What evidence is there for cognitive dysfunction in Parkinson’s disease

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Parkinson’s disease is a neurodegenerative disease, characterised by resting tremors, rigidity, slowing of physical movements (bradykinesia) and reduced or nonexistent voluntary movement (hypokinesia). 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. 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 patients (Katai, Maruyama, Hashimoto, & Ikeda, 2003).

Therefore it would follow that since the areas of the brain required for prospective memory to operate are impaired in Parkinson’s disease that these patients show deficits on tasks relying on this process. This was confirmed in Katai (1999) who found that Parkinson’s disease patients performed significantly worse than normal controls on subtests of the Rivermead Behavioral Memory Test for prospective memory, although Katai et al (2003) discovered that this deficit is restricted to event related prospective memory, with their results on time-related tasks showing no significant differences with those of the control group.

An aspect of this research into memory is the fact that it is possible that rather than these patients having a specific deficit in memory, it could be that they have a deficit in another process that must be employed in order to complete the task.

For example, Buytenhuijs et al 1994 found that Parkinson’s disease sufferers have a preference for externally guided strategies and show deficits when they have to rely on self-guided or semantic strategies instead. It has been suggested that this theory explains why Parkinson’s disease patients perform worse on recall tasks than they do on recognition ones, as it the latter rely less on self-initiated approaches (Brown and Marsden 1990).

However, another reason for the selective nature of the memory deficit in Parkinson’s disease has been suggested to be that different types of memory rely on different systems, for example recollection relies on the hippocampus proper, whereas familiarity is dependent on the parahippocampal or perirhinal cortex (Wan, Aggleton and Brown 1999) and therefore it is possible that since they are only impaired in the latter, that the parahippocampal or perirphinal areas are damaged more so than the hippocampus proper.

The possibility that the damage occurs to these areas earlier on in the disease has also been proposed (Braak, Del Tredici, Rub, de Vos, Jansen Steur and Braak 2003). Studies into the nervous system suggest that Parkinson’s disease significantly damages the entorhinal region and hippocampal formation within in the limbic system, both of which, among other things, mediate memory functions as well as motor activity (Braak and Braak 2000).

Therefore it is probable that this damage that leads to the memory deficits evident in Parkinson’s disease patients in addition to the motor related symptoms. Selective impairments in linguistic ability have also been observed in Parkinson’s disease patients. Green, McDonald, Vitek, Evatt, Freeman, Haber,et al (2002) found that compared with normal controls, those with Parkinson’s disease performed badly on confrontation naming tasks. Additionally, semantic and phonemic cuing as well as word list generation processes have been shown to be affected (Henry and Crawford 2004).

The lack of verbal fluency has been attributed to a frontal or executive deficit. Skeel et al (2001) stated that the dysfunction of the basal ganglia most associated with Parkinson’s disease could not account for this alone, suggesting that damage in another area must be responsible. Longworth, Keenan, Barker, Marslen-Wilson, and Tyler (2005) emphasize the role of neocortical regions in language related functions which would imply that these deficits could be attributed to legions in this section instead.

A study conducted by Grossman, Lee, Morris, Stern, and Hurtig (2002) showed that when comparing the brain activation of Parkinson’s disease patients and normal controls while performing linguistic tasks of sentence processing, it is apparent that the former use less of the striatal anteromedial prefrontal and posterolateral temporal cortical regions. This shows that these regions are required for or at least used in this process, and the fact that Parkinson’s disease seems to affect the recruitment of these areas suggests that they must be damaged or impaired.

Attention is another area that has been investigated. In a normal functioning person, attentional control relies on a distributed fronto-parietal network (Reza-Naghavi and Nyberg 2005). Originally it was thought that attention remains unaffected by the disease, as experiments have indicated that those with Parkinson’s disease performed as well as controls in tasks of vigilance and sustained attention.

However, Bruck, Kurki, Kaasinen, Vahlberg and Rinne (2004) noted that atrophy of the prefrontal cortex was associated with attentional disturbance on a vigilance measuring task and therefore Parkinson’s disease patients differ biologically than normal controls, casting doubt on these findings. Further deficits in attention have been found, as although Parkinson’s disease patients are able to complete complex attentional tasks with the aid of external cues, when these are absent, thus requiring self-allocation of attention, they are unable to do so (Brown and Marsden 1998).

Additionally, both the ability to perform speed cognitive processing and to maintain attention on a task despite a distracter item are severely impaired (Vingerhoets, Verleden, Santens, Miatton and De Reuck 2003). As the frontal cortex is affected by Parkinson’s disease, it would follow that these patients would be impaired in the areas for which this area is responsible. It has been shown to be integral in high level cognitive functioning and there is evidence to support that the three frontal cortical regions have strong associations with behavioural and cognitive functions.

Parkinson’s disease patients have demonstrated deficits in working memory, trail-and-error method of learning, planning, monitoring of responses and set shifting (Zgaljardic et al 2003) which are indicative of damage mainly within the dorsolateral prefrontal cortex as this governs the majority of these processes. Zgaljardic et al (2003) suggested that the impairments in secondary memory and visuospatial processing problems expressed by Parkinson’s disease patients is very similar to a dysexecutive syndrome suggesting that similar processes are damaged or remaining unused.

The serotonergic, cholinergic and noradrenergic systems are affected by Parkinson’s disease which support this theory as damage to these systems produce dysexecutive syndrome. More generally speaking, the symptoms of Parkinson’s that do not relate to the motor problems associated with the disease have been shown to not be entirely down to the dopamine deficiency as the motor-symptoms are.

This was discovered as a result of experiments requiring Parkinson’s disease patients to complete certain tasks testing the cognitive dysfunctions apparent in the disease while under different levels of dopaminergic medication. As the difference in motor ability was not reflected in mental ability, it was concluded that other systems must be responsible (Dubois and Pillon (1997) However, in experiments conducted on both monkeys and humans, dopamine reduction did induce cognitive deficiencies alongside evidence of Parkinson’s disease (Schneider and Kovelowski 1990).

Additionally, Lange, Robbins, Marsden, James, Owen, and Paul et al (1992) found that dopamine withdrawal leads to difficulties in completing executive function tests and Brozoski Brown, Rosvold and Goldman (1979) discovered that reducing the dopamine levels in the prefrontal region in monkeys produces deficits in spatial delayed alternation tasks and so although dopamine levels may not directly affect the cognitive symptoms, it seems likely that they have some effect on them.

The frontostriatal circuits that connect the basal ganglia with the frontal lobe regions are strongly associated with cognitive and behavioural processes (Alenxander DeLong and Strick 1986) and this are linked with the serotonergic, dopaminergic, cholinergic and noradrenergic systems. As these systems are affected by Parkinson’s disease, their contribution to the frontostriatal circuits will be greatly inhibited, leading to a reduced if at all existent level of information processing modulation for which they are responsible (Tekin and Cummings 2002).

This therefore is a possible reason for the cognitive deficits present in Parkinson’s disease. In conclusion, despite earlier objections, cognitive dysfunction has been found to exist in Parkinson’s disease patients. This has been made evident by investigations into their performance in a wide range of tasks involving memory, attention, verbal fluency and executive function among many others.

Although the focus of Parkinson’s disease is the dopamine deficiency in the basal ganglia, this is not the only area that is affected. The disease reaches many regions of the brain either directly or indirectly, leaving the patient with many damaged brain systems. However, this topic remains one which is debateable and so more research is necessary in order for a full understanding of the range and extent of these cognitive dysfunctions.

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