Maternal dietary omega-3 deficiency worsens the deleterious effects of prenatal inflammation on the gut-brain axis in the offspring across lifetime.

Maternal immune activation (MIA) and poor maternal nutritional habits are risk factors for the occurrence of neurodevelopmental disorders (NDD). Human studies show the deleterious impact of prenatal inflammation and low n-3 polyunsaturated fatty acid (PUFA) intake on neurodevelopment with long-lasting consequences on behavior. However, the mechanisms linking maternal nutritional status to MIA are still unclear, despite their relevance to the etiology of NDD. We demonstrate here that low maternal n-3 PUFA intake worsens MIA-induced early gut dysfunction, including modification of gut microbiota composition and higher local inflammatory reactivity. These deficits correlate with alterations of microglia-neuron crosstalk pathways and have long-lasting effects, both at transcriptional and behavioral levels. This work highlights the perinatal period as a critical time window, especially regarding the role of the gut-brain axis in neurodevelopment, elucidating the link between MIA, poor nutritional habits, and NDD.

Recovery from nonfluent aphasia after melodic intonation therapy: a PET study.

We examined mechanisms of recovery from aphasia in seven nonfluent aphasic patients, who were successfully treated with melodic intonation therapy (MIT) after a lengthy absence of spontaneous recovery. We measured changes in relative cerebral blood flow (CBF) with positron emission tomography (PET) during hearing and repetition of simple words, and during repetition of MIT-loaded words. Without MIT, language tasks abnormally activated right hemisphere regions, homotopic to those activated in the normal subject, and deactivated left hemisphere language zones. In contrast, repeating words with MIT reactivated Broca's area and the left prefrontal cortex, while deactivating the counterpart of Wernicke's area in the right hemisphere. The recovery process induced by MIT in these patients probably coincides with this reactivation of left prefrontal structures. In contrast, the right hemisphere regions abnormally activated during simple language tasks seem to be associated with the initial persistence of the aphasia. This study supports the idea that abnormal activation patterns in the lesioned brain are not necessarily related to the recovery process.

Parinaud's syndrome: electro-oculographic and anatomical analyses of six vascular cases with deductions about vertical gaze organization in the premotor structures.

Six cases of Parinaud's syndrome, with downward (Cases 1, 2), upward (Cases 3, 4) and both downward and upward gaze paralysis (cases 5, 6) are reported. Four cases (Cases 1, 2, 3, 5) were studied anatomically using serial sections of the brain and 3 cases (Cases, 1, 4, 6) analysed electro-oculographically. In all the cases there were rather small vascular lesions in the mesodiencephalic region, sparing the oculomotor nuclei. Since the rostral interstitial nuclei of the medial longitudinal fasciculus (riMLF), located above the oculomotor nuclei, contain the final relays producing all vertical saccades, it is suggested that the different aspects of Parinaud's syndrome may result from damage to their cells or to their excitatory efferent tracts, or even to their afferent pathways. Downgaze paralysis results from bilateral lesions involving the regions located just caudal, medial and dorsal to the upper poles of the red nuclei. The critical area is probably related to the mediocaudal part of the riMLF, the lateral portion of which appears to be spared. These anatomical data, combined with the clinical observation that most downward eye movements (except slow reflex movements) are affected in the case with such paralysis, lead us to propose that it is the riMLF efferent tracts mediating downgaze and projecting on to the oculomotor nuclei that are principally damaged by the lesions. Upgaze paralysis results from unilateral lesions in or near the posterior commissure. The clinical data allow us to propose that it is also the riMLF efferent tracts, mediating upgaze, that are damaged in such cases. consequently these tracts, probably originating from the dorsolateral part of the riMLF, would decussate through the posterior commissure before they reach the oculomotor nuclei. Combined downgaze and upgaze paralysis results from bilateral lesions involving the region related to the whole riMLF on both sides. The principal conclusion is that the riMLF efferent tracts mediating upward and downward gaze have clearly separate courses in the immediate premotor structures.