Essay on "Brain Structures/Systems Are Affected in Parkinsons Disease?"

Essay 7 pages (2651 words) Sources: 15

[EXCERPT] . . . .

brain structures/systems are affected in Parkinsons disease? What do the cognitive and emotional symptoms of the disease tell us about the possible functions of the different parts of these systems?"

Parkinsons Disease is a crippling, degenerative disorder that mainly affects a movement center of the brain. The disorder creates a shortage or limiting of action of the neurotransmitter dopamine which in a healthy brain triggers purposeful movement in the neurons of the region and is also shown to affect norepinepherine, to some degree. The disease is usually progressive, beginning with a single sided tremor usually in one hand, particularly when the individual is at rest and then can progress to tremors in all the limbs, all the time as well as slow movement (bradykinesia), an inability to move (akinesia), rigid limbs, a shuffling gait, and a stooped posture. It is also not uncommon for people with the disease to have reduced facial expressions and often speak in a soft voice, as a result of the neurological affect. Individuals may also experience fatigue, depression, personality changes, dementia and other cognitive function impairments. (National Institute of Neurological Disorders and Stroke, 2010)

There is some difficulty in separating the severe limitations of the disease, as well as the bleak prognosis from cognitive changes such as clinical depression as the disorder has limited treatment and can seriously affect quality of life. People with Parkinson's disease often show reduced facial expressions and speak in a soft voice. Occasionally, the disease also causes depression, personality changes, dementia, sleep disturbances, speech impairments, or sexual difficulties. It is also clear that there is only a limited knowledge of neurotransmitters and the normal function of receptors and transmitters both in the normal brain as well as the Parkinson's affected brain and cognitive manifestations, especially dementia can be positively linked with the disorder itself, rather than as a normative cognitive response to decreased quality of life and are also shown to directly affect the level of disability associated with the disease. (Weintraub, Moberg, Duda, Katz & Stern, 2004, pp. 784-788)

According to the National Institute of Neurological Disorders and Stroke:

The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 50. Early symptoms of PD are subtle and occur gradually. In some people the disease progresses more quickly than in others. As the disease progresses, the shaking, or tremor, which affects the majority of PD patients may begin to interfere with daily activities. Other symptoms may include depression and other emotional changes; difficulty in swallowing, chewing, and speaking; urinary problems or constipation; skin problems; and sleep disruptions. (NINDS, 2010)

There is also a longstanding tradition of research into the subtle cognitive changes in individuals, even in early onset untreated Parkinson's Disease, which has been identified since the 1980s and provides a great deal of insight into the normal functioning of the center of the brain affected by the disease;

No impairment of general intellectual function was found in the patients using the WAIS and New Adult Reading IQ tests and no abnormalities were apparent on cognitive estimates and two-choice Recognition Memory Tests. Patients with Parkinson's disease, however, had significantly greater difficulty in shifting conceptual sets and produced more perseverative errors on both the modified Wisconsin Card Sorting Test and Benton's Word Fluency Test. These subtle cognitive difficulties might underlie the mental inflexibility and rigidity of Parkinson's disease and could be attributed to destruction of the ascending dopaminergic meso-corticolimbic pathway. (Lees & Smith, 1983, p. 257)

Other early work attempted to identify the manner in which medical interventions slowed or changed the cognitive affects of the disease, likely with the hope that early intervention would ultimately limit, reduce or even eliminate cognitive impairments present in the disease, as it sometimes did with the motor affects of the disease. (Taylor, Saint-Cyr & Lang, 1987, pp. 35-51) Ultimately most research pointed to the idea that cognitive impairment, though often subtle through the early stages of the disease was persistent and often progressive, with the level of impairment, almost regardless of medical (pharmacological) intervention. (Gotham, Brown & Marsden, 1988, pp. 299-321) it was also made clear early on that despite initial assumptions the type of disease processes that caused the rare but persistent outcome of dementia (to a degree of impairment similar to progressive Alzheimer's) was not, contrary to previous assumptions related to the same neurological defects. Where Alzheimer's is associated with plaque deposition and tangled ganglia formations Parkinson's dementia is thought to be created by neurotransmission abnormalities:

…in Parkinsonian patients with dementia there were extensive reductions of choline acetyltransferase and less extensive reductions of acetylcholinesterase in all four cortical lobes. Choline acetyltransferase reductions in temporal neocortex correlated with the degree of mental impairment assessed by a test of memory and information but not with the extent of plaque or tangle formation. In Parkinson's but not Alzheimer's disease the decrease in neocortical (particularly temporal) choline acetyltransferase correlated with the number of neurons in the nucleus of Meynert suggesting that primary degeneration of these cholinergic neurons may be related, directly or indirectly, to declining cognitive function in Parkinson's disease. (Perry et.al. 1985, p. 413)

Cognitive function is therefore impaired by chemical rather than structural means, in that when the production of necessary neurotransmitters or the inability of cells to uptake these chemicals is impaired dementia may result, most often in late stages of the disease. Additionally the later the disease develops symptoms the more common dementia and other cognitive scale impairments are seen and these impairments can often be seen in cases where the absence of or only limited motor impairments are present. (Perry et.al. 1985, pp. 413-421) Sadly, due the fact that a great deal of knowledge on the subject is specialized and/or scholarly patients who exhibit atypical Parkinsonian cognitive impairment, such as dementia, that is not accompanied by motor impairments are often not screened for Parkinson's and can be overlooked for treatment.

In other words, because the disease develops differently in different people it can be easily misdiagnosed (especially in dementia cases) and treated as Alzheimer's which though limited in treatment does not have a treatment regimen that will positively affect Parkinsonian dementia or other symptoms. This sort of masked, atypical Parkinson's manifestation should demand more rigorous identification of etiology of Alzheimer's and other dementia diagnosis. Risk factors associated with environmental exposure and new research in genetic predisposition will likely aide in this oversight. (NINDS, 2010)

Additionally, early work on the cognitive impairments seen in Parkinson's Disease led to more substantive theory and testing regarding the affect of the disease and the centers of the brain affected by it, the substantia nigra which then sends messages (in the form of neurotransmitters) to the corpus striatum to produce purposeful smooth movement. Yet, it is clear from decades of research that this area of the brain, has multiple functioning and provides indications that cognitive functioning also has some significant links to purposeful movement and likely the reverse as well. In the following decade more research was conducted to isolate the cognitive impairments, in controlled trials with comparisons between medicated, non-medicated and early stage non-medicated patients with the disease and the results indicated that some cognitive impairments were persistent while others where shown to be progressive, in later stage medicated and non-medicated individuals, statistically dependant on the severity of the disease. The resulting research demonstrated that impairments were similar to those that had been reported in individuals (absent of disease) with frontal lobe damage. The later stage patients showed delays in the development of solutions to self-sorting problems but accuracy issues only came into play in more severe symptom sets, while all three groups, showed statistical impairment in attentional set-shifting ability but only higher degrede disability patients (medicated) showed impairment in short-term spatial memory functioning. (Owen, Leigh, Summers, Marsden, Quinn, Lange & Robbins, 1992, pp.1727-1751)

Ultimately, the early research indicates that the areas of the brain affected by Parkinson's are functionally responsible for some aspects of behavioral regulation in sorting or planning tasks, defective use of memory stores and impairment in the manipulation of internal representation of visuospatial stimuli.

These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The… READ MORE

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