacia model is proposed explaining the pathomechanical events associated with oblique tracking patellar syndrome. The authors suggest that excessive pronation is the causative factor directing asynchronous rotation between the shank and femur. This forces the patella out of its normal tracking groove, which, in turn, generates erosion between the inferior margin of the patella and femoral epicondyles.
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PMID:Excessive pronation: a major biomechanical determinant in the development of chondromalacia and pelvic lists. 297 5

An investigation was carried out into the pathogenesis of a unique locomotory disorder of sheep. Thirty sheep which had exhibited clinical signs for more than 15 months were examined for the presence of muscle atrophy, limb paresis, and spontaneous rotational behaviour. A single large dose of levodopa was administered to 12 normal and 12 affected sheep, and the drug-related effects of sedation and excitation were monitored continuously for three hours. The striatum was removed from eight normal and eight affected sheep and assayed for dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC). The findings of asymmetrical atrophy of pelvic limb extensor muscles, asymmetrical paresis of the limbs, a left:right dominance ratio of 50:50, spontaneous rotational behaviour, decreased response to levodopa loading, and decreased levels of DA (19 per cent reduction) and DOPAC (30 per cent reduction) in the striatum of affected sheep, were interpreted as indicative of a primary nigrostriatal dopaminergic disorder. It is suggested that a striatal presynaptic receptor malfunction has occurred.
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PMID:A novel nigrostriatal dopaminergic disorder in sheep affected by Tribulus terrestris staggers. 344 81

The clinical spectrum of this remarkable non-syphilitic spirochaetosis (spirochaeta infection) of the nervous system is described in light of 53 further cases with reference to our earlier description of 47 cases. As the etiological diagnosis is not possible in all cases the knowledge of clinical courses is especially important. Males are affected almost twice as often as women. The disease is especially prevalent in the sixth decade. Usually, the syndrome begins in the warm season with exquisite pain and other sensory irritations in combination with marked malaise. Initial signs during the winter as well as painless clinical courses were also noted. About one half of the patients remembered contact with arthropodes or a chronic migrating erythema. In most cases (95%), asymmetrical peripheral signs followed the painful stage. More than two thirds of the patients showed affection of cranial nerves, usually facial palsy. Twenty percent demonstrated paresis of the extremities alone, the combination of involvement of cranial nerves and extremities was noted in one third of the cases. The sensory signs were usually only mild. Occasionally, the neurological impairment was limited to isolated sensory impairment. In contrast to the closely related Lyme disease, central nervous affection as well as cardiac and arthritic involvement is rare: 34 percent demonstrated mild psychopathological impairment; in one case a Babinski-phenomenon was elicited. Knee joint pain and gonarthritis were found in one case each. Even though meningeal signs were usually absent, the CSF showed alterations suggestive of chronic lymphocytic meningitis in all cases. At the same time, local synthesis of all three immune globulins was documented, especially of IgM (85%).
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PMID:[Meningopolyneuritis (Garin-Bujadoux, Bannwarth) erythema chronicum migrans disease of the nervous system transmitted by ticks]. 389 83

An analysis of associated deformities in 74 patients with isolated microtia is reported. Microtia should be considered a microform of hemifacial microsomia because of similar (1) asymmetrical nature of the defects, (2) incidence and pattern of seventh nerve paresis, (3) correlation of the degree of seventh nerve weakness with grade of auricular deformity and not with the severity of mandibular hypoplasia, (4) right-sided preponderance, (5) incidence of associated cleft lip and palate, (6) male predilection, and (7) equivocal mode of inheritance. These clinical observations confirm the concept that microtia and hemifacial microsomia have the same etiopathogenesis which is not shared by mandibulofacial dysostosis.
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PMID:Microtia: a microform of hemifacial microsomia. 407 Apr 53

Conjugate gaze paresis was investigated in 436 patients who had suffered a severe stroke and were consecutively hospitalized for unilateral hemispheric damage. Gaze paresis was found in 120 and was associated with a high mortality, severe neurological impairment, and was more frequent in women. However, conjugate gaze paresis was also dependent on the side and locus of the lesion. It was more frequent, severe, and long-lasting in patients with right-sided brain damage. Moreover, it was preponderantly associated with post-Rolandic lesions in patients with right-sided brain damage and with involvement of the entire territory of distribution of the Sylvian artery in those with left-sided brain damage. This suggests that oculomotor centers have an asymmetrical organization in the two hemispheres, diffuse on the left and focalized on the right. It also explains why visual neglect occurs more frequently following right-sided brain damage.
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PMID:Conjugate gaze paresis in stroke patients with unilateral damage. An unexpected instance of hemispheric asymmetry. 710 96


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