Parkinson’s Diseases is a slowly progressive neurodegenerative disorder. It results from dopamine depletion caused by degeneration of dopaminergic nigrostriatal system, leading to a neurotransmitter imbalance between dopamine and acetylecholine in corpus striatum part of the brain. It is expressed in the form of symptoms and signs that include akinesia (loss or impairment of the ability to initiate voluntary movement), tremor, rigidity (inflexibility or stiffness) and unstable posture.
Parkinson’s disease is an extremely disabling neurological disease causing a steep fall in quality of life and enormous patient suffering. However there are various measures that we can take to control the disease, improve the quality of life, ensure patient independence in daily activities and reduce disease related suffering significantly. All these goals can be achieved mainly with the help of 3 strategies, including rehabilitation measures, medical treatment and surgical intervention.
Medical treatment is aimed at altering the chemical status in the brain of these patients to achieve balance between dopamine and acetylecholine with the help of certain medicines. Restoration of balance between dopaminergic and cholinergic neurons provides symptomatic relief and improves quality of life.
1. Principle of Initiation of Medical Treatment:
A consensus exists among all the experts that symptomatic medical treatment of Parkinson’s Disease should not be initiated until symptoms significantly impair the quality of life of the patient. Quality of life primarily includes ability to perform independently the activities of daily living, moving around without any danger of fall or injury, earning for oneself and managing ones own finances.
Here is a list of medicines along with their description that are used for the treatment of Parkinson’s Disease.
The first ever medicine introduced for the treatment of Parkinson’s Disease is levodopa. It still remains not only the most effective but also first line of treatment for these patients.
I. Mechanism of Action:
Levodopa activates 2 types of dopamine receptors i.e. D1 and D2, hence making up for dopamine deficiency, which is hallmark of Parkinson’s Disease pathology.
II. Adverse Effects:
Levodopa usually is marketed as a combination with carbidopa, which inhibits an enzyme named dopa decarboxylase. Dopa decarboxylase converts levodopa to dopamine in peripheral circulation. Combination with carbidopa is used to prevent conversion of levodopa to dopamine in peripheral circulation (i.e. outside of brain) because peripheral conversion of levodopa to dopamine can cause unwanted side effects, which include nausea, vomiting and low blood pressure. Other side effects result from its prolonged use, which include fluctuations in symptoms, worsening of movement impairments and psychological symptoms such as confusion.
It is marketed by the famous name of sinemet, which is available in varying combinations of levodopa/carbidopa (10/100, 25/100, 25/25o and slow release 25/100, 50/200). Dose is gradually titrated upwards until symptoms are controlled.
3. Dopamine Agonists:
Dopamine agonists are another option to makeup for dopamine deficiency in this disease. These can also be used alone or in combination with levodopa. Another advantage of these dopamine agonists is that these remain active for longer periods of time as compared to conventional type of levodopa.
I. Adverse Effects:
Their adverse effects are same as those of levodopa except bromocriptime, which causes red inflamed skin (Saint Anthony’s Fire). This skin disorder is reversible when the drug is discontinued.
There are various agents included in dopamine agonists with varying dosage regimens as mentioned below.
Bromocriptine 2.5 to 40 milligrams per day, Pergolide 0.1 to 5 milligrams per day, Cabergoline 0.5 to 1 milligram per day, Pramipexole 1.5 to 4.5 milligrams per day and Ropinirole 0.75 to 24 milligrams per day.