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Parkinson's disease is most noted for tremor, rigidity, and slow movement. Patients with Parkinson's disease often develop memory deficits and difficulties with reasoning and other intellectual functions. However, these complications are not evenly distributed among all Parkinson's patients; they tend to be more common among patients who developed Parkinson's disease later in life. A study was undertaken to compare the intellectual disturbances in patients who developed Parkinson's disease at a younger age with those who developed the disorder later in life. The cases of 11 patients who developed Parkinson's disease before the age of 45 were compared with 11 patients who developed the disorder after 65. Each group of 11 was also compared with 11 healthy control subjects matched for age. Psychological testing revealed some intellectual deficits in the younger subjects, but these deficits were mild and the patients could largely compensate for them in their daily activities. Indeed, only the more complex of the psychological tests revealed the difficulty. The same was not true of the older patients, however. Testing of the older patients revealed more total intellectual deterioration. In addition to moderate memory problems, there were intellectual deficits that were of the sort associated with abnormal function of the frontal lobes of the brain. However, the language functions of these older patients were well preserved, a pattern common among patients with Parkinson's disease. The increased deficit of the older patients cannot be attributed entirely to their age, since similar deficits were not seen in the age-matched controls. Therefore, it seems that in younger patients with Parkinson's disease the deterioration is largely confined to movement. In older patients, however, the progression of movement disorders is soon followed by progressive deterioration of intellectual function as well. (Consumer Summary produced by Reliance Medical Information, Inc.)

In order to investigate the neuronal basis of cognitive disorders in Parkinson's disease, the neuropsychological performance of 120 patients with idiopathic Parkinson's disease was analysed in relation to motor symptoms as a function of their response to levodopa. Cognitive impairment was poorly correlated with akinesia and rigidity, symptoms which respond well to levodopa treatment, and was not correlated at all with that part of the patients' motor score that could be improved by the drug. In contrast, strong correlations were found between all neuropsychological test scores and axial symptoms such as gait disorder and dysarthria, which respond little if at all to levodopa treatment. The neuropsychological test scores were also strongly correlated with the motor score of patients estimated when clinical improvement was maximal under levodopa treatment. This score is assumed to represent residual non-dopaminergic motor dysfunctions. The correlations suggest that much of the cognitive impairment in Parkinson's disease results from the dysfunction of non-dopaminergic neuronal systems. [ABSTRACT FROM AUTHOR]

In order to investigate the neuronal basis of cognitive disorders in Parkinson's disease, the neuropsychological performance of 120 patients with idiopathic Parkinson's disease was analysed in relation to motor symptoms as a function of their response to levodopa. Cognitive impairment was poorly correlated with akinesia and rigidity, symptoms which respond well to levodopa treatment, and was not correlated at all with that part of the patients' motor score that could be improved by the drug. In contrast, strong correlations were found between all neuropsychological test scores and axial symptoms such as gait disorder and dysarthria, which respond little if at all to levodopa treatment. The neuropsychological test scores were also strongly correlated with the motor score of patients estimated when clinical improvement was maximal under levodopa treatment. This score is assumed to represent residual non-dopaminergic motor dysfunctions. The correlations suggest that much of the cognitive impairment in Parkinson's disease results from the dysfunction of non-dopaminergic neuronal systems. [ABSTRACT FROM AUTHOR]

In a series of 50 cases in which nerve and/or muscle microvasculitis was seen on biopsy, seven were associated with malignancy. In two cases, the cancer was found after the discovery of microvasculitis. All patients exhibited sensory-motor neuropathy, which was often painful and asymmetrical, with a progressive course. ESR and CSF protein levels were always elevated. Motor conduction velocity was slightly reduced in three cases, unmeasurable in one case, and normal in three. Cancers involved were adenocarcinoma in five cases (three prostate and two lung), Hodgkin's disease in one and immunoblastic lymphadenopathy in one. A thorough search for cancer should be performed when microvasculitis is seen in nerve or muscle biopsy specimens, especially when ESR and CSF protein levels are elevated. [ABSTRACT FROM AUTHOR]

A 39-year-old woman experienced severe headache, epilepsy and rapidly progressive aphasia and hemianopia. Carotid angiograms displayed segmentary narrowing of intracranial arteries as previously described in benign cerebral vasculitis. Her superficial temporal artery was also involved, allowing a biopsy of the abnormal part of the vessel. Microscopical study of this artery was normal. A second carotid angiogram, 14 days later, showed normal intracranial arteries. These findings suggest arterial spasm rather than distal arteritis. [ABSTRACT FROM AUTHOR]

Among a population of 75 hospitalised Parkinsonian subjects, confusional states were observed in 46% of demented patients not receiving anticholinergic drugs and in 93% of demented patients under anticholinergic therapy. The sensitivity of demented Parkinsonians to anticholinergic drugs can be attributed to a cholinergic deficiency which has been detected in the cortex and hippocampus of Parkinsonian patients post-mortem. The observations suggest that anticholinergic medication should be avoided in Parkinsonians with intellectual impairment. [ABSTRACT FROM AUTHOR]

Blood pressure and pulse rate were studied in 20 Parkinsonian patients on no treatment, and during treatment with bromocriptine (mean dosage 148 mg/day) as the sole anti-Parkinsonian therapy. The drug was shown to reduce erect systolic and diastolic and supine systolic blood pressure and to increase erect pulse rate, in a predictable dose-dependent manner. The occurrence of episodes of significant postural hypotension was less predictable and was a transitory phenomenon in all patients. Peripheral dopamine receptor blockade with domperidone did not alter the findings, suggesting that the principal mechanism for these cardiovascular effects is a central dopaminergic one. [ABSTRACT FROM AUTHOR]