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When we behave according to rules and instructions, our brains interpret abstract representations of what to do and transform them into actual behavior. In order to investigate the neural mechanisms behind this process, we devised an fMRI experiment that explicitly isolated rule interpretation from rule encoding and execution. Our results showed that a specific network of regions (including the left rostral prefrontal cortex, the caudate nucleus, and the bilateral posterior parietal cortices) is responsible for translating rules into executable form. An analysis of activation patterns across conditions revealed that the posterior parietal cortices represent a mental template for the task to perform, that the inferior parietal gyrus and the caudate nucleus are responsible for instantiating the template in the proper context, and that the left rostral prefrontal cortex integrates information across complex relationships.

HIV-associated neurocognitive disorder remains prevalent in HIV-infected individuals despite effective antiretroviral therapy. As these individuals age, comorbid cerebrovascular disease will likely impact cognitive function. Effective tools to study this impact are needed. This study used diffusion tensor imaging (DTI) to characterize brain microstructural changes in HIV-infected individuals with and without cerebrovascular risk factors. Diffusion-weighted MRIs were obtained in 22 HIV-infected subjects aged 50 years or older (mean age = 58 years, standard deviation = 6 years; 19 males, three females). Tensors were calculated to obtain fractional anisotropy (FA) and mean diffusivity (MD) maps. Statistical comparisons accounting for multiple comparisons were made between groups with and without cerebrovascular risk factors. Abnormal glucose metabolism (i.e., impaired fasting glucose, impaired glucose tolerance, or diabetes mellitus) was associated with significantly higher MD (false discovery rate (FDR) critical p value = 0.008) and lower FA (FDR critical p value = 0.002) in the caudate and lower FA in the hippocampus (FDR critical p value = 0.004). Pearson correlations were performed between DTI measures in the caudate and hippocampus and age- and education-adjusted composite scores of global cognitive function, memory, and psychomotor speed. There were no detectable correlations between the neuroimaging measures and measures of cognition. In summary, we demonstrate that brain microstructural abnormalities are associated with abnormal glucose metabolism in the caudate and hippocampus of HIV-infected individuals. Deep gray matter structures and the hippocampus may be vulnerable in subjects with comorbid abnormal glucose metabolism, but our results should be confirmed in further studies.

Obsessive compulsive disorders (OCD) may be encountered after basal ganglia lesions of various aetiologies. These lesions are usually bilateral. We report here the case of a 24 years old man who developed a pure compulsive behavior after a unilateral left-sided caudate nucleus hemorrhage due to a cavernoma. The pathophysiology of this compulsive disorder probably reflects a frontal cortex deafferentation mechanism. Behavioral, psychological and medical (serotoninergic) treatments are usually proposed but the efficacy of such therapy remains to be investigated in secondary OCD.

Clinical-neuropsychological investigations were performed in 187 patients with arteriovenous malformations (AVM) of deep brain structures; 28 had AVM of the caudate nucleus, 35 of the thalamus, 45 of the cingulate gyrus, 43 of the hippocampus, and 36 of the corpus callosum. A total of 47 patients displayed neglect phenomena of different modalities, while unfixed neglect was demonstrated in 40 cases using special tests. The vast majority of patients showed neglect of left-sided space and the left side of the body, while only three patients showed right-sided neglect. These three patients had signs of left-handedness. In the development of neglect in all patients was associated with post-hemorrhagic or post-operative damage to the white matter (the projections of sensory bundles of the parietal and occipital lobes, the periventricular white matter) or the thalamus and corpus callosum. In hemispheric lesions, neglect developed on the background of the corresponding derangements (hemihypesthesia hemianopsia) and were of the same modality. In cases of damage to the corpus callosum, neglect could develop without accompanying sensory disturbances or the phenomenon could occur on different sides (in cases of simultaneous left hemisphere damage). This supports the independent nature of the neglect phenomenon.

Cerebral infarcts in children are rather rare and in most cases no precise etiology is established. The authors describe a case of cryptogenetic cerebral infarction in a 9-year-old boy. The child presented an acute onset of hemiplegia in the right arm and leg, central facial palsy, dysarthria and steppage. The infarction was proved by Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). Laboratory and instrumental studies rule out all known causes of brain infarction. The only possible etiopathogenetic hypothesis was a varicella arteritis which occurred 45 days before the clinical manifestation.

Three patients with symmetrical bilateral low-density areas which were the perfusion territories of Heubner's arteries are reported. The infarctions were demonstrated on computed tomography after aneurysm surgery. Two of them had an anterior communicating artery aneurysm and the other one had multiple aneurysms of both sides. They were operated upon in the acute stage after subarachnoid haemorrhage. As common factors, a thick and diffuse subarachnoid haemorrhage, an acute-stage operation, temporary clips to bilateral A1 segments or the internal carotid artery and a relatively low systemic blood pressure during operation were found. From these findings we conclude that the pathogenesis of the infarctions was due to occlusive changes affecting Heubner's arteries bilaterally.

The statistical data, obtained in seventy five brains with lacunar state, show that the lenticular nuclei and the periventricular arterial end-and borderzones are the main seats of the infarcts. In teen brains the relationship between the deep arterial angioarchitecture and the location of thirty lacunes is studied by means of the translucidation technique after filling the arterial system with a colloîdal barium sulphate solution. The deep perforating arteries are poorly filled and show several narrowings and post-stenotic dilatations. In twenty-four lacunes, an occlusion of the responsible artery is found. In the six remaining lacunes, no occlusion of the main artery is observed but the side-branches are not demonstrated. The significance of these findings and the relationship between the location of the occlusion and the topography of the lacune are discussed.

Employing the experimental set-up and the methods described - in part I of the paper, the measurements of the regional cerebral blood flow (rCBF) and evaluation of brain microcirculation were performed. The control series provided normal values and constituted the reference for the results of the post-haemorrhagic measurements. Arterial subarachnoid haemorrhage increases transitorily the intracranial pressure to values close to the diastolic blood pressure. The rise of the blood pressure (Cushing response) is not adequate to prevent the reduction in the cerebral perfusion pressure. Cerebral blood flow diminishes after arterial subarachnoid haemorrhage during the elevation of intracranial pressure. It results in numerous, disseminated areas of reduced regional cerebral blood flow. During 4 hours following arterial subarachnoid haemorrhage global cerebral blood flow returns to normal values, while focal reductions in blood flow persist in the grey matter structures of both hemispheres. These foci are accompanied by confined areas of markedly increased regional cerebral blood flow. Disseminated foci with a reduced number of patent capillaries are found in the grey matter structures of both hemispheres 1 and 4 hours following arterial subarachnoid haemorrhage. Their number decreases during the 4 hours observation.