149 research outputs found

    Interactions between mood and the structure of semantic memory: event-related potentials evidence

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    Recent evidence suggests that affect acts as modulator of cognitive processes and in particular that induced mood has an effect on the way semantic memory is used on-line. We used event-related potentials (ERPs) to examine affective modulation of semantic information processing under three different moods: neutral, positive and negative. Fifteen subjects read 324 pairs of sentences, after mood induction procedure with 30 pictures of neutral, 30 pictures of positive and 30 pictures of neutral valence: 108 sentences were read in each mood induction condition. Sentences ended with three word types: expected words, within-category violations, and between-category violations. N400 amplitude was measured to the three word types under each mood induction condition. Under neutral mood, a congruency (more negative N400 amplitude for unexpected relative to expected endings) and a category effect (more negative N400 amplitude for between- than to within-category violations) were observed. Also, results showed differences in N400 amplitude for both within- and between-category violations as a function of mood: while positive mood tended to facilitate the integration of unexpected but related items, negative mood made their integration as difficult as unexpected and unrelated items. These findings suggest the differential impact of mood on access to long-term semantic memory during sentence comprehension.The authors would like to thank to all the participants of the study, as well as to Jenna Mezin and Elizabeth Thompson for their help with data collection. This work was supported by a Doctoral Grant from Fundacao para a Ciencia e a Tecnologia - Portugal (SFRH/BD/35882/2007 to A. P. P.) and by the National Institute of Mental Health (RO1 MH 040799 to R. W. M.; RO3 MH 078036 to M.A.N.)

    Consensus Paper: Cerebellum and Social Cognition.

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    The traditional view on the cerebellum is that it controls motor behavior. Although recent work has revealed that the cerebellum supports also nonmotor functions such as cognition and affect, only during the last 5 years it has become evident that the cerebellum also plays an important social role. This role is evident in social cognition based on interpreting goal-directed actions through the movements of individuals (social "mirroring") which is very close to its original role in motor learning, as well as in social understanding of other individuals' mental state, such as their intentions, beliefs, past behaviors, future aspirations, and personality traits (social "mentalizing"). Most of this mentalizing role is supported by the posterior cerebellum (e.g., Crus I and II). The most dominant hypothesis is that the cerebellum assists in learning and understanding social action sequences, and so facilitates social cognition by supporting optimal predictions about imminent or future social interaction and cooperation. This consensus paper brings together experts from different fields to discuss recent efforts in understanding the role of the cerebellum in social cognition, and the understanding of social behaviors and mental states by others, its effect on clinical impairments such as cerebellar ataxia and autism spectrum disorder, and how the cerebellum can become a potential target for noninvasive brain stimulation as a therapeutic intervention. We report on the most recent empirical findings and techniques for understanding and manipulating cerebellar circuits in humans. Cerebellar circuitry appears now as a key structure to elucidate social interactions

    Akinetic Mutism Without a Structural Prefrontal Lesion

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    Akinetic mutism is characterized by profound apathy and a lack of verbal and motor output for action, despite preserved alertness. The condition usually follows bilateral damage to the medial frontal subcortical circuits. We report a 59-year-old right-handed woman who was admitted to the neurology ward with sudden-onset akinetic mutism. Her medical history included an ischemic stroke 3 years earlier, with residual anomia and mild agraphia but no motor dysfunction. On this admission, a cranial computed tomography scan disclosed an acute left superior cerebellar infarction embracing the vermis, and a prior left inferior parietal infarct. Electroencephalogram showed bilateral frontal delta-wave activity. Four weeks later, we performed a technetium-99m hexamethylpropyleneamine oxime single-photon emission computed tomography (Tc-99m-HMPAO SPECT) scan to study the patient's frontal lobe function. The SPECT scan revealed the causative bifrontal hypoperfusion, more prominent on the right, while the structurally evident cerebellar infarction was predictably masked by subacute hyperperfusion phenomenon. Contralateral frontal diaschisis is an established sequela of cerebellar infarction. Because this patient also had lesions in the left parietal region, her left prefrontal area was critically deprived of its major reciprocally connected cortical counterparts (right prefrontal and left parietal), and also became dysfunctional. Her resulting bilateral frontal dysfunction is a common cause of akinetic mutism

    Neurodevelopmental Influences in Psychosis: A Case of Left Cerebral Hemiatrophy and Schizoaffective Disorder

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    Cerebral hemiatrophy (or Dyke-Davidoff-Masson Syndrome) is a neurodevelopmental disorder characterized by atrophy or hypoplasia of one cerebral hemisphere accompanied by ipsilateral calvarial changes. Clinically, the condition presents with contralateral motor dysfunction, facial asymmetry, epilepsy and intellectual impairment. Psychiatric manifestations are uncommon and the neuropsychiatric aspect of the disease is not wet described. Here, we report a 26-year-old female who presented with left cerebral hemiatrophy and schizoaffective disorder. We discuss the relevance of left-sided neurodevelopmental cerebral atrophy in the context of disrupted neural development of brain lateralization, plasticity, and evidence regarding left hemisphere dysfunction in schizophrenia and schizoaffective disorder
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