Physiology of Parkinson’s Disease


A 69-year-old white male client was outpatiently admitted to a movement disorder clinic. He worked as a carpenter and reported a tremor in the right hand that later transferred to the contralateral extremity. The resting tremor lasted for one year. The client underwent neurological and oculomotor examination. The cognition was normal; oculomotor test did not reveal alarming indicators; upon the Myerson sigh test, the blinking was present.

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The client was observed to have an intermittent resting tremor in the upper right extremity. Cogwheel rigidity was also observed during the exposure to passive movement. The movements were slow (bradykinesia); the gait was normal, as were the equilibration-control reflexes. The client recalled that his late father used to have “the shakes” at approximately the same age. The client supposed, in retrospective, that his father might have had Parkinson’s disease (although no diagnosis was conducted and no treatment assigned) and feared he might have the same disorder.

It was decided that the treatment be initiated. Such decision was caused by the client’s age, occupation, and fear of adverse outcomes. The disorder itself, namely its rate of progress, present phenomenology, and the related impairments also triggered the initiation. The physician reasoned that on early stages of neurodegenerative diseases – specifically, Parkinson’s – the symptoms are generalized, and the best solution would be to prevent the disease from progression. A CR l-dopa formulation (Sinemet CR) was prescribed to curb the parkinsonism and prevent the motoric symptoms.

Background and Physiology

Parkinson’s disease is a neurodegenerative disorder with the most severe impact on CNS (Fytagoridid, Sandvik, Astrom, Bergenheim, & Blomstedt, 2012). The client described in the case is in his early stage of Parkinson’s disease, characterized by movement-related impairments. In the advanced stages, the disease manifests itself through cognitive and behavioral disorders, dementia, and clinical depression (Parkinson’s disease, 2016).

The treatment is complexified by the idiopathic nature of the disease. Genetics seems to have a part in it; some environmental factors have also been associated with the genesis of parkinsonism, such as exposure to pesticides and heavy metals (Parkinsons Anatomy, 2016).

The symptoms of Parkinson’s disease manifest themselves as a result of decreased activity of cells secreting dopamine. The decrease is caused by the death of cells in the mid-brain (namely, substantia nigra). Normally, the basal nuclei are connected to the circuits responsible for voluntary motion and provide them with protection. The ganglia normally release inhibitors permitting the activity of those circuits.

Additionally, the ganglia’s inhibition prevents the involuntary movement of various motoric systems (Quiroga-Varela, Walters, Brazhnik, Marin, & Obeso, 2013). A necessary component of the inhibition is dopamine, which is the reason high dopamine level facilitates motor capacity in a healthy person. Low levels of it (depletion) result in hypokinesia, the slow-down of motoric activity. Parkinson’s disease clients have lower levels of dopamine, meaning that the dopamine secretion is reduced, with slower and unsteadier movement as one of the ways the disease manifests itself (Obeso et al., 2008).

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The speculations on what causes the death of cells resulting in the depletion of dopamine have led to several theories. One of them is the accumulation of insoluble proteins inside the neurons. No lab tests exist to detect the disease at early stages, although tomographic scans can provide a hint by identifying the decrease in basal ganglia activity (Obeso et al., 2008).

Clinical Manifestations of Parkinson’s disease

The way Parkinson’s disease manifests itself on early stages can be seen from the case above. As the disease emerges, it mainly reveals motor dysfunctions. The four main indicators of parkinsonism are resting tremor, rigidity, hypokinesia, and an unsteady gait (Baranyi et al., 2016). These can occur in various combinations. A person on earlier stages of Parkinson’s disease can display asymmetrical extremity swing – bradykinesia – succeeded by stiffness in facial muscles and a wobbly voice.

As a rule, the mental component of Parkinson’s disease is not evident until the disease is in advanced stages (Jankovic & Poewe, 2012). Occasionally, such symptoms as fatigue, constipation, and insomnia can be present before the motoric dysfunction is evident. Such symptoms cannot be related to Parkinson’s disease until the motoric components are diagnosed. The interdependence of symptoms somewhat disencumbers the diagnosis and treatment considering that the disease has no univocal causes and cannot be cured, only curbed. On the other hand, some scholars advocate for the “premotor” manifestations and diagnosis (Obeso et al., 2010). The symptoms not related to dopamine depletion are still debatable.

A person with Parkinson’s disease in advanced stages is more subject to dementia than any other client; the longer is the Parkinson history – the higher the risk of a client being demented. Among other manifestations of an advanced-level Parkinson’s disease are altered behaviors, e.g., mood swings, cravings, eating disorders, hypersexuality, etc. (Jankovic & Poewe, 2012). In some cases, psychotic symptoms persist – such as hallucinations; these can be related with advanced age and l-dopa intake.


As evidenced by the case, the early stages of Parkinson’s disease are characterized by minor motor impairments and little or no mental dysfunction. The treatment options on the early stages of the disease include, primarily, not initiating the treatment at all or starting with symptomatic medications. These can include IR l-dopa, CR l-dopa, dopamine agonists, MAO-I, etc. Such treatment can be characterized as early symptomatic, and the client should be informed of such treatment status, as well as the prospective treatment.

At that, it is evidenced that the course of the disease cannot be reversed whatsoever; the treatment can only modify it (Korczyn & Hassin-Baer, 2015). The goal of early therapy is to curb the parkinsonism and stop the disease from progression. On subsequent stages of Parkinson’s, the symptoms are further exacerbated. Individuals with severe motoric impairments are under increased risk of falls and wearing-off (Jankovic & Poewe, 2012).

The individuals in this state receive dopamine agonists, MAO-I, l-dopa/carbidopa and other inhibitors. Additionally, ropinirole extended-release should be considered in treating of restlessness (namely, legs). Clients with prolonged Parkinson’s disease history (15 years and more) which are irresponsive to l-dopa, experience the wearing-off, fluctuate between the on/off states, can respond to combinations of entacapone and l-dopa/carbidopa (Jankovic & Poewe, 2012). NIR therapy has been also proposed as a method of disease modification, although it has not yet been generally accepted (Johnstone, Moro, Stone, Benabid, & Mitrofanis, 2016).

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Baranyi, M., Porceddu, P. F., Gölöncsér, F., Kulcsár, S., Otrokocsi, L., Kittel, Á.,… Sperlágh, B. (2016). Novel (Hetero)arylalkenyl propargylamine compounds are protective in toxin-induced models of Parkinson’s disease. Molecular Neurodegeneration 11, 6.

Fytagoridid, A., Sandvik, U., Astrom, M., Bergenheim, T., & Blomstedt, P. (2012). Long term follow-up of deep brain stimulation of the caudal zona incerta for essential tremor. Journal of Neurology, Neurosurgery & Psychiatry, 83, 258-262.

Jankovic, J., & Poewe, W. (2012). Therapies in Parkinson’s disease. Current Opinions in Neurology, 25(4), 433-447.

Johnstone, D. M., Moro, C., Stone, J., Benabid, A. L., & Mitrofanis, J. (2016). Turning On Lights to Stop Neurodegeneration: The Potential of Near Infrared Light Therapy in Alzheimer’s and Parkinson’s Disease. Frontiers in Neuroscience, 9, 500.

Korczyn, A. D., & Hassin-Baer, S. (2015). Can the disease course in Parkinson’s disease be slowed? BMC Medicine, 13, 295.

Obeso, J. A., Rodriguez-Oroz, M. C., Benitez-Temino, B., Blesa F. J., Guridi, J., Marin, C., & Rodriguez, M. (2008). Functional organization of the basal ganglia: Therapeutic implications for Parkinson’s disease. Movement Disorders, 23, 548-559.

Obeso, J. A., Rodriguez-Oroz, M. C., Goetz, C. G., Marin, C., Kordower, J. H., Rodriguez, M.,…Halliday, G. (2010). Missing pieces in the Parkinson’s disease puzzle. Nature Medicine, 16(6), 653-661.

Parkinsons Anatomy, Pathology, Prognosis and Diagnosis. (2016). Web.

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Parkinson’s disease. (2016). Web.

Quiroga-Varela, A., Walters, J.R., Brazhnik, E., Marin, C., & Obeso, J. A. (2013). What basal ganglia changes underlie the parkinsonian state? The significance of neuronal oscillatory activity. Neurobiology of Disease, 58, 242-248.

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