Thank you for your exploration of Parkinson’s disease (PD), an important neurologic disorder, especially of the elderly (Palma, 2018). Definitive diagnosis is histological, with its etiology visible as either loss of pigmented dopaminergic neurons of the substantia nigra pars compacta or the occurrence of Lewy bodies in neurons (Palma, 2018).
Genetic predisposition is likely since about 10% of patients have a family history of Parkinson’s disease. The genetic disease usually has an earlier onset with a usually more benign course compared to later-onset disease.
Secondary and tertiary prevention of illness is more feasible due to the lack of modifiable risk factors. That is important to the healthcare provider as they counsel the patient and relatives as well as health education as part of population health.
The defect is usually genetic, primarily a mutation in leucine-rich repeat kinase 2 (LRRK2; also known as PARK8), affecting the mandarin protein responsible for the neuron defects on histology and clinical presentation.
A gradual accumulation of defective protein in neurons in the illness causes an insidious onset of the disease. The degeneration that results in the dorsal aspect of the putamen on the basal ganglia is a critical cause of the characteristic motor manifestations.
It is primarily clinical, as alluded to. Palma (2018) note that it presents as tremor, reduced dexterity, reduced arm swing on the first-involved side, softening of voice, reduced facial expression, sleep disturbances, decreased olfaction, autonomic dysfunction, weakness, malaise or lassitude, depression or anhedonia, slow thinking, imaging, and lab tests are usually unremarkable therapy in the disease.