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At least 1,081 records · Page 60Linked to original sources
PubMed1996

Basal ganglia and movement disorders: an update.

A model of basal ganglia functioning proposed a few years ago suggests that increased and decreased activity in basal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic movements as seen in Huntington's disease or after treatment with L-dopa and neuroleptics, respectively. Although the basic features of this model have stood the test of time, patterns of electrophysiological activity and changes in indices of GABA-dependent transmission in the external pallidum lead to a reconsideration of the mechanisms responsible for these changes in output activity.

Basal Ganglia↗
PubMed2000

[Homocystinuria with generalized chorea and other movement disorders: a case report].

We report a 50-year-old right-handed woman who, at age 20, was diagnosed to have homocystinuria presumably due to cystathionine beta-synthase deficiency. At age 40 years, involuntary movements developed insidiously, affecting her face, neck and upper limbs. During the next 10 years, involuntary movements progressed and she could no longer walk. Examination disclosed bilateral lens dislocation and marfanoid skeletal deformity. Muscle strength was mildly decreased in the right arm and bilateral legs. There was hyperreflexia in the right upper and bilateral lower extremities without Babinski sign. Muscle tone was mildly increased in the neck and bilateral upper extremities. She had persistent generalized choreic movements, dystonia affecting the face and neck, and resting and postural tremor in the upper limbs and tongue. A cranial CT scan showed an old low density lesion in the left frontal area. Involuntary movements in homocystinuria is rare and, to our knowledge, only 9 cases have been reported. This case was unique in that involuntary movements developed in the adulthood.

Chorea↗