Biomedical subjects

R Cecchetto

Publications and source records attributed to R Cecchetto.

2 recordsLinked to original sources

PubMed1986

Plasma beta-endorphin and beta-lipotropin in patients with Parkinson's disease.

Experimental and human data in young volunteers suggest that tuberoinfundibular dopaminergic systems physiologically inhibit pituitary secretion of beta-endorphin. This hypothesis was verified in patients with Parkinson's disease, a human model of a selective deficit of dopamine. Both previously untreated patients and patients who had been without chronic treatment for 1 week showed plasma beta-endorphin levels significantly higher than those of healthy age-matched controls. Plasma beta-lipotropin levels of patients and of controls were similar. There was no correlation between plasma opioid levels and age, severity, or duration of the disease. In five patients retested during chronic treatment, plasma levels both of beta-endorphin and of beta-lipotropin significantly decreased. This decrease approximately paralleled clinical improvement. The finding that in Parkinson's disease there is a reversible disinhibition of pituitary secretion of beta-endorphin confirms that this secretion is physiologically inhibited by tuberoinfundibular dopaminergic systems.

Aged↗

PubMedDate not supplied

Cognitive processes in insulin-dependent diabetes.

Cognitive processes in a group of neurologically asymptomatic patients with relatively severe but uncomplicated insulin-dependent diabetes mellitus (IDDM) were studied. In comparison with a homogeneous group of normoglycemic controls, the diabetic group performed significantly worse in global memory, abstract reasoning, and eye-hand coordination tests. The two groups scored similarly in intelligence, concentration and attention, spatial, visual, and psychomotor tests. The neuropsychological deficits did not correlate with the duration or the severity of the disease. Whether these mild neuropsychological deficits are transient or stable or whether they are caused by central nervous system vascular or metabolic dysfunctions or by the emotional influence of the chronic illness on the intellectual and educational development of patients remains unclear. Our findings need to be cautiously interpreted and perhaps could not be extended to diabetic patients with better metabolic control.

Adolescent↗