Structure and neural mechanisms of catatonia

Abstract

Catatonia is a psychomotor syndrome associated with several psychiatric and medical conditions. Psychomotor signs range from stupor to agitation, and include pathognomonic features such as verbigeration and waxy flexibility. Disturbances of volition led to the classification of catatonia as a subtype of schizophrenia, but changes in nosology now recognise the high prevalence in mood disorders, overlap with delirium, and comorbidity with medical conditions. Initial psychometric studies have revealed three behavioural factors, but the structure of catatonia is still unknown. Evidence from brain imaging studies of patients with psychotic disorders indicates increased neural activity in premotor areas in patients with hypokinetic catatonia. However, whether this localised hyperactivity is due to corticocortical inhibition or excess activity of inhibitory corticobasal ganglia loops is unclear. Current treatment of catatonia relies on benzodiazepines and electroconvulsive therapy-both effective, yet unspecific in their modes of action. Longitudinal research and treatment studies, with neuroimaging and brain stimulation techniques, are needed to advance our understanding of catatonia.

Figure 1.. Motor network pathology in catatonia.

Left panel depicts motor system in healthy controls, right panel in current hypokinetic catatonia. Cortical (pre)motor areas are: ventromedial prefrontal cortex (vmPFC), cingulate motor area (CMA), pre-supplementary motor area (pre-SMA), supplementary motor area (SMA), primary motor cortex (M1), and inferior parietal lobe (IPL). GPe = external globus pallidus, GPi = internal globus pallidus, STN = subthalamic nucleus. Green arrows indicate net facilitatory pathways, such as the direct pathway. Red arrows indicate net inhibitory pathways, such as indirect or hyperdirect pathways. Blue arrows indicate neutral or modulatory connections. Note: in catatonia preSMA and SMA have increased neural activity concurrently with motor behavioral inhibition, which may either result from cortico-cortical inhibition or from dominant indirect/hyperdirect pathway activity.