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The long-term complications of Parkinson’s Disease

Many people do not realize that Parkinson’s Disease (PD) is one of the most complicated medical illnesses to manage. The truth is, PD is an illness that affects the body, mind and soul. Apart from the movement disorder, PD results in mental problems (depression, anxiety, hallucination), constipation, insomnia and many others. In addition, the doctor has to manage other concomitant illnesses that are commonly present in the elderly people such as high blood pressure, diabetes and heart problem.

Thus, the process of going through each Parkinson’s problems is a real challenge (and a headache as well). At the end of each clinic session, doctors often feel dizzy and exhausted after going through at least 40 problems; five complications for each of the eight Parkinson’s patients whom they treat.

As mentioned previously, most Parkinson’s patients eventually develop numerous complications especially during the late stage of the illness, such as follow:

a) motor complications

These complications are attributed to both progression of PD and long-term side effects of levodopa. Motor complications have been reported to occur in 50% of patients after three to five years of levodopa treatment (Marsden CD, Parkes JD and Quinn N, 1995). The motor complications usually appear in the later stage of illness (Parkinson Study Group, 1996).

The various types of motor complications are as follow:

i) “wearing off” effect

At the early stage of illness, patients generally feel “good” (the “on” period) for up to 12 hours after each dose of levodopa. However, the duration of the “on” period gradually shortens with time. When the “on” period becomes shorter than four hours, the patient is considered to have “wearing off” phenomenon. Patients often complain that they can walk freely for only two to three hours and need to take levodopa more frequently than before.

ii) “on and off” effect

The movement of patients fluctuates rapidly, sometimes within minutes, from “smooth” movement to “feeling stiff”. This occurs regardless of the time of ingestion of levodopa.

iii) “delayed on” effect

The effect of levodopa comes on only after more than half an hour (usually levodopa begins to work within half an hour after ingestion).

 

Picture 1. The “yo-yo” fluctuation of a Parkinson’s patient; the first photo showed that she was immobile and stiff, the second photo taken two hours later showed the dyskinesia involving both upper limbs and neck muscles. In addition, she has involuntary closure of the eyes due to dystonia.

iv) dyskinesia

Dyskinesia usually occurs after ingestion of levodopa (peak-dose dyskinesia). It manifests as uncontrollable swinging body movements which often affects all body parts. In mild to moderate cases (refer to dyskinesia-1 in the video section), patients can still carry out most of the daily activities. However, in severe cases (refer to dyskinesia-2 in the video section), dyskinesia can affect hand function (such as feeding, bathing and writing) to the extent that the quality of life is impaired. Many patients with severe dyskinesia lose weight simply because they can’t even hold the spoon steadily while eating (the excessive body movement also causes a high caloric consumption).

Dyskinesia usually lasts for about two to three hours (during “on” period) and subsides as soon as the effect of levodopa wears off. During the “off” period, the patient becomes stiff again. Thus, the patient goes through the same “yo-yo” cycle for the whole day; stages of “excessive dancing” movement that alternate with stages of “being motionless” (Picture 1).

Dyskinesia has been observed to be more common in younger Parkinson’s patients (Friedman A, 1994).

b) mental complications

PD itself only rarely causes mental complications. More often, the mental complications are attributed to the PD drugs, infection, hypoglycemia (low blood glucose) and electrolyte disturbances. The various types of mental complications are as follow:

i) depression

It is seen in about 40-60% of Parkinson’s patients (Waters CH, 1997). Typically, depression is present at two stages of PD: the early stage of illness as a manifestation of PD, and at the later stage as a reaction to increasing physical disability. In more severe cases, patients lose the will to live and may even attempt to take their own life (suicidal tendency).

ii) psychosis

It has been reported to be present in 10-50% of Parkinson’s patients (Factor SA, 1995). Some patients have delusion of persecution, that is, they are convinced that someone is out to harm them. Based on my own observation, Parkinson’s patients have a peculiar tendency to develop suspicion of their spouses; many of them feel that their spouses are conspiring with secret lovers to get rid of them! I believe this is partly due to feeling of inferiority that is an inherent problem in many Parkinson’s patients.

The most common type of hallucination is visual, such as seeing rats running under the bed. Sometimes, the visual hallucination can be frightening, for example seeing ghosts or strangers in the house. Auditory hallucination (hearing voices of non-existing people) is much less common in PD.

iii) confusion

This is a condition whereby the patient is no longer aware of the time, place and people around them – being in the “twilight zone”. Very often, the patient is also restless and agitated.

iv) dementia

This usually occurs during the late stage of PD, among about 30-40% of Parkinson’s patients (Lieberman et al, 1979; Celesia GG and Wanamaker WM, 1972). Dementia in PD (termed PD Dementia or PDD) leads to progressive memory loss, change of personality (e.g. becoming withdrawn) and poor judgment.

PDD is characterized by deficiency of Acetylcholine, a biochemical substance which acts as neurotransmitter (a “messenger” that facilitates communications between each brain cells) in the brain. Medications which increase the level of Acetylcholine in the brain, such as Rivastigmine (Exelon), have been shown to slow down the process of memory loss in PDD (Emre M, Aarsland D, Albanese A et al: 2004).

c) dysautonomia

This results in postural hypotension (low blood pressure), impotence, difficulty in passing urine and gastrointestinal problems (constipation, reflux oesophagitis and dysphagia).

  • Constipation is a very common problem in PD. It occurs because of several reasons: inadequate intake of fluids and fibre, side effect of PD drugs, poor physical mobility and PD itself.

 

  • Reflux oesophagitis (heartburn) refers to a condition in which the food and fluids from the stomach flow back to the throat and cause burning sensation in the chest. This chest pain is typically worsened by lying flat and relieved by sitting up (heartburn is usually felt while in bed).
  • Dysphagia refers to difficulty in swallowing that can be caused by PD itself. It sometimes occurs during the “off” period and disappears when levodopa becomes effective. It is important to realise that dysphagia can also be due to other diseases such as cancer of the stomach, and further investigations may be needed.

 

d) falls

This is discussed further in the following article.

e) sleep disorders

More than 75% of Parkinson’s patients have some form of sleep disorders (Pal PK et al, 1999). These can be in the form of difficulty in falling asleep, reversal of sleep cycle (sleeping during daytime and being awake during the night) and excessive daytime sleepiness (this can be due to inadequate sleep at night or side effect of PD medications).

Conclusions

It is obvious that the management of PD is not all about “slow movement”. It also includes the management of a wide range of complications that encompasses various subspecialties in Medicine. Very often, the Neurologists have to work hand in hand with psychiatrists (specialists who deal with mental problems), surgeons, geriatricians (specialists who deal with the illnesses of elderly people), etc. In other words, the best treatment is delivered by a “PD Team” that adopts a multi-disciplinary approach.

References

Celesia GG, Wanamaker WM. Psychiatric disturbances in Parkinson’s disease. Diseases of the nervous system, 1972; 33: 577-583.

Emre M, Aarsland D, Albanese A, et al. Rivastigmine for dementia
associated with Parkinson’s Disease. N Engl J Med 2004; 351: 2509-18.

Factor SA, Molho ES, Podskalny GD, Brown D. Parkinson’s disease: drug-induced psychiatric states. Adv Neurol 1995; 65: 115-38.

Friedman A. Older-onset Parkinson’s disease compared with younger-onset disease; clinical differences and similarities. Acta Neurol Scand 1994; 89: 258-61.

Lieberman A, Dziatolowski M, Coopersmith M, Cerb M, Goodgold A, Lorein J, Goldstein M. Dementia in Parkinson’s disease. Ann Neurol 1979; 6: 355-359.

Marsden CD, Parkes JD, Quinn N. Fluctuations of disability in Parkinson’s disease-clinical aspects. In: Marsden CD, Fahn S (eds) Movement Disorder 1 Reissue, Butterworth-Heinemann Ltd 1995, 96-122.

Pal PK, Calne S, Samii A and Fleming JAE. A review of the normal sleep and its disturbances in Parkinson’s disease. Parkinson Relat Disord 1999; 5: 1-17.

Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP patients requiring levodopa. Ann Neurol 1996; 39: 37-45.

Waters CH. Managing the late complications of Parkinson’s disease. Neurology 1997; 49 (Suppl 1): S49-57.