Loosen Up And De-Stress As You Are Learning The Strategies Of Tryptophan synthase

1 It is a quinolone derivative with a high affinity for dopamine D2 and D3 receptors, and Tryptophan synthase serotonin 5-HT1A, 5-HT2A and 5-HT2B receptors. The mechanism of action of aripiprazole is not yet known, but evidence suggests that its efficacy in the treatment of the positive and negative symptoms of schizophrenia and its lower propensity for extrapyramidal symptoms may be attributable to aripiprazole��s partial agonist activity at dopamine D2 receptors. At serotonin 5-HT1A receptors, in vitro studies have shown that aripiprazole acts as a partial agonist whereas at serotonin 5-HT2A receptors aripiprazole is an antagonist. Literature review revealed one documented case of treatment resistant schizophrenia who developed NMS following the start of aripiprazole.2 The case of our patient, however, was complicated by the administration of haloperidol (selective antagonism of dopamine D2 receptors), which in addition to aripiprazole may have contributed to the development of NMS. Theoretically, the abrupt discontinuation of aripiprazole could also have contributed. Despite lack of supporting evidence for this theory in patients with schizophrenia, studies reviewing malignant features occurring in patients with Parkinson's disease clearly identify the immediate triggering event as discontinuation or reduction of antiparkinsonian drugs.3 Further studies of aripiprazole are therefore required, given its relatively beneficial therapeutic profile described in the literature to date. 2. ??The development of catatonic schizophrenia and subsequent diagnosis of NMS. Opinions are clearly divided concerning the existence of a link between these two conditions. One hypothesis is that catatonia and NMS are two entities on the same spectrum.4 This postulated link clearly has implications for the use of antipsychotic medications. In the case of our patient, development of catatonic schizophrenia was closely followed by the development of NMS. We would suggest that the presence of catatonic symptoms should raise clinical suspicion for the development of NMS. Vital signs and CK levels should be monitored closely to ensure early diagnosis. Furthermore, the presence or absence of known risk factors should be used to assess risk of developing NMS. Although not an exhaustive list, known risk factors include those with concurrent infection, organic brain disease or sympathoadrenal hyperactivity,5 postpartum women6 and those with low serum iron.7 Other documented risk factors include chronic ingestion of neuroleptic agents, rapid neuroleptisation, a long history of polysubstance abuse and combination usage of haloperidol and lithium.8 Male gender in itself has not been reported as a definitive risk factor. Although NMS has been reported to be more common in men, this is thought, however, to be most likely due to increased use of neuroleptics in men.9 Young adult men in particular predominate among reported cases of NMS.