It is one of the commonest neurodegenerative disorder of the elderly and affects about 1% of the people above the age of 60 years and 4% people above the age of 40 years affecting both sexes equally.

Parkinsons disease was described in 1817 by James Parkinson as a clinical syndrome characterized by bradykinesia, tremor, and slow shuffling gait with postural instability and was given the name of ‘shaking palsy’. The disease is of world wide distribution.

Its onset is insidious usually over a period of 2-3 years with a progressive and prolonged course. It may run in families with familial incidence of 1-2%. First degree relatives have a 2-3 fold increased risk of Parkinson’s disease.


It is unknown. A number of factors ranging from Toxins, Environmental factors, infections, poisons, Drugs to trauma have been incriminated in the causation of disease. There is degenration of dopaminergic cells in the basal ganglia leading to interferance in neural transmission.

Clinical classification

Syndrome of parkinsonism is classified into primary. Secondary and parkinsonism plus syndromes. Primary parkinsonism is the idiopathic form where there is no cause to explain the degeneration of the neurons of the substantia nigra while in secondary parkinsonism a number of factors operate.

Clinical classification of parkinsons disease

I. Primary parkinsonism (Parkinsons disease)

2. Secondary parkinsonism

(a) Drug induced:

Phenothiazines, reserpine, haloperidol, lithium, metoclopramide.

(b) Toxins: Pesticides, MPTP (synthetic heroin). hexane, toluenc, petroleum products, manganese, carbon monoxide..

(c) Viral: Post encephalitic (Japanese B encephalitis), Western equine encephalities, encephalitis, lethargica, subacute scierosing panencephalitis.

(d) Trauma: Head injury, punch drunk syndrome in boxers.

(e) Vascular: Atherosclerosis.

3. Parkinsonism Plus syndrome:

(a) Progressive supranuclear palsy

(b) Multisystem atrophy

(c) Cortico basal degeneration

(d) Wilson’s disease

(e) Huntigton’s chorea

(f) Diffuse Lewy body disease

(g) Parkinsonism dementia syndromes.


Characteristically there is degeneration and loss of dopaminergic neurones in the substantia nigra. There is appearance of eosinophilic cytoplasmic inclusion bodies known as Lewy bodies and neuro fibrillary tangles. Degeneration also occurs in other brain stem nuclei (corpus striatum, caudate nucleus. Putamen and globus pallidus).

Biochemically there is loss of dopamine in the corpus striatum. The normal functioning of basal ganglia system is dependant on equilibrium between acctylcholine and dopamine secretions.

Imbalance between these results in parkinsonism. With dopamine deficiency, there is hyper activity of acetylcholine and this may be a mechanism for symptoms of parkinsonism. Other neurotrasmitters such as nor epinephrine, gamma aminobutyar acid, serotonin and enkephalins may also have a role in this.

Parkinsons disease

Clinical features

Typically Parkinson’s disease is a disorder of middle or elderly age group with a progressive and prolonged course. Early symptoms of Parkinson’s disease consist of lack of movements (akinesia), paucity of movements (bradykinesia), stiffness and rigidity of limbs, postural disturbances, pill rolling movements and typical facies.

1. Facies, attitude and movements

Patient has a mask like facies. The facial muscles exhibit an unnatural immobility (expressionless). When glabella is tapped repeatedly there is infrequent blinking as compared to a normal person (glabellar tap positive).

There is attitude of limbs lying in flexion. Voluntary movements are slow to initiate, reduced and lack precision. Movements which are carried out by small muscles suffer most such as closure of eyes, mastication, deglutation and articulation.

There is hypokinesia (poverty) or slowing down (bradykinesia) of automatic and voluntary movements. Acts of walking, dressing and even feeding are slowed down. Swinging of the arms while walking are effected markedly. Hand writing becomes smaller (micro graphia). Speech is slurred, monotonous and soft (Hypophonia) and later on becomes barely audible.

There is difficulty in initiating movements. Rapid movements such as finger tapping (Piano playing movements) opening and closing of the fist, pronation and supination of the forearm are effected. Though the movements become slow yet the motor power is usually normal.

2. Muscular rigidity

Increase in tone resulting in equal rigidity in both opposing group of muscles is characteristic. This is present uniformly throughout the whole range of movement (lead pipe rigidity) in contrast to rigidity in cases of upper motor neurone lesions where rigidily is felt maximally at the start of the movement.

Parkinsonian rigidity is often unequal on two sides. When rigidity is combined with tremors it becomes interrupted and is known as ‘cogwheel rigidily’ (Ratcheling movements)

3. Gait Patient has a slow shuffling gait and it consist of small steps

Patient may have a tendency to advance huff iedly with small steps (Festinant gait). He is unable to stop quickly when pushed gently forwards or backwards (propulsion and retropulsion).

Because of rigidity, patient often assumes a stooped posture. There may be marked degree of kyphosis. Rising from a sitting position may require several attempts. A freezing phenomenon causes the patient to suddenly stop in the middle of a movement in contrast to another phenomenon called ‘paradoxical kinesia’, where patient can suddenly move with ease for short periods.

This is seen when patient tries to cross over an obstacle. Patients of parkinsonism have difficulty in tuming round and falls are common due to poor postural adjustments.

4. Tremors

Tremors are more marked at rest. This is characteristic 4-7 Hz rest tremor. The tremor is asymmetric, seen in the beginning in the hands and later on becomes more extensive involving the lower limbs, face, lips and tongue. The classical pill rolling tremor of parkinsonism is coarse, present mainly at rest and is suppressed by voluntary movements.

Cognitive, Autonomic and Sensory disturbances. There is no loss of sensation. At least a great majority of patients suffer from slowness of thought process and inattentiveness. Depression and dementia may be seen in late stages.

Constipation and urinary difficulties and mild to moderate degree of orthostatic hypotension may occur. Reflexes are usually preserved and not affected.


Diagnosis of Parkinson’s disease is not difficult since a patient has typical features of mask like facies, Tremors, generalized rigidity and a festinant gait. The National Institute for Neurological Disorder and Stroke (NINDS) has outlined diagnostic criteria which itself is self explanatory.

Ninds diagnostic criteria for Parkinsons Disease (RD.)

Fratures characteristic of PD.

1. Resting tremor

2. Bradykinesia

3. Rigidity

4. Asymmetric onset

Criteria for diagnosis. At least two of four features and one of them is tremor or bradykinesia.

Clinical features of Parkinsonism

1. Mask like facies

2. Glabellar tap positive

3. Small, slurred, indistinct speech

4. Stooped posture

5. Poverty (Hypo) or slowing down (Brady) of automatic and voluntary movements

6. Fcstinant Gait

7. Reduced swinging of arms

8. Propulsion and retropulsion

9. Tremors: 4-7 Hz/sec at rest

10. Diminuation of tremors on movements

11. Pill rolling movements of thumbs and fingers

12. Cog wheel type of rigidity

13. Normal deep reflexes

14. Muscle power not affected

15. Emotional lability

16. Depression in third of the patients

Investigation. Routine laboratory tests, CT scan and MRI usually do not show any abnormally. Some degree of atrophy in the brain may be seen. Position emission tomography (PET) may show reduced accumulation of isotopes in the corpus striatum.


The aim of treating a case of parkinsons disease is to improve symptoms and possibly slow the progress of disease. Motor complications do not develop for many years and so drug therapy is only started once functional disability develops.

It consists mainly of:

1. Drugs

2. Surgery

3. Symptomatic

Drug therapy

The first line of therapy in P.D. is variable and it ranges from Levodopa with or without COMT inhibitors (entacapone). Anticholinergic drugs. Dopamine agonists (Ropinirole) to monoamine oxidase inhibitors (Selegiline).

Levodopa (L Dihydrocy phenylalanine) is the most widely used drug and acts by increasing the dopamine content in the corpus striatum. Dose is 500 mg two to three times a day. Treatment is started with a low dose (125 mg) and gradually increased every 4th or 5th day to reach the maximal dose (1500- 6000 mg).

Great majority of patients show improvement in their rigidity, tremors and hypokinesia. Controlled release preparations of levodopa are prescribed for over night use in those patients who experience difficulty in tuming in bed. Side effects include nausea. Vomiting anorexia, confusion, visual hallucinations and orthostatic hypotension.

L-dopa is contraindicated in patients with hepatic, renal and cardiac disease. Protein rich foods reduce the absorption of the drug. Troublesome “on-off’ phenomenon characterized by abrupt onset of bradykinesia develops in patients on long term Ldopa therapy.

Because of peripheral breakdown of L-dopa into dopamine L-dopa is usually combined with a dopa decarboxylase inhibitar (Carbidopa) to prevent its peripheral breakdown and thus not only increase its absorption but also reduce G.I. side effects.

Carbidopa is four times as potent as L-dopa alone. Dose is 300-1000 mg (carbidopa IL dopa 25/100, 25/250).

Comt Inhibitors

Adding COMT inhibitors to levodopa preparation prolongs their life since they reduce levodopa breakdown. These drugs inhibit the enzyme catecholo-methyl transferase and block central dopamine metabolism. These drugs do not have any independent effect and have to be combined with Ldopa. Entacapone (200 mg tablet) is the drug in this group. With use of COMT inhibitors the dose of Ldopa is reduced.

Dopamine Agonists

These are analogues of dopamine that directly stimulate the dopaminergic receptors. These are often the first choice and are effective, cause less long term motor complications. There are two main groups of dopamine agonists. Those derived from ergot compounds (Bromocriptine, Pergolide) and non ergot (ropinirole).

Dopamine agonists can be used as monotherapy. Bromocriptine (5-10 mg) is of benefit to patients showing severe ‘on-off’ reaction. It is started with a low dose of 1.25 mg per day and increased with 1.25 mg every week till adequate response is obtained (6-8 weeks).

Bromocriptine improves tremors, rigidity, bradykinesia and other parkinsonian symptoms at all stages of the disease. Side effects include nausea, vomiting, confusion, psychosis and, postural hypotension.

Non-ergot preparation (Ropinirole) is the one commonly used. Again used as monotherapy and usually started at 0.25-0.5 mg. Its use is associated with a reduced loss of striatal isotope uptake. Side effects include nausea, ankle swelling, hallucinations and confusion.

Apomorphine is a short acting non-ergot dopamine agonist which is given parenterally (dose 1-6 mg). It is effective in severe motor fluctuations.

Monoamine oxidase B-inhibitors. Selegiline is the only preparation available in this group (dose 5-10 mg). It reduces the disability of parkinsons disease, incidence of motor fluctuations and delays the need for levodopa. Side effects include. Hallucinations confusion and postural hypotension.

Anticholinergic drugs

Since there is imbalance because of loss of dopamine and excess of acetylcholine, anticholinergic drugs are effective in correcting this balance. Main drugs in this group are procyclidine (7.5-15 mg), pacitane (1-2 mg), diphenhydramine (Benadryl), etc. They antagonise acetylcholine at striatal interneurones.

They are more effective in controlling tremors and rigidity. Side effects include dry month, blurred vision, sphincter disturbances, hallucinations and confusion. Elderly patients are more vulnerable to cognitive side effects of these drugs and should be used in caution in them.


Stereotoxie surgery is employed in patients with failed medical therapy. It is useful in patients with dopa induced dyskinesia and various targeted areas include subthalamic nucleus and globus pallidus. Stereotoxic procedures includes ventrolateral thalamotomy, medial pallidotomy etc. Improvement occurs in patients of Parkinson’s disease with severe tremors.

Symptomatic treatment

Patient should be given physiotherapy to improve rigidity. Emphasis should be on staying physically and mentally active, maintaining mobility and care of nutrition. Constipation is managed by diet (increase in fibre diet good amount of fluids). Care should be taken about nutrition needs since many drugs are likely to cause loss of appetite.

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