The pathophysiology of NMS
The pathophysiology of NMS is still not fully understood. It is currently believed to be caused either by neuroleptic-induced dopamine depletion or a blockade in both the striatum and hypothalamus, leading to abnormal thermoregulation. Data on dosage indicate that NMS is not a result of overdosage with neuroleptics, and usually occurs with drug levels within the therapeutic range. It occurs idio-syncratically and develops in only a small number of patients among those who are receiving neuroleptics. Many physiologic and environmental factors were suggested to promote the occurrence of NMS, including dehydration, agitation, malnutrition, exhaustion, and IM injection of neuroleptics. Whether the syndrome has a genetic predisposition Viagra Pharmacy, as in the case of malignant hyperthermia, is still under investigation.
Virtually all neuroleptics are capable of inducing NMS, including phenothiazines, thioxanthenes, and the newer atypical antipsychotics, such as clozapine, risperidone, and olanzapine. In addition, NMS has also been reported in association with other drugs used in medicine that have neuroleptic properties. These include antiemetics (prochlorperazine), properistaltic agents (metoclopramide), anesthetics (droperidol), and sedatives (promethazine). Haldo-peridol, used commonly in the ICUs, is high on the list among the causative medications. Venlafaxine, a selective serotonin reuptake inhibitor, has been reported to induce NMS previously. Though rare, NMS could be an adverse reaction induced by venlafaxine. The possible mechanism was proposed to be extrapyramidal side effects of selective serotonin reuptake inhibitor and the inhibitory action of serotonin on dopamine activity.
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Although having a variable onset, NMS usually develops over a period of 24 to 72 h, and its clinical course runs from 2 to 14 days; however, the course of NMS may be prolonged in some cases. For example, patients receiving long-acting depot neuroleptics may remain ill nearly twice as long. Successful treatment of this syndrome depends on early recognition and prompt withdrawal of the neuroleptic agents. Supportive therapies including IV fluids, antipyretics, and cooling blanket are required. It is also important to properly position the patient to avoid aspiration due to the temporary loss of the gag reflex. Dopamine agonist medications such as amantadine should be continued if already in use, because their withdrawal may worsen the syndrome. www.myviagrainaustralia.com