Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscular deficit, voluntary movement disorders, abnormal movements, and global disturbance of movements are considered. A muscular deficit is part of the Dejerine-Roussy syndrome. It appears as hemiparesis, regressive within days or weeks. A juxta-thalamic capsular involvement can be considered as the origin of this deficit in most cases, especially in hemorrhagic processes even if these are located within the thalamus, on account of mass effect. The occurrence of paresis or paralysis in ischemic processes strictly situated in the thalamus, however, is discussed: the deficit may be limited to parts of limbs; most often, it is not associated with pyramidal symptomatology; recovery is observed in the hand before the inferior limb. To these anatomoclinical facts some data from animal experiments or thalamic stereotaxic surgical procedures in humans must be added. A deafferentiation from the cortex seems to be the main cause of these motor disturbances. Three types of voluntary movement disorders may be encountered: contralateral cerebellar incoordination due to the involvement of the nucleus ventrooralis posterior where the superior cerebellar peduncle ends; homolateral imitative syncinesias, not confined to thalamic lesions, but frequently observed in this location with a particular aspect; contracture. Abnormal movements include choreoathetosic movements, and exceptionally intention and action tremor, and asterixis. They primarily involve the superior limb, but reported cases are not associated with thalamic limited lesions. Global disturbance of movements is observed in the hand or gait. "Thalamic hand" consists of incessant finger movements in the vertical and horizontal planes. They are associated with thalamic dystonia and deep sensibility disorder.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Motor symptomatology of the thalamus]. 378 43

Behaviors, actions and movements may take place as purely mental events, as in the obsessions of obsessive-compulsive disorder, phantom limbs or sensory tics. In the present paper we report on the case of a 43-year-old diabetic hypertensive man who developed an incomplete form of the Dejerine-Roussy syndrome. Whenever he lay down or withdrew the leg from the ground, he experienced the illusion that the left intermediate toes painfully twisted and mounted each other. Conversely, as he stood up or firm pressure was artificially exerted against the sole, there was a dramatic relief from the "cramp" whose illusory character could he be certain of only by looking down at the foot. By passively moving his toes into the referred position we realized that the experienced deformity conformed to the pattern of a fixed dystonia not outwardly expressed through the motor system. There was severe proprioceptive loss in the same toes that harbored the cramp. MRI showed the appropriate lesion in the posteroventrolateral thalamus (VPL) and wallerian degeneration of thalamo-cortical projections. SPECT showed hypoperfusion of the overlying ipsilateral parietal cortex as well as of the basal nuclei bilaterally, besides the expected image of thalamic exclusion. We hypothesize that the infarct disconnected the somatic sensory cortex (S-1) from critical proprioceptive input with relative sparing of superficial sensibility. Lifting the foot deprived S-1 of tonic inputs conveyed by undamaged contact-pressure pathways, a functional effect promptly reversed by placing the foot back against the ground. The case illustrates how a capricious deafferentation of S-1 by a discrete VPL thalamic infarct might facilitate the emergence of autochthonous activity.
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PMID:[Virtual dystonia due to posterior ventrolateral thalamic infarct: case report]. 910 96