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Medial Frontal (medial + frontal)

Distribution by Scientific Domains

Medical Sciences	50%

Terms modified by Medial Frontal

medial frontal cortex

Selected Abstracts

Prefrontal cortex activity is reduced in gambling and nongambling substance users during decision-making,

HUMAN BRAIN MAPPING, Issue 12 2007
Jody Tanabe
Abstract Objective: Poor decision-making is a hallmark of addiction, whether to substances or activities. Performance on a widely used test of decision-making, the Iowa Gambling Task (IGT), can discriminate controls from persons with ventral medial frontal lesions, substance-dependence, and pathological gambling. Positron emission tomography (PET) studies indicate that substance-dependent individuals show altered prefrontal activity on the task. Here we adapted the IGT to an fMRI setting to test the hypothesis that defects in ventral medial and prefrontal processing are associated with impaired decisions that involve risk but may differ depending on whether substance dependence is comorbid with gambling problems. Method: 18 controls, 14 substance-dependent individuals (SD), and 16 SD with gambling problems (SDPG) underwent fMRI while performing a modified version of the IGT. Result: Group differences were observed in ventral medial frontal, right frontopolar, and superior frontal cortex during decision-making. Controls showed the greatest activity, followed by SDPG, followed by SD. Conclusion: Our results support a hypothesis that defects in ventral medial frontal processing lead to impaired decisions that involve risk. Reductions in right prefrontal activity during decision-making appear to be modulated by the presence of gambling problems and may reflect impaired working memory, stimulus reward valuation, or cue reactivity in substance-dependent individuals. Hum Brain Mapp, 2007. © 2007 Wiley-Liss, Inc. [source]

Characterization of White Matter Microstructure in Fetal Alcohol Spectrum Disorders

ALCOHOLISM, Issue 3 2009
Susanna L. Fryer
Background:, Exposure to alcohol during gestation is associated with CNS alterations, cognitive deficits, and behavior problems. This study investigated microstructural aspects of putative white matter abnormalities following prenatal alcohol exposure. Methods:, Diffusion tensor imaging was used to assess white matter microstructure in 27 youth (age range: 8 to 18 years) with (n = 15) and without (n = 12) histories of heavy prenatal alcohol exposure. Voxelwise analyses, corrected for multiple comparisons, compared fractional anisotropy (FA) and mean diffusivity (MD) between groups, throughout the cerebrum. Results:, Prenatal alcohol exposure was associated with low FA in multiple cerebral areas, including the body of the corpus callosum and white matter innervating bilateral medial frontal and occipital lobes. Fewer between-group differences in MD were observed. Conclusions:, These data provide an account of cerebral white matter microstructural integrity in fetal alcohol spectrum disorders and support extant literature showing that white matter is a target of alcohol teratogenesis. The white matter anomalies characterized in this study may relate to the neurobehavioral sequelae associated with gestational alcohol exposure, especially in areas of executive dysfunction and visual processing deficits. [source]

Classic and false memory designs: An electrophysiological comparison

PSYCHOPHYSIOLOGY, Issue 5 2004
Doreen Nessler
Abstract In false memory tasks new items either overlap with the semantic concepts of studied items (LURE) or do not (NEW). ERP differences between OLD and NEW items in false memory tasks have been interpreted as similar to episodic memory effects observed in classic recognition studies. However, NEW items in a false memory task can be rejected on the basis of semantic information alone, a strategy useless in classic tasks. Here a medial frontal (400 to 500 ms) episodic memory effect was revealed in both classic and false memory tasks, whereas a parietal (500 to 700 ms) episodic memory effect was found only in the classic task. In the false memory task a large, parietally focused positivity was evident for NEW items, assumed to reflect a targetlike response to new semantic information. The brain activity underlying false memory effects, therefore, cannot be interpreted as a straightforward example of that arising during a standard recognition task. [source]

Relationship between atrophy and ,-amyloid deposition in Alzheimer disease

ANNALS OF NEUROLOGY, Issue 3 2010
Gaël Chételat PhD
Objective Elucidating the role of aggregated ,-amyloid in relation to gray matter atrophy is crucial to the understanding of the pathological mechanisms of Alzheimer disease and for the development of therapeutic trials. The present study aims to assess this relationship. Methods Brain magnetic resonance imaging and [11C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group. Results Global and regional atrophy were strongly related to ,-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical ,-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional ,-amyloid load was related to local atrophy in the areas of highest ,-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/precuneus areas. Interpretation There is a strong relationship between ,-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated ,-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss. ANN NEUROL 2010;67:317,324 [source]