Parkinson's disease (PD) is a neurodegenerative disorder in which nerve cells in the substantia nigra, a pigmented dopamine-rich region in the brain, are destroyed gradually over a period of time. These cells are responsible for the smooth relay of nerve impulses to the next point, the corpus striatum. Loss of these neurons leads to dopamine deficiency which eventually manifests clinically. Unfortunately, at this stage, 60-80% of the cells have already died.
PD is a chronic and progressive disorder. The first symptoms are stiffness, abnormalities of movement, tremor, or problems with balance. Later on, the individual notices difficulties in walking and with speech.
The typical PD tremor is a tremor at rest. The tremor is not due to the dopamine deficiency that is characteristic of PD. In the same way, it is not easily relieved by levodopa or other dopamine agonists. While the tremor may affect various parts of the body, the frequency of tremor is separate in each part. The tremor does not start in the thalamus, but rather in the cerebellum in response to basal ganglia impulses.
As with any tremor, PD tremor is also exaggerated by hyper-adrenergic states such as hyperthyroidism, excitement or stress, or physical fatigue. It can be distinguished clinically by the following features:
- Muscles show cogwheel type of rigidity
- A latent period of 8-9 seconds before the tremor begins
- Older patient (above 60 years)
- Resting tremor
- No family history
- Unilateral onset
- Poverty of movement
Parkinson disease quite often presents with a tremor, but in approximately one-fourth of all patients it never develops at all. In patients who do display tremor, it often reduces in amplitude as the disease progresses, with increasing bradykinesia (slowness of movement).
Tremor in PD is a resting tremor made up of agonist-antagonist activation tuned precisely. A resting tremor is seen during the relaxed phase of a muscle. It is often found only in the hands or fingers. It disappears when a purposeful movement is begun, or during sleep. However, the tremor starts up again soon after the posture is maintained against gravity, and may also be called the re-emergent tremor. This is therefore considered a rest tremor as it results from holding the body posture against gravity.
PD results in a stereotypical repetition of specific movements, such as the typical pill-rolling tremor. This refers to a rhythmic rubbing of the thumb and forefinger over each other. It is quite noticeable when the hand is at rest.
The tremor of PD is commonly found to affect one hand at first. In rare cases it first involves a foot, or the chin. It disappears as a deliberate action is begun. The tremor is most frequently the presenting symptom of PD when patients seek medical help.
Some patients have a rest tremor but never develop PD, and have been thought to have another condition. This is now thought to be a subclinical form of PD.
Some PD patients may have more than one form of tremor. Again, other patients may not display any elicitable tremor during the first visit. It is quite rare but possible to have a purely kinetic tremor in this condition. For all these reasons, PD should be diagnosed only if tremor is accompanied by other features, especially bradykinesia.
PD patients have accumulations of a protein called alpha-synuclein, which are called Lewy bodies. It is possible that these are related to the disorder. Both genetic factors and environmental insults or triggers are thought to interact in the genesis of the condition. In the present state of knowledge, most cases are considered to be sporadic, or scattered, rather than clumped in a familial manner.
The tremor in PD is not a result of dopamine deficiency, which results in bradykinesia and rigidity. On the other hand, it is suggested that the tremor is a mechanism meant to compensate for the disturbance in the basal ganglia activity. It may also be a direct consequence of nerve cell degeneration itself. For this reason, the drugs used to treat PD are not always useful in controlling the tremor.
Various techniques have been evolved to manage the symptoms of PD, but as with medication, they cannot restore lost function due to brain cell death or irreversible damage.
Pallidotomy and Thalamotomy
The globus pallidum or the thalamus, which are parts of the brain that are responsible for PD symptoms, are selectively ablated to improve symptoms such as tremor.
Deep brain stimulation (DBS)
Here a fine electrode is implanted into the brain, usually deep within the subthalamic nucleus or globus pallidum, to improve PD symptoms.