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Alternatively, degeneration of the ascending cholinergic and catechola- minergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease. (Dubois & Pillon, 1996, pp.2-8)
The development of a greater understanding, over time of the causal factors as well as the manifestations and possible interventions for cognitive function in Parkinson's disease has continued since this time. Greater functional understanding of neurotransmitters and receptors as well as brain function in general have also significantly aided in the treatment Parkinson's Disease. Research has even led to the conclusion that standards dopamine (pharmacological) treatments while they improve some cognitive function (switching between two tasks "thought to depend on circuitry connecting the dorsolateral prefrontal cortex and the posterior parietal cortex to the dorsal caudate nucleus) might impair others that are usually spared by PD (probabilistic reversal learning, which; "implicates orbitofrontal cortex -- ventral striatal circuitry." involvement) (Cools, Barker, Sahakian & Robbins, 2001, p. 1136) the implications of this are that cognitive function as it related to neurotransmission and the physical aspects of the brain that it effects is a balancing act that requires substantive thought and development with regard to treatment. In 2002, research-based testing on humans began to surface on pharmacological treatments that were affective with regard to the cognitive impairments seen in PD, one such drug Donepezil (trade name Aricept a cholinesterase inhibitor) showed promise in mitigating the cognitive affects of PD when placebo was compared and improvement was shown for patients with PD in cognitive function and was well tolerated by the PD population. (Aarsland, Laake, Larsen & Janvin, 2002, pp) Surgical intervention is also a current point of study, with the development of implantation of deep subthalamic nucleus (STN) stimulation devices, yet again there were limitations on cognitive change development, with moderate improvements in depression, (in conjunction with improvement in motor function) but not on other cognitive impairments. (Funkiewiez, et.al. 2004, pp. 734-739)
Separating the emotional aspects of the disease from those that would be present in any chronic incurable disease is still more difficult than say cognitive function aspects to both interpret and research. Though previously thought to be nearly entirely associated with the degenerative nature of the disease the more that is learned about emotional and cognitive function, and the effects of multiple neurotransmission function the more it is believed that the emotional and cognitive processes are not simply associated with the bleak prognosis of PD and its limitations on quality of life. (Ishihara-Paul et. al. 2008, pp. 1148-1150) Surgical interventions involving subthalamic nucleus stimulation and the comparative research associated with them also indicate that discrete processes are at work in the whole of the system that indicate that any single area of the brain is responsible for all emotional and/or cognitive function changes but that the brain is a careful balancing act of microelectronics and chemical interactions.
Our results confirm that the STN is involved in both the apathy and emotion recognition networks. However, the absence of any correlation between apathy and emotion recognition impairment suggests that the worsening of apathy following surgery could not be explained by a lack of facial emotion recognition and that its behavioural and cognitive components should therefore also be taken into consideration. (Drapier et. al. 2008, pp. 2796-2801)
Current trends in research demonstrate that the cognitive and emotional functioning impairments may be discrete of one another but occur simultaneously and can be seen as nearly universal in PD patients, as compared to normal individuals. "The performance of the patients in memory tests and other tests evaluating cognitive capacity did not correlate either with their motor disability or with their mood. A possibility therefore exists that biological processes behind the cognitive decline and the motor disability are separate, even if they may occur simultaneously." (Hietanen, Teravainen, 2009, pp. 151-159) Further research will likely demonstrate this even more keenly as more and more diagnostic tools gain efficacy and more and more comparative research is conducted. The implications of research for the future include significant strides in understanding of the multifunctional balance of the neurotransmission centers that affect cognition, mobility and emotion.
Aarsland, D. Laake, K. Larsen, J.P. & Janvin, C. (2002) Donepezil for cognitive impairment in Parkinson's disease: a randomised controlled study. Journal of Neurology Neurosurgery & Psychiatry. 72 (6), 708-712.
Cools, R. Barker, R.A. Sahakian, B.J. & Robbins, T.W. (December 2001) Enhanced or Impaired Cognitive Function in Parkinson's Disease as a Function of Dopaminergic Medication and Task Demands. Cerebral Cortex, 11 (12), 1136-1143.
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Dubois, B. Pillon, B. (November 1996) Cognitive deficits in Parkinson's Disease. Journal of Nuerology. 244 (1), 2-8.
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National Institute of Neurological Disorders and Stroke (2010) NINDS Parkinson's Disease Information Page http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease.htm
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