El proceso metafórico.

For clinical purposes, the prefrontal cortex can be divided into three distinct neuroanatomical regions: 1) dorsolateral prefrontal cortex (Brodmann‟s areas 9, 10, 46); 2) medial prefrontal cortex (including the functionally related anterior cingulate cortex and Brodmann‟s area 24); and 3) orbital prefrontal cortex (Brodmann‟s areas 11 and 12), corresponding to the most inferior and ventral parts of the prefrontal cortex (behind the eyes, or orbits). Both medial prefrontal and orbitofrontal are part of a frontostriatal circuit that has strong connections to the amygdala and other parts of the limbic system. Consequently, these regions are anatomically well suited for the integration of affective and non-affective information, and for the regulation of appetitive/motivated responses. Functionally, these regions are often considered together, as when researchers focus on effects of damage to ventromedial prefrontal cortex (Happaney et al., 2004).

The prefrontal cortex is a heterogeneous region of the brain and the three principal frontal-subcortical circuits are involved in cognitive, emotional, and

motivational processes. The primary focus of the current research will be on the roles of the dorsolateral and orbital divisions of the prefrontal cortex, which manifest quite distinct anatomical and functional properties (Fuster, 1989; Stuss & Benson, 1986).

The dorsolateral prefrontal cortex projects primarily to the dorsolateral head of the caudate nucleus, which receives input from the posterior parietal cortex and

premotor areas. The dorsolateral circuit then connects to the dorsolateral part of the globus pallidus and rostral substantia nigra reticulate, and continues to the

parvocellular area of the medial dorsal and ventral anterior portions of the thalamus. Projections from the thalamus back to the dorsolateral prefrontal circuit close the circuit (Cummings, 1993).

Functionally, the high-level cognitive abilities mediated by the dorsolateral prefrontal cortex and its connections are those referred to as „executive functions‟, including cognitive flexibility, temporal ordering of events, planning, monitoring and inhibiting pre-programmed behaviour, set-shifting, working memory and concept formation (Smith & Jonides, 1999). According to Cummings (1995), dysfunction in the dorsolateral prefrontal circuit is associated with circuit-specific problems

including decreased verbal fluency, perseveration, difficulty shifting set, poor

recall/retrieval of information, reduced mental control, limited abstraction ability, and poor response inhibition. However, while patients with lesions restricted to this region are concrete and perseverative and show impairments in reasoning and mental

flexibility (Benton, 1986), they typically demonstrate intact perception, calculation, language abilities and storage of memories (Duke & Kaszniak, 2000).

The orbitofrontal cortex occupies the ventral region of the prefrontal cortex (Kringelbach & Rolls, 2004), which is reciprocally connected with the amygdala (Ghashghaei & Barbas, 2002). The orbitofrontal cortex projects to the ventromedial caudate nucleus, which receives input from other cortical association areas and brainstem regions, and has open interconnections with the dorsolateral prefrontal cortex, the temporal pole, and the amygdala (Davis & Whalen, 2001). The

orbitofrontal cortex contains the secondary taste cortex, in which the reward value of taste is represented. It also contains the secondary and tertiary olfactory cortical areas,

in which the identity and also the reward value of odours are represented. The orbitofrontal cortex also receives information about the sight of objects from the temporal lobe cortical visual areas (Rolls, 1999).

The orbitofrontal-subcortical circuit is said to underlie social behaviour and appears to play a critical role in the representation of the reward value of a stimulus and the way in which this representation guides goal-directed behaviour (Rolls, 1999). Lesions specific to the circuit have been found to result in marked changes in

personality, including disinhibition, impulsivity, and antisocial behaviour, and irritability and lability are often prominent (Cummings, 1995). Some of the changes may be related to difficulty in the learning and reversal of stimulus-reinforcement associations, and thus the correction of behavioural responses when they are no longer appropriate due to changes in reinforcement contingencies (Rolls, 2004; Hornak et al., 2004). Indeed, investigations in macaques have shown that lesions to the orbitofrontal cortex impair reversal learning (Dias et al., 1996a). Consistent with this, the

orbitofrontal cortex is activated by monetary rewards and punishments, and the magnitude of the reinforcers (O‟Doherty, Kringelbach, Rolls, Hornak & Andrews, 2001). The visual input to neurons in the orbitofrontal cortex is in many cases the reinforcement association of visual stimuli, one of which is information about faces. Such facial stimuli convey information that is important in social reinforcement (Rolls, 2004).

The medial circuit, begins in the anterior cingulate and projects to the nucleus accumbens. The anterior cingulate has interconnections with dorsolateral prefrontal cortex and the amygdala, and it also receives input from the ventral tegmental area (Duke & Kaszniak, 2000). The medial frontal-subcortical circuit is involved in

motivation. Lesions to this region often produce apathy, lack of motivation, decreased social interaction, and psychomotor retardation (Sbordone, 2000).

The ventromedial prefrontal region includes the medial and varying sectors of the lateral orbitofrontal cortex, encompassing Brodmann‟s areas 25, lower 24, 32, and medial aspect of 11, 12, and 10, and the white matter subjacent to all of these areas (Bechara, 2004). Patients with bilateral lesions of the ventromedial cortex develop severe impairments in personal and social decision-making, in spite of otherwise largely preserved intellectual abilities. Following damage to this region of the prefrontal cortex, patients develop difficulties in daily and future planning, and difficulties in choosing friends and activities (Bechara, Damasio & Damasio, 2000a; Bechara, Tranel & Damasio, 2002).

The identification of these adjacent circuits provides insight as to the

similarities of behavioural changes caused by lesions to different brain regions. Whilst focal lesions to the areas of the prefrontal cortex have led to what have been labelled “frontal lobe syndrome”, the involvement of multiple circuits in subcortical lesions has resulted in variable behavioural manifestations (Cummings, 1995). For example, studies of lesions to the globus pallidus have described patients with marked changes in personality and reduced activity levels with memory and executive function deficits, but with normal intelligence and language abilities (e.g., Strub, 1989).

In summary, the frontal–subcortical circuits are extensively connected to each other at the level of the frontal lobes. The circuits are discrete in subcortical regions. The dorsolateral circuit, because of its neuroanatomy, is uniquely able to integrate information from all three frontal–subcortical circuits. Here, the integrated

information from the external world and the cognitive and emotional states of the individual can be used in the production of social behaviour.