Conclusions and recommendations

Parkinson's disease is a chronic progressive neurodegenerative disorder of insidious onset, characterized by the presence of predominantly motor symptomatology (bradykinesia, rest tremor, rigidity, and postural disturbances). It is also associated with a diversity of non-motor symptoms, which, together with late-onset motor symptoms (such as postural instability and falls, freezing of gait, speech and swallowing difficulties), are presently one of the most difficult challenges the treating physician is faced with when dealing with patients with a long duration of the disease.

In addition to the motor symptomatology of Parkinson's disease (PD) (1), some non-motor symptoms such as hyposmia, rapid eye movements, sleep behaviour disorder, personality changes, pain, paresthesias and depression may be present and may even manifest before the motor symptoms (2). Urinary disturbances, orthostatic hypotension and neuropsychiatric disturbances (dementia, hallucinations and delirium) usually become evident and troublesome after several years in the course of the disease (3). Overt dementia is a late complication that most frequently affects older patients with prolonged disease duration (4). Late-onset motor symptoms include postural instability and falls, freezing of gait, speech and swallowing difficulties.

The pathophysiology of PD involves the progressive loss of dopamine-containing neurons of the pars compacta of the substantia nigra leading to denervation of the nigrostriatal tract and significant reduction of dopamine at the striatal level. The consequence of this denervation process is an imbalance in the striato-pallidal and pallido-thalamic output pathways, which is responsible for the major motor deficits (5). Genetic predisposing factors in combination with environmental factors are thought to be responsible for the cellular changes leading to progressive neuronal degeneration in which mitochondrial dysfunction, oxidative mechanisms and failure of the protein degradation machinery at the cellular level are probably involved (6). The presence of Lewy bodies (cytoplasmic proteinaceous inclusions) in surviving dopaminergic neurons is the pathological hallmark of PD.

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