All about Parkinson’s disorder

All about Parkinson’s disorder


An older man who comes to see you report a 6-month history of progressive dragging of his left leg and difficulty using his left hand for fiddly tasks. He is worried that he has a brain tumor. You find no weakness or spasticity but note that he stoops and shuffles a little when he walks and cannot wiggle the left fingers or open and close the left hand rapidly. You can tell him that he has an entirely happier diagnosis of Parkinson’s disease. Dr. Arun is the best neurosurgeon in Gurgaon, having vast experience in treating Parkinson’s disease.


Tremor is a rhythmic (or somewhat rhythmic) to and fro movement of a body part. It can range in severity from something that the patient can feel, but you cannot see through to something that causes wild involuntary movements that prevent proper limb function. 

The crucial differentiating feature of Parkinson’s disease tremor is that it is most evident at rest. It is reduced or abolished by voluntary movement. The best neurosurgeon in Delhi diagnoses this feature. Other features of Parkinson’s disease, such as bradykinesia and rigidity, are usually also present to some degree and point to the correct diagnosis.

Patients with disease in the cerebellum and its brainstem connections commonly have clumsy, uncoordinated movements of their limbs. The incoordination is present throughout the proximal and distal limb muscles, leading to large- amplitude, chaotic shaking of the stem. This is most marked on attempted movement and is therefore termed kinetic tremor, although it is almost always present on sustained posture. 

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Much the most common cause of severe kinetic tremor in multiple sclerosis.

Patients with cerebellar degenerations may have a milder kinetic tremor, where the involuntary oscillations appear as the limb approaches its intended target, a phenomenon some- times referred to as intention tremor.

In both situations, there are likely to be additional signs of cerebellar or brainstem dysfunction, such as dysarthria, gait ataxia, limb ataxia with past pointing and dysdiadochokinesia, and nystagmus.

We all have some degree of tremor on sustained posture, termed physiological tremor. This is faster than parkinsonian or cerebellar tremor, absent at rest, and most evident in the hands. Most of the predominantly postural tremors are due to an exaggeration of this phenomenon.

Postural tremors are made more obvious when circulating catecholamines are increased, such as anxiety, and by sympathomimetic drugs like salbutamol. Conversely, they are suppressed to some extent by beta-adrenergic blockade and sometimes by alcohol. The mechanisms of these effects are not understood. They are often exploited by people who require a steady hand, such as surgeons, snooker players, or musicians, who may take propranolol or alcohol on essential occasions. Reliance on alcohol to treat tremors can lead to dependency and liver disease.

The most disabling postural tremor is essential familial tremor, which tends to be dominantly inherited. A more jerky, asymmetrical variant of crucial tremor is seen in patients with a personal or family history of dystonia and is referred to as dystonic tremor; it is less responsive to beta-blockers or alcohol.

Parkinson’s disease

Parkinson’s disease is rare before the age of 40 but becomes increasingly familiar with the generation and affects 1–2% of people over 65 years old. Several genes causing familial Parkinson’s disease have been identified, and other genes probably contribute to the risk of developing the disease in those with no family history. Environmental factors that increase the risk of developing Parkinson’s disease include working with pesticides; drinking coffee and smoking cigarettes both reduce the risk.

The symptoms and signs of Parkinson’s disease reflect a highly selective pattern of degeneration in the brain. The worst damage occurs in the dopamine-producing neurons of the substantia nigra. This accounts for many of the movement abnormalities, referred to as ‘parkinsonism.’ These neurons project to the corpus striatum via the nigrostriatal pathway. The consequence of loss of neurons in the substantia nigra is dopamine deficiency in the corpus striatum. This may be unilateral, asymmetrical, or symmetrical.

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The noradrenaline- and 5HT-producing neurons in the brainstem are also affected, which may explain the high incidence of depression in Parkinson’s disease. The neurons that deliver acetylcholine to the cerebral cortex are affected as well; this, together with the involvement of the cortical neurons themselves, contributes to cognitive symptoms. In all these locations, the neurons degenerate characteristically, forming clumps of a protein called Lewy bodies.

Management of patients with Parkinson’s disease

The management of patients with Parkinson’s disease requires patience and persistence. The patient’s concerns and expectations may be very different from yours. It may take time to reach a shared understanding and objectives. Specialist nurses, the best neurosurgeons in Delhi, and patient groups like the Parkinson’s Disease Society help this. Non-drug treatments should be sought where possible, and advice from speech therapists, physiotherapists, occupational therapists, and dieticians is often required.

Drug schedules should be altered gradually. Side effects from the drugs are common, making regular consultations necessary. As the illness evolves, drug schedules can become quite complicated, needing clear explanation and written confirmation.

Most patients initially respond brilliantly to levodopa therapy. 

There are three subsequent problems:

  • Wearing off: the response becomes shorter and less marked.
  • Dyskinesia: each dose produces involuntary chorea


  • On-off effect: the transition between lack of response(off) and response (on) becomes rapid.

The oral dopamine agonists are not as potent as levodopa in alleviating parkinsonism but are less prone to cause dyskinesia and fluctuation. Young and mildly affected patients are some- times started, therefore, on a dopamine agonist initially, in the hope of postponing levodopa therapy and its complications for a while. Alternatively, the agonist drugs can be introduced later to reduce the patient’s reliance on levodopa after these complications have begun. It is not clear whether one strategy is better than the other. Dopamine agonists often cause adverse effects in older patients, especially hallucinations.

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There are two strategies for very refractory fluctuation or dyskinesia:

  • Apomorphine infusion: this parenteral dopamine agonist can be infused subcutaneously to achieve stable control. This is tricky and requires specialist medical and nursing input.
  • Surgical treatments: these are aimed at inhibiting overactive parts of the basal ganglia circuitry, either with a stereotactic lesion or by implanting an electrode with an impulse genus- tor. Targets for these operations include the internal globus pallidus within the striatum (to reduce dyskinesia) and the tiny subthalamic nucleus (to minimize the parkinsonism itself). Procedures to graft the striatum with fetal substantia nigra cells or stem cells remain experimental.

Many patients consult Dr. Arun Saroha as he is the best neurosurgeon in Delhi.

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