Current Issues in Psychopharmacology

Parkinson’s Disease (PD) affects one out of every 200 people in the United States over the age of 50, with 10% of the overall diagnosed younger than 50 years of age, for a combined total U.S. prevalence of 66 to 258/100,000 (Wickens, 2005; Berger, Dodel, & Oertel, 2001). The clinical presentation of PD usually includes loss of facial muscle tone, resting tremor of the hands, slowness of movement (bradykinesia), difficulty in initiating movement (akinesia), and increased muscle tone (rigidity). In one particular study in Canada, a mortality ratio of 2.5 was observed for those diagnosed with PD versus an age-adjusted control group (Furukaw, Guttman, & Kish, 2003). In 2003, PD became the 14th leading cause of death in the United States, accounting for nearly 7 out of every 100,000 deaths (QuickStats, 2003). The exact cause of PD is not yet known, but several factors have been implicated in the development and progression of the disease. However, in order to understand the onset, progression, and treatment of PD a foundational understanding of the neurological and synaptic systems involved must be laid.      

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The human nervous system is divided into two main sections: the peripheral nervous system, comprising the autonomic and somatic nervous systems, and the central nervous systems, which entails the spinal cord and brain. The main function of the spinal cord is to connect the peripheral nervous system with the brain. Furthermore, the brain can be sub-divided into sections: the forebrain, the midbrain, and the brain stem. It is the forebrain that is most implicated in the development of PD. The forebrain encompasses the cerebral cortex, thalamus, the basal ganglia, and the limbic system. If the spinal cord can be thought of like the front door and the various cranial nerves as the back door of a house, then the basal ganglia are the internal doorways that connect the various rooms. The basal ganglia does not have access to the direct manipulation of movement but appear only to modulate activity in other parts of the brain (Wickens, 2005). Furthermore, the basal ganglia consist of the striatum, globus pallidua, sub-thalamus, and the substantia nigra. It is the substantia nigra and the striatum that is the site of PD development and progression. However, before the disease itself can be considered the neural interactions of the basal ganglia must be taken into account. 

Neurons, the building blocks of the nervous system, conduct electrical impulses from their cell bodies (soma), down their axons, and into the synapses. The synapsis is the gap between the neurons, which is the site of sometimes intense neurochemical interactions. One of the neurotransmitters used in the neural synapsis to communicate between neurons is dopamine. Dopamine has a wide variety of uses in the human brain, with roles ranging from cognition, sleep, and attention—to reward, motivation, and voluntary movement (Dopamine, 2009). In the case of the basal ganglia, the substantia nigra creates dopamine, which is then transported to the innervated striatum. It is this dopaminergic pathway that is at the heart of PD and its proposed treatments. 

Now that a neurological and synaptic foundation has been laid, the actual causes and treatments of PD can be addressed. The causes of PD do not appear to be genetic but rather environmental, except in cases of early-onset (before 45 years) where a genetic correlation seems to be apparent (Furukaw, Guttman, & Kish, 2003). The causes of PD are reminiscent of the ecumenical position that all roads lead to heaven. For instance, a virus called encephalitis lethargica, similar to influenza at the onset ravaged much of the world in the early 20th century. What is odd is that the ones that survived the illness developed PD after the illness abated. Years later post-mortem examinations revealed PD-like deterioration of the substantia nigra in those afflicted with the virus. Then in the early 1980s, a group of Californians developed a drug (MPTP) which also caused PD symptoms and deterioration of the substantia nigra. However, the general causes of the deterioration of the substantia nigra in late-onset PD are not fully known as of yet. It is clear though that deterioration of the substantia nigra, leading to dopaminergic deficiency in the striatum is the source of the illness. One proposed hypothesis is that a special enzyme in the substantia nigra, called MAO-B, is deficient in those with late-onset PD. This particular enzyme bonds to free radicals in dopaminergic substantia nigra neurons to create non-toxic materials. It is interesting that MPTP works by causing an overabundance of free radicals in the substantia nigra, which leads to the degeneration of the substantia nigra. 

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The first line of treatment for PD is pretty straightforward. The substantia nigra is degraded and has lost the ability to make sufficient amounts of dopamine to supply the striatum, so give the patient more dopamine. The problem with this pretty straightforward approach is that dopamine cannot cross the blood-brain barrier created by the endothelial and astrocyte cells that line the vesicle walls of the brain (Blood-brain barrier, 2009). The solution for this problem was the implementation of levodopa, a precursor to dopamine which can pass through the blood-brain barrier. Then the striatum could have a steady supply of dopamine precursor from which to facilitate normal dopaminergic neural processes. The problem with this treatment is that it only treats the symptoms. Eventually, parts of the basal ganglia deteriorate beyond repair and the person succumbs to the effects of the disease. However, another treat, borne from the research concerning MPTP, is the MAO-B inhibitor selegiline (deprenyl). This pharmacological treatment works by inhibiting monoamine oxidase, which in turn controls the flow of harmful free radicals in the substantia nigra. Lenovadopa and MAO-B inhibitors are now the standard drug therapy preferred by most medical professionals who treat PD (Wickens, 2005). Other, more experimental, procedures include deep brain stimulation (DBS), adrenal gland grafts, foetal grafts, and stem cell research. Of which stem cell research is the most promising, offering a way to regenerate neurons in the substantia nigra, which can then produce dopamine without further assistance (Furukawa, Guttman, & Kish, 2003) 

There is currently no cure for PD, only medications and therapies that can slow the progression of the illness. PD is caused primarily by a degeneration of the substantia nigra, which in turn slows dopaminergic activity in the striatum. The effect of this degeneration is that voluntary movement is restricted substantially and control of posture is inhibited (resting tremors). Once the clinical presentation of the illness has been observed MAO-B inhibitors and levodopa are the standard treatments for the disease. The only proposed cure which offers more than ‘mild to moderate’ results is stem cell research, which is controversial at times because of the embryonic source of the stem cells (Wickens, 2005).   

References

Berger, K., Dodel, R., & Oertel, W. (2001). Health-related quality of life and healthcare utilization in patients with Parkinson’s Disease: Impact of motor fluctuations and dyskinesias. PharmacoEconomics, 19, 1013-1038. Retrieved April 7, 2009, from EBSCOHost Database. 

Blood-brain barrier. (2009). In Wikipedia, The Free Encyclopedia. Retrieved April 14, 2009, from http://en.wikipedia.org/w/index.php?title=Blood-brain_barrier&oldid=281333247

Dopamine. (2009). In Wikipedia, The Free Encyclopedia. Retrieved April 13, 2009, from http://en.wikipedia.org/w/index.php?title=Dopamine&oldid=283625287

Furukawa, Y., Guttman, M., & Kish, S. J. (2003). Current concepts in the diagnosis and management of Parkinson’s disease. CMAJ: Canadian Medical Association Journal, 168(3), 293. Retrieved April 7, 2009, from EBSCOHost Database. 

QuickStats: Age-adjusted death rates for Parkinson’s Disease—United States, 1973—2003. (2003). Retrieved April 13, 2009, from CDC.gov Web site: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5506a7.htm

Wickens, A. (2005). Foundations of biopsychology, 2e. Upper Saddle River, N.J.: Pearson Hall. 

Paper Topic

  • In preparation for this paper, select a current issue in psychopharmacology. Be sure to obtain faculty approval of your selected issue prior to beginning this assignment.
    • Prepare a 1,050 to 1,400-word paper in which you analyze your selected issue and its impact on the field of biological psychology. Additionally, be sure to address the following items in your analysis:
    • Describe the role of postsynaptic potentials (excitatory and inhibitory), synaptic transmission, and receptors in producing and regulating behavior.
    • Describe the primary neurotransmitters and their role in brain function and behavior.

Include at least two references in your paper from scholarly (peer-reviewed) sources, and be prepared to discuss this assignment in class.

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