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Sommaires des Revues - Neurology

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Clinical Reasoning: A 15-month-old boy with progressive lethargy and spasticity  Voir?

A previously healthy and developmentally normal 15-month-old boy presented to the emergency department with 5 days of worsening altered mental status in the setting of an upper respiratory infection. He initially developed cough, rhinorrhea, and irritability without fever, vomiting, or diarrhea. His mental status at home had slowly declined, with increased sleepiness and progressively decreased activity. At the time of presentation, he had stopped playing, walking, sitting, or drinking. On his initial examination, he was breathing comfortably on room air and was afebrile with normal vital signs. He did not respond to stimuli and had developed intermittent rhythmic shaking of his arms, concerning for seizures. He had no visual tracking and minimal pupil reactivity. He had diffuse hypertonia with bilateral flexion of the upper extremities and extension of the lower extremities without spontaneous movement, minimal withdrawal to noxious stimuli, diffuse hyperreflexia, and several beats of left Achilles tendon clonus.

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Clinical Reasoning: A 50-year-old woman with SLE and a tumefactive lesion  Voir?

A 50-year-old woman with a history of systemic lupus erythematosus (SLE) treated with methotrexate and hydroxychloroquine presented to the emergency department for evaluation of numbness and weakness of the left hand that began 12 hours earlier.

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Opinion and Special Articles: Creation of a diversity and inclusion certificate program for neurology residents  Voir?

Neurologists must provide excellent care to an increasingly diverse patient population. According to census projections, the United States will become a majority–minority nation by 2060, with no single ethnic or racial group making up a majority of the population.1 Diversity of gender, sex, sexual orientation, race, ethnicity, socioeconomic status, age, ability, and religion must be acknowledged and understood in order to provide equitable patient care.

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Teaching NeuroImages: RCVS causing simultaneous convexity subarachnoid hemorrhage and hemimedullary infarction  Voir?

A 34-year-old previously healthy man presented with thunderclap headache, dysphagia, dysarthria, and oscillopsia. Neurologic examination revealed right-beating nystagmus, dysphagia, hypophonia, right hemianesthesia, and left hemiparesis. Brain imaging showed convexity subarachnoid hemorrhage (figure 1A) and left hemimedullary infarct (figure 1B). Catheter angiography showed tapering of left vertebral artery and diffuse segmental vasoconstriction (figure 2). Routine serum and CSF results were unremarkable. Thorough infectious, immunologic, and coagulopathy workup was negative. Reversible cerebral vasoconstriction syndrome (RCVS) is associated with severe headache, stroke, brain edema, and hemorrhage characterized by transient, multifocal intracranial vessel vasoconstriction.1 RCVS can cause simultaneous ischemic and hemorrhagic stroke.2

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Spotlight on the September 19 issue  Voir?

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The "plus" side of epilepsy phenotyping  Voir?

The first clinical description of generalized epilepsy with febrile seizures plus (GEFS+) by Scheffer and Berkovic1 in their landmark Brain article of 1997 represented a major step forward in the understanding of the genetic basis of the epilepsies. Coming 2 years after their identification, with collaborators, of the genetic basis for a relatively homogenous syndrome, autosomal dominant nocturnal frontal lobe epilepsy, the detailed phenotypic description of a single large Australian family with heterogeneous febrile seizure plus epilepsy phenotypes and a clear dominant pattern of inheritance put a novel perspective on genotype–phenotype relationships in the epilepsies.2 Shortly after, the SCN1A and SCN1B genes were linked to the syndrome, and subsequently the last 2 decades has confirmed that the majority of epilepsy genes show phenotypic heterogeneity and the majority of syndromes reveal genetic heterogeneity.3 Why one individual in a GEFS+ family has a severe developmental and epileptic encephalopathy such as Dravet syndrome and another has simple self-limited febrile seizures is unknown, but is likely to be determined by other genetic factors influencing the SCN1A, or other major genes identified in a family.

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Vertebral artery stenosis: The hurdles of stenting are too high  Voir?

Up to a quarter of patients with vertebrobasilar ischemic stroke or TIA have a symptomatic stenosis of the vertebrobasilar arteries.1,2 Patients with vertebral artery (VA) stenosis >50% have a high risk of recurrent stroke, comparable to patients with symptomatic carotid artery stenosis, with the highest risk during the first weeks after the initial TIA or ischemic stroke.3 Endovascular treatment of symptomatic VA stenosis has appeal as a treatment option that is widely performed, despite the scarcity of evidence for its safety or benefit.

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Medication overuse headache: An ongoing debate  Voir?

Medication overuse headache (MOH) has incited passionate debate among headache clinicians and researchers in recent years. The existence of MOH as a diagnostic category1 and as a potentially modifiable risk factor for headache chronification is well-recognized by most headache specialists.2 However, the greatest controversies seem to exist over whether medication overuse should be regarded as cause or consequence; and over the treatment strategies, including advice about withdrawal of frequently used symptomatic (acute pain relieving) medication and whether prophylactic treatment should be initiated during withdrawal or after detoxification.3,4 This ongoing debate is undoubtedly a symptom of a lack of high-quality evidence, as Scher et al.5 state in this issue of Neurology®. Other contributing factors include the difficulty of disentangling retrospectively the underlying primary headache type predating medication overuse and cultural differences regarding types of overused symptomatic medication. Most notably, the advice to patients to stop symptomatic medication that may provide transient benefits seems to counter the mission of headache practitioners to minimize pain.

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Jean Holowach Thurston, MD (1917-2017)  Voir?

Jean Holowach Thurston, MD, Emeritus Professor of Neurology and Pediatrics at Washington University in St. Louis, died on April 29, 2017, two months short of her 100th birthday. Her career encompassed a spectrum of disciplines that is unfathomable in our current era of subspecialization.

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Genetic epilepsy with febrile seizures plus: Refining the spectrum  Voir?

Objective:

Following our original description of generalized epilepsy with febrile seizures plus (GEFS+) in 1997, we analyze the phenotypic spectrum in 409 affected individuals in 60 families (31 new families) and expand the GEFS+ spectrum.

Methods:

We performed detailed electroclinical phenotyping on all available affected family members. Genetic analysis of known GEFS+ genes was carried out where possible. We compared our phenotypic and genetic data to those published in the literature over the last 19 years.

Results:

We identified new phenotypes within the GEFS+ spectrum: focal seizures without preceding febrile seizures (16/409 [4%]), classic genetic generalized epilepsies (22/409 [5%]), and afebrile generalized tonic-clonic seizures (9/409 [2%]). Febrile seizures remains the most frequent phenotype in GEFS+ (178/409 [44%]), followed by febrile seizures plus (111/409 [27%]). One third (50/163 [31%]) of GEFS+ families tested have a pathogenic variant in a known GEFS+ gene.

Conclusion:

As 37/409 (9%) affected individuals have focal epilepsies, we suggest that GEFS+ be renamed genetic epilepsy with febrile seizures plus rather than generalized epilepsy with febrile seizures plus. The phenotypic overlap between GEFS+ and the classic generalized epilepsies is considerably greater than first thought. The clinical and molecular data suggest that the 2 major groups of generalized epilepsies share genetic determinants.

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Incidence and management of seizures after ischemic stroke: Systematic review and meta-analysis  Voir?

Objective:

We conducted a meta-analysis of the incidence of early and late seizures following ischemic stroke as well as a systematic review of their pharmacologic treatment.

Methods:

Observational studies that reported incidence of seizures following ischemic stroke and those that reported treatment response to any particular antiepileptic drugs (AEDs) were included. Risk of bias was assessed by predefined study characteristics. Random effects meta-analysis was conducted for all studies where data were available for the incidence of early and late stroke-related seizures. Heterogeneity was measured with I2 statistic and sensitivity analyses were performed using prespecified variables. A qualitative synthesis of studies reporting use of AEDs for stroke-related seizures was performed.

Results:

Forty-one studies from 10,554 articles were identified; 35 studies reported incidence of stroke-related seizures and 6 studies reported effects of specific AEDs. Most studies were of low to moderate quality. Rate of early seizures was 3.3% (95% confidence interval 2.8%–3.9%, I2 = 92.8%), while the incidence of late seizures or epilepsy was 18 per 1,000 person-years (95% confidence interval 1.5–2.2, I2 = 94.1%). The high degree of heterogeneity could not be explained from the sensitivity analyses. For management of stroke-related seizures, no single AED was found to be more effective over others, though newer AEDs were associated with fewer side effects.

Conclusions:

The burden of stroke-related seizures and epilepsy due to ischemic stroke is substantial. Further studies are required to determine risk factors for epilepsy following ischemic stroke and optimal secondary prevention.

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Stenting for symptomatic vertebral artery stenosis: The Vertebral Artery Ischaemia Stenting Trial  Voir?

Objective:

To compare in the Vertebral Artery Ischaemia Stenting Trial (VIST) the risks and benefits of vertebral angioplasty and stenting with best medical treatment (BMT) alone for symptomatic vertebral artery stenosis.

Methods:

VIST was a prospective, randomized, open-blinded endpoint clinical trial performed in 14 hospitals in the United Kingdom. Participants with symptomatic vertebral stenosis ≥50% were randomly assigned (1:1) to vertebral angioplasty/stenting plus BMT or to BMT alone with randomization stratified by site of stenosis (extracranial vs intracranial). Because of slow recruitment and cessation of funding, recruitment was stopped after 182 participants. Follow-up was a minimum of ≥1 year for each participant.

Results:

Three patients did not contribute any follow-up data and were excluded, leaving 91 patients in the stent group and 88 in the medical group. Mean follow-up was 3.5 (interquartile range 2.1–4.7) years. Of 61 patients who were stented, stenosis was extracranial in 48 (78.7%) and intracranial in 13 (21.3%). No periprocedural complications occurred with extracranial stenting; 2 strokes occurred during intracranial stenting. The primary endpoint of fatal or nonfatal stroke occurred in 5 patients in the stent group vs 12 in the medical group (hazard ratio 0.40, 95% confidence interval 0.14–1.13, p = 0.08), with an absolute risk reduction of 25 strokes per 1,000 person-years. The hazard ratio for stroke or TIA was 0.50 (p = 0.05).

Conclusions:

Stenting in extracranial stenosis appears safe with low complication rates. Large phase 3 trials are required to determine whether stenting reduces stroke risk.

ISRCTN.com identifier:

ISRCTN95212240.

Classification of evidence:

This study provides Class I evidence that for patients with symptomatic vertebral stenosis, angioplasty with stenting does not reduce the risk of stroke. However, the study lacked the precision to exclude a benefit from stenting.

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Erenumab (AMG 334) in episodic migraine: Interim analysis of an ongoing open-label study  Voir?

Objective:

To assess long-term safety and efficacy of anti–calcitonin gene-related peptide receptor erenumab in patients with episodic migraine (EM).

Methods:

Patients enrolled in a 12-week, double-blind, placebo-controlled clinical trial (NCT01952574) who continued in an open-label extension (OLE) study will receive erenumab 70 mg every 4 weeks for up to 5 years. This preplanned interim analysis, conducted after all participants had completed the 1-year open-label follow-up, evaluated changes in monthly migraine days (MMD), achievement of ≥50%, ≥75%, and 100% reductions, Headache Impact Test (HIT-6) score, Migraine-Specific Quality of Life (MSQ), Migraine Disability Assessment (MIDAS), and safety. Data reported as observed without imputation for missing data.

Results:

Of 472 patients enrolled in the parent study, 383 continued in the OLE with a median exposure to erenumab of 575 days (range 28–822 days). Mean (SD) MMD were 8.8 (2.6) at parent study baseline, 6.3 (4.2) at week 12 (beginning of OLE), and 3.7 (4.0) at week 64 (mean change from baseline [reduction] of 5.0 days). At week 64, 65%, 42%, and 26% achieved ≥50%, ≥75%, and 100% reduction in MMD, respectively. Mean HIT-6 scores were 60.2 (6.3) at baseline and 51.7 (9.2) at week 64. MSQ and MIDAS improvements from baseline were maintained through week 64. Safety profiles during the OLE were similar to those in the double-blind phase, which overall were similar to placebo.

Conclusions:

One-year efficacy, supported by functional improvements and favorable safety and tolerability profiles, supports further investigation of erenumab as a preventive treatment in patients with EM.

Clinicaltrials.gov identifier:

NCT01952574.

Classification of evidence:

This study provides Class IV evidence that for patients with episodic migraine, erenumab reduces long-term MMD and improves headache-related disability and migraine-specific quality of life.

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Sleep architecture and the risk of incident dementia in the community  Voir?

Objective:

Sleep disturbance is common in dementia, although it is unclear whether differences in sleep architecture precede dementia onset. We examined the associations between sleep architecture and the prospective risk of incident dementia in the community-based Framingham Heart Study (FHS).

Methods:

Our sample comprised a subset of 321 FHS Offspring participants who participated in the Sleep Heart Health Study between 1995 and 1998 and who were aged over 60 years at the time of sleep assessment (mean age 67 ± 5 years, 50% male). Stages of sleep were quantified using home-based polysomnography. Participants were followed for a maximum of 19 years for incident dementia (mean follow-up 12 ± 5 years).

Results:

We observed 32 cases of incident dementia; 24 were consistent with Alzheimer disease dementia. After adjustments for age and sex, lower REM sleep percentage and longer REM sleep latency were both associated with a higher risk of incident dementia. Each percentage reduction in REM sleep was associated with approximately a 9% increase in the risk of incident dementia (hazard ratio 0.91; 95% confidence interval 0.86, 0.97). The magnitude of association between REM sleep percentage and dementia was similar following adjustments for multiple covariates including vascular risk factors, depressive symptoms, and medication use, following exclusions for persons with mild cognitive impairment at baseline and following exclusions for early converters to dementia. Stages of non-REM sleep were not associated with dementia risk.

Conclusions:

Despite contemporary interest in slow-wave sleep and dementia pathology, our findings implicate REM sleep mechanisms as predictors of clinical dementia.

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Effect of simvastatin on CSF Alzheimer disease biomarkers in cognitively normal adults  Voir?

Objective:

To examine potential disease-modifying effects of statin drugs, we conducted a 12-month randomized, placebo-controlled clinical trial of simvastatin in cognitively normal adults using change in CSF Alzheimer disease biomarkers as primary outcome measure.

Methods:

Participants were 45–64 years old and statin-naive with normal cognition and normal or mildly elevated cholesterol. Forty-six participants completed the 1-year study per protocol (25 in the simvastatin and 21 in the placebo group). Simvastatin was titrated to 40 mg/d. CSF Aβ42, total tau, and p-tau181 were measured at baseline and after 12 months of treatment using the INNO-BIA AlzBio3 assay. We used analysis of covariance to assess differences in biomarker change from baseline between treatment groups, adjusting for age, sex, and APOE 4 status.

Results:

Changes from baseline did not differ significantly between treatment groups for any CSF biomarker, with p values of 0.53, 0.36, and 0.25 for CSF Aβ42, total tau, and p-tau181, respectively. There was no significant modifying effect of sex, APOE 4, or baseline high-density lipoprotein or triglycerides on treatment group for any of the biomarkers (all p > 0.18). However, a significant interaction between treatment group and baseline low-density lipoprotein (LDL) was observed for p-tau181 (p = 0.003), where greater decreases from baseline in CSF p-tau181 concentrations were associated with higher baseline LDL level for the simvastatin group.

Conclusions:

Simvastatin-related reductions in CSF p-tau181 concentrations may be modulated by LDL cholesterol. The potential disease-modifying effects of simvastatin on CSF phospho-tau should be further investigated in persons with hypercholesterolemia.

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Cognition and gray and white matter characteristics of presymptomatic C9orf72 repeat expansion  Voir?

Objective:

To investigate cognitive function, gray matter volume, and white matter integrity in the presymptomatic stage of chromosome 9 open reading frame 72 repeat expansion (C9orf72RE).

Methods:

Presymptomatic C9orf72RE carriers (n = 18) and first-degree family members without a pathogenic expansion (healthy controls [HC], n = 15) underwent a standardized protocol of neuropsychological tests, T1-weighted MRI, and diffusion tensor imaging within our cohort study of autosomal dominant frontotemporal dementia (FTD). We investigated group differences in cognitive function, gray matter volume through voxel-based morphometry, and white matter integrity by means of tract-based spatial statistics. We correlated cognitive change with underlying gray or white matter.

Results:

Our data demonstrate lower scores on letter fluency, Stroop card I, and Stroop card III, accompanied by white matter integrity loss in tracts connecting the frontal lobe, the thalamic radiation, and tracts associated with motor functioning in presymptomatic C9orf72RE compared with HC. In a subgroup of C9orf72RE carriers above 40 years of age, we found gray matter volume loss in the thalamus, cerebellum, and parietal and temporal cortex. We found no significant relationship between subtle cognitive decline and underlying gray or white matter.

Conclusions:

This study demonstrates that a decline in cognitive functioning, white matter integrity, and gray matter volumes are present in presymptomatic C9orf72RE carriers. These findings suggest that neuropsychological assessment, T1-weighted MRI, and diffusion tensor imaging might be useful to identify early biomarkers in the presymptomatic stage of FTD or amyotrophic lateral sclerosis.

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MRI substrates of sustained attention system and cognitive impairment in pediatric MS patients  Voir?

Objective:

To explore the structural and functional integrity of the sustained attention system in patients with pediatric multiple sclerosis (MS) and its effect on cognitive impairment.

Methods:

We enrolled 57 patients with pediatric MS and 14 age- and sex-matched healthy controls (HCs). Patients with >3 abnormal tests at neuropsychological evaluation were classified as cognitively impaired (CI). Sustained attention system activity was studied with fMRI during the Conners Continuous Performance Test (CCPT). Structural integrity of attention network connections was quantified with diffusion tensor (DT) MRI.

Results:

Within-group analysis showed similar patterns of recruitment of the attention network in HCs and patients with pediatric MS. Diffuse network DT MRI structural abnormalities were found in patients with MS. During CCPT, with increasing task demand, patients with pediatric MS showed increased activation of the left thalamus, anterior insula, and anterior cingulate cortex (ACC) and decreased recruitment of the right precuneus compared to HCs. Thirteen patients (23%) were classified as CI. Compared to cognitively preserved patients, CI patients with pediatric MS had decreased recruitment of several areas located mainly in parietal and occipital lobes and cerebellum and increased deactivation of the ACC, combined with more severe structural damage of white matter tracts connecting these regions.

Conclusions:

Our results suggest that the age-expected level of sustained attention system functional competence is achieved in patients with pediatric MS. Inefficient regulation of the functional interaction between different areas of this system, due to abnormal white matter integrity, may result in global cognitive impairment in these patients.

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Human dorsal root ganglion in vivo morphometry and perfusion in Fabry painful neuropathy  Voir?

Objective:

To evaluate functional and morphometric magnetic resonance neurography of the dorsal root ganglion and peripheral nerve segments in patients with Fabry painful neuropathy.

Methods:

In this prospective study, the lumbosacral dorsal root ganglia and proximal peripheral nerve segments of the lower extremity were examined in 11 male patients with Fabry disease by a standardized 3T magnetic resonance neurography protocol. Volumes of L3 to S2 dorsal root ganglia, perfusion parameters of L5-S1 dorsal root ganglia and the spinal nerve L5, and the cross-sectional area of the proximal sciatic nerve were compared to healthy controls.

Results:

Dorsal root ganglia of patients with Fabry disease were symmetrically enlarged by 78% (L3), 94% (L4), 122% (L5), 115% (S1), and 119% (S2) (p < 0.001). In addition, permeability of the blood-tissue interface was decreased by 53% (p < 0.001). This finding was most pronounced in the peripheral zone of the dorsal root ganglion containing the cell bodies of the primary sensory neurons (p < 0.001). Spinal nerve permeability showed no difference between patients with Fabry disease and controls (p = 0.7). The sciatic nerve of patients with Fabry disease at the thigh level showed an increase in cross-sectional area by 48% (p < 0.001).

Conclusions:

Patients with Fabry disease have severely enlarged dorsal root ganglia with dysfunctional perfusion. This may be due to glycolipid accumulation in the dorsal root ganglia mediating direct neurotoxic effects and decreased neuronal blood supply. These alterations were less pronounced in peripheral nerve segments. Thus, the dorsal root ganglion might play a key pathophysiologic role in the development of neuropathy and pain in Fabry disease.

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A case-control study of hormonal exposures as etiologic factors for ALS in women: Euro-MOTOR  Voir?

Objective:

To investigate the role of hormonal risk factors for amyotrophic lateral sclerosis (ALS) among women from 3 European countries.

Methods:

ALS cases and matched controls were recruited over 4 years in Ireland, Italy, and the Netherlands. Hormonal exposures, including reproductive history, breastfeeding, contraceptive use, hormonal replacement therapy, and gynecologic surgical history, were recorded with a validated questionnaire. Logistic regression models adjusted for age, education, study site, smoking, alcohol, and physical activity were used to determine the association between female hormones and ALS risk.

Results:

We included 653 patients and 1,217 controls. Oral contraceptive use was higher among controls (odds ratio [OR] 0.65, 95% confidence interval [CI] 0.51–0.84), and a dose-response effect was apparent. Hormone replacement therapy (HRT) was associated with a reduced risk of ALS only in the Netherlands (OR = 0.57, 95% CI 0.37–0.85). These findings were robust to sensitivity analysis, but there was some heterogeneity across study sites.

Conclusions:

This large case-control study across 3 different countries has demonstrated an association between exogenous estrogens and progestogens and reduced odds of ALS in women. These results are at variance with previous findings, which may be partly explained by differential regulatory, social, and cultural attitudes toward pregnancy, birth control, and HRT across the countries included. Our results indicate that hormonal factors may be important etiologic factors in ALS; however, a full understanding requires further investigation.

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Quality improvement in neurology: Essential Tremor Quality Measurement Set  Voir?

Essential tremor (ET) is one of the most common movement disorders in the world, with prevalence rates in the general population ranging from 0.4% to 4.6%.1,2 The incidence of ET increases with age,1 with the average age at onset in mid-to-late 40s.3 ET is estimated to affect as many as 7 to 10 million Americans.3,4 Clinically, ET is characterized by bilateral, symmetric, postural tremor in hands and forearms, with or without kinetic tremor, in the absence of abnormal posturing or task specificity.5 ET can also affect lower extremities, head, and voice.6,7 Symptoms may be barely noticeable, or severe and disabling.

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Medication overuse headache: An entrenched idea in need of scrutiny  Voir?

It is a widely accepted idea that medications taken to relieve acute headache pain can paradoxically worsen headache if used too often. This type of secondary headache is referred to as medication overuse headache (MOH); previously used terms include rebound headache and drug-induced headache. In the absence of consensus about the duration of use, amount, and type of medication needed to cause MOH, the default position is conservative. A common recommendation is to limit treatment to no more than 10 or 15 days per month (depending on medication type) to prevent headache frequency progression. Medication withdrawal is often recommended as a first step in treatment of patients with very frequent headaches. Existing evidence, however, does not provide a strong basis for such causal claims about the relationship between medication use and frequent headache. Observational studies linking treatment patterns with headache frequency are by their nature confounded by indication. Medication withdrawal studies have mostly been uncontrolled and often have high dropout rates. Evaluation of this evidence suggests that only a minority of patients required to limit the use of symptomatic medication may benefit from treatment limitation. Similarly, only a minority of patients deemed to be overusing medications may benefit from withdrawal. These findings raise serious questions about the value of withholding or withdrawing symptom-relieving medications from people with frequent headaches solely to prevent or treat MOH. The benefits of doing so are smaller, and the harms larger, than currently recognized. The concept of MOH should be viewed with more skepticism. Until the evidence is better, we should avoid dogmatism about the use of symptomatic medication. Frequent use of symptom-relieving headache medications should be viewed more neutrally, as an indicator of poorly controlled headaches, and not invariably a cause.

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Tetrabenazine and subthalamic stimulation in graft-induced dyskinesias  Voir?

Putaminal fetal ventral mesencephalic stem cell transplantation has been advocated as a sustainable treatment for Parkinson disease (PD). Double-blind randomized clinical trials have inconclusively proven their benefit in the motor symptoms of PD despite evidence of graft viability, as shown by [18F]-fluorodopa PET.1 At variable intervals after grafting, 15%–57% of patients develop graft-induced dyskinesias (GID), which are characterized by violent, choreo-ballistic dyskinesias occurring regardless of the patient's medication state.2 GID are particularly difficult to manage: they do not respond to withdrawal of antiparkinsonian medication and deep brain stimulation (DBS) of the pars interna of the globus pallidus produces variable results.3 The etiopathogenesis of GIDs is debated and implicates both excessive dopaminergic neural transmission and nondopaminergic mechanisms. As for the latter, animal models and imaging studies on grafted patients have hypothesized that grafted tissues comprise a heterogeneous population of neurons, including serotoninergic ones, which in turn may contribute to GID.4 This notion led to the 5HT1A agonist buspirone to be trialed, successfully, to acutely reduce GID.2,4 Chronic treatment with buspirone has not improved all patients experiencing GID.5

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Optical coherence tomography angiography in pituitary tumor  Voir?

A 32-year-old man with a pituitary tumor had bitemporal hemianopia (figure 1). Peripapillary retinal nerve fiber layer (RNFL) in optical coherence tomography (OCT) was reduced, which corresponded to visual field defects. OCT angiography showed a dropout of capillaries and correlated well with RNFL loss in the OCT (figure 2). Compressive optic neuropathy may be associated with loss of the retinal ganglion cell layer and impaired peripapillary retinal perfusion. OCT angiography may be helpful to detect various optic neuropathies and in analyzing the vascular status of the optic nerve head and RNFL.1

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Editors' Note  Voir?

Editors' Note: In "Long-term cerebral white and gray matter changes after preeclampsia," the authors found that preeclampsia was associated with chronic temporal lobe white matter changes and reduced cortical volume in young women; the changes were consistent with persistent inflammation.

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Letter re: Long-term cerebral white and gray matter changes after preeclampsia  Voir?

The article by Siepmann et al.1 identified long-term cerebral white matter changes and reduced cortical volume, presumably of vascular origin, in young women after pregnancy complicated by preeclampsia. The authors invoked persistent inflammation as the putative agent. Sleep apnea may be a link among pregnancy, preeclampsia, and cerebrovascular disease.

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Author response: Long-term cerebral white and gray matter changes after preeclampsia  Voir?

We thank Dr. Culebras for the comment on our article.1 Sleep apnea might be among the pathophysiologic pathways linking preeclampsia with increased risk of cerebrovascular disease in previously preeclamptic women. In fact, research recently focused on the role of sleep apnea in the etiopathogenesis of cerebrovascular and cardiovascular disease and demonstrated an increased stroke risk in patients with obstructive sleep apnea (OSA).2,3 Intermittent hypoxia with consecutive vascular dysregulation has been identified as a possible mechanism whereby OSA increases risk of stroke. This might be relevant to previously preeclamptic mothers in whom autonomic neurovascular dysfunction, inter alia mediated by functional changes to the sympathetic nervous system, was also demonstrated.4 It remains to be answered whether this similarity among pathologies indeed points to a causative link between preeclampsia and cerebrovascular disease.

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Letter re: The autism "epidemic": Ethical, legal, and social issues in a developmental spectrum disorder  Voir?

Graf et al.1 wrote an interesting review on autism spectrum disorder (ASD), emphasizing the term "autism epidemic," supported by an editorial.2 Among other factors, increasing ASD diagnoses can be attributed to broader diagnostic criteria and the recognition of ASD existence differentiated from other neurodevelopmental diseases.2–4 One important issue, defended by the authors, is early screening and diagnosis with emphasis on the evolving practice of genetic testing for ASD.1

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Author response: The autism "epidemic": Ethical, legal, and social issues in a developmental spectrum disorder  Voir?

We thank Machado et al. for the comments on our review,1 and for the observations of abnormal anatomic and functional connectivity using diffusion-weighted MRI (DW-MRI). Innumerable studies have compared patients with autism spectrum disorders (ASD) and nonaffected controls at rest or while performing particular tasks, most often in small selected subject samples. For example, studies linked autism with the retino-collicular magnocellular visual pathways that project via the pulvinar to the amygdala, occipital V1, and multiple other areas, including the dorsal occipito-parietal/midtemporal streams, which participate with the frontal eye fields in processing spatial attention, moving targets, and dynamic facial expression (with inputs from the amygdala and other limbic pathways).2 However, no results consistently demonstrated specific neural networks that are uniquely pathognomonic of autism in the brain despite the fact that broad networks were linked with deficient social cognition in autism.3 Complex behaviors, like ASD, do not have a single endophenotype linked to one discrete neocortical location.4 The critical need for more research in autism should be balanced by caution about generalizing interpretations of neuroimaging findings that suggest the dysregulation of specific neural pathways. At present, DW-MRI and similar techniques, such as diffusion compartment imaging, are considered beneficial for research but not for routine clinical diagnostics.

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Mystery Case: CSF-1R mutation is a cause of intracranial cerebral calcifications, cysts, and leukoencephalopathy  Voir?

The authors retract the article "Mystery Case: CSF-1R mutation is a cause of intracranial cerebral calcifications, cysts, and leukoencephalopathy" by X. Ayrignac et al., which appeared in the Resident & Fellow Section in volume 86, page e262, because 4 of the figures were previously published in another journal (European Neurology 2012;67:151–153).2 The earlier article was not cited and there were 3 common authors (Magnin, Berger, and Labauge) on the papers. In addition to the duplicate publication, 1 image attributed to the index case in this article was attributed to his mother in the earlier article and 3 images attributed to his mother in this article were attributed to the index case in the earlier article.

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Does compensatory hyperparathyroidism predispose to ischemic stroke? Decreased bone mass and increased bone turnover with valproate therapy in adults with epilepsy; An alternative to vitamin D supplementation to prevent fractures in patients with MS; High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease  Voir?

Because of known issues leading to several retractions of papers by Y. Sato et al., the editors of Neurology® have, as a matter of due diligence, researched other papers that this group published in Neurology. To ensure that the scientific literature is correct, the Editor chooses to publish an Expression of Concern regarding 3 observational studies and a Letter to the Editor published in Neurology prior to the retracted clinical trials.1–4

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Dernière mise à jour : 20/09/2017 : 06:22


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