Reserpine parkinsonism caused

The mechanism of the neurological symptoms in Parkinson s disease was discovered from the ability of reserpine to cause akinesia in humans by the depletion of central catecholamine stores. The dopamine levels in patients who died from parkinsonism were found to be extremely low because of deterioration of the dopaminergic neuronal cell bodies and the pathways connecting the substantia nigra with the corpus striatum. 

Depletion of peripheral amines probably accounts for much of the beneficial antihypertensive effect of reserpine, but a central component cannot be ruled out. Reserpine readily enters the brain, and depletion of cerebral amine stores causes sedation, mental depression, and parkinsonism symptoms. 

Depletion of peripheral amines probably accounts for much of the beneficial antihypertensive effect of reserpine, but a central component cannot be ruled out. The effects of low but clinically effective doses resemble those of centrally acting agents (eg, methyldopa) in that sympathetic reflexes remain largely intact, blood pressure is reduced in supine as well as in standing patients, and postural hypotension is mild. Reserpine readily enters the brain, and depletion of cerebral amine stores causes sedation, mental depression, and parkinsonism symptoms. 

Reserpine acts on the dopamine transporter to cause release of the amine, so that free dopamine accumulates extracellularly. The binding appears to be non-covalent [247, 263]. (-)-Cathinone acts similarly [264]. Nicotine and, even more, some quaternary, N-methylated products of nicotine metabolism, inhibit dopamine uptake. This may help to explain why smoking relieves some symptoms of Parkinsonism [265, 266, 267]. In another way, nicotine acting on certain acetylcholine receptors evokes release of dopamine from rat striatal cells [268], Veratridine has a similar effect [142]. 

Reserpine is sometimes used in the treatment of hypertension. In addition to depleting vesicular stores of norepinephrine in sympathetic nerve endings, reserpine depletes brain dopamine and causes parkinsonism-like adverse effects. Reserpine also decreases vesicular stores of norepinephrine and serotonin in CNS neurons, which can result in depression of mood. The answer is (E). 

It has a mixed chemieal features of both diphenhydramine elass of antihistaminies and atropine. It has been used successfully in the treatment of parkinsonism, to arrest tremor and rigidity, oculogyric crises and pain secondary to muscular spasm. It is also employed to control extrapyramidal dyskinesia caused by tranquillizers, namely, chlorpromazine or reserpine. Its aetions and uses are similar to those of benzhexol and is preferred to that of the later due to its inherent sedative effeetive at its normal dose. 

It is employed in the symptomatie eontrol and management of Parkinson s disease. It has also been used in the treatment of acute spastic disorders of the skeletal muscles caused hy trauma, tension, and vertebral disk dislocation. It is also used alleviate the extrapyramidal syndrome induced by drugs, e.g., reserpine and phenothiazine derivatives. 

The drug exerts its distinet eentral actions to suppress tremor as well as rigidity that are gainfully employed therapeutically in Parkinsonism. It is also employed for the treatment of extrapyramidal dyskinesia but certainly not tardive dyskinesia which is caused due to the administration of various potent tranquillizers, namely reserpine, chlorpromazine (CPZ) ete. It may be worthwhile to mention here that the drug fails to cause any sort of central stimulation Q.e., a definite plus point), and instead produces the characteristic sedative effect normally seen amongst the antihistaminics. 

The primary actions of reserpine alkaloids are caused by inhibition of noradrenaline and depletion of amines in the central nervous system. While the hypotensive effects have a slow onset their duration is long, and the effective dose is sufficiently low to limit any side effects. It was previously used as a tranquilliser however, the much higher doses required often resulted in depression and Parkinson disease-like symptoms (Huang 1993). As a result Rauwolfia has become a restricted herb in Australia and has no place in current herbal prescribing. 

Phenothiazines and butyrophenones may cause various movement disturbances in man. Dystonia in children and young adults and parkinsonism or restlessness in older subjects may occur during treatment and are reversible. The facial dyskinesia which may occur in elderly subjects, especially those with evidence of brain damage, is often irreversible (see ref. 225 for review). Unlike reserpine, these substances have little effect on brain amine levels in animals. They behave as if they block amine receptors so that there is a compensatory activation of monoaminergic neurones with increased but functionally ineffective release of amines into the synaptic cleft. Thus,... 

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