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Background: Children with fetal alcohol spectrum disorders (FASD) often have deficits associated with multisensory processing. Because ethanol (EtOH) disrupts activity‐dependent neuronal plasticity, a process that is essential for refining connections during cortical development, we hypothesize that early alcohol exposure results in alterations in multisensory cortical networks, which could explain the multisensory processing deficits seen in FASD. Here, we use a gyrencephalic animal model to test the prediction that early alcohol exposure alters the functional connectivity and microstructural features of the rostral posterior parietal cortex (PPr), a visual‐tactile integrative area. Methods: Ferrets were exposed to moderate doses of EtOH during the brain growth spurt period. Functional connectivity and microstructural features were assessed using resting‐state functional magnetic resonance imaging and ex vivo diffusion kurtosis imaging (DKI), respectively, when the animals reached juvenile age and adulthood, respectively. Results: While the whole brain volume was smaller in alcohol‐treated animals, the relative size of the frontal brain area was larger when compared to control animals. Altered functional connectivity was observed in alcohol‐treated animals, where increased connectivity was observed between PPr and the region that provides its major visual inputs (the caudal portion of the parietal cortex), but not with the region that provides its major somatosensory inputs (tertiary somatosensory cortex). DKI revealed reduced microstructural tissue complexity in all investigated sensory areas of alcohol‐treated animals. Conclusions: In this study, we observed alterations in cortical functional connectivity and microstructural integrity in a cortical area involved in multisensory processing in a ferret FASD model. These findings indicate an alteration in cortical networks that may be related to the multisensory processing deficiencies observed in FASD. [ABSTRACT FROM AUTHOR]

Introduction: Bidirectional effects between cognition and pain have been extensively reported. Although brain regions involved in cognitive and pain processing seem to partly overlap, it is unknown what specific brain regions are involved in the interaction between pain and cognition. Furthermore, the role of gonadal hormones on these interacting effects has not been examined. This study investigated brain activation patterns of the interaction between pain and cognition over different phases of the naturally occurring menstrual cycle. Methods: Fifteen healthy normally cycling females were examined over the course of 4 different cycle phases. Sensory stimulation was applied using electrical pulses and cognitive performance was assessed using the Multi‐Source Interference Task. Brain imaging consisted of functional magnetic resonance imaging using a repeated measures ANOVA group analysis approach. Results: Sensory stimulation was found to interact with task performance in the left precuneus, left posterior cingulate cortex and right inferior parietal lobule. No effects of cycle phase were observed to interact with main effects of stimulation, task or interaction effects between task performance and sensory stimulation. Conclusion: Potential neural correlates of shared resources between pain and cognition were demonstrated providing further insights into the potential mechanisms behind cognitive performance difficulties in pain patients and opening avenues for new treatment options including targeting specific cognitive factors in pain treatment such as cognitive interference. [ABSTRACT FROM AUTHOR]

High-force lengthening contractions are associated with muscle damage and pain, and the muscle-tendon junction is commonly cited as the primary area where myofiber damage occurs. We induced injury in the rat tibialis anterior muscle and acquired magnetic resonance imaging (MRI) images postinjury. We also assayed membrane damage and quantified the number of centrally nucleated myofibers throughout the injured muscles. Results suggest that myofiber injury occurs primarily in the middle portion of the muscle, with interstitial edema in the middle and distal portions. Muscle Nerve, 2009 [ABSTRACT FROM AUTHOR]

Background: People with fetal alcohol spectrum disorder (FASD) often have structural or functional alterations of the central nervous system, including changes in brain network organization. These have been associated with neuropsychological deficits, but outcomes are not consistent across studies. We used a rat model of FASD to assess brain network alterations in males and females following ethanol exposure during a prenatal period similar to the first half of gestation in humans. Methods: Pregnant Long Evans rats were given an ethanol‐containing or isocaloric non‐ethanol diet from gestation day 6 to 20. Resting‐state functional magnetic resonance imaging was performed on offspring in young adulthood. Graph theoretical analysis was used to assess properties associated with the whole brain network organization, with a focus on segregation, integration, and small‐world organization—a feature which allows specialized local information processing (segregation) and simultaneously efficient global information sharing (integration). Results: Ethanol‐exposed females showed a significant decrease in small‐worldness compared with control females or with ethanol‐exposed males. Compared to control females, the proportion of animals with atypically high path length (1 standard deviation higher than the grand average) was significantly higher in ethanol‐exposed females, indicating that the alteration in small‐world organization is driven by decreased network integration. No significant effects were seen in males. Conclusion: The results revealed that prenatal ethanol exposure disrupts the balance between network segregation and integration in young adult female rats. The whole brain network is less integrated after ethanol exposure in the females, suggesting wide‐spread reduction of long‐range regional communication. [ABSTRACT FROM AUTHOR]

Organophosphorus ( OP) insecticides are pest-control agents heavily used worldwide. Unfortunately, they are also well known for the toxic effects that they can trigger in humans. Clinical manifestations of an acute exposure of humans to OP insecticides include a well-defined cholinergic crisis that develops as a result of the irreversible inhibition of acetylcholinesterase ( AChE), the enzyme that hydrolyzes the neurotransmitter acetylcholine ( ACh). Prolonged exposures to levels of OP insecticides that are insufficient to trigger signs of acute intoxication, which are hereafter referred to as subacute exposures, have also been associated with neurological deficits. In particular, epidemiological studies have reported statistically significant correlations between prenatal subacute exposures to OP insecticides, including chlorpyrifos, and neurological deficits that range from cognitive impairments to tremors in childhood. The primary objectives of this article are: (i) to address the short- and long-term neurological issues that have been associated with acute and subacute exposures of humans to OP insecticides, especially early in life (ii) to discuss the translational relevance of animal models of developmental exposure to OP insecticides, and (iii) to review mechanisms that are likely to contribute to the developmental neurotoxicity of OP insecticides. Most of the discussion will be focused on chlorpyrifos, the top-selling OP insecticide in the United States and throughout the world. These points are critical for the identification and development of safe and effective interventions to counter and/or prevent the neurotoxic effects of these chemicals in the developing brain. This is an article for the . [ABSTRACT FROM AUTHOR]

Fragile X syndrome ( FXS) is the most common form of inherited mental retardation and is studied in the Fmr1 knockout ( KO) mouse, which models both the anatomical and behavioral changes observed in FXS patients. In vitro studies have shown many alterations in synaptic plasticity and increased density of immature dendritic spines in the hippocampus, a region involved in learning and memory. In this study, magnetic resonance imaging ( MRI) and 1H magnetic resonance spectroscopy ( MRS) were used to determine in vivo longitudinal changes in volume and metabolites in the hippocampus during the critical period of early myelination and synaptogenesis at post-natal days ( PND) 18, 21, and 30 in Fmr1 KO mice compared with wild-type (WT) controls. MRI demonstrated an increase in volume of the hippocampus in the Fmr1 KO mouse compared with controls. MRS revealed significant developmental changes in the ratios of hippocampal metabolites N-acetylaspartate ( NAA), myo-inositol (Ins), and taurine to total creatine ( tCr) in Fmr1 KO mice compared with WT controls. Ins was decreased at PND 30, and taurine was increased at all ages studied in Fmr1 KO mice compared with controls. An imbalance of brain metabolites in the hippocampus of Fmr1 KO mice during the critical developmental period of synaptogenesis and early myelination could have long-lasting effects that adversely affect brain development and contribute to ongoing alterations in brain function. [ABSTRACT FROM AUTHOR]

Functional magnetic resonance imaging (fMRI) was used to compare cortical nociceptive responses to painful contact heat in healthy young (ages 22–30, n= 7) and older (ages 56–75, n= 7) subjects. Compared to young subjects, older subjects had significantly smaller pain-related fMRI responses in anterior insula (aINS) ( P < 0.04), primary somatosensory cortex (S1) ( P= 0.03), and supplementary motor area ( P= 0.02). Gray matter volumes in S1 and aINS were significantly smaller for the older group ( P= 0.02 and 0.0001, respectively), suggesting reduced processing capacity in these regions that might account for smaller pain-related fMRI responses. [ABSTRACT FROM AUTHOR]

Objective: Diffusion-weighted magnetic resonance imaging (MRI) has shown increased sensitivity in detecting brain white matter disease compared to traditional T2-weighted MRI. Diffusion-weighted imaging (DWI) can quantitatively assess the microstructural integrity of white matter using the average apparent diffusion coefficient (ADCav), a measure of the extent to which water molecules move freely within tissue. On the basis of numerous studies suggesting white matter disease in bipolar patients, particularly patients with more severe illness, this study aimed to test the utility of DWI in assessing the white matter integrity of bipolar patients with severe illness. Methods: The existing MRI scans of eight bipolar patients and eight age-matched controls with neurological illness were examined retrospectively. ADCav values for pixels within white matter regions of interest (ROIs) were calculated and used to plot ADCav frequency histograms for each ROI. Mean ADCav values for the two groups were then compared by ANCOVA. Results: The bipolar mean ADCav (0.855 ± 0.051 × 10−3 mm2/s) for combined white matter ROIs significantly exceeded that of controls (0.799 ± 0.046 × 10−3 mm2/s), while covarying for age ( F = 4.47, df = 3, p = 0.025). Conclusions: This is the first report of an elevated ADCav in the white matter of a group of patients with bipolar disorder. In this group of patients with severe illness, increased white matter ADCav suggests microstructural changes consistent with decreased white matter integrity. DWI may be an additional, useful tool to assess white matter abnormalities in bipolar disorder. [ABSTRACT FROM AUTHOR]