Mood disorders such as a bipolar disorder and depression are the most common etiologies to progress to catatonia. Other psychiatric associations include schizophrenia and other primary psychotic disorders. It also is related to autism spectrum disorders.Catatonia is also seen in many medical disorders, including infections (such as encephalitis), autoimmune disorders, meningitis, focal neurological lesions (including strokes), alcohol withdrawal, abrupt or overly rapid benzodiazepine withdrawal, cerebrovascular disease, neoplasms, head injury, and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia). Pathogenesis
The pathophysiology that leads to catatonia is still poorly understood and a definite mechanism remains unknown. Neurologic studies have implicated several pathways; however, it remains unclear whether these findings are the cause or the consequence of the disorder.Abnormalities in GABA, glutamate signaling, serotonin, and dopamine transmission are believed to be implicated in catatonia.Furthermore, it has also been hypothesized that pathways that connect the basal ganglia with the cortex and thalamus is involved in the development of catatonia. Diagnosis
There is not yet a definitive consensus regarding diagnostic criteria of catatonia. In the American Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the World Health Organizations eleventh edition of the International Classification of Disease (ICD-11) the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggesions for diagnostic criteria.DSM-5 classification
The DSM-5 does not classify catatonia as an independent disorder, but rather it classifies it as catatonia associated with another mental disorder, due to another medical condition, or as unspecified catatonia.
Some of the rarer auto-antibodies (e.g., NMDAR) have no commercially available assay and can only be measured by a very small number of research laboratories worldwide, further delaying diagnosis by weeks or months. Most patients with limbic encephalitis are initially diagnosed with herpes simplex encephalitis, because the two syndromes cannot be distinguished clinically. HHV-6 (human herpes virus 6) encephalitis is also clinically indistinguishable from limbic encephalitis.There are two sets of diagnostic criteria used. The oldest are those proposed by Gultekin et al. in 2000. A revised set of criteria were proposed by Graus and Saiz in 2005. The main distinction between the two sets of criteria is whether or not the detection of a paraneoplastic antibody is needed for diagnosis. Antibodies against intracellular neuronal antigens
The main antibodies within this group are those against Hu, Ma2, CV2, amphiphysin and Ri. The syndrome of anti-Ma2 encephalitis may be clinically mistaken for Whipples disease. Antibodies against cell membrane antigens
The main antibodies within this group are those against N-methyl-D-aspartate receptors (NMDAR) and the voltage-gated potassium channel-complex (VGKC-complex). Anti-NMDAR encephalitis is strongly associated with benign tumours of the ovary (usually teratomata or dermoid cysts). Anti-VGKC-complex encephalitis is most often not associated with tumours.Patients with NMDAR encephalitis are frequently young women who present with fever, headache and fatigue. This is often misdiagnosed as influenza, but progresses to severe behavioural and personality disturbance, delusions, paranoia and hallucinations. Patients may therefore initially be admitted to a psychiatric ward for acute psychosis or schizophrenia. The disease then progresses to catatonia, seizures and loss of consciousness.