Parkinson's disease

Parkinson's Disease

Parkinson's disease was first described by James Parkinson in his essay on the shaking palsy. The age of onset is around the age of 50, with incidence peaking during the mid-seventies. The prevalence is 190 by 100,000 population with the sex ratio of three is to two (male to female) with a five per cent familial incidence.

The cause of Parkinson's disease is unknown. Discordance in identical twins suggests that genetic factors are not important. Environmental mechanisms appear to play a role.

Increased interest in the role of exogenous toxins has arisen through the recent observation that in drug users Parkinsonism is reduced by selectively destroying nigral cells and their striatal projections. Virus infection seems an unlikely explanation in view of the worldwide distribution, lack of viral antibodies in the brain and inability to transmit the disease to primates.

In view of the unclear etiology of Parkinson's disease it is referred to as Idiopathic Parkinson's diseases as opposed to Secondary Parkinsonism where the possible causes are available (drugs like reserpine and haloperidol and the repetitive trauma to the head like in boxing).

There are visible changes in the brain of persons with Idiopathic Parkinson's disease. The substantia nigra contains the pigmented cells (neuromelanin) which give it a characteristic black appearance. These cells are lost in Parkinson's disease and the substantia nigra becomes pale. The remaining cells contain atypical eosinophilic inclusions in the cytoplasm called Lewy bodies. The presence of cortical inclusions is linked with dementia. There are also minor changes seen in other basal nuclei.

The initial symptoms of Parkinson's disease are vague, with the patient oftentimes complaining of aches and pains. The posture of the patient is bent. The face is expressionless with drooling (mask like facie). There are fine tremors in the hands described as pill rolling tremor. The legs are stiff and the gait is shuffling.

Early in the disease, a coarse tremor at a rate of four per second usually develops. The tremor begins unilaterally in the upper limbs and eventually spreads to all four limbs. The pill rolling tremor can be observed on the hands with the thumb moving rhythmically backwards and forwards on the palm of the hand. This tremor occurs at rest, improves with movement and disappears during sleep.

The rigidity of the body can be detected by examination. The body is in a typical flexed posture. The flexor muscles of the neck, trunk and limbs are in the semi-contracted position. The person is in the posture like that of a boxer.

When the facial muscles of expression are affected the face becomes expressionless. Also affected were the muscles of mastication, speech, voluntary swallowing and muscles of the trunk and limbs. The gait becomes robot like. Every step seems very heavy with little associated movements like arm swinging.

Signs and symptoms will worsen affecting every aspect of the patient's life. The handwriting will become smaller. The gait becomes shuffling with smaller rapid steps giving the impression that the patient is trying to keep up with the centre of gravity. The posture will become more bent. Initiating movements from a stationary position will become harder. Even rising from a chair becomes laborious. The movements of the eyeballs may also be affected. In some cases, although rare, there may be acute ocular deviation. There may also be excessive sweating and greasy skin. Patients may also have depression, postural hypotension and encephalitis.

Diagnosis of Parkinson's depends on high degree of suspicion based on complete history, physical examination and exclusion of other disease entities that mimic or can produce tremors and bradykinesia. Senile tremor, essential tremor and metabolic tremor are not visible during rest and will appear only and become more pronounced on voluntary movement. Distinguish also rigidity from spasticity. In spasticity, the resistance is felt towards the end of motion. In rigidity, resistance is present through the full range of movement.

Management is aimed to restore the balance between dopamine and acetycholine. Treatment is symptomatic and will not stop the pathologic process. The goal is to reduce acetycholine and its effects and increase dopamine. Anticholinergic drugs will reduce tremors but have minimal effect on the rigidity and bradykinesia. Dopamine and dopamine agonists will improve bradykinesia and rigidity with some degree of control of tremor. Good nursing care and the regular consultation to prevent complications are essential.