There are only 2 cases in the whole series (22 and 23) that deserve attention, on the basis that an experienced clinician would want more information before giving an opinion, eg, case 22, “Sertraline lithium methysergide 6 mg of sumatriptan sc. On examination, she was dysarthric, excited, hypomanic, shivering, with dilated pupils, weakness of all limbs more pronounced on the right . . . frequent myoclonic jerking in all limbs with hemiballistic movements in the right upper extremity. She was diffusely hyperreflexic . . . ataxia

of limb and gait.” Applying the Hunter ST Criteria decision rules17: rule 1, the cardinal sign of clonus was not present. Rule 2 requires “inducible clonus Torin 1 order with agitation or diaphoresis” (negative), and rule 3 requires “other clonus with agitation” (also negative). Rule 4 requires tremor and hyperreflexia (negative) and the criteria state if these are not present, the case is “not SS”; so this case fails to meet the criteria. Also, it does not

appear likely to be SS on the basis of “clinical judgment. It is also relevant to note that the HSTC symptoms have been defined by experienced toxicologists. The threshold for assigning pathological significance to particular signs such as hyperreflexia and SCH772984 nmr agitation is likely to be different (lower) in less experienced hands, so the bias is likely to be toward including false positives (cf. nefazodone below). Different classes of drugs exhibit distinct degrees to which they can elevate serotonin. The 3 relevant categories of drugs

are: (1) releasers (eg, MDMA, 3,4-methylenedioxymethamphetamine); 上海皓元医药股份有限公司 (2) MAOIs; and (3) SSRIs. Altering each of these mechanisms (that is, catecholamine release, breakdown, and uptake) each produces a characteristic maximum effect. Thus overdoses of SSRIs do not precipitate either severe or fatal SS, or temperature elevation beyond 38.5°C. No other classes of serotonin enhancing drugs have ever been demonstrated to produce severe SS, neither l-tryptophan, lithium, 5-HT1A antagonists or agonists, nor catechol-O-methyltransferase inhibitors. Three types of data support such deductions: (1) the presence of serotonergic side effects at therapeutic doses; (2) serotonergic side effects or toxicity after overdose; and (3) serotonergic effects on coadministration with MAOIs. All other drugs that produce SS exhibit congruent findings in these 3 categories which, for instance, predict those tricyclic antidepressants that do, or do not, precipitate SS, for discussion and elaboration of this point see Gillman.10,71,72 There is no good evidence that triptans produce serotonergic side effects at therapeutic doses; serotonergic side effects, or toxicity after overdose; or, likewise on coadministration with MAOIs.