Cortical Subcortical Factors in the Generation of Emotionality

Given that acquired brain lesions (such as strokes and tumors) are typically large and don't respect the boundaries of known cytoarchitectonic and functional areas (such as Brodmann areas; see Fig. 2.1), a main focus of lesion-behavior correlation studies in emotion studies has been hemispheric laterality. Studies in the sixties and early seventies found that lesions in the left hemisphere were associated with catastrophic emotional reactions (tears, depression, despair, anger), while damage to the right hemisphere was accompanied more by emotional indifference (lack of concern, emotional unawareness, and at times an unrealistic euphoria/hypomania). These early findings were explained by expressive difficulties in the patients with left-side damage, and by neglect and anosognosia in the right-damaged ones. However, at about the same time, a group of neurosurgeons in Italy reported similar emotional changes following unilateral hemispheric sedation with amobarbital sodium for the assessment of speech dominance (Rosadini and Rossi, 1967). Discounting cognitive or functional factors, they proposed that the left and right hemispheres exert opposite influences on emotional tone, with the left hemisphere subserving expressions of positive affect, and the right hemisphere organizing expressions of negative affect.

This view was further advanced by Gainotti (1972, 2001) and Sackheim et al. (1982), who reviewed the literature on pathological laughing and crying produced by nuclear brainstem (pseudo-bulbar) lesions. They confirmed a statistical association of pathological laughing with right hemisphere lesions and pathological crying with left hemispheric damage. In addition, they reviewed the literature on emotional outbursts as ictal components in epilepsy, leading to a significant association of ictal laughing with left-sided foci and ictal crying with right-sided foci. Thus, Sackheim et al. (1982) concluded that mood changes following unilateral lesions reflect disinhibition of contralateral regions and not ipsilateral subcortical release. More recently it has been proposed that lateralized hemispheric mood changes result from release of ipsilateral subcortical centers within a vertical hierarchy of emotional control rather than contralateral disinhibition (Liotti and Tucker, 1995). This issue remains empirically unresolved, although it has long been recognized that in animals certain types of bilateral cortical damage leads to the intensification of emotional behaviors (e.g., decorticate rage).

Cases of pseudo-bulbar palsy, a condition in which patients have uncontrollable episodes of laughter or crying without an apparent triggering stimulus and without associated feelings of happiness or sadness (reviewed in Poeck, 1969; Rinn, 1984), have been interpreted as reflecting damage to pathways that arise in the motor areas of the cerebral cortex, descend to the brainstem, and inhibit motor "output" systems for laughter and crying. In that view, the lesions placed mostly in subcortical structures (basal ganglia and the internal capsule), would disinhibit or release the laughter

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Figure 2.1. Representation of the Brodmann areas in the human brain: lateral surface (/eft); medial surface (right). See ftp site for color image.

u> ■»j and crying response systems (Poeck, 1969; Rinn, 1984). Recently, Parvizi et al. (2001) described a case of restricted damage to the cerebro-ponto-cerebellar pathways, highlighting a role for cerebellar structures in the automatic programming of crying and laughter. Although these studies emphasize the nonaffective subcortical motor output systems in such emotional responses, they should not be taken to indicate that subcortical systems have no role in the generation of affect. As discussed later, there is abundant evidence that parts of the subcortical instinctual action apparatus are critical for the generation of emotional feelings.

Other lesion-behavior correlations have emphasized different hemispheric contributions to the regulation of noncognitive emotional influences, such as arousal and emotional expression. Right hemisphere patients have been found to be underaroused, with reduced cortical and autonomic responsivity, particularly to emotionally charged stimuli (Heilman et al., 1978; Morrow et al., 1981; Caltagirone et al., 1989), with less avoidant eye movements to aversive stimuli (Caltagirone et al., 1989) and greater dysfunction in sexual arousal (see review in Tucker and Dawson, 1984). In addition, patients with right hemisphere damage are less facially expressive than patients with left hemisphere damage (Borod et al., 1985; Borod, 1992, 2000). Similarly, normal adults have been found to express emotions more intensely on the left side of the face, particularly during spontaneous displays, which is innervated predominantly by the contralateral right hemisphere (Borod et al., 1983). Interestingly, the left side of the face appears also to be more expressive in rhesus monkeys and in chimpanzees (Fernandez-Carriba et al., 2002), providing evidence for evolutionary continuity that argues for the ethological approach to the analysis of emotional behavior. On the other hand, voluntary emotional displays such as social smiling, are typically more intense on the right side of the face.

Another line of evidence on hemispheric asymmetry for emotion derives from half-field and dichotic studies in healthy volunteers and research on deficits of emotion recognition in brain-injured patients. Tachistoscopic studies in normal participants have shown that the right hemisphere is typically faster and more accurate than the left hemisphere in discriminating facial expressions of emotion, even when the effect of face identity is partialled out (e.g., Ley and Bryden, 1979; Strauss and Moscovitch, 1981). Similarly, patients with right hemisphere damage showed greater deficits in recognizing facial expressions of emotion (e.g., Bowers et al., 1985; Kolb and Taylor, 1981). Recently Adolphs et al. (2000) used an automated three-dimensional lesion reconstruction algorithm in a large group of right- and left-brain-damaged patients to identify a critical role for ventral primary and secondary somatosensory cortices (extending to the insular cortex), particularly on the right, in deficits of facial emotion recognition. These regions presumably contain neural maps of the bodily state associated with an emotion, in agreement with a theoretical framework emphasizing the role of somatic representation in feeling emotions (somatic marker hypothesis; Damasio, 1996).

Recognition of emotional prosody in speech has also been associated with predominantly right hemisphere lesion foci (Ross, 1981; Borod, 1992, 2000) and recently confirmed by neuroimaging studies in healthy participants (Morris et al., 1999; Buchanan et al., 2000; Rama et al., 2001).

Anxiety and Depression 101

Anxiety and Depression 101

Everything you ever wanted to know about. We have been discussing depression and anxiety and how different information that is out on the market only seems to target one particular cure for these two common conditions that seem to walk hand in hand.

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