There is no specific test for<unk> . Diagnosis is by symptom observation and investigation of the person's history. Several criteria have been proposed. The first evaluated criteria were introduced in 1991 by Harvey Sternbach. Researchers later developed the Hunter Toxicity Criteria Decision Rules, which have better sensitivity and specificity, 84% and 97%, respectively, when compared with the gold standard of diagnosis by a medical toxicologist. As of 2007, Sternbach's criteria were still the most commonly used. The most important symptoms for diagnosing<unk>  are tremor, extreme aggressiveness, akathisia, or clonus (spontaneous, inducible and ocular). Physical examination of the patient should include assessment of deep-tendon reflexes and muscle rigidity, the dryness of the mucosa of the mouth, the size and reactivity of the pupils, the intensity of bowel sounds, skin color, and the presence or absence of sweating. The patient's history also plays an important role in diagnosis, investigations should include inquiries about the use of prescription and over-the-counter drugs, illicit substances, and dietary supplements, as all these agents have been implicated in the development of<unk> . To fulfill the Hunter Criteria, a patient must have taken a serotonergic agent and meet one of the following conditions: * Spontaneous clonus, or * Inducible clonus plus agitation or diaphoresis, or * Ocular clonus plus agitation or diaphoresis, or *Tremor plus hyperreflexia, or * Hypertonism plus temperature > plus ocular clonus or inducible clonus Differential diagnosis<unk>  toxicity has a characteristic picture which is generally hard to confuse with other medical conditions, but in some situations it may go unrecognized because it may be mistaken for a viral illness, anxiety disorders, neurological disorder, anticholinergic poisoning, sympathomimetic toxicity, or worsening psychiatric condition. The condition most often confused with<unk>  is neuroleptic malignant<unk>  (NMS). The clinical features of neuroleptic malignant<unk>  and<unk>  share some features which can make differentiating them difficult. In both conditions, autonomic dysfunction and altered mental status develop. However, they are actually very different conditions with different underlying dysfunction<unk>  excess vs dopamine blockade). Both the time course and the clinical features of NMS differ significantly from those of<unk>  toxicity.<unk>  toxicity has a rapid onset after the administration of a serotonergic drug and responds to<unk>  blockade such as drugs like chlorpromazine and cyproheptadine. Dopamine receptor blockade (NMS) has a slow onset, typically evolves over several days after administration of a neuroleptic drug, and responds to dopamine agonists such as bromocriptine. Differential diagnosis may become difficult in patients recently exposed to both serotonergic and neuroleptic drugs. Bradykinesia and extrapyramidal "lead pipe" rigidity are classically present in NMS, whereas<unk>  causes hyperkinesia and clonus; these distinct symptoms can aid in differentiation.
Serotonin syndrome
Malignant hyperthermia
Cannabinoid hyperemesis syndrome
Neuroleptic malignant syndrome
Post-acute-withdrawal syndrome
Methanol toxicity
Glycine encephalopathy
Anticonvulsant hypersensitivity syndrome