Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 52-year-old man with posttraumatic parkinsonism. He was admitted to our department because of right-sided hand tremor and gait disturbance. He had suffered from a severe head injury incurred in a traffic accident with brief unconsciousness 6 months before admission. Three weeks after his injury, tremor and rigidity in the right upper limb developed, and he walked dragging his right leg. Five months after his injury, he received 1-dopa therapy, exhibiting a moderate improvement in parkinsonian symptoms. On admission, he was demented to a mild degree with masked face and monotonous speech. He presented with resting-postural-kinetic tremor and muscle rigidity on the right side. Cranial CT and MRI showed no abnormality. Inter-peak latencies of waves III to V of BAEP were significantly longer in this patient than in normal subjects. This BAEP findings suggested an upper brainstem lesion. 123I-IMP SPECT disclosed decreased cerebral blood flow in the left thalamus, bilateral frontal and parietal cortices. We diagnosed this case as having posttraumatic parkinsonism. Parkinsonism in the present case may be due to the involvement of multiple neuronal circuits of the extrapyramidal system at the level of the midbrain to the thalamus.
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PMID:[A case of posttraumatic parkinsonism]. 176 60

We report a 65-year-old female who have suffered from progressive gait disturbance for 3 years, followed by disorientation and forgetfulness. Neurological examination revealed dementia, constructional disability, limb kinetic apraxia, supranuclear gaze palsy, especially on downward gaze, symmetrical muscle rigidity and bradykinesia. Involuntary movements were undetectable. Brain MRI showed significant brain atrophy in the left fronto-parietal lobe. The three-dimensional surface display with 131I-IMP demonstrated decreased cerebral blood flow in the left frontoparietal cortex. The diagnosis of this case is discussed with regard to either progressive supranuclear palsy or corticobasal degeneration or both.
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PMID:[A case with clinical features of progressive supranuclear palsy with apraxia--corticobasal degeneration?]. 772

A 63-year-old man was admitted to the hospital with a 1,5-year history of progressive dementia, supranuclear ophthalmoplegia, pseudobulbar palsy, rigidity and dystonia in the neck and the upper trunk. Magnetic resonance imagings showed severe atrophy of the frontal lobe and the brainstem. He was diagnosed as having progressive supranuclear palsy (PSP). Rigidity, nuchal dystonia, frequent micturition, and profuse sweating ameliorated after trazodone administration. Furthermore, additional administration of L-dopa and droxidopa improved his pseudobulbar palsy, akinesia, and lack of initiative. Single photon emission tomography using IMP after medication showed increased IMP-uptake in the frontal areas and the basal ganglia compared with that before medication. This patient illustrates a substantial role of impairments in the serotonin system in the production of some PSP symptoms.
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PMID:[A case of progressive supranuclear palsy showing improvement of rigidity, nuchal dystonia and autonomic failure with trazodone]. 783 44

We reported a 67-year-old male, who suffered from apraxia and amnesia for 2 years and for muscle rigidity of right extremities for a year. Neurological examination revealed dysarthria, dysphagia, marked dystonia of right arm, hyperreflexia of all limbs and ataxic gait. He also had dementia and many other higher cortical dysfunction mostly due to left hemisphere damage. No impairment of eye movement was disclosed. Brain MRI as well as CT showed the significant brain atrophy in the left parieto-occipital region. A degenerative atrophy was suspected by 123I-IMP-SPECT and 18F-FDG-PET. By FDG-PET, the decrease of cerebral blood flow and glucose metabolism was detected not only affected unilateral cerebral cortex including primary motor area but ipsilateral basal ganglia and thalamus. Although, it is difficult to distinguish clinically CBD from atypical case of Alzheimer's disease, we speculated that in early stage of dementia, significant unilateral hypoperfusion and hypometabolism of basal ganglia and thalamus is characteristic of CBD.
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PMID:[Clinically diagnosed corticobasal degeneration (CBD)]. 833 74