Impact on quitting smoking of cognitive impairment in stroke patients.

INTRODUCTION: Smoking is a well-established risk factor for strokes, leading to a high incidence of cognitive deficits. Since the impact of cognitive impairment on the effectiveness of interventions for smoking cessation is not yet known, we considered important to assess it. METHODS: We compared, from April 2012 to November 2015, the success rate of quitting smoking in two groups of acutely hospitalised adult smokers. The first group consisted of stroke patients (SP, n = 54) with lesions confirmed by cerebral imaging. The second used as a control group (NSP, n = 38), included patients hospitalised for any reason other than stroke and characterised by normal global cognition. All participants were assessed twice, in acute phase (T0) and 3 months later (T1), using exhaled carbon monoxide (CO) and several questionnaires. RESULTS: At T1, we observed in SP group an inverse correlation between the Montreal Cognitive Assessment (MoCA) and CO (r = -0.33, p = 0.015). Amongst patients who continued smoking, a higher increase in CO between T0 and T1 was observed in SP group (average 20 ± 15, p < 0.001) than NSP (average 9 ± 13, p = 0.002). CONCLUSIONS: The inverse correlation between CO and cognitive parameters at T1 in SP group suggests an increased susceptibility to tobacco dependency in case of residual cognitive impairment. The global cognitive assessment should thus be taken into consideration when providing assistance with quitting smoking, especially in case of stroke patients.

Rituximab Responsive Relapsing-Remitting IgG4 Anticontactin 1 Chronic Inflammatory Demyelinating Polyradiculoneuropathy Associated With Membranous Nephropathy: A Case Description and Brief Review.

ABSTRACT: Nodal/paranodal IgG4-related chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) rarely involves anticontactin (CNTN1) subtype and exceptionally complicates with nephrotic syndrome. A 65-year-old man developed weakness, facial palsy, and balance impairment; after spontaneous recovery, he severely relapsed 1 month later. Electroneuromyography confirmed CIDP. Proteinorachy (462 mg/dL; N < 45), proteinuria (3.5 g/g creatine), and biopsy-proven membranous nephropathy were identified. Intravenous immunoglobulins, corticosteroids, and plasmaphereses did not allow recovery. Anti-CNTN1 immunoglobulin G4 (IgG4) assay was positive. Rituximab (375 mg/m2/week, 4 weeks) provided obvious improvement. Relapsing-remitting anti-CNTN1-CIDP co-occurring with nephrotic syndrome is exceptional, and its identification is essential because efficient therapies such as rituximab are available for this severe condition.

Contactin-1 is a novel target antigen in membranous nephropathy associated with chronic inflammatory demyelinating polyneuropathy.

Primary membranous nephropathy (MN) is an autoimmune glomerular disease in which autoantibodies are directed against podocyte proteins. In about 80% of cases the main targeted antigen is the phospholipase A2 receptor 1 (PLA2R1). Anti-PLA2R1 antibodies are mainly immunoglobulin G type 4 (IgG4). However, the antigenic target remains to be defined in 20% of cases. MN can be associated with chronic inflammatory demyelinating polyneuropathy, an autoimmune disease of the peripheral nervous system where a common antigenic target has yet to be identified. To ascertain a possible novel target antigen, we analyzed kidney biopsies from five patients positive for anti-contactin 1 antibodies and presenting with MN combined with chronic inflammatory demyelinating polyneuropathy. Eluted IgG from biopsy sections against contactin 1 and nerve tissue were screened. Western blot revealed contactin 1 expression in normal kidney glomeruli. Confocal microscopic analysis showed the presence and colocalization of contactin 1 and IgG4 on the glomerular basement membrane of these patients. Glomerular contactin 1 was absent in patients with anti-PLA2R1-associated MN or membranous lupus nephritis or a healthy control. The eluted IgG from contactin 1-positive biopsy sections but not the IgG eluted from patients with PLA2R1 MN bound contactin 1 with the main eluted subclass IgG4. Eluted IgG could bind paranodal tissue (myelinated axon) and colocalized with commercial anti-contactin 1 antibody. Thus, contactin 1 is a novel common antigenic target in MN associated with chronic inflammatory demyelinating polyneuropathy. However, the precise pathophysiology remains to be elucidated.

The characteristics of patients with bilateral absent evoked potentials after post-anoxic brain damage: A multicentric cohort study.

OBJECTIVES: Patients with bilateral absence of cortical response (N20ABS) to somatosensory evoked potentials (SSEPs) have poor neurological outcome after cardiac arrest (CA). However, SSEPs are not available in all centers. The aim of this study was to identify predictors of N20ABS. METHODS: Retrospective analysis of institutional databases (2008-2015) in three ICUs including all adult admitted comatose patients undergoing SSEPs between 48 and 72 h after CA. We collected clinical (i.e. absence of pupillary reflexes, PLR, myoclonus and absent or posturing motor response and myoclonus on day 2-3), electroencephalographic (EEG; i.e. unreactive to painful stimuli; presence of a highly malignant patterns, such as burst-suppression or flat tracings) findings during the first 48 h, and the highest NSE levels on the first 3 days after CA. Unfavorable neurological outcome (UO) was assessed at 3 months using the Cerebral Performance Categories of 3-5. RESULTS: We studied 532 patients with SSEPs, including 143 (27%) without N20ABS; UO was observed in 334 (63%) patients. Median time to SSEPs was 72 [48-72] h after CA. No patient with absent PLR and myoclonus during the ICU stay had N20 present; similar results were observed with the combination of absent PLR, myoclonus and any EEG pattern (i.e. unreactive or highly malignant). Similar results were observed in the subgroup of patients where NSE was available (n = 303). In a multivariate logistic regression, non-cardiac etiology of arrest, unreactive EEG to painful stimuli, absence of pupillary reflexes and posturing motor response, were independent predictors of N20ABS. When available, the highest NSE was also an independent predictor of N20ABS. CONCLUSIONS: Clinical and EEG findings predicting patients with N20ABS, confirm that N20ABS reflects a severe and permanent cerebral damage after CA.

Charcot-Marie-Tooth hereditary neuropathy revealed after administration of docetaxel in advanced breast cancer.

Charcot-Marie-Tooth (CMT) neuropathy is the most common hereditary cause of neuropathy. Diagnosis is usually not made during the childhood but in adolescence or late adulthood. It is reported in the literature that some neurotoxic chemotherapeutical agents can reveal an asymptomatic CMT IA hereditary neuropathy. To our knowledge, we report here the first case of CMT IA revealed in a 55-year-old woman after the administration of docetaxel/trastuzumab/pertuzumab for metastatic breast cancer. This case stresses again the necessity to obtain a complete personal and familial anamnesis and to perform a neurologic examination before the administration of neurotoxic chemotherapeutical agents to prevent the clinical expression of these hereditary neuropathies.

Evolution of clinical, electrophysiological, and radiological aspects of the carpal tunnel syndrome before and after surgery.

The aim of the study was to analyze the evolution of the clinical, electrophysiological, and ultrasound aspects of carpal tunnel syndrome (CTS) before and 4 and 8 weeks after surgery. A Boston Carpal Tunnel Questionnaire, an ultrasound scan, and an electrophysiological exam were performed in 14 patients the day of surgery, 4 and 8 weeks after. The nerve conduction study included: median nerve sensory conduction stimulating digit 3 and 4, median motor conduction from the abductor pollicis brevis, ulnar nerve sensory, and motor conduction. A significant improvement of the symptoms and a significant decrease of the median nerve proximal cross-sectional area on the ultrasound scan were observed 4 weeks after surgery. Distal motor latency (DML) was > 4.2 ms in six patients and decreased along the three visits. DML was ≤ 4.2 ms in the eight others and stayed stable after surgery. We observed a significant increase of the sensory median nerve amplitude response at the wrist stimulating the third digit 8 weeks after surgery. When operated patients are referred for control, we recommend to perform: (1) 4 weeks after surgery, an ultrasonography, and a measure of the DML of the median nerve; (2) 8 weeks after surgery, a measure of the sensory conduction velocity of the median nerve.

The Prognostic Value of 48-h Continuous EEG During Therapeutic Hypothermia After Cardiac Arrest.

BACKGROUND: The aim of this study was to evaluate the prognostic value of continuous electroencephalogram (cEEG) during the first 48 h following cardiac arrest (CA) in patients treated with targeted temperature management (TTM). METHODS: We reviewed data from 92 comatose post-CA patients over a 6 year-period; cEEG recordings were performed during TTM and restoration of normothermia. EEG findings were divided into four time-periods: 0-8, 8-16, 16-24, and 24-48 h after CA. Background EEG findings were defined as moderate encephalopathy (diffuse slowing with reactivity/variability), severe encephalopathy (diffuse slowing without reactivity/variability), burst suppression or suppression, and dichotomized as malignant (suppression/burst suppression/severe encephalopathy) or benign (moderate encephalopathy). Epileptiform activity was defined as the presence of seizures, sporadic epileptiform discharges, or periodic discharges. Neurological outcome was assessed at 3 months using the cerebral performance categories (CPC) score (good outcome: CPC 1-2). RESULTS: 26/92 (28%) patients had a good outcome. Malignant patterns were associated with a poor outcome at all time-points, with a high positive predictive value (94-97%) but a poor negative predictive value (44-56%). Epileptiform activity did not influence the prognostic value of EEG patterns. All patients with moderate encephalopathy and seizures or generalized periodic discharges had a poor outcome. CONCLUSIONS: cEEG can identify patients with poor outcome from the first hours following CA, with limited predictive value for good outcome. Epileptiform activity did not improve the prognostic accuracy of EEG, but seizures and generalized periodic discharges were associated with poor outcome even when developing on a benign EEG pattern.

Distal acquired demyelinating symmetric neuropathy associated with anti-GM1 antibodies: is this a CIDP variant?

Distal acquired demyelinating symmetric (DADS) neuropathy is clinically characterised by distal motor and sensory disturbances. Typically DADS does not respond or responds poorly to intravenous immunoglobulins (IVIg). We report the case of a 58-year-old patient who developed distal paraparesis. Serum electrophoresis demonstrated monoclonal IgM paraproteinemia having an anti-GM1 but no anti-MAG activity. Conduction velocities showed demyelinating pattern. Work-up excluded a lymphoproliferative disorder After IVIg treatment we observed a clinical and neurophysiological improvement. Regarding these peculiar findings, we suggest that DADS needs to be splitted in several forms determined among others by clinical, neurophysiological and antiganglioside profile and therapeutic response. We advocate to perform systematic antiganglioside antibodies assay additionnaly to anti-MAG when DADS is suspected in order to improve dysimmune neuropathies classification.