Vous êtes ici :   Accueil » Sommaires des Revues - Neurology
 
Prévisualiser...  Imprimer...  Imprimer la page...
Menu Principal
Recherche
Recherche
Journal de Neurochirurgie

couv01.jpg

Publications
Sommaires des Revues - Neurology

Neurology current issue


Neurology RSS feed -- current issue


Clinical Reasoning: An 82-year-old man with worsening gait  Voir?

An 82-year-old man with hypothyroidism presented with difficulty walking.

(???)

Teaching NeuroImages: Myeloperoxidase-anti-neutrophil cytoplasmic antibody-positive hypertrophic pachymeningitis  Voir?

A 49-year-old woman with chronic epistaxis presented with painless left monocular vision loss. Notable findings on examination of the left eye included visual acuity of 20/200 and relative afferent pupillary defect. MRI of the brain revealed enhancement of the left optic nerve sheath and diffuse dural thickening (figure). Laboratory workup yielded only lymphocytic pleocytosis (12 white blood cells) and positive serologies for perinuclear anti-neutrophil cytoplasmic antibodies (ANCA) and anti-myeloperoxidase (MPO) antibodies. Dural biopsy showed multifocal dense lymphoplasmacytic infiltration with vasculitis and reactive fibroplasia. A diagnosis of MPO-ANCA-positive hypertrophic pachymeningitis was made. This phenotypic variant of granulomatosis with polyangiitis is typically restricted to the CNS and upper airway; treatment involves immunosuppression.1 The patient improved clinically and radiographically with prednisone and rituximab.

... / ... Lire la suite

(???)

Spotlight on the November 21 issue  Voir?

(???)

Ischemic lesions and superficial siderosis in CAA: Partners in crime or innocent bystanders?  Voir?

Cerebral amyloid angiopathy (CAA), first described in 1927 as a congophilic angiopathy associated with amyloid plaque in brains of patients with Alzheimer dementia,1 has an association with large and small intracranial hemorrhages (ICH). The differential diagnosis of ICH therefore includes CAA, especially in older patients or those without hypertension. The widely used Boston Criteria for diagnosis of CAA in vivo rely on the hemorrhagic characteristics of the disease.2 The pathophysiology of ICH in CAA remains uncertain. Thus, its prognosis, risk stratification, and clinical management present a challenge. Additional imaging features of CAA have contributed potential new perspectives on pathophysiology. The report of ischemic lesions in CAA may represent a novel concept for most clinicians accustomed to thinking about CAA as a hemorrhagic disease. The observation that Alzheimer dementia brains with severe amyloid angiopathy had more prevalent infarcts3–5 prompted subsequent investigations suggesting that amyloid deposition in small and medium-sized cortical vessels may play an active role in ischemia through pathologic thickening of the vessel wall, producing reduction or obliteration of the vessel lumen.6,7 Cortical superficial siderosis (cSS), easy to detect with modern MRI, is a striking and common feature of CAA. How these additional imaging features fit into a larger model of CAA remains unclear. Are they an epiphenomenon or can they teach us about the disease? In the current issue of Neurology®, a pair of articles suggest that CAA might be a multifaceted vascular entity in its own right, and elucidation of these newer features may increase our understanding of its pathophysiology, leading to better prognosis and management.

... / ... Lire la suite

(???)

Neurofilaments in blood: (Almost) facing clinical application  Voir?

Neurodegeneration is a critical pathophysiologic process of Alzheimer disease (AD) and related dementias, and correlates better with cognitive symptoms than the sole presence of pathologic proteins such as β-amyloid or α-synuclein. Thus, the identification of a biomarker that tracks with neurodegeneration is critical for following disease progression from the preclinical through the clinical phases and assessing rate of progression or therapeutic utility. The identification of a blood-based biomarker of neurodegeneration would be the Holy Grail. Compared to neuroimaging CSF collection, a blood draw is much less invasive and costly, has minimal side effects, is available in rural areas, and is feasible and acceptable by patients for serial testing to monitor disease progression and therapeutic response.

... / ... Lire la suite

(???)

Cortical superficial siderosis multifocality in cerebral amyloid angiopathy: A prospective study  Voir?

Objective:

In order to explore the mechanisms of cortical superficial siderosis (cSS) multifocality and its clinical implications for recurrent intracerebral hemorrhage (ICH) risk in patients with cerebral amyloid angiopathy (CAA), we used a new rating method that we developed specifically to evaluate cSS extent at spatially separated foci.

Methods:

Consecutive patients with CAA-related ICH according to Boston criteria from a single-center prospective cohort were analyzed. The new score that assesses cSS multifocality (total range 0–4) showed excellent interrater reliability (k = 0.87). The association of cSS with markers of CAA and acute ICH was investigated. Patients were followed prospectively for recurrent symptomatic ICH.

Results:

The cohort included 313 patients with CAA. Multifocal cSS prevalence was 21.1%. APOE 2 allele prevalence was higher in patients with multifocal cSS. In probable/definite CAA, cSS multifocality was independently associated with neuroimaging markers of CAA severity, including lobar microbleeds, but not with acute ICH features, which conversely, were determinants of cSS in possible CAA. During a median follow-up of 2.6 years (interquartile range 0.9–5.1 years), the annual ICH recurrence rates per cSS scores (0–4) were 5%, 6.5%, 13.5%, 16.2%, and 26.9%, respectively. cSS multifocality (presence and spread) was the only independent predictor of increased symptomatic ICH risk (hazard ratio 3.19; 95% confidence interval 1.77–5.75; p < 0.0001).

Conclusions:

The multifocality of cSS correlates with disease severity in probable CAA; therefore cSS is likely to be caused by discrete hemorrhagic foci. The new cSS scoring system might be valuable for clinicians in determining annual risk of ICH recurrence.

... / ... Lire la suite

(???)

Evolution of DWI lesions in cerebral amyloid angiopathy: Evidence for ischemia  Voir?

Objective:

To address the pathophysiologic nature of small diffusion-weighted imaging (DWI) lesions in patients with cerebral amyloid angiopathy (CAA) who underwent serial MRI. Specifically, we tested (1) whether DWI lesions occurred preferentially in individuals with prior DWI lesions, (2) the cross-sectional association with chronic cortical cerebral microinfarcts (CMIs), and (3) the evolution of DWI lesions over time.

Methods:

Patients with probable CAA (n = 79) who underwent at least 2 MRI sessions were included. DWI lesions were assessed at each available time point. Lesion appearance and characteristics were assessed on available structural follow-up images. Presence and burden of other neuroimaging markers of small vessel disease (white matter hyperintensities, cerebral microbleeds, cortical superficial siderosis, and chronic cortical CMIs) were assessed as well.

Results:

Among 221 DWI scans (79 patients with 2 DWI scans; 40 with ≥3), 60 DWI lesions were found in 28 patients. Patients with DWI lesions at baseline were not more likely to have additional DWI lesions on follow-up compared to patients without DWI lesions at baseline. DWI lesions were associated with chronic cortical CMIs and cortical superficial siderosis, but not with other markers. For 39/60 DWI lesions, >1 MRI sequence was available at follow-up to determine lesion evolution. Twenty-four (62%) were demarcated as chronic lesions on follow-up MRI. Five appeared as cavitations, 18 as noncavitated infarcts, and 1 underwent hemorrhagic transformation.

Conclusions:

Based on their neuroimaging signature as well as their association with chronic cortical CMIs, DWI lesions appear to have an ischemic origin and represent one part of the CMI spectrum.

... / ... Lire la suite

(???)

Blood-brain barrier leakage increases with small vessel disease in acute ischemic stroke  Voir?

Objective:

In patients with acute ischemic stroke, we aimed to investigate the relation between preexisting small vessel disease (SVD) and the amount of blood–brain barrier (BBB) leakage in ischemic and nonischemic area before IV thrombolysis.

Methods:

We retrospectively accessed anonymous patient-level data from the Stroke Imaging Repository and the Virtual International Stroke Trials Archive resources and included patients treated with IV thrombolysis with pretreatment MRI. We rated SVD features using validated qualitative magnetic resonance (MR) scales. Leakage of BBB was assessed with postprocessing of perfusion-weighted images. We evaluated associations between SVD features (individually and summed in a global SVD score) and BBB leakage using linear regression analysis, adjusting for major clinical confounders.

Results:

A total of 212 patients, mean age (±SD) 69.5 years (±16.1), 102 (48%) male, had available MR before IV thrombolysis. Evidence of BBB leakage was present in 175 (80%) and 205 (94%) patients in the ischemic and nonischemic area, respectively. Lacunar infarcts (β = 0.17, p = 0.042) were associated with BBB leakage in the ischemic area, and brain atrophy was associated with BBB leakage in both ischemic (β = 0.20, p = 0.026) and nonischemic (β = 0.27, p = 0.001) areas. Increasing SVD grade was independently associated with BBB leakage in both ischemic (β = 0.26, p = 0.007) and nonischemic (β = 0.27, p = 0.003) area.

Conclusions:

Global SVD burden is associated with increased BBB leakage in both acutely ischemic and nonischemic area. Our results support that SVD score has construct validity, and confirm a relation between SVD and BBB disruption also in patients with acute stroke.

... / ... Lire la suite

(???)

GABA alterations in pediatric sport concussion  Voir?

Objective:

To evaluate whether frontal-lobe magnetic resonance spectroscopy measures of -aminobutyric acid (GABA) would be altered in a sample of adolescents scanned after sport concussion because mild traumatic brain injury is often associated with working memory problems.

Methods:

Eleven adolescents (age 14–17 years) who had sustained a first-time sport concussion were studied with MRI/magnetic resonance spectroscopy within 23 to 44 days after injury (mean 30.4 ± 6.1 days). Age- and sex-matched healthy controls, being seen for sports-related injuries not involving the head and with no history of concussion, were also examined. GABA/creatine + phosphocreatine (Cre) was measured in left-sided frontal lobe and central posterior cingulate regions. The frontal voxel was positioned to overlap with patient-specific activation on a 1-back working memory task.

Results:

Increased GABA/Cre was shown in the frontal lobe for the concussed group. A decreased relationship was observed in the parietal region. High correlations between GABA/Cre and task activation were observed for the control group in the frontal lobe, a relationship not shown in the concussed participants.

Conclusions:

GABA/Cre appears increased in a region colocalized with working memory task activation after sport concussion. Further work extending these results in larger samples and at time points across the injury episode will aid in refining the clinical significance of these observations.

... / ... Lire la suite

(???)

Multiparametric MRI changes persist beyond recovery in concussed adolescent hockey players  Voir?

Objective:

To determine whether multiparametric MRI data can provide insight into the acute and long-lasting neuronal sequelae after a concussion in adolescent athletes.

Methods:

Players were recruited from Bantam hockey leagues in which body checking is first introduced (male, age 11–14 years). Clinical measures, diffusion metrics, resting-state network and region-to-region functional connectivity patterns, and magnetic resonance spectroscopy absolute metabolite concentrations were analyzed from an independent, age-matched control group of hockey players (n = 26) and longitudinally in concussed athletes within 24 to 72 hours (n = 17) and 3 months (n = 14) after a diagnosed concussion.

Results:

There were diffusion abnormalities within multiple white matter tracts, functional hyperconnectivity, and decreases in choline 3 months after concussion. Tract-specific spatial statistics revealed a large region along the superior longitudinal fasciculus with the largest decreases in diffusivity measures, which significantly correlated with clinical deficits. This region also spatially intersected with probabilistic tracts connecting cortical regions where we found acute functional connectivity changes. Hyperconnectivity patterns at 3 months after concussion were present only in players with relatively less severe clinical outcomes, higher choline concentrations, and diffusivity indicative of relatively less axonal disruption.

Conclusions:

Changes persisted well after players' clinical scores had returned to normal and they had been cleared to return to play. Ongoing white matter maturation may make adolescent athletes particularly vulnerable to brain injury, and they may require extended recovery periods. The consequences of early brain injury for ongoing brain development and risk of more serious conditions such as second impact syndrome or neural degenerative processes need to be elucidated.

... / ... Lire la suite

(???)

Serum neurofilament light in familial Alzheimer disease: A marker of early neurodegeneration  Voir?

Objectives:

To investigate whether serum neurofilament light (NfL) concentration is increased in familial Alzheimer disease (FAD), both pre and post symptom onset, and whether it is associated with markers of disease stage and severity.

Methods:

We recruited 48 individuals from families with PSEN1 or APP mutations to a cross-sectional study: 18 had symptomatic Alzheimer disease (AD) and 30 were asymptomatic but at 50% risk of carrying a mutation. Serum NfL was measured using an ultrasensitive immunoassay on the single molecule array (Simoa) platform. Cognitive testing and MRI were performed; 33 participants had serial MRI, allowing calculation of atrophy rates. Genetic testing established mutation status. A generalized least squares regression model was used to compare serum NfL among symptomatic mutation carriers, presymptomatic carriers, and noncarriers, adjusting for age and sex. Spearman coefficients assessed associations between serum NfL and (1) estimated years to/from symptom onset (EYO), (2) cognitive measures, and (3) MRI measures of atrophy.

Results:

Nineteen of the asymptomatic participants were mutation carriers (mean EYO –9.6); 11 were noncarriers. Compared with noncarriers, serum NfL concentration was higher in both symptomatic (p < 0.0001) and presymptomatic mutation carriers (p = 0.007). Across all mutation carriers, serum NfL correlated with EYO ( = 0.81, p < 0.0001) and multiple cognitive and imaging measures, including Mini-Mental State Examination ( = –0.62, p = 0.0001), Clinical Dementia Rating Scale sum of boxes ( = 0.79, p < 0.0001), baseline brain volume ( = –0.62, p = 0.0002), and whole-brain atrophy rate ( = 0.53, p = 0.01).

Conclusions:

Serum NfL concentration is increased in FAD prior to symptom onset and correlates with measures of disease stage and severity. Serum NfL may thus be a feasible biomarker of early AD-related neurodegeneration.

... / ... Lire la suite

(???)

Alzheimer disease brain atrophy subtypes are associated with cognition and rate of decline  Voir?

Objective:

To test the hypothesis that cortical and hippocampal volumes, measured in vivo from volumetric MRI (vMRI) scans, could be used to identify variant subtypes of Alzheimer disease (AD) and to prospectively predict the rate of clinical decline.

Methods:

Amyloid-positive participants with AD from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) 1 and ADNI2 with baseline MRI scans (n = 229) and 2-year clinical follow-up (n = 100) were included. AD subtypes (hippocampal sparing [HpSpMRI], limbic predominant [LPMRI], typical AD [tADMRI]) were defined according to an algorithm analogous to one recently proposed for tau neuropathology. Relationships between baseline hippocampal volume to cortical volume ratio (HV:CTV) and clinical variables were examined by both continuous regression and categorical models.

Results:

When participants were divided categorically, the HpSpMRI group showed significantly more AD-like hypometabolism on 18F-fluorodeoxyglucose-PET (p < 0.05) and poorer baseline executive function (p < 0.001). Other baseline clinical measures did not differ across the 3 groups. Participants with HpSpMRI also showed faster subsequent clinical decline than participants with LPMRI on the Alzheimer's Disease Assessment Scale, 13-Item Subscale (ADAS-Cog13), Mini-Mental State Examination (MMSE), and Functional Assessment Questionnaire (all p < 0.05) and tADMRI on the MMSE and Clinical Dementia Rating Sum of Boxes (CDR-SB) (both p < 0.05). Finally, a larger HV:CTV was associated with poorer baseline executive function and a faster slope of decline in CDR-SB, MMSE, and ADAS-Cog13 score (p < 0.05). These associations were driven mostly by the amount of cortical rather than hippocampal atrophy.

Conclusions:

AD subtypes with phenotypes consistent with those observed with tau neuropathology can be identified in vivo with vMRI. An increased HV:CTV ratio was predictive of faster clinical decline in participants with AD who were clinically indistinguishable at baseline except for a greater dysexecutive presentation.

... / ... Lire la suite

(???)

Spaceflight-induced changes in white matter hyperintensity burden in astronauts  Voir?

Objective:

To assess the effect of weightlessness and the respective roles of CSF and vascular fluid on changes in white matter hyperintensity (WMH) burden in astronauts.

Methods:

We analyzed prespaceflight and postspaceflight brain MRI scans from 17 astronauts, 10 who flew a long-duration mission on the International Space Station (ISS) and 7 who flew a short-duration mission on the Space Shuttle. Automated analysis methods were used to determine preflight to postflight changes in periventricular and deep WMH, CSF, and brain tissue volumes in fluid-attenuated inversion recovery and high-resolution 3-dimensional T1-weighted imaging. Differences between cohorts and associations between individual measures were assessed. The short-term reversibility of the identified preflight to postflight changes was tested in a subcohort of 5 long-duration astronauts who had a second postflight MRI scan 1 month after the first postflight scan.

Results:

Significant preflight to postflight changes were measured only in the long-duration cohort and included only the periventricular WMH and ventricular CSF volumes. Changes in deep WMH and brain tissue volumes were not significant in either cohort. The increase in periventricular WMH volume was significantly associated with an increase in ventricular CSF volume ( = 0.63, p = 0.008). A partial reversal of these increases was observed in the long-duration subcohort with a 1-month follow-up scan.

Conclusions:

Long-duration exposure to microgravity is associated with an increase in periventricular WMH in astronauts. This increase was linked to an increase in ventricular CSF volume documented in ISS astronauts. There was no associated change in or abnormal levels of WMH volumes in deep white matter as reported in U-2 high-altitude pilots.

... / ... Lire la suite

(???)

Caudate nucleus as a component of networks controlling behavior  Voir?

The striatum participates in parallel corticobasal ganglia–thalamocortical loops interconnecting its different territories with areas of the frontal lobe, forming partially segregated motor, oculomotor, associative, and limbic circuits.1 Human studies using resting-state fMRI2–4 and diffusion tensor imaging5–10 confirm the presence of a functional parcellation of the human striatum, particularly the caudate nucleus,11 based on segregated corticostriatal connections. However, the corticostriatal connections are complex, and there are extensive interactions among functional territories.12 Furthermore, the distinct territories of the striatum are functionally linked to cortical networks rather than specific cortical regions.13 There are specific patterns of coactivation of different portions of the striatum and cerebral cortex across distinct psychological tasks, which only partially overlap the parcellation of the striatum based on steady-state connectivity.14 The caudate nucleus contains several neuronal clusters that are functionally connected to cortical areas that are part of distributed networks involved in cognitive and emotional processing. This extensive connectivity explains the profound impairment in multiple cognitive and behavioral domains resulting from lesions of the caudate nucleus in humans.15,16 The following 2 representative cases illustrate the profound consequences of caudate lesions in cognition and behavior and the associated widespread changes in frontal lobe metabolism.

... / ... Lire la suite

(???)

Epidemiology of recurrent traumatic brain injury in the general population: A systematic review  Voir?

Objective:

To comprehensively assess recurrent traumatic brain injury (rTBI) risk and risk factors in the general population.

Methods:

We systematically searched MEDLINE, EMBASE, and the references of included studies until January 16, 2017, for general population observational studies reporting rTBI risk or risk factors. Estimates were not meta-analyzed due to significant methodologic heterogeneity between studies, which was evaluated using meta-regression.

Results:

Twenty-two studies reported recurrence risk and 11 reported on 27 potential risk factors. rTBI risk was heterogeneous and varied from 0.43% (95% confidence interval [CI] 0.19%–0.67%) to 41.92% (95% CI 34.43%–49.40%), with varying follow-up periods (3 days–55 years). Median time to recurrence ranged from 0.5 to 3.8 years. In studies where cases were ascertained from multiple points of care, at least 5.50% (95% CI 4.80%–6.30%) of patients experienced a recurrence after a 1-year follow-up. Studies that used administrative data/self-report surveys to ascertain cases tended to report higher risk. Risk factors measured at time of index traumatic brain injury (TBI) that were significantly associated with rTBI in more than one study were male sex, prior TBI before index case, moderate or severe TBI, and alcohol intoxication. Risk factors reported in a single study that were significantly associated with rTBI were epilepsy, not seeking medical care, and multiple factors indicative of low socioeconomic status.

Conclusions:

rTBI is an important contributor to the general population TBI burden. Certain risk factors can help identify individuals at higher risk of these repeated injuries. However, higher quality research that improves on rTBI surveillance methodology is needed.

... / ... Lire la suite

(???)

TRMT5 mutations are associated with features of complex hereditary spastic paraparesis  Voir?

Mitochondrial DNA (mtDNA) encodes for 22 tRNAs (mt-tRNA) that undergo posttranscriptional modification.1,2 A specific nucleotide adjacent to the anticodon of mt-tRNA (position 37) is methylated (m1G37) to enhance translational efficiency/fidelity.3 The gene tRNA methyltransferase 5 (TRMT5) encodes a protein involved in m1G37 formation for some mitochondrial tRNAs3,4 and has been associated with combined oxidative phosphorylation deficiency 26 (COXPD26) (OMIM 616539).

... / ... Lire la suite

(???)

Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy  Voir?

A 9-month-old boy with migrating partial seizures of infancy due to a de novo KCNT1 mutation c.2278A>T (p.Ile760Phe) developed bluish discoloration of the hands, feet, and lips (figure) during a 9-month trial of quinidine (40 mg/kg/d; level 3.4 μg/mL).1 There was no exposure to other medications that cause pigmentary changes. Given minimal improvement in seizures and development, quinidine was stopped. Discoloration persisted at 3 months but markedly improved by the 6-month follow-up. Though common with other potassium channel blockers (ezogabine and quinine), such discoloration has only rarely been reported with quinidine, all in adults.2 Epileptologists should be aware of this potential complication of quinidine therapy.

... / ... Lire la suite

(???)

Editors' Note  Voir?

Editors' Note: In the American Academy of Neurology and the American Epilepsy Society practice guideline on sudden unexpected death in epilepsy (SUDEP) incidence rates and risk factors, Harden et al. made recommendations to clinicians caring for people with epilepsy including the need to inform their patients about SUDEP, the most common cause of epilepsy-related death. Commenting on the guideline, Stanton et al. note that certain pediatric populations (children with Dravet syndrome, Dup15q syndrome) face a significantly higher risk of SUDEP.

... / ... Lire la suite

(???)

Letter re: Practice guideline summary: Sudden unexpected death in epilepsy incidence rates and risk factors: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Epilepsy Society  Voir?

The new guideline by the American Academy of Neurology (AAN) and the American Epilepsy Society (AES) on sudden unexpected death in epilepsy (SUDEP) is a landmark.1 The communication between medical professionals and patients about SUDEP risk remains unacceptably low. Tragically, family members often first learn about SUDEP after their loved one's death. Every patient and parent deserves to know the risks of epilepsy. For the first time, the AAN and AES recommend that neurologists inform them about SUDEP, the most common cause of epilepsy-related death.1

... / ... Lire la suite

(???)

Author response: Practice guideline summary: Sudden unexpected death in epilepsy incidence rates and risk factors: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Epilepsy Society  Voir?

We wholeheartedly agree with the comments of Stanton et al. on our sudden unexpected death in epilepsy guideline article.1

(???)

Letter re: Dementia risk in renal dysfunction: A systematic review and meta-analysis of prospective studies  Voir?

Deckers et al.1 conducted random effects meta-analyses on the prospective association between potential markers of renal dysfunction and development of cognitive impairment or dementia. Pooled odds ratios (95% confidence intervals) of albuminuria and estimated glomerular filtration rate <60 mL/min/1.73 m2 for cognitive impairment or dementia were 1.35 (1.06–1.73) and 1.28 (0.99–1.65), respectively.1 As the number of studies was not sufficient, meta-analyses could not be done for serum creatinine, creatinine clearance, or cystatin C.1 The authors concluded that albuminuria was a useful marker of renal dysfunction for screening the development of cognitive impairment or dementia.1 I have 2 concerns about their study.

... / ... Lire la suite

(???)

Author response: Dementia risk in renal dysfunction: A systematic review and meta-analysis of prospective studies  Voir?

We thank Prof. Kawada for the interest in our article,1 and agree that the exact mechanisms underlying the relationship between renal dysfunction and cognitive impairment or dementia are not fully understood. In our article, we discussed several suggested potential mechanisms.1 These might work additively, or synergistically, and include shared vascular risk factors or a direct effect of uremic toxins.1,2

... / ... Lire la suite

(???)

Dernière mise à jour : 22/11/2017 : 13:57


Préférences

Se reconnecter :
Votre nom (ou pseudo) :
Votre mot de passe
Captcha reload
Recopier le code :


  Nombre de membres 406 membres
Connectés :
( personne )
Snif !!!
Lettre d'information
Pour avoir des nouvelles de ce site, inscrivez-vous à notre Newsletter.
Captcha reload
Recopier le code :