Delayed onset of late movement-related cortical potentials and abnormal response to lorazepam in catatonia

Catatonia is a psychomotor syndrome with an inability to execute and termin ate movements completely, leading consecutively to akinesia and posturing, which both respond almost immediately to benzodiazepines, i.e. gaba-potenti ators like lorazepam. However, pathophysiological mechanisms of cortical mo tor and gaba-ergic dysfunction remain unclear. We therefore investigated mo vement-related cortical potentials (MRPs) and movement kinematics during a motor task before and after lorazepam. Ten akinetic catatonic patients were compared with 10 psychiatric (similar age, sex, medication, and underlying psychiatric disease but without catato nic syndrome) and 20 healthy controls. MRPs from frontal (F), central(C), a nd parietal (P) sites were recorded to obtain measures of early and late re adiness potential and movement potential. Kinematic measures included param eters for amplitude of movements, peak velocity, average duration of moveme nts, elevation angle, and angle velocity. The motor task consisted in self- initiated extension of the right index finger. All catatonic and psychiatri c control patients received intravenous lorazepam (1 mg), whereas healthy c ontrols were subjected to a placebo-controlled (10 received lorazepam, 10 r eceived placebo) double-blind study design. Catatonics showed a significantly delayed onset of late readiness and movem ent potential in central electrodes (Cz, C3) compared with psychiatric and healthy controls. This delayed onset correlated significantly with catatoni c motor symptoms and movement duration. Lorazepam led to significantly stro nger delays in onset of late readiness potential in left fronto-parietal (F 3, C3, P3) electrodes in catatonic patients than in psychiatric and healthy controls. It is concluded that delayed latencies in late MRP components in catatonic patients may reflect their inability to execute and terminate movements com pletely. Differential and stronger response to lorazepam in catatonia sugge sts dysfunction in inhibitory control of cortical motor function with incre ased gaba-ergic sensitivity. (C) 2000 Elsevier Science B.V. All rights rese rved.