[Facial palsy: diagnostic traps]. / Paralysie faciale : pièges diagnostiques.

Peripheral facial palsy is a common, often idiopathic and self-limiting mononeuropathy. However, secondary facial palsies require specific management: they are most often of infectious, vascular or dysimmune causes. The presence of red flags in the history, clinical examination or medical follow-up should alert clinicians. Because of the high incidence of Lyme disease in our region, this etiology deserves special attention. The management is based on general measures (eye protection, rehabilitation) and corticosteroid therapy; antivirals may provide additional benefit.

La paralysie faciale périphérique (PFP) est une mononeuropathie fréquente, souvent idiopathique et autorésolutive. Cependant, les paralysies faciales secondaires nécessitent une prise en charge spécifique : elles sont le plus souvent de causes infectieuses, vasculaires ou dysimmunes. La présence de drapeaux rouges à l'anamnèse, à l'examen clinique ou lors du suivi médical doivent alerter les cliniciens. En raison de l'incidence élevée de la borréliose dans nos régions, cette étiologie mérite une attention particulière. La prise en charge repose sur des mesures générales (protection oculaire, rééducation) et sur la corticothérapie ; l'ajout d'antiviraux pourrait apporter un bénéfice supplémentaire.

Antisaccade, a predictive marker for freezing of gait in Parkinson's disease and gait/gaze network connectivity.

Freezing of gait is a challenging sign of Parkinson's disease associated with disease severity and progression and involving the mesencephalic locomotor region. No predictive factor of freezing has been reported so far. The primary objective of this study was to identify predictors of freezing occurrence at 5 years. In addition, we tested whether functional connectivity of the mesencephalic locomotor region could explain the oculomotor factors at baseline that were predictive of freezing onset. We performed a prospective study investigating markers (parkinsonian signs, cognitive status and oculomotor recordings, with a particular focus on the antisaccade latencies) of disease progression at baseline and at 5 years. We identified two groups of patients defined by the onset of freezing at 5 years of follow-up; the 'Freezer' group was defined by the onset of freezing in the ON medication condition during follow-up (n = 17), while the 'non-Freezer' group did not (n = 8). Whole brain resting-state functional MRI was recorded at baseline to determine how antisaccade latencies were associated with connectivity of the mesencephalic locomotor region networks in patients compared to 25 age-matched healthy volunteers. Results showed that, at baseline and compared to the non-Freezer group, the Freezer group had equivalent motor or cognitive signs, but increased antisaccade latencies (P = 0.008). The 5-year course of freezing of gait was correlated with worsening antisaccade latencies (P = 0.0007). Baseline antisaccade latencies was also predictive of the freezing onset (χ2 = 0.008). Resting state connectivity of mesencephalic locomotor region networks correlated with (i) antisaccade latency differently in patients and healthy volunteers at baseline; and (ii) the further increase of antisaccade latency at 5 years. We concluded that antisaccade latency is a predictive marker of the 5-year onset of freezing of gait. Our study suggests that functional networks associated with gait and gaze control are concurrently altered during the course of the disease.

[Current developments in Parkinson's disease]. / Actualité de la maladie de Parkinson.

Our understanding of Parkinson's disease has considerably evolved in the last few years. While the cardinal motor features bradykinesia, rigidity, and tremor define the disease and respond to dopamine replacement therapy, there is a wider-spread neurodegeneration causing non motor symptoms and their impact on the quality of life of patients is being increasingly recognized. The follow-up requires a good collaboration between primary care physicians and neurologists. The purpose of this article is to offer a practical treatment guide of uncomplicated Parkinson's disease for general practitioners and internal medicine specialists. The management of late complications of Parkinson's disease will be addressed in another article.

Notre compréhension de la maladie de Parkinson a été bouleversée ces dernières années. Alors que les manifestations motrices cardinales (bradykinésie, rigidité, tremblement) définissent toujours la maladie et sont traitées efficacement avec la substitution dopaminergique, nous reconnaissons de plus en plus l'importance des symptômes non moteurs, qui résultent d'une neurodégénérescence plus étendue et qui grèvent substantiellement la qualité de vie des patients. Ces connaissances renouvellent la collaboration entre le médecin traitant et le neurologue. Nous proposons ici un vade-mecum de la maladie de Parkinson non compliquée, à l'attention du médecin généraliste et interniste. Le traitement des complications est le sujet d'un autre article.

Hepatitis E virus infection as a direct cause of neuralgic amyotrophy.

INTRODUCTION: We describe a patient who developed neuralgic amyotrophy (NA) related to hepatitis E virus (HEV) infection. METHODS: The patient underwent neurological and electrodiagnostic examinations, high-resolution analysis of serological changes, and HEV load profile, and was treated with intravenous immunoglobulin. RESULTS: There was evidence of bilateral, asymmetric acute inflammatory cervical polyradiculopathy and possible brachial plexopathy. Positive serum anti-HEV IgM was followed by seroconversion to anti-HEV IgG positivity. A calculated anti-HEV antibody index was compatible with intrathecal synthesis, and HEV genotype 3 RNA was found in serum and cerebrospinal fluid (CSF). Liver function tests returned to normal within 6 weeks. CONCLUSIONS: Bilateral involvement of cervical nerve roots and/or plexus, elevated liver function tests, and abnormal CSF are typical features of HEV-associated NA. The pathogenesis involves possible immune-mediated mechanisms. However, our findings support the hypothesis that HEV-related NA is associated with direct infection. Muscle Nerve 54: 325-327, 2016.

[Follow-up of nerve and muscle disorders: the collaboration between general practitioner and specialist]. / Suivi des malades neuromusculaires: collaboration entre praticien et spécialiste.

The follow-up of neuromuscular diseases varies widely as the etiologies and requires specialized care. Yet, the inter-disciplinary and collaborative approach with the General Practitioner (GP) is indispensable, and we may review the international recommandations according to the Evidence-based Medicine (EBM) of frequent symptoms like cramps and neuropathic pain. Besides, we discuss some principles of our daily pratice, which--we hope--would facilitate the communication with the GPs.

Principles of gait encoding in the subthalamic nucleus of people with Parkinson's disease.

Disruption of subthalamic nucleus dynamics in Parkinson's disease leads to impairments during walking. Here, we aimed to uncover the principles through which the subthalamic nucleus encodes functional and dysfunctional walking in people with Parkinson's disease. We conceived a neurorobotic platform embedding an isokinetic dynamometric chair that allowed us to deconstruct key components of walking under well-controlled conditions. We exploited this platform in 18 patients with Parkinson's disease to demonstrate that the subthalamic nucleus encodes the initiation, termination, and amplitude of leg muscle activation. We found that the same fundamental principles determine the encoding of leg muscle synergies during standing and walking. We translated this understanding into a machine learning framework that decoded muscle activation, walking states, locomotor vigor, and freezing of gait. These results expose key principles through which subthalamic nucleus dynamics encode walking, opening the possibility to operate neuroprosthetic systems with these signals to improve walking in people with Parkinson's disease.