What evidence is there for cognitive dysfunction in Parkinson's disease? What brain systems might be affected in these patients to cause these deficits?

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What evidence is there for cognitive dysfunction in Parkinson’s disease? What brain systems might be affected in these patients to cause these deficits?

        Parkinson’s disease is a neurodegenerative disease, characterised by resting tremors, rigidity, slowing of physical movements (bradykinesia) and reduced or nonexistent voluntary movement (hypokinesia) (Ramírez-Ruiz). Although depletion of dopaminergic neurons within the substantia nigra are predominantly the cause of these symptoms, the damage is not isolated as the peripheral, central, and enteric nervous systems are also affected (Braak and Braak 2000). The disease affects the neuronal cytoskeleton and as only selective cells can form this cytoskeleton abnormality, the damage caused by Parkinson’s disease creates a particular pattern of lesions, making the symptoms and cognitive deficits roughly consistent between patients (Braak and Braak 2000). The dopamine depletion is continual, but for the symptoms to be sunstantial enough to be noticed the levels must have been reduced by around 90% (Gazziniga, Ivry and Mangun, 2002). Although Parkinson’s disease has been linked to drug abuse and genetic factors, in most cases it is idiopathic (Gazzaniga et al, 2002). When Parkinson’s disease was first described it was not appreciated that it had any affect on the mental state of the individual, with the original statement regarding it stating ‘the senses and intellect are uninjured’ (Parkinson, 1817). However, it was found that Parkinson’s disease did cause cognitive deficits in memory, verbal, attention and executive function among many other areas. (Lezak, 1995). 

There is evidence to suggest that many areas of memory are affected including working memory, episodic memory, procedural learning, recall and prospective memory (Dujardin and Laurent, 2003; Whittington, Podd and Stewart-Williams 2006). However, there is much debate on this topic, with many contradictory conclusions generated as a result. An example of this is whether recognition memory is disturbed by Parkinson’s disease. The widely held view was that it remains unaltered despite the deterioration of other forms of memory (e.g. Flowers, Pearce and Pearce 1984). However, through a meta-analysis of data, Whittington, Podd, and Kan (2000) concluded that in fact procedural memory does indeed decline, with only the statistical power of the experiments that making it appear otherwise. Whittington et al (2006) confirmed this theory, as it found significant differences between Parkinson’s disease sufferers and normal controls in a recognition memory task.

The poor performance in this area has been attributed to various possible causes. One is the lapses of attention common in Parkinson’s disease, which will be discussed later, as it may have occurred during debriefing or during presentation of stimuli (Serrano and Garcia-Borreguero, 2004).  The impairments witnessed in this experiment could be do to deterioration of the cholinergic (Bedard et al 1999) or noradrenergic systems (Agid 1991) which is a feature of Parkinson’s disease. As the basal ganglia is the area most affected by this disease, it could be assumed that most deficits occurring as a result could be due to this, but very few experiments have been conducted into what processes the basal ganglia is responsible for, leaving it an ambiguous and underdeveloped area of study. Hay et al (2002), however is one of these few and found that a patient without Parkinson’s disease but with damage to the basal ganglia reflected similar memory deficits as he was impaired in recognition but not in recall tasks. This shows that memory impairments are likely to be a consequence of damage to the caudate.It has also been shown that frontal regions are affected by the disease and studies have shown that previously normal patients who have received frontal legions share some of the same deficits as those with Parkinson’s (Zgaljardic et al 2003). It is for this reason that executive functioning in Parkinson’s disease has been thought to be affected and this has been a suggestion as to why memory impairments are apparent as they cannot strategically retrieve memories to fit the task.

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        The presence and deterioration of prospective memory is another aspect that has been investigated. This refers to remembering to carry out postponed actions at a later point (Kerns, 2000) and has been an important area of study as it is thought to be governed by the frontal lobes and the connections from them to various other cortical and subcortical areas which have been associated with damage in Parkinson’s disease (McDaniel, Glisky, Rubin, Guynn, & Routhieaux, 1999). It has also been thought that prospective memory involves utilization of the central executive in working model which again is usually impaired in Parkinson’s disease ...

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