Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology
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Catatonia was originally described as a psychomotor syndrome in the 19th century by Kahlbaum including motor, affective and behavioral symptoms. Later, at the beginning of the 20th century, catatonia was rather considered as the motoric manifestation of schizophrenia. Accordingly, neuropathological research focused predominantly on those neuroanatomical substrates, i.e. the basal ganglia being primarily involved in the generation of movements. Even though some authors observed minor alterations in the basal ganglia, consistent findings in these subcortical structures could not be obtained.
Since neuroleptics can induce catatonic-like symptoms i.e. neuroleptic malignant syndrome (NMS), there has been a recent re-emergence in clinical and scientific interest in catatonia. However, exact psychopathological and pathophysiological characterization of both NMS and catatonia remains unclear.
Clinically, catatonia and NMS show more or less similar motor symptoms i.e. akinesia. These may be accounted for by dysregulation in cortical-subcortical circuits between motor/premotor cortex and basal ganglia i.e. the so-called “motor loop”. While in NMS the “motor loop” may be dysregulated by neuroleptic blockade of subcortical striatal D-2 receptors one may rather assume cortical gaba-ergic alteration in catatonia. The premotor/motor cortex and consecutively the “motor loop” may be dysregulated by gaba-ergic abnormalities in orbitofrontal cortex. Gaba-ergic cortical dysfunction may account for affective and behavioural abnormalities in catatonia which cannot be observed as such in NMS. Consequently, one may characterize catatonia as a cortical “psychomotor syndrome” while NMS may rather be regarded as subcortical “motor syndrome”.
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