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Parkinson’s disease Treatment

Physical and speech therapy can help patients with moderate to severe Parkinson’s disease. In advanced cases, the quality of life can be enhanced by some aids such as extra handrails in home, table cutlery with larger handles, non-slippery table surfaces, voice amplifiers and chairs that can easily lift the occupant.

Medication in Parkinson’s disease

parkinson treatmentNon-selective muscarinic antagonists (anticholinergic drugs) are often useful, especially in improvement of tremor. There are many preparations, including trihexyphenidyl, benztropine, procyclidine and orphenadrine.

Most common side effects are dry mouth, constipation, urinary retention, blurred vision. Glaucoma with a closed angle may be aggravated. In the elderly, mental confusion and hallucinations are particularly troublesome. Treatment begins with the chosen preparation, with a small starting dose, increased gradually according to response and tolerance of the patient. If the drug is not effective, it must be replaced with another anticholinergic drug.

Amantadine alone or in combination with an anticholinergic agent, it is sometimes useful in mild Parkinsonism; it enhances the release of endogenous dopamine. Can improve all clinical manifestations of the disease; relatively rare side effects (restlessness, confusion, rash, edema, heart rhythm disturbances); the standard dose is 100 mg, two times a day. However, the benefit, if it occurs, is transient in many patients.

Levodopa, the metabolic precursor of dopamine brings symptomatic benefit in most of the patients with Parkinsonism. It is particularly useful for the relief of bradykinesia. Because of this dopa decarboxylase the intestinal mucosa (the enzyme which converts levodopa into dopamine), the biggest of the ingested dose of levodopa is lost before entering the systemic circulation.

The administration of levodopa in combination with an inhibitor of dopa-decarboxylase extra cerebral reduces extra cerebral metabolism of levodopa, reducing also the incidence of adverse effects and peripherals. Thus, levodopa is routinely administered in combination with an inhibitor of peripheral dopa decarboxylase (carbidopa in the United States; benserazide in Europe).

Medications that act as dopamine agonist such as ergot derivatives, bromocriptine and pergolide can cause symptomatic benefit by direct stimulation of dopamine receptors, although the benefit is not obvious unless you are receiving levodopa. Absorption and brain distribution are less volatile than those of levodopa. It does not require enzymatic conversion to an active metabolite.

Bromocriptine, which stimulates dopamine D2 receptors, are inserted at a dose of 1.25 mg / daily for a week and 2.5 mg / day, the next week. Then, the daily dose is increased by 2.5 mg every two weeks depending on the response and tolerance.

Side effects of agonists are similar to levodopa, but psychiatric effects as delusions or hallucinations are more common; dyskinesias are rarer than levodopa.

Dopamine agonists are contraindications to patients with psychotic disorders and should be avoided in patients with recent myocardial infarction, severe peripheral vascular disease and active peptic ulcer.

New symptomatic therapies have recently been evaluated or are being evaluated; including selective inhibitors of catechol-Ometil transferase (COMT), which may increase the benefit of the therapy with levodopa by reducing the conversion of levodopa to 3-O-methyldopa (which competes with levodopa for an active transport mechanism) and by increasing the availability of levodopa in the brain. Experimental studies have shown that glutamate antagonists may be beneficial for patients with Parkinson’s disease. GM1 ganglioside and varied neurotrophic factors influences striatal dopaminergic cells. They are working to develop the management system that will allow them to treat Parkinson’s disease.

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