What catatonia can tell us about “top-down modulation”: A neuropsychiatric hypothesis

Abstract

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called “conflict of paradigms.” Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting “horizontal modulation” of cortico-cortical relation. Furthermore, alteration in “top-down modulation” reflecting “vertical modulation” of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered “bottom-up modulation” between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation – “vertical” and “horizontal” modulation, respectively.

Psychosis and catatonia in fragile X: Case report and literature review

“…ECT is a well-established treatment for catatonia across the age span including children and adolescents (73,74). This is the first report of catatonia and ECT therapy in a premutation carrier, although the neurochemical changes that occur in both FXS and in premutation carriers (lower GABA and elevated glutamate, specifically mGluR5 up-regulation because of an FMRP deficit) is likely to predispose to catatonia (40). We would suggest testing for the FMR1 mutation or at least checking FMRP levels when they become clinically available for those who experience catatonia.…”

“…dopamine hypoactivity, GABA hypoactivity, and glutamate hyperactivity (40,41). The second and the third alteration are similar to the FMRP deficient phenotype that is seen in the majority of FXS and the minority of fragile X-associated disorders individuals.…”

Recurrent opisthotonus in catatonia: An atypical presentation

“…[17] Compromised GABAergic (neuron producing gamma-aminobutyric acid) inhibition in the spinal cord has also been suggested as a possible etiological factor in opisthotonic posturing. [2] The dramatic improvement in opisthotonic posturing following intravenous lorazepam in this patient provides strong support to the above theory.…”

Deep Brain Stimulation in Schizophrenia

“…Here ECT is thought to reinforce GABAergic modulation of dopaminergic transmission in thalamo-cortical circuits (Daniels, 2009;Sanacora et al, 2003). The putatively causative dysregulation of GABA emerges primarily from cortical regions (Northoff, 2002), which are inaccessible for DBS.…”