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The term “Gilles de la Tourette syndrome”, or the more commonly used term “Tourette syndrome” (TS) refers to the association of motor and phonic tics which evolve in a context of variable but frequent psychiatric comorbidity. The syndrome is characterized by the association of several motor tics and at least one phonic tic that have no identifiable cause, are present for at least one year and appear before the age of 18. The presence of coprolalia is not necessary to establish or rule out the diagnosis, as it is present in only 10% of cases. The diagnosis of TS is purely clinical and is based on the symptoms defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). No additional tests are required to confirm the diagnosis of TS. However, to exclude certain differential diagnoses, further tests may be necessary. Very frequently, one or more psychiatric comorbidities are also present, including attention deficit hyperactivity disorder, obsessive-compulsive disorder, anxiety, explosive outbursts, self-injurious behaviors, learning disorders or autism spectrum disorder. The condition begins in childhood around 6 or 7 years of age and progresses gradually, with periods of relative waxing and waning of tics. The majority of patients experience improvement by the end of the second decade of life, but symptoms may persist into adulthood in around one-third of patients. The cause of TS is unknown, but genetic susceptibility and certain environmental factors appear to play a role. The treatment of TS and severe forms of tics is often challenging and requires a multidisciplinary approach (involving the general practitioner (GP), pediatrician, psychiatrist, neurologist, school or occupational physicians, psychologist and social workers). In mild forms, education (of young patients, parents and siblings) and psychological management are usually recommended. Medical treatments, including antipsychotics, are essential in the moderate to severe forms of the disease (i.e. when there is a functional and/or psychosocial discomfort linked to tics). Over the past decade, cognitive-behavioral therapies have been validated for the treatment of tics. For certain isolated tics, botulinum toxin injections may also be useful. Psychiatric comorbidities, when present, often require a specific treatment. For very severe forms of TS, treatment by deep brain stimulation offers real therapeutic hope. If tics are suspected and social or functional impairment is significant, specialist advice should be sought, in accordance with the patient's age (psychiatrist/child psychiatrist; neurologist/pediatric neurologist). They will determine tic severity and the presence or absence of comorbidities. The GP will take over the management and prescription of treatment: encouraging treatment compliance, assessing side effects, and combating stigmatization among family and friends. They will also play an important role in rehabilitation therapies, as well as in ensuring that accommodations are made in the patient's schooling or professional environment.

The association between the pattern of cortical thickness (CT) and executive dysfunction (ED) in mild cognitive impairment (MCI) and subjective cognitive complaints (SCC) is still poorly understood. We aimed to investigate the association between CT and ED in a large French cohort (MEMENTO) of 2323 participants with MCI or SCC.

Évaluer les pratiques de prescription et de surveillance d’antipsychotiques (AP) en psychiatrie générale chez les patients schizophrènes âgés et les facteurs susceptibles d’influer sur elles.

Évaluer la qualité de vie liée à la santé en France de sujets de 65ans et plus vivant à domicile, à l’aide d’une échelle auto-administrée spécifique validée en français, la LEIPAD.

L’émigration est le processus qui mène un individu ou un groupe à s’installer sur le long terme dans un territoire ou un pays dont il n’est pas originaire. La personne qui émigre est – si elle souhaite réussir – soumise aux multiples processus organisant l’adaptation à son nouvel environnement de vie, ainsi qu’à un juste détachement de son environnement d’origine. Le cas de la personne d’âge avancé est particulier. Il l’est par la rareté de la migration à cet âge et par le terrain psychologique à part qu’il représente. Ce travail tente d’apporter à travers un cas clinique un éclairage sur les enjeux liés à l’émigration en âge avancé.

The age-related changes in the ventral cochlear nucleus (VCN) as revealed by glial fibrillary acid protein (GFAP) immunoreactivity were analyzed in the following age groups: 3-, 6-, 12-, 18-, and 24-month-old Sprague-Dawley rats. A cartographic and a quantitative analysis showed a significant increase in the number of GFAP positive astrocytes during the first year of life and a significant decrease in older rats. We also observed an age-induced modification in the spatial distribution of GFAP positive astrocyte. In the anterior part of the VCN of the 3- and 6-month-old rats, we observed a significant decrease in the rostro-caudal as well in the dorso-ventral axes. In the posterior part of the VCN, a significant decrease in the dorso-ventral axis could be also observed, but no significant difference in the spatial distribution was obtained in the rostro-caudal axis. In older rats, the distribution appeared homogeneous throughout the nucleus. Additionally, aging was associated with a significant increase in GFAP positive astrocyte sizes, except for immunolabelled astrocytes in the granule cell layer. The different levels of GFAP expression occurring in the VCN during normal aging could reflect a progressive decline of cellular activity in the VCN, without severe cell degeneration or synaptic loss.

The age-related change in glial fibrillary acidic protein (GFAP) immunoreactivity was analyzed in young (3 months) and old (24 months) adult rat cochlear nuclei (CN). Quantitative analyses show a significant increase with age, in the number of GFAP positive astrocytes and processes in the old adult when compared with the young adult rat. There was also a differential distribution of GFAP immunoreactivity in the young adult CN where it predominates in the granular cell region, whereas in old rats, the GFAP immunoreactivity distribution was homogeneous in all parts of the nucleus. There was no change in the total number of neurons between these two stages in any part of the nucleus except for the antero-ventral CN, where a decrease in neuronal number was observed in the aged rats. The increase in GFAP immunoreactivity was related to an increase of both GFAP positive astrocyte number and processes. The increase of GFAP positive astrocytes may be due either to an alteration of auditory nerve fibers, changing the trophic interactions with post-synaptic cells, or to intrinsic alterations of CN neurons and local circuits reflecting aging of the CN.