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.
Part of parkinsonian patients develops, over time, subcortical dementia.
It was 