Prefrontal and orbitofrontal cortex often bear the brunt of damage in traumatic brain injuries. Also, the system may degrade in patients with stroke, multiple sclerosis, the cortical and subcortical dementias, and other cerebral disorders. Behavioral and mood syndromes caused by frontal lobe injury are recapitulated by lesions in subcortical structures of the circuits.
The primary structures in the circuitry for emotional regulation include the orbital and ventromedial prefrontal cortex (BA 12), regions of the DLPFC, and the amygdala, hippocampus, and anterior cingulate. Other interconnected structures implicated in aspects of emotion, affective style, and the maintenance, amplification, and attenuation of an emotion include the hypothalamus, insular cortex, and ventral striatum. This system also suppresses negative emotions such as anger and impulsive aggression, partly through seroton-ergic neuromodulation.363 Antidepressant and antianxiety medications act on the system through such modulation.
Three distinct neurobehavioral syndromes have been described that involve frontal-subcortical circuits.364 Mixed behavioral features suggest the involvement of more than one circuit.
1. The prefrontal syndrome includes deficits in motor programming, especially evident in alternating, reciprocal, and sequential motor tasks. Executive function impairments include the inability to generate hypotheses and show flexibility in maintaining or shifting sets required by changes in the demands of a task. Patients also exhibit poor organizational strategies for learning tasks and copying complex designs, as well as diminished verbal and drawing fluency. Lesions span the circuit from BA 9 and 10 to the dorsolateral caudate nucleus, to the globus pallidus, and to the ventral anterior and dorsomedian thalamus and back to DLPFC. This circuit is shown to be hypometabolic in Figure 3-3 after an anterior thalamic stroke. Indirect pathways extend from globus pallidus externa to lateral subthalamic nucleus, then to globus pallidus interna and substantia nigra.
2. The orbitofrontal syndrome especially affects personality. The range of characteristics include a change in interests, initiative, and conscientiousness, as well as disinhibition, tactless words, irritability, lability, and euphoria. Patients tend to be enslaved by environmental cues. They may automatically imitate the gestures and actions of others. Lesions span the same structures as the dorsolateral syndrome, but in different sectors. Impul-sivity and aggression may accompany lesions that affect this area and adjacent prefrontal cortex. Orbitofrontal cortex provides a social context for perceptual information and, through its connections with the prefrontal cortex and amygdala, plays a key role in constraining impulsive outbursts.363 The frontal-subcortical circuit includes the lateral orbitofrontal cortex (BA 10, 11, and 47) to ventromedial caudate to globus pallidus to ventral anterior and dorsomedian thalamus and back to the orbitofrontal region. Figure 3-4 shows the resting hypometabolic activity that may result from interruption of elements of this circuit after a stroke in duced by an anterior communicating aneurysm.
3. The anterior cingulate syndrome includes profound apathy, even akinetic mutism. The circuit includes the anterior cingulate (BA 24) to nucleus accumbens to globus pallidus to dorsomedian thalamus and back to BA 24. Other striatal loops are involved as well. Both DLPFC and orbitofrontal subcortical circuits may be part of the substrate of depression.
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