The neural mechanisms and progressive nature of symptoms of Parkinson's disease--based on clinical, neurophysiological and morphological studies.
The neural mechanism of parkinsonian motor symptoms, i.e., rigidity, tremor and akinesia, which are the result of nigrostriatal dopamine deficiency, is interpreted from long-term observations on the effect of surgical and pharmacological treatment of the disease in relation to the neuropathological findings within the substantia nigra zona compacta (SNc). Rigidity, tremor and secondary akinesia start first with degeneration of the ventral tier of the SNc followed by spread of the pathology to the dorsal tier, which may produce primary akinesia. Later, locus ceruleus pathology will be added. Spread of pathology is extremely slow in the juvenile or early onset parkinsonism (JP) compared with that in Parkinson's disease (PD). This spreading of pathology from one functional system to another might be one of the key factors responsible for the progressive worsening of the disease, which is different in speed between JP and PD.
Narabayashi
H
H
Neurological Clinic, Tokyo, Japan.
D004295:Dihydroxyphenylalanine / Q000009:adverse effects; D018450:Disease Progression; D004409:Dyskinesia, Drug-Induced; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D009069:Movement Disorders / Q000503:physiopathology; D009420:Nervous System / Q000503:physiopathology*; D010300:Parkinson Disease / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery
D007980:Levodopa; D004295:Dihydroxyphenylalanine