Chronic inflammatory demyelination polyradiculoneuropathy (CIDP), the most common chronic inflammatory neuropathy—though still rare overall—is an autoimmune demyelinating neuropathy that causes at least two months of progressive, monophasic, or relapsing-remitting weakness and sensory symptoms. Most patients have “typical” CIDP with symmetric proximal and distal weakness, sensory loss, and areflexia. Atypical variants include A-CIDP, sensory-predominant CIDP, motor CIDP, multifocal forms such as multifocal-acquired demyelinating sensory and motor polyneuropathy/Lewis–Sumner syndrome, and distal acquired-demyelinating polyneuropathy. Prevalence is low (about 0.7–7.7 per 100,000), and the distribution of variants varies by region. Misdiagnosis is frequent—especially in variants—and practice patterns differ, with many clinicians still unfamiliar with the 2021 European Federation of Neurological Societies/Peripheral Nerve Society guidelines.

This review outlines a structured, guideline-based diagnostic approach that relies on clinical features plus electrodiagnostic evidence of demyelination, with cerebrospinal fluid studies, monoclonal protein testing, antibody panels, imaging, and occasionally nerve biopsy as supportive tools. The 2021 criteria collapse certainty into “CIDP” and “possible CIDP,” acknowledging the lack of a gold standard and providing variant-specific differentials. First-line treatment for typical and many atypical forms centers on intravenous immunoglobulin, corticosteroids, or plasma exchange, with response tracked using validated disability and impairment scales. Recognizing the different phenotypes and their mimics is critical to avoiding misdiagnosis and using immunotherapy appropriately.

Reference: Roman-Guzman RM, Martinez-Mayorga AP, Guzman-Martinez LD, Rodriguez-Leyva I. Chronic Inflammatory Demyelinating Polyneuropathy: A Narrative Review of a Systematic Diagnostic Approach to Avoid Misdiagnosis. Cureus. 2025 Jan 1;17(1):e76749. doi: 10.7759/cureus.76749.

Myasthenia gravis (MG) is an autoimmune neuromuscular junction disorder causing painless, fluctuating, fatigable weakness—most often starting with ptosis and binocular diplopia, and progressing to bulbar, limb, and sometimes respiratory involvement. It has an incidence up to approximately 30 million person-years and prevalence of 150 to 250 million, with early-onset disease predominating in younger women and late-onset in older men. Disease heterogeneity is defined by distribution of weakness (ocular vs generalized), antibody, age at onset, and thymic pathology. Diagnosis relies on recognizing fatigable patterned weakness, confirming antibodies when present, demonstrating impaired neuromuscular transmission on repetitive nerve stimulation or single-fiber EMG, and imaging the chest for thymoma.

Treatment targets “minimal manifestation status” using pyridostigmine for symptomatic relief plus immunotherapy. Intravenous immunoglobin and plasma exchange are used for crisis, perioperative optimization, or bridging. Thymectomy is mandatory for thymoma and recommended for many younger patients with nonthymomatous AChR-positive generalized MG. Newer biologics and FcRn inhibitors offer faster, targeted control for refractory disease. Special considerations apply to ocular MG, pregnancy, myasthenic crisis, and checkpoint inhibitor–associated MG, but with timely, tailored therapy, most patients can achieve good long-term outcomes and near-normal life expectancy.

Reference: Juel VC. Autoimmune Myasthenia Gravis. Continuum (Minneap Minn). 2025 Oct;31(5):1270–1302.

Myasthenia gravis (MG) is a chronic neuromuscular disease that causes fluctuating muscle weakness. It often starts with drooping eyelids and double vision and sometimes progresses to difficulties with speaking, chewing, swallowing, breathing, and everyday activities like climbing stairs. Most people with generalized MG have detectable antibodies against structures at the neuromuscular junction, but some have “seronegative” MG, where antibodies aren’t found even though symptoms are the same. In ocular MG, weakness is limited to the eye muscles, causing ptosis and diplopia, and in some people this later generalizes.

In children, MG can appear in several ways. Transient neonatal MG affects some babies born to mothers with MG when maternal antibodies cross the placenta. Symptoms such as poor feeding, weak cry, and breathing difficulty usually resolve over weeks to months as these antibodies clear. Congenital MG is not autoimmune but genetic, and it can appear from birth through childhood with MG-like weakness. Juvenile MG begins before age 18 and may start subtly with eyelid drooping and double vision, sometimes progressing to more generalized fatigue and swallowing difficulties. Understanding these types can help patients, families, and caregivers recognize symptoms earlier and work with healthcare providers on appropriate management and support.

Reference: MG United. Understanding the six types of myasthenia gravis. MG United US Global. Published April 2022. Accessed December 11, 2025. https://www.mg-united.com/disease-and-treatment/the-six-types-of-myasthenia-gravis