Non motors symptoms of Parkinson disease (PD)can precede the symptoms related to dopamine deficiency by several years3and are the main determinants of qual­ity of life and institutionalization.            The non-motor symptoms are:Olfactory deficits hyposmia or anosmia, PD individual show a loss of mitral cells and substance P?containing cells in the olfactory bulb, amygdala and a reduction in the level of calcium-binding protein and this may be linked to ??synuclein-mediated pathology and to altered neurogenesis. Hallucinations have been linked to the presence of Lewy bodies in the occipital lobe and in ret­inal neurons, and to the loss of dopaminergic amacrine cells and the regulatory role of D1 dopamine receptors D1Rs and D2Rs in the eye. Pain and somatosensory disturbances: Nociceptive and neuropathic pain which can whether have a musculoskeletal ori­gin or central origin.

Other sensory changes are peripheral paraesthesia, burning sensation. The basal ganglia, locus coeruleus, raphe, nucleus, amygdala and thalamus are the implicate brain region. Dopamine, serotonin and noradrenaline are the neurotransmitter implicated.  Anxiety encompasses generalized anxiety, panic attacks and social phobias. Basal ganglia are affected and dopamine and noradrenaline are implicated.

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Depression is related to changes in dopaminergic, noradrenergic and serotonergic systems. Dopamine transporter availability in the striatum and limbic brain is reduced in PD patients with depression. Apathy may coexist with depression and dementia. Fatigue, basal ganglia dysfunction has been implicated in fatigue, reduced 5?HT transporter levels in the caudate nucleus, putamen, ventral striatum, thalamus, cingu­late and amygdala has been observed.

Cognitive deficits the affected area is the profontal cortex and dopamine is affected. Dementiais accompanied by a substantial reduction in cortical cholinergic markers. The severity of demetia in PD has been link to the density of Lewy bodies present. The areas aaffected are the temporal, parietal and occipital lobe. Acetylcholine is the implicated neurotransmitter.Psychosis include visual hallucinations and delusions, little structural change in cortical regions.

Decreases in retinal dopamine concentrations may also contribute to changes in visual perception. Sleep disorders: daytime somnolence, night-time sleep disorders include insomnia, Dopaminergic neurons in the ventral tegmental area–substantia nigra receive inputs from hypothalamic hypocretin neurons, reticula formation are affected as well. Dopamine and serotonin are the neurotransmitter implicated.Autonomic dysfunction Bladder dysfunction includes nocturia, and increased frequency and urgency of mictu­rition, which are associated with detrusor hyper-reflexia is thought to be related to loss of the inhibitory role of the basal ganglia.

specifically, the D1R?mediated output and the dopamine and acetylcholine are implicatedGastrointestinal dysfunction includes excessive salivation, dysphagia, impaired gastric emptying, constipation and impaired defecation. Multiple neurotransmitters and neuromodulators for example, acetylcholine, 5?HT, dopamine, noradrenaline, vasoactive intestinal peptide (VIP) and nitric oxide. con­trol bowel function. Cardiovascular features This dysfunction encompasses orthostatic hypotension and labile hypertension. Hyposmia presence and progression could represent a biomarker for early pre-motor PD Orthostatic hypotension is a marker of sympathetic dysfunction raised, cardiovascular may serve as a marker of early PD. The presence of ??synuclein aggregations along the gastrointestinal tract has been proposed as a diagnos­tic tool allowing early detection of the disease process before the onset of motor symptoms.

Schapira, A. H. V., K. R. Chaudhuri and P.

Jenner (2017). “Non-motor features of Parkinson disease.” Nat Rev Neurosci 18(7): 435-450.  

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