Introduction/Aims: Chronic inflammatory demyelinating polyneuropathy (CIDP) may be rarely preceded by infection. A causative link remains unproven, in contrast to Guillain‐Barré syndrome (GBS), which is commonly postinfectious with well‐demonstrated pathophysiological mechanisms of molecular mimicry following Campylobacter jejuni enteritis. Uncommonly, infections are reported before the onset of CIDP. In this study we aimed to determine the frequency and characteristics of CIDP occurring after antecedent infections or vaccinations in two large European cohorts.Methods: We reviewed the records of 268 subjects with “definite” or “probable” CIDP from the Inflammatory Neuropathy Clinic, Birmingham, UK (129 subjects), and from the Serbian national CIDP database (139 subjects).Results: Twenty‐five of 268 (9.3%) subjects had a respiratory or gastrointestinal infection in the 6 weeks preceding CIDP onset, and 3 of 268 (1.1%) had received an influenza vaccination. CIDP disease onset occurred at a younger age (mean [standard deviation], 44.25 [17.36] years vs 54.05 [15.19] years; P < .005) and acute‐onset CIDP was more common (42.9% vs 12.1%; odds ratio, 5.46; 95% confidence interval, 2.35‐12.68; P < .001) in subjects with preceding infections or vaccinations. No differences in CIDP subtype, rates of cerebrospinal fluid protein level elevation, disability, or likelihood of treatment response, were observed.Discussion: Antecedent infections or vaccinations may precede about 10% of cases of CIDP and are more common in younger subjects. Acute‐onset CIDP is more frequent after antecedent events. These findings may suggest specific pathophysiological mechanisms in such cases.

Background: Spinal muscular atrophy type 3 (juvenile SMA, Kugelberg–Welander disease) is a genetic disease caused by changes in the survival motor neuron 1 (SMN) gene. However, there is increasing evidence of metabolic abnormalities in SMA patients, such as altered fatty acid metabolism, impaired glucose tolerance, and defects in the functioning of muscle mitochondria. Given that data in the literature are scarce regarding this subject, the purpose of this study was to estimate the prevalence of glucose and lipid metabolism disorders in adult patients with SMA type 3. Methods: We conducted a cross-sectional study of 23 adult patients with SMA type 3 who underwent a comprehensive evaluation, including a physical examination, biochemical analysis, and an oral glucose tolerance test during 2020–2023. Results: At least one lipid abnormality was observed in 60.8% of patients. All four lipid parameters were atypical in 4.3% of patients, three lipid parameters were abnormal in 21.7% of patients, and two lipid parameters were altered in 8.7% patients. A total of 91.3% of SMA3 patients met the HOMA-IR criteria for insulin resistance, with 30.43% having impaired glucose tolerance. None of the patients met the criteria for a diagnosis of overt DM2. Conclusions: The prevalence of dyslipidemia and altered glucose metabolism in our study sets apart the adult population with SMA3 from the general population, confirming a significant interplay between muscle, liver, and adipose tissue. Ensuring metabolic care for aging patients with SMA 3 is crucial, as they are vulnerable to metabolic derangements and cardiovascular risks.

Background: Recent literature data highlights metabolic changes in amyotrophic lateral sclerosis (ALS). To explore possible early metabolic changes, we aimed to analyse the fatty acids (FA) composition of erythrocytes in newly diagnosed als patients and to see whether fatty acid levels correlate with the ALSFRS-R score or disease duration. Methods: The severity of motor function involvement was assessed by the ALSFRS-R scale at the initial evaluation. The fatty acid profile of erythrocyte membranes was analysed by gas-liquid chromatography. The study comprised 26 clinically diagnosed als patients, with mean ALSFRS-R 38±8. The control group included 26 healthy volunteers. Results: Significantly higher levels of palmitic acid and total saturated FAs were detected in als patients. In als patients, total monounsaturated FA, palmitoleic, vaccenic, and oleic acid were also significantly increased. The levels of eicosapentaenoic acid, docosapentaenoic acid, total polyunsaturated FA (PUFA) and n-6 PUFA were significantly lower in als patients. Additionally, a-linolenic acid, the precursor of the n-3 PUFA family, was not detected in als patients. We found no significant correlation between the ALSFRS-R score and the abundance of individual FAs analysed. A moderate negative correlation was found between disease duration and DHA level, and a positive correlation was detected with MUFA. Conclusion: Experimental evidence presented may contribute to shaping a beneficial nutritional intervention.

Background and Aims: This study aimed to systematically phenotype autonomic nervous system (ANS) involvement in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), monoclonal gammopathy of undetermined significance‐associated neuropathy (MGUS‐PNP), Charcot–Marie–Tooth disease Type 1A (CMT1A), and hereditary neuropathy with liability to pressure palsies (HNPP). Methods: Autonomic symptoms were assessed using the SCales for Outcomes in Parkinson's Disease‐Autonomic Dysfunction (SCOPA‐AUT). Muscle strength and functional disability were evaluated using the Medical Research Council (MRC) scale, the Inflammatory Neuropathy Cause and Treatment (INCAT) disability scale, and the Overall Neuropathy Limitation Scale (ONLS). Results: A total of 343 participants were included: 98 with CIDP (mean age: 59.2 ± 13.2 years), 51 with MGUS‐PNP (66.0 ± 11.3 years), 51 with CMT1A (51.2 ± 13.1 years), 18 with HNPP (40.6 ± 15.1 years), and 125 healthy controls (58.2 ± 13.3 years). Compared with healthy controls, patients with CIDP, MGUS‐PNP, and CMT1A showed significantly higher total SCOPA‐AUT scores ( p < 0.01). Distinct, disease‐specific ANS symptom patterns were observed across neuropathy subtypes. Overall disability was independently associated with overall autonomic symptom burden in MGUS‐PNP ( β = 0.42, p < 0.05) and CMT1A ( β = 0.68, p < 0.05). In CIDP, patients with active disease showed higher autonomic symptom burden than those with inactive disease (12.7 ± 11.7 vs. 8.6 ± 7.9, p = 0.042). Interpretation: Patients with CIDP, MGUS‐PNP, and CMT1A exhibit a substantial autonomic symptom burden with distinct disease‐specific ANS patterns. These findings highlight the relevance of autonomic dysfunction in immune‐mediated and hereditary neuropathies and warrant further studies to clarify their clinical and prognostic significance.