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Lobe Areas (lobe + area)
Selected AbstractsSerotonin and dopamine transporter binding in children with autism determined by SPECTDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 8 2008Ismo Makkonen MD Disturbances in the serotonergic system have been recognized in autism. To investigate the association between serotonin and dopamine transporters and autism, we studied 15 children (14 males, one female; mean age 8y 8mo [SD 3y 10mo]) with autism and 10 non-autistic comparison children (five males, five females; mean age 9y 10mo [SD 2y 8mo]) using single-photon emission computed tomography (SPECT) with [123I] nor-,-CIT. The children, with autism were studied during light sedation. They showed reduced serotonin transporter (SERT) binding capacity in the medial frontal cortex, midbrain, and temporal lobe areas. However, after correction due to the estimated effect of sedation, the difference remained significant only in the medial frontal cortex area (p=0.002). In the individuals with autism dopamine transporter (DAT) binding did not differ from that of the comparison group. The results indicate that SERT binding capacity is disturbed in autism. The reduction is more evident in adolescence than in earlier childhood. The low SERT binding reported here and the low serotonin synthesis capacity shown elsewhere may indicate maturation of a lesser number of serotonergic nerve terminals in individuals with autism. [source] From learning to forgetting: Behavioral, circuitry, and molecular properties define the different functional states of the recognition memory traceHIPPOCAMPUS, Issue 5 2010Rocío Romero-Granados Abstract Neuropsychological analyses of amnesic patients, as well as lesion experiments, indicate that the temporal lobe is essential for the encoding, storage, and expression of object recognition memory (ORM). However, temporal lobe structures directly involved in the consolidation and reconsolidation of these memories are not yet well-defined. We report here that systemic administration of a protein synthesis inhibitor before or up to 4 h after training or reactivation sessions impairs consolidation and reconsolidation of ORM, without affecting short-term memory. We have also observed that ORM reconsolidation is sensitive to protein synthesis inhibition, independently of the ORM trace age. Using bdnf and egr-1 gene expression analysis, we defined temporal lobe areas related to consolidation and reconsolidation of ORM. Training and reactivation 21 days after ORM acquisition sessions provoked changes in bdnf mRNA in somatosensory, perirhinal, and hippocampal cortices. Reactivation 2 days after the training session elicited changes in bdnf and egr-1 mRNA in entorhinal and prefrontal cortices, while reactivation 9 days post-training provoked an increase in egr-1 transcription in somatosensory and entorhinal cortices. The differences in activated circuits and in the capacity to recall the memory trace after 9 or 21 days post-training suggest that memory trace suffers functional changes in this period of time. All these results indicate that the functional state of the recognition memory trace, from acquisition to forgetting, can be specifically defined by behavioral, circuitry, and molecular properties. © 2009 Wiley-Liss, Inc. [source] Cortical mapping of naming errors in aphasia,HUMAN BRAIN MAPPING, Issue 8 2009Julius Fridriksson Abstract Persons with aphasia vary greatly with regard to clinical profile; yet, they all share one common feature,anomia,an impairment in naming common objects. Previous research has demonstrated that particular naming errors are associated with specific left hemisphere lesions. However, we know very little about the cortical activity in the preserved brain areas that is associated with aphasic speech errors. Utilizing functional magnetic resonance imaging (fMRI), we show for the first time that specific speech errors are associated with common cortical activity in different types and severities of aphasia. Specifically, productions of phonemic errors recruited the left posterior perilesional occipital and temporal lobe areas. A similar pattern of activity was associated with semantic errors, albeit in the right hemisphere. This study does not discount variability in cortical activity following left hemisphere stroke; rather, it highlights commonalities in brain modulation in a population of patients with a common diagnosis but vastly different clinical profiles. Hum Brain Mapp 2009. © 2009 Wiley-Liss, Inc. [source] Unawareness in schizophrenia: Neuropsychological and neuroanatomical findingsPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 5 2006LORENZO PIA phd Abstract, The lack of insight in schizophrenia has so far been interpreted as a primary symptom of the illness, namely a defensive mechanism rather than a neurologically-based condition. However, recent findings have emphasized its relationship with damage to specific brain areas as well as the domain specificity in which it may occur. This supports a neuropsychological interpretation of the lack of insight in schizophrenia. The present article reviews the foregoing data, and takes into account the most relevant anatomo-clinical results. There is evidence that the lack of insight in schizophrenia may occur as a neurological disease per se following brain damage that seems related to frontal lobe areas. Additionally, it could either be related to all aspects of the disease or be domain-specific, occurring for one kind of symptom but not for others. These data indicate several analogies with the phenomenon called anosognosia for a neurological deficit. [source] |