This review examines how chronic immune-mediated neuropathies, especially chronic inflammatory demyelinating polyneuropathy (CIDP), can occur alongside other autoimmune diseases, raising the possibility that some cases reflect broader systemic immune dysregulation rather than an isolated peripheral nervous system disorder. Reported CIDP associations include diabetes, thyroid disease, systemic lupus erythematosus, Sjögren’s syndrome, sarcoidosis, inflammatory bowel disease, celiac disease, autoimmune liver disease, nephrotic syndromes, myasthenia gravis, autoimmune hemolytic anemia, and idiopathic thrombocytopenic purpura. However, the authors emphasize that much of the evidence comes from case reports, small series, and tertiary-care cohorts, so many associations may be coincidental rather than causal.

The review highlights important diagnostic and management implications. In patients with chronic inflammatory neuropathies, clinicians may need to look for systemic autoimmune disease when symptoms, labs, or treatment response suggest a broader immune process. This is especially relevant in conditions such as diabetes, where diabetic neuropathy can complicate CIDP recognition, and autoimmune nodopathies, where antibodies against nodal/paranodal proteins may be linked with nephrotic syndrome or central nervous system demyelination and may respond poorly to intravenous immunoglobulin but potentially better to rituximab. The authors conclude that systematic screening may identify treatable comorbidities, but larger epidemiologic and mechanistic studies are needed before these reported overlaps can meaningfully guide routine treatment decisions.

Reference: Freiha J, Min YG, Rajabally YA, Osman C. The spectrum of autoimmune disorders in chronic immune-mediated neuropathies. Expert Rev Clin Immunol. 2026 Apr;22(4):393-405. doi: 10.1080/1744666X.2026.2641535.

In this video, Jeffrey Allen, MD, emphasizes that chronic inflammatory demyelinating polyneuropathy (CIDP) is heterogeneous, frequently misdiagnosed, and challenging to confirm because there is no single diagnostic test. Accurate diagnosis depends on matching the clinical picture with electrophysiologic evidence of peripheral nerve demyelination while carefully excluding mimics. Early recognition matters because disability can become substantial, and about half of patients may eventually lose the ability to live independently. Typical CIDP presents with relatively symmetric proximal and distal weakness and numbness progressing over at least two months, but distal, multifocal, sensory, and motor variants can complicate diagnosis.

For initial management, Dr. Allen recommends starting with evidence-based therapies such as immunoglobulin, corticosteroids, or plasma exchange, then closely assessing response over three to six months. Treatment response should be measured through patient-reported improvement, validated disability scales, and objective strength measures such as MRC strength scoring or handheld grip strength. If there is no clear improvement, clinicians should reassess the diagnosis before moving to another therapy, since lack of response may indicate the diagnosis is incorrect. When treatment works, the goal is to individualize therapy by adjusting dose and frequency to achieve the lowest effective, tolerable, and safe regimen, with newer options such as efgartigimod alfa potentially useful for patients who respond to immunoglobulin but struggle with its logistics or tolerability.

Reference: Allen J. Early diagnosis and management of chronic inflammatory demyelinating polyneuropathy (CIDP). Medscape. Published April 23, 2026. Accessed June 22, 2026. https://reference.medscape.com/viewarticle/cidp-first-line-treatment-adults-2026a1000909

This review outlines how hereditary spastic paraplegia (HSP) care has evolved from a largely symptom-based model to an emerging precision-medicine framework. Historically, diagnosis relied on clinical observation and family history, while treatment focused on managing spasticity, gait impairment, and secondary complications through medications, physical therapy, botulinum toxin, intrathecal baclofen, and select surgical approaches. However, evidence for many interventions remains limited by small, heterogeneous studies, inconsistent outcome measures, and a lack of validated biomarkers. Recent advances in next-generation sequencing, long-read sequencing, MRI, preclinical models, and multi-omics are improving genetic diagnosis, disease classification, and understanding of HSP pathophysiology.

The article also highlights the future direction of HSP care, including gene therapy, antisense oligonucleotides, drug repurposing, artificial intelligence, digital gait analysis, wearable sensors, telemedicine, patient registries, and digital twin technology. Early examples, such as AAV9-based therapy for SPG50 and allele-specific ASOs in KIF1A-associated disease, suggest that individualized treatments may be feasible for selected ultra-rare subtypes, though most remain experimental and require long-term safety monitoring. The authors conclude that while current HSP management is still dominated by symptomatic care, advances in genetics, biomarkers, digital health, and patient-centered outcomes are laying the groundwork for more personalized, data-driven, and potentially disease-modifying approaches.

Reference: Cipriano L, Angelini C, Maria Santorelli F. Hereditary spastic paraplegia: from decades of therapy to future innovations. Ther Adv Neurol Disord. 2026 Jan 12;19:17562864251406589. doi: 10.1177/17562864251406589.