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Introduction: Executive function impairments and high level of impulsivity may constitute heritable endophenotypes that confer predisposition for alcohol dependence. Brain volume abnormalities have also been reported in young, alcohol-naïve subjects at high risk (HR) for alcohol dependence, and linked to cognitive dysfunction., Methods: This paper presents a literature review of magnetic resonance imaging (MRI) studies that examined brain volumes in adolescent/young adult HR offspring from families with multiple cases of alcohol dependence compared to low risk controls with no family history of alcohol or drug misuse. In some of these studies, executive functioning and externalizing symptoms were also assessed., Results: In HR subjects, local white matter volume deficits were found in the corpus callosum and in the right orbito-frontal cortex, and lower fractional anisotropy in the left inferior longitudinal fasciculus and in the right optic radiation. Altered fronto-cerebellar connectivity has also been reported. Diminished gray matter volume of the cerebellar cortex was found in HR subjects, in the frontal, cyngulate and para-hippocampal gyri, and also in the amygdala, the thalamus and the cerebellum. These structural abnormalities have been associated with higher impulsivity level and executive function impairments, themselves markers of vulnerability to alcoholism. These premorbid cerebral abnormalities may increase the risk for developing an alcohol use disorder in HR subjects through atypical control processing., Conclusion: Brain abnormalities may potentially constitute an abnormal neural network that might underlie the risk towards alcohol dependence. These circuitry abnormalities might contribute to the reward deficiency, as well as impaired response inhibition that predict impulsive spectrum behavior, which are thought to represent the inherited vulnerability to alcohol dependence in HR individuals., (Copyright © 2013 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

The number of structural neuroimaging studies of bipolar disorder have increased during recent years, expanding the literature on the nature of cerebral abnormalities underlying this disorder. The purpose of this paper is to provide a selective review on the main issues concerning this literature. Consistent findings are higher rate of periventricular and deep subcortical white matter hyperintensites seen on MRI. Although there is strong evidence for links between hyper-intense lesions and age or cardio-vascular risk factors, some authors have observed the presence of these abnormalities early in the course of the illness. There are also frequent reports on ventricular enlargement, which has been described as mild and predominant in the right lateral ventricle. Total cerebral volume appears to be preserved. Whereas changes in total grey matter volume are uncertain, evidence suggests that reduced white matter volume reflects genetic factors predisposing to the disorder. Recent studies have reported volume changes in several cortical areas including the subgenual cingular, frontal and temporal cortices. Additionally, a number of reports described morphometric abnormalities in various subcortical structures, such as amygdala, basal ganglia and thalamus. Part of the variability in the morphometric abnormalities might be attributable to differences in clinical status and demographic characteristics of patient groups. Despite some inconsistencies across the studies, it emerges that abnormalities are asymmetrically distributed throughout the two cerebral hemispheres. When increase in volume is reported, it is preferentially localised in the left cerebral hemi-sphere and more specifically in prefrontal and temporal cortices and in amygdala. By contrast, when structural abnormalities concern the right cerebral hemisphere, they are identified as deficits. These latter results are in direct line with those of studies of mania following brain injuries, which report that these secondary mania result mainly from right cerebral lesions. It is also important to notice that most of the abnormalities concern both the cortical and subcortical level, ie frontal, striatal, thalamic and limbic regions. These abnormalities highlight the role in the pathophysiology of bipolar disorder of the loops involved in emotional information processing. The particular role of fronto-limbic loops in the phenomenology of bipolar disorder have been emphasised by recent data from functional neuroimaging studies.

Over the last years, technical advances in neuroimaging have allowed drastic improvements in the assessment of acute ischemic cerebral events. Beyond conventional morphological analysis, diffusion-weighted and perfusion-weighted MRI now enable routine functional assessment of brain tissue; spectroscopy and diffusion tensor imaging still remains in the domain of clinical research. During acute ischemia events, diffusion-weighted MRI can detect the movements of water molecules and cytotoxic edema related to cell injury enabling rapid diagnosis and early assessment of cerebral ischemia. In conjunction with perfusion imaging, which detects hypoperfusion areas, diffusion-weighted MRI provides a means to identify areas of penumbra ischemia. More recent multislice computed tomographic (CT) scans with multimodal analysis are also very competitive for assessment of cerebral ischemia (non-enhanced CT, CT angiography and perfusion CT). The purpose of this paper is to describe the CT and MRI patterns during the different stages of cerebral infarcts.

A good knowledge of the brain anatomy is necessary for all physicists interested in neurologic pathology, and especially for the radiologists. The aim of this paper is to summarize the important data in morphological but also in functional brain anatomy. The main neurologic pathways are represented on MR standard slices for practical application. The international anatomica nomenclatura (french terms) is used.

We describe in this paper how the STEAM sequence can be an efficient tool to obtain images free of flow artifacts in anatomical situation where the spin echo failed. The simplest way to eliminate flow artifacts is to exploit the dephasing induced by motion in magnetic field gradients and to reduce to zero the signal from moving tissues. This can be achieve by increasing the time elapsed between the spin excitation and the signal observed. Because of T2 relaxation, such an increase results in a signal decrease when the spin echo sequence is used. The STEAM sequence has the unique property that the time elapsed between observation and excitation can be increased without change in T2 value and so allows a good suppression of signals from the moving spins with short TE. Our results demonstrate that, although the stimulated echo intensity is only half that of a spin echo taken at the same read out time, the advantages of STEAM imaging can compensate for this partial loss in signal to noise in some particular clinical situations. The influence of mixing time on contrast has been evaluated using thoracic spine imaging and it has been shown that contrast between spine and CSF can be significantly improved (+ 60%) when TM is increased (from 17 ms to 50 ms). In the same time, the contrast between spine and fat issue decreases (40%). This last effect facilitates the adjustment of contrast window. Suppression of motion artifacts has first been evaluated with thoracic spine imaging, using a whole body coil. Suppression of artifacts was better than that obtained with a flow compensated spin echo sequence, especially in the case of kyphotic patients when a presaturation band was inefficient. In a second step suppression of motion artifacts has been evaluated from posterior fossa examination after injection of a paramagnetic contrast agent. The images obtained with the stimulated echo sequence show a dramatic reduction of signal from blood in the lateral sinus, and therefore an increase of quality by elimination of motion artifacts.