Recently, catatonia is considered as a neuropsychiatric syndrome, instead of a subtype of schizophrenia, associated with psychiatric disorders or medical conditions. In DSM-5, catatonia is classified into three categories: 1) catatonia associated with another mental disorder, 2) catatonic disorder due to another medical condition, and 3) unspecified catatonia. According to DSM-5, catatonia is diagnosed if the clinical picture is dominated by three (or more) of the 12 characteristic symptoms. Some symptoms in the diagnostic criteria could occur in other neuropsychiatric conditions, like delirium or akinetic mutism. Therefore, the criteria should be cautiously applied in diagnostic procedures.
 Catatonia may occur in association with delirium, especially in the presence of medical conditions. However, in DSM-5, catatonia is defined as a disturbance, which does not occur exclusively during the course of delirium. This criterion may occasionally cause diagnostic confusion, especially in medical conditions.
 The neurobiology of catatonia is still not fully known. Derangements of neurotransmitters, including GABAA, NMDA, and dopamine, with disturbances of the neuronal network, such as the orbitofrontal and posterior parietal cortex and cortico-thalamic tract, are suspected as neurobiological bases of catatonia.
 Malignant catatonia is the most serious complication of catatonia. Furthermore, a similar somatic condition, neuroleptic malignant syndrome, may occur in catatonic patients. A common pathophysiology is suspected in malignant catatonia and neuroleptic malignant syndrome, although some differences in clinical features exist. Serotonin excess is suspected as a cause of this condition.
 Some types of encephalitis may cause various psychiatric symptoms. In the late 1960s, several cases of acute lymphocytic encephalitis, clinically mimicking malignant catatonia, were reported in Japan. Also, a large number of cases of anti-NMDA receptor encephalitis with catatonia were recently reported, suggesting an association between NMDA derangement and psychotic symptoms.
 The treatment of underlying medical and neurological disorders as well as somatic complications should be a priority for patients with catatonia. Derangements of neurotransmitters, especially imbalances of GABA_A and NMDA, are corrected by the administration of GABA_A receptor agonists and NMDA receptor antagonists to ameliorate the symptoms of catatonia. Modified electroconvulsive therapy should be cautiously employed after examination of the physical condition, especially the cardiovascular function.
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