Affective disturbances are frequently reported in diseases of the basal ganglia. Symptoms common to many basal ganglia diseases include depression, anhedonia, apathy, and withdrawal. While a reaction to the physical impairments caused by these diseases may account for certain aspects of depression, there is evidence to suggest biological systems may underlie mood disturbances. Depression in Parkinson's disease appears to be the result of depletion of serotonin. Evidence of hypometabolism of the frontal cortex with bilateral lesions of the basal ganglia is reviewed and neuroanatomical and biochemical mechanisms underlying depressive pathology in basal ganglia diseases are postulated.
76 patients suffering from different basal ganglia diseases (28 cases with M. Parkinson, secondary parkinsonism and Parkinson diseases; 5 cases with Chorea Huntington; 5 cases with Fahr disease and 38 cases with M. Wilson) MRI featured 2 characteristical patterns: 1. abnormal deposition of minerals, 2. focal atrophies of involved organs. Thus MRI provides with informations about: 1. differential diagnosis in clinically misleading courses, 2. stage and, as a consequence, prognosis of some diseases, 3. biochemical processes of diseases in vivo.
Abstract In July 1957, at the First International Congress of Neurological Sciences in Brussels, J. N. Cumings summarized the state of our knowledge on the biochemistry of basal ganglia diseases in one sentence: "The biochemical pathologist has so far been of practical assistance to the clinical neurologist and to the patient in only one of the group of extrapyramidal disorders, namely hepato-lenticular degeneration."1 Progress in the understanding of Wilson's disease, which had been hesitant for many years,2 has been rapid and constant since 1957 but very little has been added to the biochemistry of the other basal ganglia diseases. For that reason we feel that some recent developments in this field must be brought to the attention of neurologists. As is well known, biochemical changes in mental disease, especially alterations in catechol-amine and serotonin metabolism, are becoming increasingly important, and it may be that the present findings will give References 1. Cumings, J. 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