By Colin Farrell B.Sc.

Parkinson’s Disease (PD) is a neurodegenerative disease with symptomatic features including impaired motor and autonomic function, cognitive impairment, and psychiatric disturbances (Cronin-Golomb, 2013). Juvenile-onset (occuring before age 20) and early-onset (occuring before age 40) are variants of the condition, which in its typical form classically occurs around age 60. Increasing age is the biggest risk factor for development of PD (Grosset, Fernandez, & Okun, 2009). It is the second most common neurodegenerative disease after Alzheimer’s Disease (Simuni & Pahwa, 2009). The leading cause of death in PD is pneumonia, frequently due to impairment of the swallowing muscles (Walker, 2013). Worldwide prevalence of PS  is generally accepted as 200 cases per 100,000 individuals, with men 1.5 times more likely than women to develop it (Chaudhuri, Clough, & Sethi, 2011). The number of individuals with PD in the Republic of Ireland is slightly lower than average and has been estimated at approximately 7,000 (Gustavsson et al., 2011).

Clinical features of PD include physical symptoms such as tremor, which most often occurs in the extremities but can also affect the lips, tongue, and face (Tuite, Thomas, & Reukert, 2009); and progressively slowed/reduced movement (Ling, Massey, Lees, Brown, & Day, 2012). The trademark Parkinsonian tremor or “resting tremor” occurs during muscle relaxation (Nistico et al., 2011); posture, balance, and gait are also facets of motor ability which are impaired (Mille et al. 2012). Patients have sometimes reported an internal tremor sensation, which can cause restlessness, discomfort, and distress (Friedman, 2009). Muscle rigidity is a common feature of PD, with increased tone and decreased strength resulting in likelihood of falls and slower walking speed (Paul, Canning, Sherrington, & Fung, 2012). Such motor symptoms often appear unilaterally at onset of the disease and usually progress to affect both sides of the body (Tuite, Thomas, & Reukert, 2009). Nonmotor symptoms which occur early in disease manifestation include olfactory deficit, Rapid Eye Movement sleep disorders, and erectile dysfunction; these are often manifest before diagnosis and have been identified as potential early indicators of PD (Chaudhuri & Naidu, 2008).

Cognitive impairment is increasingly recognised as a symptom of PD (Archibald, Hutton, Clarke, Mosimann, & Burn, 2013); with 1 in every 4-5 patients suffering from dementia to some extent (Weiner, Shulman & Lang, 2006). Mild cognitive impairment is also prevalent, and is associated with more accompanying neuropsychiatric symptoms (Maranon, Amayra, Uterga & Gomez-Esteban, 2011). Such symptoms include sleep disturbances, anxiety, dysphoria/depression, delusions, and hallucinations (Leroi, Pantula, McDonald, & Harbishettar, 2012).

PD is caused by the loss of dopiminergenic neurons in the area of the midbrain known as the substantia nigra; while several genes have been identified in the pathogenesis of this neuronal loss, specific understanding of disease activation and progression are not well defined (Filatova, Alieva, Shadrina, & Slominsky, 2012). Also implicated in PD is the dysfunction and accumulation of alpha-synuclein proteins in the brainstem and basal ganglia to the cerebral cortex (Shoji et al., 2000). Alpha-synuclein aggregates to form what are known as Lewy Bodies, cytotoxic materials which cause cell death in surrounding cortical areas (Wakabayashi et al., 2013).

In terms of neuropharmacological treatment for PD, the biochemical Levodopa is still the clinicians’ standard in reduction and management of parkinsonian symptoms (Kääriäinen, et al., 2012). This occurs through restoration of extracellular dopamine levels in the PD affected cortical areas (Navailles, Carta, Guthrie, & De Deurwaerdère, 2011); however, a complication arising from this treatment is eventual persistence of involuntary movements due to neural plasticity in these areas (Iravani, McCreary, & Jenner, 2012). In addition, the drug rasagiline has been found to have rapid and significant efficacy in reduction of motor symptoms – particularly in problems with slowness of movement (Silver & Buck, 2011; Zambito Marsala et al., 2013). Treatment utilising both drugs simultaneously has also shown positive results (Zhang et al., 2013).

As symptoms often present at an advanced stage of disease progression in PD, this inhibits the efficacy of treatments; therefore further exploration of its pathogenesis is a priority for research in the near future (Khaindrava et al, 2011). A solution to this issue may lie in combining neuroimaging techniques such as transcranial sonography and scintigraphy (Behnke et al., 2013). Other recent advances in early diagnosis have been achieved through identification of blood based biomarkers using identification of specific proteins and autoantibodies (Pagan, 2012).



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