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The frequency of dementia, the clinical characteristics and the pattern of cognitive impairment were studied in 147 unselected Parkinsonian patients. Twenty-one patients (14.28%) were judged to be demented. They had a more severe and widespread cognitive deficit although they were affected particularly in those tests that already discriminated Parkinsonian patients from controls. A direct comparison of Parkinsonian dementia with other types of dementia is needed to validate the concept of subcortical dementia. [ABSTRACT FROM AUTHOR]

Twenty-one Parkinsonian patients were tested in on and off phases during chronic levodopa therapy for cognitive function, affective status, and evaluation of motor performance with reaction and movement times. A worsening of mood was observed from the on to the off phase. No variation in cognitive performance was observed from the on to the off phase in spite of evident motor changes. Mood changes during on-off variations may reflect involvement of mesocortical and mesolimbic dopaminergic systems. [ABSTRACT FROM AUTHOR]

Eighteen patients with Huntington's chorea were examined before and after neuroleptic treatment (haloperidol, pimozide, tiapride) to study the effect of such treatment on hyperkinesia and motor performance. Pimozide and haloperidol improved hyperkinesia; none of the drugs significantly affected motor performance. No correlation was found between the severity of hyperkinesia and motor performance scores, or between hyperkinesia and intelligence score, before and after therapy. [ABSTRACT FROM AUTHOR]

Madopar, a combination of levodopa with benserazide, induced an inconsistent rise in plasma growth hormone in unmedicated patients with Parkinson's disease and in controls, and a greater growth hormone rise in Parkinsonian subjects on chronic Madopar therapy. In subjects on chronic therapy with levodopa and carbidopa (Sinemet), the growth hormone releasing effect of Madopar was blunted. Madopar increased plasma prolactin (PRL) in controls, unmedicated patients and patients on Madopar therapy while in patients on Sinemet therapy the PRL-releasing effect of Madopar was strikingly reduced. Since these data were interpreted as due to a defective dopamine tone in the hypothalamus of Parkinsonian subjects on Madopar but not Sinemet therapy, a direct dopamine receptor agonist, lisuride was administered. Lisuride, however, elicited a blunted growth hormone response both in patients on Madopar and Sinemet therapy, without revealing a state of supersensitivity of dopamine receptors for growth hormone control in Parkinsonian subjects on Madopar therapy. No difference was present in the PRL-lowering effect of lisuride in the different experimental groups. These findings suggest that: (1) hypothalamic dopamine function is impaired in Parkinsonian subjects on Madopar therapy, preserved in unmedicated patients and enhanced in patients on Sinemet therapy; (2) the endocrine effects observed in Parkinsonian subjects on chronic Madopar therapy may be due to some penetration of benserazide across the blood brain barrier in the region of the hypothalamus; (3) since Madopar and Sinemet are in essence equally effective antiparkinsonian remedies, penetration of benserazide does not occur across the blood brain barrier surrounding the nigrostriatal system. [ABSTRACT FROM AUTHOR]

Electro-oculographic recordings were obtained from 11 patients with Huntington's disease. Significant reduction of saccadic velocity was constantly found. In all the patients vertical saccades were much more impaired than horizontal. When present, vertical saccades showed long latency, low amplitude, low velocity, and disturbances related to blinking. Following movements were jerky, and ability to perform repeated rhythmic movements was impaired. These results are in agreement with previous observations and underline the selective defect of rapid movements as a characteristic feature of Huntington's disease. Further, they suggest a possible correlation between the difficulty in performing repeated ocular movements and the impaired execution of gestural sequences involving a succession of different fundamental movements. [ABSTRACT FROM AUTHOR]

A double-blind crossover trial with 2-dimethylaminoethanol (Deanol), a possible precursor of brain acetylcholine, was carried out in nine patients with Huntington's chorea. It was found to be ineffective in inducing any alteration in hyperkinesia. [ABSTRACT FROM AUTHOR]

Twenty-six patients affected by Parkinson's disease were treated with a 2-Br-alpha-ergocriptine (CB 154): 14 cases were given CB 154 alone, and 12 were given CB 154 along with L-dopa plus benserazide (Madopar). Both CB 154 and combined therapy (CB 154+Madopar) induced a significant improvement in total disability score, tremor, rigidity, akinesia, self-sufficiency, and some motor performance tests (dynamic tests). No significant difference was found between results obtained with CB 154 therapy and with Madopar treatment, while the improvement induced by combined therapy (CB 154+Madopar) was significantly higher than that obtained by Madopar alone. The averse reactions caused by CB 154 alone or associated with Madopar are similar to those observed during other dopaminergic treatment. CB 154 alone or combined with Madopar appears to be a useful advance in the management of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Fifteen patients affected by Huntington's chorea were divided into two groups, 'slow' and 'fast', according to IQ scores on the Wechsler-Bellevue scale, and scores on some motor performance tests. A possible correlation was looked for between some biochemical data (cerebrospinal fluid (CSF), homovanillic acid (HVA), and 5-hydroxyindolacetic acid (5HIAA) levels, plasma dopamine-beta-hydroxylase (DBH), dopamine (DA) uptake by platelets), and clinical data (duration of illness, severity of symptoms, age of patients, IQ scores, 'slow' and 'fast' groups). The CSF, HVA, and 5HIAA levels were found to be significantly lowered in comparison with normal controls. DBH activity and DA uptake by platelets did not differ significantly from normal subjects. Treatment with haloperidol in all patients and with dipropylacetic acid in three patients did not appear to modify the CSF, HVA, and 5HIAA concentrations, the plasma DBH activity, or the DA uptake. There were no significant differences in the CSF, HVA, and 5HIAA contents between the two groups of patients, and there was no correlation between biochemical data and clinical features. [ABSTRACT FROM AUTHOR]