What Can Different Motor Circuits Tell Us About Psychosis? 

An RDoC Perspective

Vijay A. Mittal; Jessica A. Bernard; Georg Northoff


Schizophr Bull. 2017;43(5):949-955. 

In This Article

Cortico-motor Circuits and Changes in Psychomotor Organization and Speed

Both the basal ganglia and cerebellum provide major inputs to cortical regions including motor cortex and other regions like the prefrontal cortex.[5–7,23] This accounts for bottom-up modulation of cortical motor regions by subcortical regions which, as we have seen, accounts for motor excitation/inhibition and timing. Additionally, the reverse modulation also takes place, namely from cortical to subcortical motor regions. Specifically, cortical regions implicated in cognitive, social, and affective functions exert top-down modulatory effects on cortical and subcortical regions implicated in motor function.[44] Though research is still in its infancy in this regard, we describe such circuits as cortico-motor circuits and assume them to be closely related to psychomotor function. In the following, we will give 2 examples of cortico-motor circuits (ie, orbitofrontal-motor connectivity, and default-mode network [DMN]—sensorimotor balance) and how they are involved in different forms of psychomotor modulation (ie, psychomotor organization and speed).

Anterior medial prefrontal cortical regions like the ventromedial prefrontal cortex and pre/subgenual anterior cingulate cortex are strongly implicated in emotional processing.[45] At the same time these regions show strong functional connectivity with premotor, supplementary, and motor cortex.[44] One can thus speak of a medial prefrontal—motor cortico-cortical circuit (MPMCCC) which, functionally, may allow to link emotion and movements allowing for psychomotor modulation. The MPMCCC has been found abnormal in patients with catatonia who, correspondingly, show both affective-emotional and motor abnormalities: they remain unable to control their abnormal emotional intensity and show abnormal hypo- and hyperkinetic movements with catalepsy, flexibilitas cerea, posturing, and hyperkinetic changes.[44,46,47] This perspective is also supported by multimodal imaging studies that have pinpointed an important role for the supplementary motor area in catatonia.[48,49] Moreover, data in catatonia indicate that the MPMCCC can be modulated by GABA-ergic drugs such as Lorazepam in both healthy[44] and catatonic[50] subjects—this is of high interest given that Lorazepam has been proven therapeutically highly beneficial in acute catatonic patients.[51] Accordingly, the MPMCCC may serve as a possible candidate for a construct that can be related to both specific behavior (ie, psychomotor organization) and biochemical levels (ie, GABA).

Yet another example of psychomotor modulation can be found in a related circuit, ie, the relationship between different neural networks in the brain's spontaneous activity.[52,53] Among these are the DMN and the sensorimotor network (SMN). While the SMN is related to motor and sensory functions,[53] the DMN is strongly implicated in internal cognition including self-related processing,[54] spontaneous thoughts or mind wandering,[55] and mental time travel or episodic simulation.[56] A recent investigation[57] demonstrated reciprocal balance between DMN and SMN in BD: high levels of neuronal variability in DMN are accompanied by low variability levels in SMN in depressed BD while the reverse constellation (ie, low DMN and high SMN variability) can be observed in manic BD. Both constellations exert major impact on psychomotor function: manic BD is featured by psychomotor agitation while depressed BD shows psychomotor retardation. Hence, the balance between DMN and SMN (DMN-SMN ratio) is related to psychomotor speed while both neuronal and behavioral levels are abnormally altered in opposite ways in manic and depressed BD. Recent work designed to also understand the role structural connectivity abnormalities play in contributing to slowing in affective disorder populations will also be important for providing a more comprehensive perspective.[58]

In sum, domain construction is warranted for the psychomotor features of psychiatric disorders. Psychological changes in affective, social, and/or cognitive functions can affect and modulate motor functions in an abnormal way. This may be related to cortico-motor circuits like MPMCCC and DMN-SMN ratio. However, the investigation of such psychomotor circuits has been largely neglected so far. They may be crucial in order to understand the motor changes including their close relation to psychological abnormalities in psychosis and various other psychiatric disorders though. Of course, it is also possible that motor systems affected across psychiatric illness may also drive deficits in important high-order functions as well. Future work aimed at teasing apart if motor abnormalities are secondary or primary to psychological symptoms is sorely needed, and will certainly provide a more holistic perspective for understanding aberrant human behavior.