Clinical manifestations of cholinergic deficiency in patients with Parkinson's disease

Abstract

Background. According to the new concept of Parkinson's disease, the brain suffers from a generalized deficit of neuromediators inclusively serotonergic, adrenergic, dopaminergic, cholinergic and monoaminergic. An important role in the pathophysiology and biocellular mechanisms of Parkinson's disease is played by the cholinergic deficit that becomes evident later than the dopaminergic deficit Case report. An important role in the pathophysiology and biocellular mechanisms of Parkinson's disease is played by the cholinergic deficit that becomes evident later than the dopaminergic deficit. Cholinergic neurons that are diffusely distributed in the cerebral parenchyma play an important role by its involvement in numerous brain processes, the most important being the accomplishment of the superior brain functions. Thus, with the progress ofthe disease a large part of the patients develop cognitive disorders / dementia due to cholinergic deficit. In this paper, the features of cholinergic deficits in patients with Parkinson's disease and their clinical correlations are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions refer to cholinergic neurotransmission at the synaptic level, pathway and circuit. Of interest would be the fact that there is evidence of the connection between cholinergic changes and motor symptoms, gait dysfunction, levodopa-induced dyskinesia, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction and impaired olfactory function. The pathophysiology of these symptoms is related to the alteration of cholinergic tone in striated and degeneration of cholinergic nuclei, the most important being the magnocellular basal nucleus and pedunculopontine nucleus. Finally, several drugs acting on muscarinic receptors have been shown to be effective in the treatment of levodopa-induced dyskinesia and cognitive impairment but also as neuroprotective agents in experiments made on humans. However experimental results on patients are missing. Conclusions. Parkinson's disease is a neurodegenerative disease with diffuse damage of the cholinergic system. Thus, with the progression of the disease occurs an expressed heterogeneity of clinical manifestations.