Although no distinct cause has been determined, Parkinson’s disease is due to gradual loss of cells in an area deep within the brain called substantia nigra, which normally produces a chemical called dopamine. Once produced, dopamine travels to other portions of the brain.

One portion called the striatum is the coordination center for various brain circuits. As there is insufficient dopamine in the striatum, the chemical imbalance leads to the symptoms of Parkinson’s disease. Later in the disease, cells in other portion of the brain and nervous system also degenerate.

No one knows why this dopamine producing cells die. Scientists are exploring several theories including chemical reactions within the body, exposure to toxic substances and certain genetic factors. A new gene in certain families suffering from Parkinson’s disease known as “Parkin gene” has been identified to be the positive factor for Parkinson’s disease.

However this has been found to be positive in a small group of patients with young onset of Parkinson’s disease. The research is still going on to find out the real cause for Parkinson’s disease in large patient population

Parkinson’s disease (PD) even to date essentially remains a clinical diagnosis and there are no definitive laboratory tests or brain scans to confirm the diagnosis. Most of these tests are diagnosed to eliminate other diseases that mimic PD.

Patients of PD patients may experience the following symptoms:

Tremor – Slight shaking or tremor in fingers, thumb, hand, chin or lip. Legs shake on sitting down or when relaxing. Tremors is a common and early sign of PD. The typical PD tremors are also called peel rolling tremors, as if one is rolling peels. The tremors are experienced at rest and usually are mild in nature. They disappear on action and activities like drinking and eating.

Micrographia – Sudden change in handwriting which becomes much smaller than the earlier one. The letter sizes become smaller and words tend to be crowded together. Sudden change in handwriting is often a sign of PD. The handwriting diminishes in height from the beginning to the end of the sentence. This is called micrographia.

Rigidity – Patients of PD describe that their body to have become very stiff and the coordinated body movements are lacking making them difficult to carry out their day to day activities like difficulty in arising from chair, turning in bed etc.

Bradykinesia – It is characterized by slowness of movements. The patient has decreased arm swing whilst waking.. It is also manifested in other activities of daily living. The relatives often describe that the patient has slowed down considerably in past few months.

Advanced aging – Young adults rarely experience Parkinson’s disease. It usually demonstrates itself in the middle to late years of life. The risk continues to increase the older one gets. Investigators assume that people with Parkinson’s have neural damage from genetic or ecological factors that get worse as they age. People usually develop the disease around age 60 or older.

Heredity – Having a close relative with Parkinson’s Disease increases the chances that you’ll develop the disease. However, your risks are still small unless you have many relatives in your family with Parkinson’s disease.

Sex – Men are more likely to get Parkinson’s than women. Potential reasons for this may be that males have larger exposure to other risk factors such as toxin exposure or head trauma. It has been hypothesized that oestrogen may have neuro-protective effects OR in the case of hereditary predisposition, a gene predisposing someone to Parkinson’s may be linked to the X chromosome

Selection of medication and their dosage is tailored to each individual patient. In deciding the treatment, the physician considers factors such as severity of symptoms, the patient’s age, and presence of other medical conditions. No two patients will respond identically to any particular drug, so this process involves experimentation with different drugs, persistence and patience. As the disease progresses, drug dosages may have to be altered and a combination of drugs can be given.

A combination of Levodopa and Carbidopa is the mainstay of treatment in Parkinson’s disease. Levodopa is rapidly converted into dopamine, by the enzyme dopa decarboxylase, which is present in the central and peripheral nervous system, however much of the levodopa is metabolized before it reaches the brain.

Carbidopa blocks the peripheral metabolism of levodopa i.e. in the liver, and increases the amount of levodopa that reaches the brain. Levodopa is most effective in treating bradykinesia and rigidity, less effective in reducing tremor, and very less effective in relieving problems with balance.

Side effects include nausea, low blood pressure (hypotension) and abnormal movement’s i.e. dyskinesias.

Slow dosage adjustment and taking medication with food can reduce these effects. Depression, confusion and visual hallucinations are the side effects which may occur with these medications, especially in the elderly.

The key pathology in Parkinson’s Disease (PD) is α-synuclein accumulation. Large α-synuclein aggregates form round lamellate eosinophilic cytoplasmic inclusions, Lewy bodies (LBs) in the neuronal body. α-synuclein is toxic. Its accumulation impairs the functions of the cell. The core pathology of PD affects the dopamine-producing neurons of the substantia Nigra (SN). In advanced PD, loss of pigmented neurons results in gross depigmentation of the SN.

The triad of rigidity, bradykinesia and tremor at rest correlates with degeneration of the dopaminergic nigrostriatal pathway and dopamine depletion in the striatum. α-synuclein deposits and LBs are also present in the cerebral cortex, limbic system and in many extra-nigral neuronal groups. This is the underlying pathology for PD.

Parkinson’s Disease (PD) is just one of several neurologic movement disorders that produce similar symptoms. It is important that the physician you are seeing has experience with all of the different disorders that can masquerade as Parkinson’s disease.

The diagnosis of PD is entirely clinical. It is characterized by tremors, slowness of movements (bradykinesia), stiffness (rigidity), postural imbalance and gait disturbances. In various patients combination of any of the above symptoms can be seen. One of the distinguishing feature of PD from other Parkinson’s like diseases, is its classical response to medical treatment in the early years. According to one estimate, there can be an error of upto 40% in diagnosis when the patient is seen by non-specialist. As there are no radiological (i.e. CT scan, MRI) or blood investigations that can confirm the diagnosis of PD, the onus of diagnosis rests on the physician.

It is very important to make a correct diagnosis. As in some of these diseases, like Progressive supranuclear palsy, Cortico-basal ganglionic degeneration or Multiple system atrophy, people quickly become totally disabled and the surgical interventions in such cases can be disastrous to say the least.