Parkinson’s disease was first described in 1817 by James Parkinson and is the second most common neurodegenerative disease in the world, after Alzheimer’s disease. The disease currently affects 1% of the UK population aged over 65 years and more than 2% aged over 80 years. At this time there are 110, 000 cases in the UK, however, the disorder appears to be less common in China and West Africa.
Parkinson’s disease can result from a range of states including; idiopathic Parkinson’s disease, drug induced neuroleptic effects and dopamine depleters, such as reserpine and methyldopa, and after post-encephalytic viral infection. The pathology of the disorder results in a shift in balance from dopamine to acetylcholine in the striatum of the brain. The current rationale approach in treating this pathology is to increase dopamine levels in the body and block cholinergic actions using a variety of pharmaceutical treatments. Drug induced Parkinsonism is often seen in psychiatric patients taking anti-psychotic drugs, such as, neuroleptic chlorpromazine. These effects are reversible by stopping the offending drug. The pathological hallmark of Parkinson’s disease is the lewy body usually present in the striatal parts of the brain. Classic, clinical features of the disease include; rigidity, resting tremor, bradykinesia and postural instability.
Depression is also a very common, yet under-diagnosed, facet of Parkinson’s disease, occurring in 40-50% of cases. Patients with Parkinson’s disease are generally responsive to treatment with levo-dopa, which is used in combination with physiotherapy and social support. Levodopa is the immediate precursor to dopamine in the catecholamine synthesis pathway of the brain which is decarboxylated to replenish the lack of dopamine. Dopamine itself is not given to overcome the deficit as it is hydrophilic and will not pass through the blood/brain barrier so it is manufactured to be more hydrophobic to aid uptake into the brain. Peripheral side effects of levo-dopa treatment are minimal through administration of selective peripheral decarboxylases, carbidopa or benserazide. The benefits of a decarboxylase include the reduction in extra cerebral adverse effects including, nausea, arrhythmias, hypertension and reduced required dose of levo-dopa.