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The Impact of Medical Illness on Executive Function -- Schillerstrom et al. 46 (6): 508 -- Psychosomatics

The Impact of Medical Illness on Executive Function -- Schillerstrom et al. 46 (6): 508 -- Psychosomatics

The functional loss associated with executive functional impairment may be behaviorally mediated by apathy. Apathy has been associated with executive functional impairment in patients with dementia, depression, and traumatic brain injury.42, 51,52 Boyle et al. 43 demonstrated that executive impairment and apathy scores contributed to 44% of the variance in instrumental activities of daily living in patients with Alzheimer's disease. Executive function may control the behaviors associated with motivation, and disruption of the neural circuits maintaining executive function may lead to apathy and subsequent functional impairment, resistance to care, and impaired decision-making capacity.

PATHOPHYSIOLOGY OF EXECUTIVE IMPAIRMENT

Frontal Circuit Anatomy and Physiology
The prefrontal cortex and related subcortical structures comprise striatal-cortical-frontal "control" circuits that are associated with specific executive functions. 53 These circuits run from the dorsolateral, orbitofrontal, and mesial prefrontal cortex to the striatum. From there, the path continues to the globus pallidus and the thalamus and then back to the prefrontal cortex. Damage to either gray or white matter in these circuits can be associated with executive deficits. These circuits are partially modulated by several monoaminergic neurotransmitters, particularly dopamine. Dopamine disruption in the prefrontal circuits accounts for a substantial portion of the variance in executive impairment. 54

Frontal Circuit Perfusion and Oxygenation
The structures within the frontal circuits are particularly sensitive to hypoperfusion and hypoxia. 55 Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, is oxygen dependent, and decreased dopamine levels are observed in brain tissue during chronic hypoxic conditions.56 Furthermore, as the brain adapts to hypoxia, N-methyl-D-aspartate (NMDA) glutamate receptors become more "excitable," which can lead to calcium-mediated oxidative cell death. 57 Significant metabolic impairment has been observed in the cerebral cortex in patients with chronic obstructive pulmonary disease and in cerebral white matter in patients with obstructive sleep apnea.58, 59 Oxidative disturbances in the frontal circuit may explain the executive impairments observed in patients with decreased cerebral perfusion, decreased respiratory function, or increased oxygen demand.
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