Discuss The Causes Of Psychological Disturbances In Parkinson’s Disease

Discuss The Causes Of Psychological Disturbances In Parkinson’s Disease

In order to address the above the request it is important to define Parkinson’s disease; it’s known causes and main physiological symptoms. Many sufferers of PD experience cognitive and mental dysfunctions from a long list. The causes of such deficits are being debated to a great extent. There is no clear conclusion that states they are caused by chemical changes in the brain associated with PD or if the stressors of living and dealing with a difficult chronic illness cause them.

Much research has been undertaken in this area in order to improve our understanding of the causes f these phenomena and lots of new and contradictory results have been found. A discussion of depression in PD will highlight some of these. Parkinson’s Disease is defined as a “progressive neurodegenerative disorder” (Factor & Weiner, as cited in Hefti & Weiner, 1988). It is unclear whether there is a genetic or environmental cause. The four symptoms that classically define PD are tremor, rigidity, bradykinesia, and gait and postural abnormalities.

The underlying cause of PD seems to be a degeneration of parts of the basal ganglia – specifically, damage to the igra pars compacta – with a consequent loss of dopaminergic input to the neostriatum and ventral tegmental area of the midbrain (Forno, as cited in Hefti et al, 1988). Motor programs, which allow us to perform automatic actions, are contained within the basal ganglia. Hence, although the brain structures involving motor schema are intact, the lack of the neurotransmitter dopamine causes them to be poorly activated, resulting in the motor deficits described above (Hefti & Weiner, 1988).

When around 80 per cent of the cells have died in the substantia nigra the physical ymptoms start to appear. So the disease is actually quite advanced when these become apparent. Schwab & England (1958, as cited in Marsh & Markham, 1973) list a number of psychological disorders they believe to be symptomatic of PD, including changes in personality, depression, agitation, anxiety, confusion, dementia, paranoia and delusions. Due to the paucity of space this essay will concentrate on and discuss the causes of depression in PD.

Depression is marked by deep feelings of hopelessness and pessimism; it can be viewed in two ways. Some patients may become demoralized with the diagnosis of PD and experience a ‘reactive depression’. Reactive depressions are linked to external events and are short in duration. Typically the patient experiencing a reactive depression is able to resolve the issue and accept the diagnosis. Individuals experiencing a reactive depression may benefit from supportive psychotherapy (Bunting & Fitzsimmons, 1991). The most typical depression experienced by the patient with PD is endogenous depression.

Endogenous depression is caused by a iochemical imbalance in the brain and can be life threatening if not treated. When James Parkinson (1817, as cited in, Strange) first described, “the shaking palsy,” he said, “the senses and intellect remain intact. ” He did, however, note a high incidence of depression in his case studies, and even some suicidal tendencies. Since then, the incidence of depression in PD has been estimated to be as low as twenty per cent and as high as ninety per cent (Gotham, Brown, & Marsden, 1986) as compared to seven per cent in the general population.

The severity of depression in PD is almost always escribed as mild or moderate (Mayeux, as cited in Heilman & Satz, 1983). There have been many contradictory reports on the specifics of depression in PD, though almost all agreed that degrees of depression were found in PD above the normal rate, there is disagreement as to its cause. Some researchers argue that depression was one of the symptoms of PD, while others claim that depression is a reasonable emotional response to such a disabling condition as PD, and is not specifically a symptom of the disease.

Horn (1974) evaluated patients with PD for depression, and compared heir scores to those of a control group of healthy subjects and a group of paraplegics. The aim was to compare the depression present in PD patients with that of a group similarly physically disabled, in order to determine whether PD caused depression beyond that which would be reasonably expected from the degree of physical disability alone. It was found that, while the paraplegic group was more depressed than the control group, the PD patients were significantly more depressed than either of the two other groups.

Beyond showing that depression in PD was not a direct result of the degree f physical disability, her data in fact demonstrated that the degree of depression in PD was entirely unrelated to the degree of physical disability, the duration of the disease, or the age or sex of the sufferer. In other words, it seems that depression is not simply a psychological reaction to the presence of PD and its corresponding physical disability; it seems that depression is one of the psychological reactions directly caused by PD.

Robins (1976) discovered more about depression in PD while investigating the monoamine theory of depression. The monoamine theory sserts that depression (or at least some kinds of it) is caused by deficiencies of noradrenaline, dopamine, and seratonin in the brain. Robins noted that all three of these neurotransmitters are reduced in the brains of PD patients (especially dopamine), and that therefore the presence of depression in PD patients would lend support to the monoamine theory.

A control group of patients with severe chronic or permanent disability was chosen, and both groups are tested for depression. Although it was found that the degree of depression did not correlate to the degree of disability n either group, the results did clearly demonstrate that the PD patients exhibited significantly greater depression than the control group, even though the control group had a greater degree of physical disability.

Thus, while the depression in PD “may be partly reactive to the motor disability, its exaggerated nature when compared to that in patients with other more sever disabilities suggests that a further mechanism is operative” (Robins, 1976: 144). The severity of depression in PD is too great to be explained merely as a reaction to physical disability, and must be considered to be a esult of other damage.

Contradictory research has reported that there does seem to be a correlation between the severity of PD and depression within the sufferer. Schrag, Jahanshahi & Quinn (2001) conclude that depression in PD patients is associated with disease severity, recent disease deterioration and occurrence of falls. It does seem that depression is more strongly influenced by the patients’ perception of the handicap than by actual disability.

This report takes into account that the actual depression may be causing these patients to view their disabilities more severely than hey actually are, not vice versa. The researchers also discuss the inventory’s reliability; especially the ones requiring the patients to self rate their symptoms of PD and depression. The prevalence of depression in this sample appeared to be bimodal in distribution, with a higher percentage being depressed at the initial stages of the disease and a larger percentage at later stages.

This may indicate reactive depression soon after diagnosis, improvement of depression in the process of adaptation to a slowly advancing disease and improvement of parkinsonian eatures after initial treatment and subsequent recurrence of depression as the disease and it’s response to medication deteriorates. While there has been no reliable or valid correlation demonstrated between depression in PD and the duration or severity of the disease, Mayeux et al. (1981) did succeed in correlating the severity of depression to impairment of intellectual function.

Using the spouses of the patients as a control group, Mayeux et al. tested the subjects for neuropsychological skills (digit span, object naming, recall and epetition, language skills, etc), psychiatric abnormalities, and neurological dysfunction. While there was no correlation found between depression and severity of PD, there was a significant relationship between the degree of depression and performance on several cognitive tasks: calculation, digit span, constructions, and word recall.

This correlation between severity of depression and intellectual impairment again shows that depression is not simply a psychological reaction to a physical condition, but rather a direct result of specific brain damage. Gotham et al (1986) performed a similar test, but used self-rated tests to determine the degree of emotional dysfunction and the degree of physical disability. In contrast to other studies, the results indicated that PD patients had equal prevalence and severity of depression as other disabled patients, and that depression was correlated to the severity and duration of the disability in both groups.

This significant difference between self- and clinic-rated severity may cast doubt on the reliability of the patients’ self-rated depression, and hence on Gotham et al’s onclusion that depression in PD is resultant only from physical disability (a conclusion based on comparison to the self-rated arthritic patients’ scores). It is then still reasonable to believe that PD does cause depression apart from that caused by the degree of physical disability, and that this depression is not correlated to the severity of the PD.

Because it seems that depression is unrelated to the severity of PD, treatment of PD does not tend to decrease depression. Levadopa is the leading treatment of PD, and often produces improvements in the motor unction of patients. There have been many widely varied reports on how levadopa affects the psychological aspects of PD, however; some have reported a decrease in depression, and some an increase. Marsh and Markham (1973) tested PD patients for depression after three months of levadopa therapy, and again after fifteen months.

Although the PD group showed marked improvement of motor function after levadopa therapy, their depression score did not change after three or fifteen months. Marsh and Markham cite several studies that indicate both increased and decreased epression resulting from levadopa, and conclude that levadopa has an unreliable effect on depression. The evidence is fairly clear that depression is one of the most common effects of PD, depression accounting for the majority of psychiatric referrals in patients with PD.

There is indeed some indication that depression can be attributed to the deficiencies of dopamine and other neurotransmitters in the basal ganglia, which characterise PD. There are a few studies that report a correlation between severity of depression and severity of motor symptoms in PD, but these findings have mainly been eliant on self rated questionnaires, could the depressive symptoms be an indicator in the fact that PD patients rate their physical symptoms much worse than they actually are?

It could be argued that depression appearing before motor symptoms develop is most likely caused by the neurological changes of the disease itself, while depression or anxiety that occurs after the disease is diagnosed are due to the natural reaction to having a chronic and debilitating illness. Reactive depression does seem that it is bimodal, reacting do different stages of the disease may be a good ndicator of this.

The mechanism of depression in PD is poorly understood, if depression was solely due to neurochemical changes then surely all PD sufferers would have depressive symptoms. It may be that there is a neurochemical predisposition for depression in PD but the way in which the physiological symptoms are dealt with by each patient will affect the onset of PD. Maybe there isn’t such a distinct line between ‘reactive’ and ‘endogenous’ depression at all. It may be stated that endogenous depressive tendencies must exist before reactive depression can manifest itself.

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Discuss The Causes Of Psychological Disturbances In Parkinson's Disease. (2019, Mar 16). Retrieved December 15, 2019, from https://essaysonline.net/discuss-the-causes-of-psychological-disturbances-in-parkinsons-disease/