Cognitive therapy can be successful in promoting clinically meaningful improvements in functional outcome, motivation, and positive symptoms in low-functioning patients with significant cognitive impairment. Trial Registration  clinicaltrials.gov Identifier: NCT00350883.

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Recent reports of improvement in the negative symptoms of schizophrenia following targeted cognitive interventions have prompted interest in the cognitive underpinnings of these symptoms. This review integrates current experimental research with the phenomenological accounts of patients participating in cognitive therapy for these specific symptoms. We propose that, in addition to the well-established role of neurobiological factors in their development and maintenance, specific cognitive appraisals and beliefs play a role in the expression and persistence of negative symptoms. This cognitive model of negative symptoms is based on a diathesis-stress formulation: a continuum of predispositional traits from the premorbid personality to the full-blown negative symptomatology, the incorporation of negative social and performance attitudes within these traits, and low expectancies for pleasure or success in goal-oriented activities. We suggest that negative symptoms represent, in part, a compensatory pattern of disengagement in response to threatening delusional beliefs, perceived social threat, and anticipated failure in tasks and social activities. A psychological aspect of this motivational and behavioural inertia appears to be the patient's perception of limited psychological resources--a perception that motivates patients to conserve energy by minimizing investment in activities requiring effort.

Past studies of the neural determinants of discriminative avoidance conditioning in rabbits have fostered a theoretical model that describes the interactive functioning of the cingulate cortex (Brodmann's Areas 24 and 29), the anterior ventral and medial dorsal thalamic nuclei (AVN and MDN) and the hippocampus. Here we test hypotheses of the model concerning the influence of the hippocampus on cortical and thalamic information processing. The rabbits learned to perform locomotory conditioned responses (CRs) in an activity wheel in response to an acoustic (pure tone) positive conditional stimulus (CS+). A shock unconditional stimulus (US) was given 5 s after CS+ onset, but locomotion during the CS+ - US interval prevented the US. The rabbits also learned to ignore a second tone (a negative conditional stimulus, CS-) of different auditory frequency than the CS+, that did not predict the US. Multi-unit activity and intracranial macropotentials were recorded in the cingulate cortex and the AVN during acquisition, overtraining, extinction, reacquisition and reversal training. Data were obtained in intact rabbits and in rabbits with bilateral lesions of the subicular complex, the origin of projections of the hippocampal formation to the cingulate cortex and AVN. In addition, the activity in the AVN was recorded in a separate group of rabbits with posterior cingulate cortical (Area 29) lesions. Subicular and Area 29 lesions were associated with an enhancement of the training-induced CS+ elicited neuronal response in the AVN. The frequency of CRs was enhanced in animals with subicular lesions. CS elicited unit responses in the cingulate cortices were attenuated in rabbits with subicular lesions. Both of the lesions were associated with significantly increased amplitudes of the CS elicited average cortical and thalamic macropotentials. These results suggested the following conclusions: subiculocortical afferents provide an enabling influence that is essential for CS elicited excitation in the cingulate cortex; the cingulate cortical excitatory response in intact animals exerts a limiting influence on the activity in the AVN; the enhanced AVN neuronal response in rabbits with lesions is due to the absence of the limiting influence and it contributes to the increased CR frequency in those animals. It is hypothesized that the hippocampus via subiculocortical projections, governs the flow of CR-inducing thalamocortical excitatory volleys. This governance determines the timing of CR output. The results of hippocampal processing of contextual information acting through the subiculocortical projection determines the moment most appropriate for the CR.

Objective Impaired facial expressions of emotions have been described as characteristic symptoms of schizophrenia. Differences regarding individual facial muscle changes associated with specific emotions in posed and evoked expressions remain unclear. This study examined static facial expressions of emotions for evidence of flattened and inappropriate affect in persons with stable schizophrenia. Methods 12 persons with stable schizophrenia and matched healthy controls underwent a standardized procedure for posed and evoked facial expressions of five universal emotions, including happy, sad, anger, fear, and disgust expressions, at three intensity levels. Subjects completed self-ratings of their emotion experience. Certified raters coded images of facial expressions for presence of action units (AUs) according to the Facial Action Coding System. Logistic regression analyses were used to examine differences in the presence of AUs and emotion experience ratings by diagnosis, condition and intensity of expression. Results Patient and control groups experienced similar intensities of emotions, however, the difference between posed and evoked emotions was less pronounced in patients. Differences in expression of frequent and infrequent AUs support clinical observations of flattened and inappropriate affect in schizophrenia. Specific differences involve the Duchenne smile for happy expressions and decreased furrowed brows in all negative emotion expressions in schizophrenia. Conclusion While patterns of facial expressions were similar between groups, general and emotion specific differences support the concept of impaired facial expressions in schizophrenia. Expression of emotions in schizophrenia could not be explained by impaired experience. Future directions may include automated measurement, remediation of expressions and early detection of schizophrenia.

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