PARKINSON’S DISEASE: CLINICAL PRESENTATION AND MANAGEMENT

Abstract

James Parkinson described a disease called shaking palsy in 1817, which showed clinical signs of muscular rigidity, poverty of movements, postural imbalance and resting tremors. The pathological hallmark of PD is loss of dopaminergic neurons of the substantia nigra pars compacta, with the appearance of intracellular inclusions known as Lewy bodies. We find mention of Kampavatta a disorder resembling Parkinsonism in ancient Charak Sanhita also. Levodopa, the metabolic precursor of dopamine, is the single most effective agent in the treatment of PD. levodopa is almost always administered in combination with a peripherally acting inhibitor of aromatic L-amino acid decarboxylase, such as carbidopa or benserazide. Levodopa therapy can have a dramatic effect on all the signs and symptoms of PD. An alternative to levodopa is the use of drugs such as Bromocriptine, Pergolide, Ropinirole and Pramipexole. The therapeutic action of the COMT inhibitors is to block peripheral conversion of levodopa to 3-O-methyl DOPA. A recently developed class of drugs for the treatment of PD consists of inhibitors of COMT like Tolcapone and Entacapone. MAO-B is the predominant form in the striatum and is responsible for most of the oxidative metabolism of dopamine in the brain. Therefore, Selegiline the selective irreversible inhibitor of enzyme MAO-B also find a place as an effective anti-parkinsonian agent. The present review focuses on clinical signs, symptoms and drug therapy of PD in detail. At present, the pharmacological therapy of neurodegenerative disorders is limited mostly to symptomatic treatments that do not alter the course of the underlying disease.