Side effects parkinsonian

Antipsychotics can be safe and effective for the treatment of psychosis in the elderly, if used at lower doses than those commonly used in younger adults. Older adults are particularly vulnerable to the side effects of FGAs. Parkinsonian symptoms... 

The only common side effect associated with IFN-y is the characteristic flu-like symptoms. However, in rare instances and at high doses, adverse clinical reactions have been noted. These have included heart failure, central nervous system complications (confusion disorientation, Parkinsonian-like symptoms), metabolic complications (e.g. hyperglycaemia), and various other symptoms. 

Many DA receptor antagonists (neuroleptics) for treating psychoses (for example, schizophrenia) have become efficient medicines. However, most of them induce severe extrapyramidal side-effects (EPS) akin to parkinsonian symptoms and also, more seriously, they induce tardive dyskinesias (TD). There is a need for improvements in the neuroleptics in the clinic. The substituted benzamides are D2 antagonists, some of which display a high degree of limbic selectivity. Such a regional selectivity has been suggested to be beneficial from the side-effects point of view [11,12]. 

Side effects include fatigue, insomnia, and altered motor coordination. Parkinsonian side effects and acute dys-tonic reactions also have been reported. Metoclopramide stimulates prolactin secretion, which can cause galactorrhea and menstrual disorders. Extrapyramidal side effects seen following administration of the phenothiazines, thioxanthenes, and butyrophenones may be accentuated by metoclopramide. 

The working assumption that the striatal system is only involved with extrapyramidal function (e.g., parkinsonian side effects, dystonias, and TD) and that the mesolimbic or mesocortical systems are only involved with psychosis may be an oversimplification. Many of the neuroanatomical studies on the identified dopaminergic tracts are done with rats. In the monkey, by contrast, there are many more DA tracts that are either absent in the rat or at least markedly different human systems could be different from the rat s or monkey s. Understanding the neuropharmacology of the antipsychotics is further complicated, given that neither the mesolimbic-mesocortical nor the striatal systems are homogeneous but may also include various subsystems. 

In fact, the SSRI-RBD link sounds a lot like the Thorazine-tardive dyskinesia tie-in, doesn t it What possibly common underlying mechanism could unite these apparently disparate phenomena One answer is dopamine, whose production by the substantia nigra is deficient in spontaneous Parkinsonism. Dopamine is blocked, hence rendered functionally deficient, by the antipsychotics that produce both immediate and delayed Parkinsonian side effects. Serotonin inhibits dopamine, which means that potentiating serotonin with SSRIs could also render dopamine less functionally efficacious. Acetylcholine is in dynamic reciprocity with both serotonin and dopamine. Acetycholine causes an increase in dopamine s efficacy in some circuits and a decrease in others. 

The first generation antipsychotics, now known as typical drugs, were all D2 receptor blockers and, as such, very likely to produce Parkinsonian side effects. Because antipsychotic potency was associated with D2 receptor affinity, it was assumed that dopamine overactivity was the essential defect in schizophrenia and that a direct dopamine blockade was the definitive route to treatment. But these drugs affected both the target dopamine pathways of the mesolimbic projection and the uninvolved nigrostriatal projection. Unfortunately, that meant that movement disorders were the price that had to be paid for antipsychosis. 

The effectiveness of the second generation antipsychotics (now called atypicals, because they have weak D2 blocking properties) show that this concept is not valid. Drugs like clozapine do not cause the Parkinsonian side effects even though they are very successful in terminating psychosis. 

Drug Levodopa Mechanism of Action Resolves dopamine deficiency by being converted to dopamine after crossing blood-brain barrier. Special Comments Still the best drug for resolving parkinsonian symptoms long-term use limited by side effects and decreased efficacy. 

Chlorpromazine, the first modern drug to be used in the treatment of schizophrenia and other psychotic disorders, was introduced into psychiatry in 1952 [61]. It was followed by a number of other drugs for the treatment of these conditions (e.g., haloperidol, thioridazine). These were also called neuroleptics because of their neurological side effects, such as parkinsonian syndrome and tardive dyskinesia. Tardive dyskinesia is a movement disorder characterized by involuntary movements of the face and limbs. The antipsychotic properties of these drugs were inseparable from the extrapyramidal effects. 

Teusink JP, Alexopoulos GS, Shamoian CA. Parkinsonian side effects induced by a monoamine oxidase inhibitor. Am J Psychiatry 1984 141(l) 118-9. 

In particular, antihistamines, anti-Parkinsonian drugs, and medications for dementia affect this system, as do numerous medications for general medical conditions. Many psychiatric medications have side effects that occur because of their influence on the acetylcholine receptors. 

Nigrostriatal tract Substantia nigra and striatum. Motor control. Hypoactivity implicated in parkinsonian-like side effects of antipsychotics. 

The primary treatment for schizophrenia involves use of antipsychotic medications. These are classified as typical or first generation, and atypical. The atypical antipsycho tics differ from the typical in having relatively less extrapyramidal side effects, such as rigidity, dystonia (muscle spasm), akathi-sia (motor restlessness), and pseudo-Parkinsonian symptoms. 

Reserpine is an alkaloid from plants of the genus Rauwolfia, used in medicine since ancient times in southern Asia, particularly for insanity more recently, reserpine was extensively used in psychiatry but is now obsolete. Reserpine depletes adrenergic nerves of noradrenaline primarily by blocking amine storage within vesicles present in the nerve ending, so reducing stores of releasable transmitter. Its antihypertensive action is due chiefly to peripheral action, but it enters the CNS and depletes catecholamine stores there too this explains the sedation, depression and parkinsonian (extrapyramidal) side effects that can accompany its use. The effects on catecholamine storage persist for days to weeks after it is withdrawn. 

Miyoshi Y, Zhang Z, Ovadia A, Lapchak PA, Collins F, Hilt D, Lebel C, Kryscio R, Gash DM (1997) Glial cell line derived neurotrophic factor-levodopa interactions and reduction of side effects in parkinsonian monkeys. Ann Neurol 42 208-214. 

Breier AF, MaUiotra AK, Su TP, Pinals DA, Elman I, Adler CM, Lafargue RT, Clifton A, Pickar D. Clozapine risperidone in chronic schizophrenia effects on symptoms, parkinsonian side effects, and neuroendocrine response. Am J Psychiatry 1999 156(2) 294-8. 

The neuroleptics produce extrapyramidal side effects due to the blocking of dopamine receptors. In addition to producing a reduction in positive psychotic symptoms by blocking dopamine in the mesolimbic region, they unfortunately produce extrapyramidal symptoms by dopamine blockade in the basal ganglia. There are three types of acute extrapyramidal symptoms Parkinsonian side effects are those that resemble Parkinson s disease, with slowed movements, decreased facial expres-... 

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