Cortical influences in emotion.

Emotions may be classified into two major divisions: experience and behavior. Because the brain is critical for mediating emotional experience and behavior, diseases of the brain may induce changes in emotional behavior and experience. Disorders of almost all portions of the cerebral hemisphere, including the cortex, limbic system, and basal ganglia, have been associated with changes of emotional experience and behavior. Dysfunction of the cerebral cortex may be associated with disorders of emotional communication. Whereas deficits of the left hemisphere appear to impair the comprehension and expression of propositional language, deficits of the right hemisphere may be associated with an impaired ability to comprehend and express emotional gestures such as facial expression and emotional prosody. Some patients have either prosodic or facial emotional deficits. Some have only expressive or receptive deficits. However, others may be globally impaired, either within or across modalities. The posterior portions of the neocortex appear to be important for comprehension and the anterior for expression of both emotional prosody and faces. Injury and dysfunction of the limbic system may also alter emotional communication and experience. For example, damage to the amygdala may be associated with an impaired ability to recognized emotional faces and a reduction of affect, especially anger, rage, and fear. In contrast, lesions of the septal region may be associated with increased ragelike behaviors. Seizures frequently emanate from the limbic system, and seizures that start in the amygdala can induce fear and perhaps even rage. Disorders of the basal ganglia may also be associated with defects of emotional communication and experience. Patients with Parkinson's disease not only may be impaired at communicating emotions with both expressive and receptive deficits but also are often depressed and anxious. Patients with Huntington's disease may have emotional comprehension deficits with an impaired ability to recognize emotional faces and prosody. Patients with Huntington's disease may have mood changes even before motor dysfunction becomes manifest. Many of the defects in emotional experience may be related to the associated changes in neurotransmitter systems. Unfortunately, how alteration of neurotransmitters induce mood changes remains unknown. In this chapter we review the feedback and central theories of emotional experience. Although we argue against the postulates that feedback is critical to the experience of emotions, we do suspect that feedback may influence emotions. Emotions may be conditioned and may use thalamic-limbic circuits, as proposed by LeDoux. However, most emotional behaviors and experiences are induced by complex stimuli that an isolated thalamus could not interpret. The cerebral cortex of humans has complex modular systems that analyze stimuli, develop percepts, and interpret meaning. We discuss the proposal that the experience of emotions is dimensional. Almost all primary emotions can be described with two or three factors, including valence, arousal, and motor activation.