Reorganization of the auditory, visual and multimodal areas in early deaf individuals.

Plasticity resulting from early sensory deprivation has been investigated in both animals and humans. After sensory deprivation, brain areas that are normally associated with the lost sense are recruited to carry out functions in the remaining intact modalities. Previous studies have reported that it is almost exclusively the visual dorsal pathway which is affected by auditory deprivation. The purpose of the current study was to further investigate the possible reorganization of visual ventral stream functions in deaf individuals in both the auditory and the visual cortices. Fifteen pre-lingual profoundly deaf subjects were compared with a group of 16 hearing subjects. We used fMRI (functional magnetic resonance imaging) to explore the areas underlying the processing of two similar visual motion stimuli that however were designed to evoke different types of processing: (1) a global motion stimulus (GMS) which preferentially activates regions of the dorsal visual stream, and (2) a form-from-motion (FFM) stimulus which is known to recruit regions from both visual streams. No significant differences between deaf and hearing individuals were found in target visual and auditory areas when the motion and form components of the stimuli were isolated (contrasted with a static visual image). However, increases in activation were found in the deaf group in the superior temporal gyrus (BA 22 and 42) and in an area located at the junction of the parieto-occipital sulcus and the calcarine fissure (encompassing parts of the cuneus, precuneus and the lingual gyrus) for the GMS and FFM conditions as well as for the static image, relative to a baseline condition absent of any visual stimulation. These results suggest that the observed cross-modal recruitment of auditory areas in deaf individuals does not appear to be specialized for motion processing, but rather is present for both motion and static visual stimuli.

Functional reorganization of the auditory pathways following late callosotomy.

Injuries at various levels of the auditory system have been shown to lead to functional reorganization of the auditory pathways. In particular, it has recently been shown that such reorganization can occur in callosal agenesis. The pattern of cortical activity following callosotomy is however still unknown, but behavioral results suggest that it could be significantly different from that observed in callosal agenesis. We aimed to confirm this hypothesis by investigating fMRI responses to complex sounds presented binaurally and monaurally in a callosotomized patient. In the binaural condition, the callosotomized subject showed patterns of auditory cortical activation that were similar to those of neurologically intact individuals. However, in both monaural conditions, the callosotomized individual showed a significant increase of the asymmetries favoring the contralateral pathways. Such patterns of cortical responses are only partially consistent with the results obtained from callosal agenesis subjects using the exact same procedure. Indeed, the latter show differences compared with normals in both binaural and monaural conditions. These findings provide neurological evidence that callosotomy could lead to distinctive functional reorganization of the human auditory pathways.

Functional reorganization of the human auditory pathways following hemispherectomy: an fMRI demonstration.

The present study investigated the functional reorganization of ipsilateral and contralateral auditory pathways in hemispherectomized subjects. Functional reorganization was assessed using functional Magnetic Resonance Imaging (fMRI) and stimulation with complex sounds presented binaurally and monaurally. For neurologically intact control subjects, results showed that binaural stimulations evoked balanced activity in both hemispheres while monaural stimulations induced strong contralateral activity and weak ipsilateral activity. The results obtained from hemispherectomized subjects were substantially different from those obtained from control subjects. Specifically, activity in the intact hemisphere showed a significant decrease in response to contralateral stimulation but, concomitantly, an increase in response to ipsilateral stimulation. The present findings suggest that a substantial functional reorganization takes place in the auditory pathways following an early hemispherectomy. The exact nature of this functional reorganization remains to be specified.

Neural basis of emotional self-regulation in childhood.

Emotional self-regulation plays a pivotal role in socialization and moral development. This capacity critically depends on the development of the prefrontal cortex (PFC). The present functional magnetic resonance imaging study was conducted to identify the neural circuitry underlying voluntary self-regulation of sadness in healthy girls (aged 8-10). A 2 x 2 factorial design was implemented with Emotion (No Sadness vs. Sadness) and Regulation (No Reappraisal vs. Reappraisal) as factors. In the No Reappraisal conditions, subjects were instructed to react normally to neutral and sad film excerpts whereas in the Reappraisal conditions, subjects were asked to voluntarily suppress any emotional reaction in response to comparable stimuli. A significant interaction of the Emotion and Regulation factors revealed that reappraisal of sad film excerpts was associated with bilateral activations of the lateral PFC (LPFC; Brodmann areas [BA] 9 and 10), orbitofrontal cortex (OFC; BA 11), and medial PFC (BA 9 and 10). Significant loci of activations were also detected in the right anterior cingulate cortex (BA 24/32) and right ventrolateral PFC (BA 47). In an identical study previously conducted by our group in adult women [Biol Psychiatry 53 (2003) 502], reappraisal of sad film excerpts was associated with activation of the right OFC (BA 11) and right LPFC (BA 9). The greater number of prefrontal loci of activation found in children relative to adults during voluntary self-regulation of sadness may be related to the immaturity of the prefronto-limbic connections in childhood.

Neural correlates of sad feelings in healthy girls.

Emotional development is indisputably one of the cornerstones of personality development during infancy. According to the differential emotions theory (DET), primary emotions are constituted of three distinct components: the neural-evaluative, the expressive, and the experiential. The DET further assumes that these three components are biologically based and functional nearly from birth. Such a view entails that the neural substrate of primary emotions must be similar in children and adults. Guided by this assumption of the DET, the present functional magnetic resonance imaging study was conducted to identify the neural correlates of sad feelings in healthy children. Fourteen healthy girls (aged 8-10) were scanned while they watched sad film excerpts aimed at externally inducing a transient state of sadness (activation task). Emotionally neutral film excerpts were also presented to the subjects (reference task). The subtraction of the brain activity measured during the viewing of the emotionally neutral film excerpts from that noted during the viewing of the sad film excerpts revealed that sad feelings were associated with significant bilateral activations of the midbrain, the medial prefrontal cortex (Brodmann area [BA] 10), and the anterior temporal pole (BA 21). A significant locus of activation was also noted in the right ventrolateral prefrontal cortex (BA 47). These results are compatible with those of previous functional neuroimaging studies of sadness in adults. They suggest that the neural substrate underlying the subjective experience of sadness is comparable in children and adults. Such a similitude provides empirical support to the DET assumption that the neural substrate of primary emotions is biologically based.

The functional neuroanatomy of major depression: an fMRI study using an emotional activation paradigm.

An important issue regarding the neural basis of major depression is whether the functional brain changes associated with the affect disturbance seen in this syndrome are similar to those that accompany transient sadness in normal subjects. To address this question, we carried out an fMRI study using an emotional activation paradigm. Brain activity associated with passive viewing of an emotionally laden film clip aimed at inducing a transient state of sadness was contrasted with that associated with passive viewing of an emotionally neutral film clip in patients suffering from unipolar depression and in normal control subjects. Results showed that transient sadness produced significant activation in the medial and inferior prefrontal cortices, the middle temporal cortex, the cerebellum and the caudate in both depressed and normal subjects. They also revealed that passive viewing of the emotionally laden film clip produced a significantly greater activation in the left medial prefrontal cortex and in the right cingulate gyrus in depressed patients than in normal control subjects. These findings suggest that these two cortical regions might be part of a neural network implicated in the pathophysiology of major depression. Taken together, these results strongly support the view that activation paradigms represent an extremely useful and powerful way of delineating the functional anatomy of the various symptoms that characterize major depression.

Assay of free-radical toxicity and antioxidant effect on the Hep 3B cell line: a test survey using lindane.

The content of reduced glutathione and of glutathione disulfide as well as the activities of glutathione reductase, glutathione peroxidase, glutathione S-transferases, catalase and superoxide dismutases were determined in human hepatoma Hep 3B cells in relation to free-radical toxicity in order to appreciate the defense capacities of these cells compared to data on normal hepatocytes. When Hep 3B cells were exposed to lindane, a known inducer of free-radical production, superoxide dismutase activity appeared as the best-adapted cellular parameter for early detection of the resulting free-radical toxicity.