Brain imaging in catatonia: systematic review and directions for future research

Abstract

Background Catatonia is a frequent, complex and severe identifiable syndrome of motor dysregulation. However, its pathophysiology is poorly understood. Methods We aimed to provide a systematic review of all brain imaging studies (both structural and functional) in catatonia. Results We identified 137 case reports and 18 group studies representing 186 individual patients with catatonia. Catatonia is often associated with brain imaging abnormalities (in more than 75% of cases). The majority of the case reports show diffuse lesions of white matter, in a wide range of brain regions. Most of the case reports of functional imaging usually show frontal, temporal, or basal ganglia hypoperfusion. These abnormalities appear to be alleviated after successful treatment of clinical symptoms. Structural brain magnetic resonance imaging studies are very scarce in the catatonia literature, mostly showing diffuse cerebral atrophy. Group studies assessing functional brain imaging after catatonic episodes show that emotional dysregulation is related to the GABAergic system, with hypoactivation of orbitofrontal cortex, hyperactivation of median prefrontal cortex, and dysconnectivity between frontal and motor areas. Conclusion In catatonia, brain imaging is abnormal in the majority of cases, and abnormalities more frequently diffuse than localised. Brain imaging studies published so far suffer from serious limitations and for now the different models presented in the literature do not explain most of the cases. There is an important need for further studies including a better clinical characterisation of patients with catatonia, functional imaging with concurrent catatonic symptoms and the use of novel brain imaging techniques.

Altered Functional Connectivity of the Orbital Cortex and Striatum Associated with Catalepsy Induced by Dopamine D1 and D2 Antagonists

“…26,27) Drug-induced parkinsonism is also known to be frequently occurred with catatonia. 28) In this study, during high-dose raclopride-induced catalepsy, the interregional correlation of ORB-ACC was reduced, implying that high-dose D2 receptor antagonists may lead to a cortico-cortical network dysfunction (Fig. 3C).…”

Catatonia in a hospitalized patient with COVID-19 and proposed immune-mediated mechanism

“…While the exact neurobiological mechanism of catatonia is unknown, alterations in both GABA-ergic and dopaminergic modulation of the cortico-basal ganglia-thalamo-cortical circuit have been implicated in its pathogenesis ( Northoff, 2002 , Haroche et al, 2020 ). Exposure to proinflammatory cytokines has been associated with altered GABA-ergic transmission in the basal ganglia ( Rossi et al, 2011 ).…”

“…Exposure to proinflammatory cytokines has been associated with altered GABA-ergic transmission in the basal ganglia ( Rossi et al, 2011 ). Other proinflammatory mediators such as interferon-alpha have been associated with a hypodopaminergic state in the basal ganglia ( Felger and Miller, 2012 ), which is postulated to be a potential precipitating factor to the development of catatonia and neuroleptic malignant syndrome (NMS) ( Caroff et al, 2004 , Haroche et al, 2020 ). NMS in a patient with COVID-19 has been recently described ( Kajani et al, 2020 ), further implicating a hyper-inflammatory state in the pathogenesis of these neuropsychiatric complications of severe COVID-19 illness.…”

The fMRI signature of acute catatonic state and its response to benzodiazepines

“…Catatonia is a complex syndrome of severe psychomotor dysregulation seen in various neuropsychiatric conditions. 1,2 Irrespective of the nature of the underlying primary neuropsychiatric disorder, the acute retarded catatonic syndrome shows a remarkable similarity in clinical presentation across all patients suffering from the condition. Moreover, it is a unique psychiatric syndrome that dramatically responds fully to acute treatment in a matter of hours to days, and therefore offers a very promising disease model for studying neuroimaging markers that predict treatment response.…”

“…Structural imaging studies in catatonia have reported inconsistent findings (for review, see). 2 A measure of cortical folding complexity known as cortical surface complexity 4 capable of detecting relatively small local differences, has been proposed as a temporally stable neurodevelopmental marker of cortical shape and abnormal gyrification in various neuropsychiatric disorders. [4][5][6][7][8][9] .…”