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It's called Mast Cell Activation Syndrome (MCAS). The most frequent comorbidity of #MCAS is #POTS. Both POTS/#dysautonomia and MCAS are pathophysiologic mechanisms of #LongCOVID.

Dr. Svetlana Blitshteyn Published 05 Oct 2026 Relevancy: 85%

It's called Mast Cell Activation Syndrome (MCAS). The most frequent comorbidity of #MCAS is #POTS . Both POTS/ #dysautonomia and MCAS are pathophysiologic mechanisms of #LongCOVID . Tove Harris 🕊😷 (@NFMai) COVID-19 linked to increased risk of six allergic conditions in children and adults: atopic dermatitis, asthma, food allergy, rhinoconjunctivitis, medication allergy, urticaria. emjreviews.com/allergy-immun… Link COVID-19 Linked to Increased Risk of Six Allergic Conditions COVID-19 was associated with increased allergic disease risk over 18 months, with differing findings in children and service members. emjreviews.com — https://x.com/NFMai/status/2106760404462403807#m

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Small Fiber Neuropathy

PubMed - small fiber neuropathy Published 02 Oct 2026 Relevancy: 80%

OBJECTIVE: Small fiber neuropathy is a common disorder; however, its diagnosis and treatment can be challenging. This article outlines the pain pathways involved in small fiber neuropathy and provides an overview of its various causes, diagnostic tools, and therapeutic interventions.

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Chronic Inflammatory Demyelinating Polyradiculoneuropathy

PubMed - autoimmune encephalitis AND misdiagnosis Published 02 Oct 2026 Relevancy: 82%

OBJECTIVE: This article describes the cardinal clinical, electrophysiologic, and supportive features of typical CIDP and its variants, how to review and apply CIDP diagnostic criteria, objective measures that can be used in practice to follow patients with CIDP, and current and emerging treatment practices.

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RT by @ZacharyGrinDPT: Here I outline principles evidence-based medicine, my lived experience, the mess with NICE #mecfs guidance @NICEComms and impacts on #longcovid guidance https://paulgarner.co.uk/sirpa-conference/

Zachary Grin Published 30 Sep 2026 FND proponent source Relevancy: 85%

Here I outline principles evidence-based medicine, my lived experience, the mess with NICE #mecfs guidance @NICEComms and impacts on #longcovid guidance paulgarner.co.uk/sirpa-confe… Link SIRPA Conference - Paul Garner In May 2025, an Association of practitioners of mind-body medicine, SIRPA, invited me to talk about my post-covid-19 condition and controversies in the field. The video is available here. paulgarner.co.uk

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Air pollution and the risk of multiple sclerosis relapses in the Paris region, the CONFISEP study

Journal of Neurology, Neurosurgery & Psychiatry - Online First Published 30 Sep 2026 Relevancy: 48%

Background Air pollution has been proposed as a short-term trigger of multiple sclerosis (MS) relapses, but delayed effects remain poorly studied in the era of modern disease-modifying therapies (DMTs). We investigated whether weekly air pollution exposure was associated with delayed MS relapse risk up to 15 weeks. Methods We conducted a bicentric retrospective cohort study in the Île-de-France region (2018–2021) including adults with relapsing MS from the Observatoire Francais de la Sclérose en Plaques registry. Weekly exposure to particulate matter (PM)10, PM2.5, nitrogen dioxide (NO2) and ozone (O3) was estimated using Airparif street-level modelling data. Associations (lags 0–15 weeks) were assessed using self-controlled case series and cohort analyses adjusted for time-varying DMTs, disease duration, number of relapses during the previous year, respiratory infections, temperature, sunlight exposure, lockdown and holiday periods and additionally for age, sex, deprivation index and urbanicity in cohort analyses. Results Among 1152 patients (73.6% women; median age 37 years), 898 relapses occurred (0.20/patient-year). In self-controlled analyses, PM10 exposure was associated with increased relapse risk at 2-week (incidence rate ratio (IRR) 1.28, 95% CI 1.05 to 1.57) and 11-week lags (IRR 1.26, 95% CI 1.02 to 1.54), PM2.5 exposure was associated with increased risk at 2-week (IRR 1.20, 95% CI 1.03 to 1.39), while NO2 exposure was associated with increased risk at 2-week (IRR 1.21, 95% CI 1.02 to 1.44), 3-week (IRR 1.26, 95% CI 1.04–1.52) and 12-week lags (IRR 1.32, 95% CI 1.12 to 1.56). Cohort analyses showed similar but weaker associations for PM10 and PM2.5. DMTs were strongly associated with lower relapse risk, with effect sizes greater than those observed for air pollution exposure. Conclusions Weekly exposure to PM10, PM2.5 and NO2 was associated with increased MS relapse risk over delayed time windows ranging from 2– 3 weeks to 11–12 weeks. These temporal windows should be considered exploratory given the multiple lag-specific analyses. DMTs remained the strongest determinants of relapse risk. Trial registration number NCT05033782.

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PABPN1 pathogenic expansion in the UK Biobank: reframing genetic prevalence of oculopharyngeal muscular dystrophy

Journal of Neurology, Neurosurgery & Psychiatry - Online First Published 30 Sep 2026 Relevancy: 66%

Background Oculopharyngeal muscular dystrophy (OPMD) is a rare, late-onset, mostly autosomal dominant muscular dystrophy caused by a trinucleotide GCN repeat expansion in PABPN1 . OPMD affects approximately 1:100 000 individuals in Europe, with substantially higher prevalence in specific founder populations. Pathogenic alleles encoding 12–18 alanine residues within the first exon show dosage effect, incomplete dominance and expression variability. The (GCN)11 allele has a prevalence of 1%–2% in the European population and is considered pathogenic in homozygosity. Conversely, heterozygous carriers might display mild, late-onset phenotypes, suggesting reduced penetrance. Methods We investigated whole exome sequencing data from 470 000 individuals in the UK Biobank cohort, by extracting PABPN1 rare (Minor Allele Frequency (MAF) < 0.001) coding (NM_004643.3) variants and focusing on the polyalanine tract. Demographic data and neuromuscular International Classification of Diseases, Tenth Revision (ICD-10) codes were collected. Results We identified 46 individuals with a genotype compatible with OPMD: 35 with a (GCN)12 genotype, 10 with a (GCN)13 genotype and 1 with a homozygous (GCN)11 genotype. In addition, 1896 individuals were heterozygous carriers of the (GCN)11 allele. The majority of (GCN)11 carriers did not present OPMD-compatible diagnostic codes, while OPMD-compatible diagnostic codes occurred in 11.4% of (GCN)12 carriers and rose to 70% of (GCN)13 carriers, showing a positive correlation between polyalanine tract length and clinical expression. Conclusions The cumulative genetic prevalence of pathogenic expansion was 1:10 200, 10 times higher than the estimated clinical prevalence. This analysis is relevant in the context of emerging therapeutic strategies targeting the PABPN1 polyalanine expansion.

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Beyond a single biomarker: a milestone toward precision medicine in aneurysmal subarachnoid haemorrhage

Journal of Neurology, Neurosurgery & Psychiatry - Online First Published 30 Sep 2026 Relevancy: 37%

HeMoVal demonstrates that CSF hemoglobin alone is insufficient for reliable real-time monitoring of secondary brain injury after aSAH. Its major legacy may therefore be the transition from single biomarkers toward multiparametric biological signatures and biomarker-guided precision therapies. The search for reliable biomarkers capable of predicting and monitoring secondary brain injury (SBI) after aneurysmal subarachnoid haemorrhage (aSAH) has been one of the major challenges in neurocritical care over the past decade.1–3 The HeMoVal (Haemoglobin Monitoring after Subarachnoid Haemorrhage Validation) study represents, in my view, an important milestone in this field, prospectively evaluating cerebrospinal fluid haemoglobin (CSF-Hb) in a large international multicentre cohort using a rigorous preregistered design. Such methodological strength is still uncommon in biomarker research and substantially increases the credibility and translational relevance of its findings. Perhaps the most important contribution of HeMoVal is not simply the validation or lack thereof of previous observations, but...

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Hereditary spastic paraplegia: a practical approach

Practical Neurology - Online First Published 30 Sep 2026 Relevancy: 82%

Hereditary spastic paraplegia (HSP) comprises a clinically and genetically diverse group of inherited neurodegenerative disorders unified by slowly progressive, usually symmetrical lower-limb spasticity secondary to corticospinal tract degeneration. For practising neurologists, the first step is recognising when a presentation is consistent with HSP and when it is not, and then carefully excluding treatable causes. We outline a pragmatic approach to assessing HSP, highlighting the broad clinical spectrum, ‘red flags’ that should trigger re-evaluation and the common acquired and genetic mimics. We summarise the relevant clinical and supportive investigations that can narrow the differential diagnosis. We also discuss the strengths and limitations of contemporary genetic testing. Finally, we focus on practical management: multidisciplinary care, spasticity treatments, and proactive recognition and management of additional symptoms outside of spasticity.

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Nocturnal behaviours, stridor and recurrent respiratory failure in anti-IgLON5 disease

Practical Neurology - Online First Published 29 Sep 2026 Relevancy: 93%

Anti-IgLON5 disease is a rare autoimmune encephalopathy with concurrent tauopathy, characterised by sleep dysfunction and brainstem involvement. A 77-year-old woman developed obstructive sleep apnoea and recurrent hypercapnic respiratory failure requiring repeated intubation, initially misdiagnosed as epilepsy. Video recordings captured elaborate nocturnal behaviours, including praying and offering alms during sleep, alongside inspiratory stridor and sleep attacks during eating. Serial polysomnography documented progressive loss of sleep spindles and undifferentiated non-rapid eye movement sleep. Brain imaging showed only mild cortical, cerebellar and brainstem atrophy. She had anti-IgLON5 antibodies in serum and cerebrospinal fluid. Her condition partially improved after intravenous methylprednisolone and then rituximab, and she remains under follow-up. Patients with treatment-resistant sleep-disordered breathing, laryngeal dysfunction and nocturnal motor behaviours should be tested for anti-IgLON5 disease.

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RT by @ZacharyGrinDPT: The interview with UK doctor Dr Anna Smith talking about her recovery from chronic fatigue is now sitting at over 450k views. Just brilliant. https://youtu.be/8JaOgnHWeZg?si=QJLqytx6JSfygotQ via @YouTube

Zachary Grin Published 28 Sep 2026 FND proponent source Relevancy: 65%

The interview with UK doctor Dr Anna Smith talking about her recovery from chronic fatigue is now sitting at over 450k views. Just brilliant. inv.kareem.one/8JaOgnHWeZg?si=QJLq… via @YouTube Link A Doctor Recovered From Chronic Fatigue. Here's What She Has Her... 👉 Get the key takeaways from the latest recovery interview in my FR... youtube.com

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