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Sommaires des Revues - Neurology

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Clinical Reasoning: A 46-year-old man with persistent hiccups, cognitive dysfunction, and imbalance  Voir?

A 46-year-old, right-handed, African American man presented to the emergency department after 1 week of persistent hiccups and 3 days of nausea and vomiting. His family member also noted that he had been experiencing right-hand tremor and gait imbalance for the last 3 months. Over the 6 months prior to presentation, the patient's coworkers had noticed that he was completing his work more slowly, that he was forgetting how to perform simple tasks, and that several times he had come to work at the wrong hours. The patient had a history of HIV diagnosed 10 years earlier and reported good adherence to an antiretroviral regimen consisting of tenofovir, emtricitabine, and atazanavir boosted by ritonavir, without any changes for several years. His viral load was undetectable when tested 8 months prior to presentation.

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Teaching NeuroImages: Artery of Percheron thrombosis causing selective downgaze palsy  Voir?

A 47-year-old man with migraines presented with sudden onset of vertical diplopia, dysarthria, right facial weakness, and downgaze palsy (figure 1). Brain MRI revealed ischemic strokes in the midbrain periaqueductal gray, bilateral thalamic–midbrain junction, and thalamus (figure 2, A–C). Gradient echo and T1 MRI showed hypointensity in the interpeduncular fossa (figure 2, D and E). No flow could be visualized in this structure on CT angiogram or catheter angiogram, demonstrating a thrombosed artery of Percheron (figure 2, F–H). Downgaze palsy, which improved 18 months later, may result from bilateral lesions of the mesencephalic–diencephalic junction involving the rostral interstitial nucleus of the medial longitudinal fasciculus.1,2

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Teaching NeuroImages: Spontaneous involution of symptomatic delayed tumefactive cyst following radiosurgery for AVM  Voir?

A 65-year-old woman underwent radiosurgery for a left temporal arteriovenous malformation (AVM) (figure 1A). Follow-up MRI/magnetic resonance angiography 3 years later demonstrated postradiation changes (figure 1B) and AVM resolution (figure 2). Six years posttreatment, she had progressive headaches and aphasia and a large cyst (figure 1C). Her symptoms resolved acutely without treatment. MRI 3 months later showed reduction of the cyst with mass effect resolution related to spontaneous fenestration in the ventricle (figure 1D).

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Teaching NeuroImages: MR neurography for the diagnosis of hypertrophic neuropathies  Voir?

A 25-year-old woman presented with a 10-year history of frequent falls and deafness. Her mother had a similar neurologic picture. Examination showed peroneal amyotrophy, pes cavus, and hearing loss. Magnetic resonance (MR) neurography showed diffuse nerve enlargement in the lower limbs (figure). Genetic analysis revealed heterozygous mutation c.82T>C (p.Trp28Arg) in the PMP22 gene, defining diagnosis of Charcot-Marie-Tooth disease (CMT) type 1A.

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Teaching Video NeuroImages: My weeping patient: Avoiding the pitfalls of a functional diagnosis  Voir?

A 54-year-old man presented with symptoms of a posterior circulation stroke. A right facial palsy and horizontal right end gaze nystagmus was noted. On resolution, episodes of uncontrolled weeping without a provoking stimulus was observed (video at Neurology.org). These were initially unremitting, lasting minutes, with complete resolution after 1 month. An early consideration was of a functional neurologic disorder. Subsequent MRI brain demonstrated bilateral anterior pontine infarcts (figure). It has been hypothesized that pseudobulbar affect (PBA) results from the loss of frontal cortex input to the cerebellum during emotional expression.1 This disruption in descending pathways is postulated in pontine infarcts.2 PBA should not be considered an incongruent sign.

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Spotlight on the October 17 issue  Voir?

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An improved way to predict neurologic recovery in acute spinal cord injury  Voir?

In North America alone, spinal cord injury affects well over 1 million patients, with the average annual incidence expected to rise secondary to an increasing amount of falls in an aging population.1,2 Spinal cord injury (SCI) has detrimental health consequences that can frequently leave the injured patient with a lifetime of medical expenses exceeding $4 million.2 Although the current practice in treating SCI is to elevate a patient's mean arterial pressure (MAP) to 85–90 mm Hg for the first 7 days in an effort to maintain spinal cord perfusion, this treatment strategy has uncertain efficacy, as the actual spinal cord perfusion pressure (SCPP) remains unknown.3 In this issue of Neurology®, Squair et al.4 propose an improved treatment approach using the calculated SCPP that can provide patients with an increased likelihood of having restoration of function after an SCI.

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Smoking cessation and secondary stroke prevention  Voir?

The 7 million adult stroke survivors in the United States remain at high risk for a recurrent stroke. The increased morbidity and cost associated with recurrent stroke, in addition to the 5% to 20% yearly stroke recurrence, support the need for additional investigations into secondary stroke prevention.1,2 Stroke prevention guidelines, whether primary or secondary, focus on risk factor control of modifiable risk factors. The American Heart Association/American Stroke Association guidelines for secondary stroke prevention indicate evidence-based risk factor control, interventional approaches, and treatment options as approaches to secondary stroke prevention.1 Risk factor control for secondary stroke prevention includes managing hypertension, diabetes mellitus, and hyperlipidemia, as well as lifestyle modifications, including weight management, alcohol consumption, and smoking cessation.3 A cornerstone of recurrent stroke reduction, and lifetime cardiovascular disease (CVD) risk, is modification of lifestyle behaviors such as abstaining from tobacco, adopting a healthy diet, and exercising regularly. While these healthy lifestyle behaviors should start in childhood and continue through one's lifetime, modifying these health behaviors after a stroke can reduce the risk of recurrent stroke and other CVD-related illnesses.3

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Preventing burnout increases the desirability of neurology as a career  Voir?

Neurologic diseases comprise a major percentage of disease burden in the United States, and one that is predicted to increase as our population ages. The need for physicians with expertise in the recognition, diagnosis, and management of neurologic diseases also will increase. Over the next decade, the number of neurologists in the United States will grow from the current 16,000 to 18,000. However, even this number represents a predicted 20% shortfall in number of neurologists needed by 2025.1,2 Our neurology workforce therefore must increase to address this current and future need.

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Spinal cord perfusion pressure predicts neurologic recovery in acute spinal cord injury  Voir?

Objective:

To determine whether spinal cord perfusion pressure (SCPP) as measured with a lumbar intrathecal catheter is a more predictive measure of neurologic outcome than the conventionally measured mean arterial pressure (MAP).

Methods:

A total of 92 individuals with acute spinal cord injury were enrolled in this multicenter prospective observational clinical trial. MAP and CSF pressure (CSFP) were monitored during the first week postinjury. Neurologic impairment was assessed at baseline and at 6 months postinjury. We used logistic regression, systematic iterations of relative risk, and Cox proportional hazard models to examine hemodynamic patterns commensurate with neurologic outcome.

Results:

We found that SCPP (odds ratio 1.039, p = 0.002) is independently associated with positive neurologic recovery. The relative risk for not recovering neurologic function continually increased as individuals were exposed to SCPP below 50 mm Hg. Individuals who improved in neurologic grade dropped below SCPP of 50 mm Hg fewer times than those who did not improve (p = 0.012). This effect was not observed for MAP or CSFP. Those who were exposed to SCPP below 50 mm Hg were less likely to improve from their baseline neurologic impairment grade (p = 0.0056).

Conclusions:

We demonstrate that maintaining SCPP above 50 mm Hg is a strong predictor of improved neurologic recovery following spinal cord injury. This suggests that SCPP (the difference between MAP and CSFP) can provide useful information to guide the hemodynamic management of patients with acute spinal cord injury.

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Comorbidity in multiple sclerosis is associated with diagnostic delays and increased mortality  Voir?

Objective:

To investigate the effect of chronic comorbidity on the time of diagnosis of multiple sclerosis (MS) and on mortality in MS.

Methods:

We conducted a population-based, nationwide cohort study including all incident MS cases in Denmark with first MS symptom between 1980 and 2005. To investigate the time of diagnosis, we compared individuals with and without chronic comorbidity using multinomial logistic regression. To investigate mortality, we used Cox regression with time-dependent covariates, following study participants from clinical MS onset until endpoint (death) or to the end of the study, censuring at emigration.

Results:

We identified 8,947 individuals with clinical onset of MS between 1980 and 2005. In the study of time of diagnosis, we found statistically significant odds ratios for longer diagnostic delays with cerebrovascular comorbidity (2.01 [1.44–2.80]; <0.0005), cardiovascular comorbidity (4.04 [2.78–5.87]; <0.0005), lung comorbidity (1.93 [1.42–2.62]; <0.0005), diabetes comorbidity (1.78 [1.04–3.06]; 0.035), and cancer comorbidity (2.10 [1.20–3.67]; 0.009). In the mortality study, we found higher hazard ratios with psychiatric comorbidity (2.42 [1.67–3.01]; <0.0005), cerebrovascular comorbidity (2.47 [2.05–2.79]; <0.0005), cardiovascular comorbidity (1.68 [1.39–2.03]; <0.0005), lung comorbidity (1.23 [1.01–1.50]; 0.036), diabetes comorbidity (1.39 [1.05–1.85]; 0.021), cancer comorbidity (3.51 [2.94–4.19]; <0.0005), and Parkinson disease comorbidity (2.85 [1.34–6.06]; 0.007).

Conclusions:

An increased awareness of both the necessity of neurologic evaluation of new neurologic symptoms in persons with preexisting chronic disease and of optimum treatment of comorbidity in MS is critical.

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Analysis of blood-based gene expression in idiopathic Parkinson disease  Voir?

Objective:

To examine whether gene expression analysis of a large-scale Parkinson disease (PD) patient cohort produces a robust blood-based PD gene signature compared to previous studies that have used relatively small cohorts (≤220 samples).

Methods:

Whole-blood gene expression profiles were collected from a total of 523 individuals. After preprocessing, the data contained 486 gene profiles (n = 205 PD, n = 233 controls, n = 48 other neurodegenerative diseases) that were partitioned into training, validation, and independent test cohorts to identify and validate a gene signature. Batch-effect reduction and cross-validation were performed to ensure signature reliability. Finally, functional and pathway enrichment analyses were applied to the signature to identify PD-associated gene networks.

Results:

A gene signature of 100 probes that mapped to 87 genes, corresponding to 64 upregulated and 23 downregulated genes differentiating between patients with idiopathic PD and controls, was identified with the training cohort and successfully replicated in both an independent validation cohort (area under the curve [AUC] = 0.79, p = 7.13E–6) and a subsequent independent test cohort (AUC = 0.74, p = 4.2E–4). Network analysis of the signature revealed gene enrichment in pathways, including metabolism, oxidation, and ubiquitination/proteasomal activity, and misregulation of mitochondria-localized genes, including downregulation of COX4I1, ATP5A1, and VDAC3.

Conclusions:

We present a large-scale study of PD gene expression profiling. This work identifies a reliable blood-based PD signature and highlights the importance of large-scale patient cohorts in developing potential PD biomarkers.

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Randomized open-label trial of dextromethorphan in Rett syndrome  Voir?

Objective:

To determine safety and perform a preliminary assessment of dose-dependent efficacy of dextromethorphan in normalizing electrographic spikes, clinical seizures, and behavioral and cognitive functions in girls with Rett syndrome.

Methods:

We used a prospective randomized, open-label trial in fast metabolizers of dextromethorphan to examine the effect of dextromethorphan on core clinical features of Rett syndrome. Interictal spike activity and clinical seizures were determined using EEG and parent reporting. Cognitive data were obtained using the Mullen Scales of Early Learning and Vineland Adaptive Behavior Scales, while behavioral data were obtained from parent-completed checklists, the Aberrant Behavior Checklist–Community Version, and the Screen for Social Interaction. Anthropometric data were obtained according to the National Health and Nutrition Examination Survey. The Rett Syndrome Severity Scale provided a clinical global impression of the effect of dextromethorphan on clinical severity.

Results:

Dextromethorphan is safe for use in 3- to 15-year-old girls with Rett syndrome. Thirty-five girls were treated with 1 of 3 doses of dextromethorphan over a period of 6 months. Statistically significant dose-dependent improvements were seen in clinical seizures, receptive language, and behavioral hyperactivity. There was no significant improvement in global clinical severity as measured by the Rett Syndrome Severity Scale.

Conclusions:

Dextromethorphan is a potent noncompetitive antagonist of the NMDA receptor channel that is safe for use in young girls with Rett syndrome. Preliminary evidence suggests that dextromethorphan may improve some core features of Rett syndrome.

Classification of evidence:

This study provides Class IV evidence that dextromethorphan at various doses does not change EEG spike counts over 6 months, though precision was limited to exclude an important effect.

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Variable course of Unverricht-Lundborg disease: Early prognostic factors  Voir?

Objective:

To explore the course of Unverricht-Lundborg disease (EPM1) and identify the risk factors for severity, we investigated the time course of symptoms and prognostic factors already detectable near to disease onset.

Methods:

We retrospectively evaluated the features of 59 Italian patients carrying the CSTB expansion mutation, and coded the information every 5 years after the disease onset in order to describe the cumulative time-dependent probability of reaching disabling myoclonus, relevant cognitive impairment, and inability to work, and evaluated the influence of early factors using the log-rank test. The risk factors were included in a Cox multivariate proportional hazards regression model.

Results:

Disabling myoclonus occurred an average of 32 years after disease onset, whereas cognitive impairment occurred a little later. An age at onset of less than 12 years, the severity of myoclonus at the time of first assessment, and seizure persistence more than 10 years after onset affected the timing of disabling myoclonus and cognitive decline. Most patients became unable to work years before the appearance of disabling myoclonus or cognitive decline.

Conclusions:

A younger age at onset, early severe myoclonus, and seizure persistence are predictors of a more severe outcome. All of these factors may be genetically determined, but the greater hyperexcitability underlying more severe seizures and myoclonus at onset may also play a role by increasing cell damage due to reduced cystatin B activity.

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Pretreatment behavior and subsequent medication effects in childhood absence epilepsy  Voir?

Objective:

To characterize pretreatment behavioral problems and differential effects of initial therapy in children with childhood absence epilepsy (CAE).

Methods:

The Child Behavior Checklist (CBCL) was administered at baseline, week 16–20, and month 12 visits of a randomized double-blind trial of ethosuximide, lamotrigine, and valproate. Total problems score was the primary outcome measure.

Results:

A total of 382 participants at baseline, 310 participants at the week 16–20 visit, and 168 participants at the month 12 visit had CBCL data. At baseline, 8% (95% confidence interval [CI] 6%–11%) of children with CAE had elevated total problems scores (mean 52.9 ± 10.91). At week 16–20, participants taking valproic acid had significantly higher total problems (51.7 [98.3% CI 48.6–54.7]), externalizing problems (51.4 [98.3% CI 48.5–54.3]), attention problems (57.8 [98.3% CI 55.6–60.0]), and attention-deficit/hyperactivity problems (55.8 [98.3% CI 54.1–57.6]) scores compared to participants taking ethosuximide (46.5 [98.3% CI 43.4–49.6]; 45.8 [98.3% CI 42.9–48.7]; 54.6 [98.3% CI 52.4–56.9]; 53.0 [98.3% CI 51.3–54.8]). Lack of seizure freedom and elevated week 16–20 Conner Continuous Performance Test confidence index were associated with worse total problems scores. At month 12, participants taking valproic acid had significantly higher attention problems scores (57.9 [98.3% CI 55.6–60.3]) compared to participants taking ethosuximide (54.5 [95% CI 52.1–56.9]).

Conclusions:

Pretreatment and ongoing behavioral problems exist in CAE. Valproic acid is associated with worse behavioral outcomes than ethosuximide or lamotrigine, further reinforcing ethosuximide as the preferred initial therapy for CAE.

Clinicaltrials.gov identifier:

NCT00088452.

Classification of evidence:

This study provides Class II evidence that for children with CAE, valproic acid is associated with worse behavioral outcomes than ethosuximide or lamotrigine.

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Comparison of symptomatic and asymptomatic persons with primary age-related tauopathy  Voir?

Objective:

To conduct a clinicopathologic study to characterize clinical and neuropathologic features associated with cognitive impairment in participants with no neuritic amyloid plaques (primary age-related tauopathy [PART] definite) and sparse neuritic plaques (amyloid sparse).

Methods:

Using the National Alzheimer's Coordinating Center database, we identified 377 individuals who were PART definite (n = 170) or amyloid sparse (n = 207), clinically examined within 1 year of death, and autopsied at 1 of 26 National Institute on Aging–funded Alzheimer's Disease Centers. Factors associated with the odds of being symptomatic (global Clinical Dementia Rating [CDR] score >0) were identified with multivariable logistic regression.

Results:

PART-definite participants less often had a high Braak neurofibrillary tangle stage V or VI (4%) compared to amyloid sparse participants (28%, p < 0.001). Of the PART-definite participants, 98 were symptomatic and 72 asymptomatic according to their global CDR scores. PART-definite participants were less often symptomatic (58%) compared with amyloid sparse participants (80%, p < 0.001). Within the PART-definite group, independent predictors of symptomatic status included depression (adjusted odds ratio [aOR] 4.20, 95% confidence interval [CI] 2.15–8.19), Braak stage (aOR 1.42, 95% CI 1.04–1.95), and history of stroke (aOR 8.09, 95% CI 2.63–24.82). Within the amyloid sparse group, independent predictors of symptomatic status included education (aOR 0.80, 95% CI 0.65–0.99), Braak stage (aOR 1.91, 95% CI 1.07–3.43), and amyloid angiopathy (aOR 2.75, 95% CI 1.14–6.64).

Conclusions:

These findings support the hypothesis that participants with PART have an amyloid-independent dementing Alzheimer disease–like temporal lobe tauopathy.

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Serum magnesium is associated with the risk of dementia  Voir?

Objective:

To determine if serum magnesium levels are associated with the risk of all-cause dementia and Alzheimer disease.

Methods:

Within the prospective population-based Rotterdam Study, we measured serum magnesium levels in 9,569 participants, free from dementia at baseline (1997–2008). Participants were subsequently followed up for incident dementia, determined according to the DSM-III-R criteria, until January 1, 2015. We used Cox proportional hazard regression models to associate quintiles of serum magnesium with incident all-cause dementia. We used the third quintile as a reference group and adjusted for age, sex, Rotterdam Study cohort, educational level, cardiovascular risk factors, kidney function, comorbidities, other electrolytes, and diuretic use.

Results:

Our study population had a mean age of 64.9 years and 56.6% were women. During a median follow-up of 7.8 years, 823 participants were diagnosed with all-cause dementia. Both low serum magnesium levels (≤0.79 mmol/L) and high serum magnesium levels (≥0.90 mmol/L) were associated with an increased risk of dementia (hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.02–1.69, and HR 1.30, 95% CI 1.02–1.67, respectively).

Conclusions:

Both low and high serum magnesium levels are associated with an increased risk of all-cause dementia. Our results warrant replication in other population-based studies.

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Smoking cessation and outcome after ischemic stroke or TIA  Voir?

Objective:

To assess whether smoking cessation after an ischemic stroke or TIA improves outcomes compared to continued smoking.

Methods:

We conducted a prospective observational cohort study of 3,876 nondiabetic men and women enrolled in the Insulin Resistance Intervention After Stroke (IRIS) trial who were randomized to pioglitazone or placebo within 180 days of a qualifying stroke or TIA and followed up for a median of 4.8 years. A tobacco use history was obtained at baseline and updated during annual interviews. The primary outcome, which was not prespecified in the IRIS protocol, was recurrent stroke, myocardial infarction (MI), or death. Cox regression models were used to assess the differences in stroke, MI, and death after 4.8 years, with correction for adjustment variables prespecified in the IRIS trial: age, sex, stroke (vs TIA) as index event, history of stroke, history of hypertension, history of coronary artery disease, and systolic and diastolic blood pressures.

Results:

At the time of their index event, 1,072 (28%) patients were current smokers. By the time of randomization, 450 (42%) patients had quit smoking. Among quitters, the 5-year risk of stroke, MI, or death was 15.7% compared to 22.6% for patients who continued to smoke (adjusted hazard ratio 0.66, 95% confidence interval 0.48–0.90).

Conclusion:

Cessation of cigarette smoking after an ischemic stroke or TIA was associated with significant health benefits over 4.8 years in the IRIS trial cohort.

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Qualitative study of burnout, career satisfaction, and well-being among US neurologists in 2016  Voir?

Objective:

To understand the experience and identify drivers and mitigating factors of burnout and well-being among US neurologists.

Methods:

Inductive data analysis was applied to free text comments (n = 676) from the 2016 American Academy of Neurology survey of burnout, career satisfaction, and well-being.

Results:

Respondents providing comments were significantly more likely to be older, owners/partners of their practice, solo practitioners, and compensated by production than those not commenting. The 4 identified themes were (1) policies and people affecting neurologists (government and insurance mandates, remuneration, recertification, leadership); (2) workload and work–life balance (workload, electronic health record [EHR], work–life balance); (3) engagement, professionalism, work domains specific to neurology; and (4) solutions (systemic and individual), advocacy, other. Neurologists mentioned workload > professional identity > time spent on insurance and government mandates when describing burnout. Neurologists' patient and clerical workload increased work hours or work brought home, resulting in poor work–life balance. EHR and expectations of high patient volumes by administrators impeded quality of patient care. As a result, many neurologists reduced work hours and call provision and considered early retirement.

Conclusions:

Our results further characterize burnout among US neurologists through respondents' own voices. They clarify the meaning respondents attributed to ambiguous survey questions and highlight the barriers neurologists must overcome to practice their chosen specialty, including multiple regulatory hassles and increased work hours. Erosion of professionalism by external factors was a common issue. Our findings can provide strategic direction for advocacy and programs to prevent and mitigate neurologist burnout and promote well-being and engagement.

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Genome editing technologies and their potential to treat neurologic disease  Voir?

Genome editing refers to a process of making precise and permanent changes in the genetic code of cells, tissues, and whole organisms. The first step in this process is to program an enzyme called a nuclease to bind to a precise DNA sequence, whereby the enzyme will cut the DNA. This double-stranded break will in turn induce the cell to make a repair at that site, which will change the DNA sequence. The repair mechanism can be utilized to either knock out or introduce selected genes. Given how rapidly gene editing systems are influencing diverse applications in biomedical research, biotechnology, and agriculture,1 clinical applications in neurology to repair genetic mutations causing disease, or to incorporate genes that might be of therapeutic benefit, are on the near horizon. The following cases illustrate how such an approach may be used to develop new ex vivo (case 1) and in vivo (case 2) therapies for neurologic disease, respectively, and highlight some of the translational challenges of using these molecular reagents safely and ethically in patients.

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Did Jules Dejerine describe AMAN at the end of the 19th century?  Voir?

Guillain-Barré syndrome (GBS) is a heterogeneous group of acute immune-mediated neuropathies, including acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). AMAN is an axonal subtype of GBS that has been known since the 1990s; this term was first used to describe a summer epidemic of acute ascending paralysis observed in children in northern China (and Mexico). It is pathologically characterized by noninflammatory axonal degeneration of the motor nerves (with little or no demyelination). The French neurologist Jules Dejerine (1849–1917) conducted a clinical and pathologic description of AMAN in the late 19th century. We describe his observations, which provide us with valuable information on the course of pathologic lesions in this disease.

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Fatigable ptosis as an initial presentation of adult-onset Leigh syndrome  Voir?

A 20-year-old man presented with bilateral fatigable ptosis for 1 month. On examination, there was bilateral incomplete ptosis, which deteriorated during upward gaze and improved at rest (figure, A and B). Tests for myasthenia gravis were all negative. Brain MRI showed symmetric hyperintensities at periaqueductal gray matter on T2- and diffusion-weighted images (figure, C). CSF lactic acid was elevated. Mitochondrial genome test demonstrated a homoplasmic T9176C mutation in the MT-APT6A gene, known as pathogenic mutation of Leigh syndrome.1 In our patient, fatigable ptosis may be ascribed to the dysfunction at centrally located synapse between the nuclear complex of the third nerve and supranuclear pathways.2

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Editors' Note  Voir?

Editors' Note: In "Ischemic lesions, blood pressure dysregulation, and poor outcomes in intracerebral hemorrhage," the authors concluded that acute blood pressure (BP) dysregulation in primary intracerebral hemorrhage (ICH) patients was associated with the development of diffusion-weighted imaging (DWI) lesions and, subsequently, worse outcomes.

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Letter re: Ischemic Lesions, blood pressure dysregulation, and poor outcomes in intracerebral hemorrhage  Voir?

We appreciated the article by Kidwell et al.1 that showed higher first-recorded blood pressure (BP) and greater delta mean arterial pressure are associated with the development of diffusion-weighted imaging (DWI) lesions in acute intracerebral hemorrhage (ICH). The most desirable BP target and optimal antihypertensive strategy in ICH are controversial.2 The relationship between BP and outcome is more complex than simply linear, and mechanisms other than BP reduction play a role. There is accruing evidence that not only absolute BP levels but their variation over time affect ICH prognosis.3 Besides increasing the risk of hematoma enlargement, BP fluctuations could favor remote ischemia by working synergistically with preexistent burden of cerebral small angiopathy, namely leukoaraiosis and microbleeds, and influence the stroke outcome. Both systolic and diastolic BP dysregulation deserve more comprehensive assessment through the proper measures of variability, such as standard and residual deviation, variation coefficient, average real variability, and variation independent of the mean.4 In addition, time to MRI differed among DWI+ and DWI– patient subgroups, which could represent a meaningful bias: it would be appropriate to include this variable among the controlling factors of the multivariable predictive model for DWI lesions development.

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Author response: Ischemic Lesions, blood pressure dysregulation, and poor outcomes in intracerebral hemorrhage  Voir?

We appreciate the comments by Drs. Lattanzi and Silvestrini on our article,1 and agree that further research is needed to better understand the complex relationship among blood pressure (BP) dysregulation, small vessel disease, and development of remote ischemic lesions in the setting of acute intracerebral hemorrhage.2

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Letter re: Efficacy and safety of brivaracetam for partial-onset seizures in 3 pooled clinical studies  Voir?

We thank Dr. French1 for her Epilepsy Currents commentary on our article.2 We agree that time will tell regarding the usefulness of brivaracetam's (BRV's) addition to the antiepileptic drug (AED) armamentarium, as there is no substitute for real-world clinical experience.

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Dernière mise à jour : 16/10/2017 : 21:51


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