Pathophysiology of Parkinson`s Disease

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Pathophysiologyof Parkinson’s Disease

Thebrain plays an important role in the coordination of the bodyactivities. Various chemicals transmit signals across nerve cells ofthe brain. These chemicals are known as neurotransmitters withdopamine being one of them. Dopamine is a monoamine neurotransmitterproduced in the brain by dopaminergic neurons in the substantia nigrapart of the brain. It plays an important role in the coordination ofmuscle activities, emotional responses, and regulation of the brain’sreward and pleasure center (Gilman). Its deficiency leads toParkinson’s disease. This essay discusses the pathophysiology ofParkinson’s disease with its associated features.

Parkinson’sdisease is a neurodegenerative disease affecting the motor systemcaused by a deficiency in dopamine (Thomas and Beal). Such deficiencyis primarily associated with the degeneration of 25% of dopaminergicneurons responsible for dopamine production in the substantia nigra.Degeneration of neurons is associated with aging and normally occursin the sixth and seventh decades of life. However, in Parkinson’sdisease, such degeneration is highly accelerated leading to reduceddopamine levels. In addition, possible dysfunction in the remainingneurons causes the further reduction of dopamine levels, which inturn leads to neurologic deficits and manifestations of Parkinson’sdisease.

Lewybodies are found in the cytoplasm of some neurons and are evidence ofcell damage. Therefore, they are associated with the disease. Freeradicals produced during normal chemical reactions of the body candamage neurons as well leading to reduced dopamine production. Inaddition, genetic predisposition increases the risk of the disease.Environmental toxins such as manganese dust and carbon disulphidealso damage dopaminergic neurons and can lead to Parkinson’sdisease.

Thedeficiency of dopamine in the stratum leads to an abnormal firing ofneurons leading to uncoordinated movements (Thomas and Beal).Dopamine is also antagonistic to acetylcholine, anotherneurotransmitter. The overall effect of dopamine is the inhibition ofmuscle contraction while that of acetylcholine is muscle stimulation.In Parkinson’s disease, the dopamine levels are low while those ofacetylcholine are normal (Viartis). This leads to excessive musclecontraction from stimulation by acetylcholine.

Thedisease manifests itself in many forms. Motor manifestations includetremors while at rest, muscle rigidity arising from continuous musclestimulation by acetylcholine, bradykinesia which is slowed movements,and unstable posture (Hasegawa p. 1165). Motor weakness and stiffnessare witnessed after the loss of more than 25% of dopaminergic neuronsand is normally the first classical sign of Parkinson’s diseasefollowed by postural instability.

Muscletremors at rest occur in more than 70% of the patients. Musclerigidity is usually unilateral and is easily diagnosed by theclinician during the physical examination by resistance to passivemovement (Thomas and Beal). Patients may also experience “motorblock” characterized by the sudden inability to step forward whilewalking. Of all the motor symptoms, gait instability is the mostpotentially dangerous as it can lead to falls with resulting injuriesand fractures.

Cognitiveand psychiatric manifestations of Parkinson’s disease includedepression, hallucinations, delusions, irritability, memory loss, andanxiety. These results from the interruption of parallel circuitswithin the basal ganglia controlled by dopamine (Hasegawa p. 1167).Other manifestations, though not highly prevalent include autonomicnervous system failure signs such as orthostatic hypertension,constipation, urinary retention, and impotence.

Inconclusion, Parkinson’s disease is caused by the gradual loss ofdopaminergic neurons leading to a dopamine imbalance withacetylcholine. This leads to symptoms of tremors at rest, musclerigidity, postural instability, and slowed movements. Diagnosis ismade clinically through history taking and physical examination.Since the disease is as a result of dopamine deficiency, it canthereby be treated with dopamine replacement.


Gilman,Sid. “Neurobiologyof Disease”Burlington, Mass.: Elsevier Academic Press, 2007. Print.

Hasegawa,Takafumi. `&quotPathophysiology and Clinical Presentation ofParkinson`s Disease-Up to Date&quot Pathomechanisms of Parkinson`sdisease`. RinshoShinkeigaku51.11 (2011): 1165-1167. Web.

Thomas,B., and M. F. Beal. “Parkinson`s Disease”. HumanMolecular Genetics16.R2 (2007): R183-R194. Web. 12 Oct. 2015.,“Biochemistry of Parkinson`s Disease”. N. p., 2014. Web. 12 Oct.2015.