These results show that early cortical neuromodulation with anodal tDCS combined with rPNS can promote motor hand recovery and that the benefit is still present 1 month after the stroke.

Introduction: Small fiber neuropathies (SFN) induce pain and/or autonomic symptoms. The diagnosis of SFN poses a challenge because the role of skin biopsy as a reference method and of each neurophysiological test remain to be discussed. This study compares six methods evaluating small sensory and autonomic nerve fibers: skin biopsy, Quantitative Sensory Testing (QST), quantitative sweat measurement system (Q-Sweat), Laser Evoked Potentials (LEP), Electrochemical Skin Conductance (ESC) measurement and Autonomic CardioVascular Tests (ACVT). Methods: This is a single center, retrospective study including patients tested for symptoms compatible with SFN between 2013 and 2016 using the afore-mentioned tests. Patients were ultimately classified according to the results and clinical features as "definite SFN," "possible SFN" or "no SFN." The sensitivity (Se) and specificity (Sp) of each test were calculated based on the final diagnosis and the best diagnostic strategy was then evaluated. Results: Two hundred and forty-five patients were enrolled (164 females (66.9%), age: 50.4 ± 15 years). The results are as follows: skin biopsy: Se = 58%, Sp = 91%; QST: Se = 72%, Sp = 39%; Q-Sweat: Se = 53%, Sp = 69%; LEP: Se = 66%, Sp = 89%; ESC: Se = 60%, Sp = 89%; Cardiovascular tests: Se = 15%, Sp = 99%. The combination of skin biopsy, LEP, QST and ESC has a Se of 90% and a Sp of 87%. Conclusion: Our study outlines the benefits of combining skin biopsy, ESC, LEP and QST in the diagnosis of SFN.

Cortical florbetapir uptake is increased in patients with CAA-related ICH relative to those with deep ICH. Although F-florbetapir PET can label vascular β-amyloid and might serve as an outcome marker in future clinical trials, its diagnostic value in acute CAA-related ICH seems limited in clinical practice.

Interest in the use of antidepressants after stroke has been renewed by better knowledge of poststroke depression, but mainly by the capacity of some of them to promote functional recovery of nondepressed subjects. Recombinant tissue plasminogen activator thrombolysis within the first few hours after the stroke is currently the only validated treatment able to improve the spontaneous--and most of the time incomplete--recovery of neurological functions after stroke. However, we have learned from research over the last decade, in part based on the considerable improvement of neuroimaging techniques, that spontaneous recovery of neurological functions is associated with a large intracerebral reorganization of the damaged human brain. The question of whether lesioned-brain plasticity can be modulated by external factors such as pharmacological antidepressant agents is now being addressed with the aim of improving recovery and reducing the final disability of patients. Poststroke depression is known to be frequent and deleterious for patient outcome. We review the interest in the use of antidepressants after stroke in classic but often neglected poststroke depression and we strongly underline the action of some antidepressants in promoting functional recovery of nondepressed patients after stroke.

Zika virus (ZIKV) infection has been associated with neurologic disorders including Guillain-Barré syndrome (GBS). In New Caledonia during the ZIKV outbreak (2014-2015), case-control and retrospective studies have been performed to assess the link between ZIKV and GBS. Among the 15 cases included, 33% had evidence of a recent ZIKV infection compared to only 3.3% in the 30 controls involved. All patients were Melanesian, had facial diplegia and similar neurophysiological pattern consistent with acute inflammatory demyelinating polyneuropathy, and recovered well. Furthermore, during the peak of ZIKV transmission, we observed a number of GBS cases higher than the calculated upper limit, emphasizing the fact that ZIKV is now a major trigger of GBS.

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Today, administering rTPA thrombolytic therapy within the first hours of a stroke is the only validated drug therapy for improving the spontaneous--and most of the time incomplete--recovery of neurological functions post-stroke. However in the past decade, thanks in part to the considerable advances of neuroimaging techniques, we have learned that spontaneous recovery of neurological functions was associated with a wide intracerebral reorganization of the damaged human brain. The question of whether lesioned-brain plasticity can be modulated by external factors like pharmacological agents is now addressed in the hope of improving recovery and reducing the chronic impairments of stroke patients. In this paper, we review the preclinical and clinical evidence for a direct action of SSRIs in promoting recovery in ischemic stroke patients.

IntroductionDry immersion is a ground-based experiment simulating the effects of weightlessness, and it is a model of acute symmetrical bilateral deafferentation. This exploratory study aimed to investigate the effects of three days of dry immersion (DI) on sensory thresholds and the functioning of lemniscal pathways, assessed by somatosensory evoked potentials (SEPs).MethodsTwelve healthy male volunteers (32+/-4.8 years) participated in the study. Sensory thresholds and SEPs of the tibial nerve of both limbs were recorded before (D-1) and on the third day of dry immersion (D3).ResultsSensory thresholds significantly decreased on D3 (-20.75 +/-21.7%; z = -2.54; p = 0.0109 on the right side and -22.18+/-17.28%; z = -3.059; p = 0.002 on the left side). The amplitude of P40 responses did not differ between D-1 and D3. Latencies of all central responses until P30 were shortened on D3 (N21 right:-0.57+/-0.31; z = -3.06; p = 0.002; N21 left -0.83+/-0.53; z = -2.94; p = 0.003; P30 right: -1.26+/-1.42; z = -3.059; p = 0.002; P30 left: -1.11+/-1.55; z = -2.27; p = 0.02)ConclusionThree days of dry immersion can induce hyperexcitability of lemniscal pathways.SignificanceThis may be explained by a change in the expression of membrane channels and/or medullar plasticity and/or hypersensitization of peripheral sensory receptors induced by this acute deafferentation. Additional studies are needed to further elucidate the mechanisms.