Parkinsonism Drug
The diagnosis of Parkinson’s disease should not be sure until it is known in detail all drugs that the patient, consciously or inadvertently, come take at the time of the query.
It is well known that neuroleptics (phenothiazines, butyrophenones) may trigger events and parkinsonian tremor by blocking postsynaptic dopamine receptors in the striatum. The same happens with the depleting dopamine (reserpine, tetrabenazine).
Selective blockers of calcium channels (cinnarizine, flunarizine), masked in various commercial preparations of routine administration can produce similar manifestations full or partial recovery in all patients after discontinuation of medication and within a variable.
Some authors argue that drug-induced parkinsonism may be a latent or subclinical parkinsonism revealed by antidopaminergic medication. It is noteworthy that late buccolingual dyskinesia caused by prolonged use of neuroleptics may be associated with parkinsonian manifestations but hardly reason for misdiagnosis is the presence of stereotyped slow and continuous movements that occur in the lower face (lips , jaw and tongue).
The distal parts of the body and trunk tend to show small movements of flexion and extension, while the proximal muscles are not compromised. When the patient is standing may have repetitive movements of the lower extremities (go hard). The patient often develops secondary akathisia. It is assumed that tardive dyskinesia was given to a hypersensitivity of postsynaptic receptors for dopamine and its increased secretion secondary to blockade of these receptors.
In particular, nerve tracts and neural systems involved in the pathophysiology of the disease: the efferent fibers of the substantia nigra to the anterior horn cells of spinal cord, the substantia nigra receives numerous stimuli of various cortical regions and striatum inhibitory stimuli ; the efferent fibers pass from the front of the substantia nigra to the medial region of the globus pallidus, where stimuli are converted into impulses that are transmitted to the premotor cortex.
These circuits may explain the different symptoms of the disease. The akinesia may be explained by the lack of stimuli that regulate involuntary automatic movements, since the passage through the substantia nigra to the bone is altered. The stiffness is the result of hyperactivity, producing clumsy movements.
“The treatment of Parkinson’s disease is symptomatic. Levodopa combined with peripheral decarboxylase inhibitor is the most effective medicine. These are enzyme inhibitors carbidopa and benzeracida. By not crossing the blood brain barrier preventing thus, the metabolism of levodopa to dopamine outside the central nervous system, allowing a higher concentration of levodopa in the latter, favoring its conversion to dopamine in the striatum (JCFustinoni).
Posted in 
Tags: