Objectives
This review has the aim of improving early recognition and effective treatment of catatonia, critically going through its historical descriptions and revisiting its nosographical collocation in current classification systems.
Methods
A PubMed search was done using the keywords “catatonia”, “catatonic schizophrenia”, “stupor”, “catalepsy” and “catatonia treatment” (until 2011).
Results
In 1874, Kahlbaum first described catatonia as a disease of its own, characterized by specific disturbances in motor and behavioural functioning; in contrast, Emil Kraepelin classified catatonic features as a clinical expression of dementia praecox, with a chronic course and poor prognosis. Catatonia occurs in children, adolescents and adults, and develops in association with a wide variety of psychiatric, neurologic and general medical conditions. The neurobiological pathways of catatonia are still unclear. In particular the role of GABA and other neurotrasmitters has been explored, but not completely defined. Nosological and diagnostic definition of disorder are still argued by clinicians and researchers. Although the main psychiatric classifications continue to sustain Krapelin’s view of catatonia as a clinical subtype of schizophrenia, in a clinical setting, catatonic symptoms are more commonly observed in patients with mood disorders and general medical conditions. Symptomatology is characterized by a wide array of manifestations: negativism, mutacism and stupor represent the most common symptoms. The lack of consensus about diagnostic criteria often complicates recognition of catatonic symptoms. The issue in diagnostic assessment is to differentiate catatonia from other overlapping psychomotor disorders and to identify the underlying psychiatric and general medical disorders. Early and correct diagnosis is crucial to start effective treatments and avoid potentially severe (sometimes lethal) somatic complications. Benzodiazepines and electroconvulsive therapy are the therapeutic mainstay for catatonia. Intravenous administration of BDZ is first-line treatment, where ECT is commonly used in non-responders to BDZ, malignant catatonia and malignant neuroleptic syndrome. Nonetheless, many authors suggest that ECT, preferably in combination with BDZ, should be considered in the early course of all types of catatonia to improve prognosis and avoid complications.
Conclusions
Further research should better define the neurobiological basis and improve clinical and nosographical collocation of catatonia; evidence-based therapeutic protocols are needed that would allow adequate and early treatment to prevent somatic complications of catatonia.