Frontal-subcortical circuitry and behavior

Abstract

The neuropsychiatric manifestations of neurodegenerative diseases are closely linked to neurocircuitry defects. Frontal-subcortical circuits, in particular, are effector mechanisms that allow the organism to act on its environment. In this paper, we present the three main frontal-subcortical circuits: the dorsolateral prefrontal circuit allows the organization of information to facilitate a response; the anterior cingulate circuit is required for motivated behavior; and the orbitofrontal circuit allows the integration of limbic and emotional information into behavioral responses. Impaired executive functions, apathy, and impulsivity are hallmarks of frontal-subcortical circuit dysfunction. A variety of other neuropsychiatric disorders, such as Tourette's syndrome, Huntington's disease, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, schizophrenia, and mood disorders may result from disturbances that have a direct or indirect impact on the integrity or functioning of these loops.

Neuropsychological and neurophysiological correlates of fatigue in post-acute patients with neurological manifestations of COVID-19: Insights into a challenging symptom

“…AES scores were found to be higher in patients compared to HC. Apathy is a disorder associated with the disruption of the frontal-subcortical circuit involved in the generation of motivation [ 51 ].…”

Vascular Cognitive Impairment through the Looking Glass of Transcranial Magnetic Stimulation

“…As known, white matter hyperintensities, commonly seen on brain T2-weighted magnetic resonance imaging (MRI), are associated with varying degrees of cognitive impairment in patients with stroke, cerebral small vessel disease, and dementia [ 10 ], although the pathophysiological mechanisms within the white matter accounting for cognitive dysfunction remain unclear. Nevertheless, the strong relationship between vascular white matter lesions (WMLs) and nonmotor sequelae has been established in large community-based populations [ 11 – 14 ], showing that cognitive and mood-behavior abnormalities may arise from the ischemic disruption of the prefrontal cortical-subcortical circuits [ 15 ]. Medial temporal lobe atrophy was also found to be a significant imaging predictor of early cognitive dysfunction in stroke survivors [ 16 ].…”

Validation Study of a German Cognitive Battery for Huntington’s Disease: Relationship Between Cognitive Performance, Functional Decline, and Disease Burden

“…The degrees of dystonia and rigidity were less strongly associated with cognitive deficits (see Table 5 ). This is reasonable, because the brain regions involved in motor and cognitive performance are the regions that are predominantly affected by the neurodegenerative process in HD ( Bonelli & Cummings, 2007 ; Georgiou-Karistianis et al., 2013 ; Rüb et al., 2015 ) and the cortical loops serve to coordinate motor and cognitive function integrated in the basal ganglia ( Alexander, 1986 ; Klempíř, Klempířová, Štochl, Špačková, & Roth, 2009 ; Ross, Pantelyat, Kogan, & Brandt, 2014 ). Moreover, our findings seem to be consistent with clinical practice and studies, which demonstrated that motor impairment, especially bradykinesia, is a factor contributing to the decline in cognitive performance of HD ( Baake et al., 2017 ; Long et al., 2014 ; van Vugt et al., 2004 ).…”