The pathological anatomy of posthemiplegic athetosis.
Disorders of movement after hemiplegia have been described for more than a century, but their pathological anatomy and physiology have remained poorly understood because of ambiguous terminology and incomplete studies. We examined the brains of 5 patients which had been serially sectioned where there had been well documented pure motor hemiplegia acquired in childhood. In 4 patients handicapped by hemiathetosis the main lesion was partial destruction of the caudate nucleus and putamen. In the fifth case, where non-disabling involuntary movements only appeared in later life, there was gliosis of the caudate nucleus and thalamus. Striatal lesions produce involuntary movement disorders if the corticospinal and other major motor tracts are partly intact. We propose that degeneration of the thalamic nuclei receiving striatal efferents (ventralis anterior, ventralis lateralis and centrum medianum), wheter primary or secondary, appears to remove an essential modulating influence on the corticospinal system which can only become manifest if this system is relatively preserved.
D000328:Adult; D001264:Athetosis / Q000150:complications / Q000473:pathology*; D001921:Brain / Q000098:blood supply / Q000473:pathology*; D001930:Brain Injuries / Q000150:complications; D002421:Caudate Nucleus / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000150:complications; D003342:Corpus Striatum / Q000473:pathology; D005260:Female; D005911:Gliosis; D005917:Globus Pallidus / Q000473:pathology; D006429:Hemiplegia / Q000150:complications / Q000473:pathology*; D006801:Humans; D007238:Infarction / Q000150:complications / Q000209:etiology; D008297:Male; D008875:Middle Aged; D009434:Neural Pathways; D009494:Neurosyphilis / Q000150:complications; D011699:Putamen / Q000473:pathology; D011712:Pyramidal Tracts / Q000473:pathology; D013787:Thalamic Nuclei / Q000473:pathology