BackgroundGuillain-Barré syndrome (GBS) can be difficult to recognise in advanced untreated HIV, particularly where cerebrospinal fluid analysis and electrophysiology are unavailable.MethodsWe retrospectively reviewed adults with advanced HIV who were not receiving antiretroviral therapy and presented with acute symmetrical weakness at an Indian HIV specialty centre during 2019-2020. Cases were classified as clinically probable GBS with Brighton Collaboration level 3 diagnostic certainty.ResultsEight cases were identified among 139 admissions (5.8%). Mean CD4 count 78 cells/mm3. All eight had multiple concurrent infectious conditions. Herpesvirus-associated syndromes included ulcerative oesophagitis compatible with a herpesvirus-associated process (n=5), antecedent herpes zoster (n=2), or diarrhoeal illness with supportive CMV IgG serology (n=1). Seven recovered after multimodal treatment; one died.ConclusionsThis repeated clinical pattern of coexistence is hypothesis-generating but does not establish active viral reactivation, directionality, or causality. Pragmatic syndromic recognition and treatment remain necessary when definitive diagnostics are unavailable.

Diaphragm dysfunction includes diaphragmatic eventration, weakness, and paralysis, a set of disorders which are often challenging to diagnose clinically due to their varied presenting symptoms including dyspnea, positional orthopnea, cough, or even chest pain. Given the clinical challenge in diagnosing these conditions, diaphragm dysfunction is often suggested incidentally on initial imaging for workup of these symptoms. Imaging can play an important role both in raising the initial suspicion for diaphragm dysfunction as well as in making the diagnosis through real-time evaluation of the diaphragm's function. This document focuses on the initial imaging of suspected diaphragm dysfunction to confirm the diagnosis and evaluate for underlying leading to the dysfunction. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed annually by a multidisciplinary expert panel. The guideline development and revision process support the systematic analysis of the medical literature from peer reviewed journals. Established methodology principles such as Grading of Recommendations Assessment, Development, and Evaluation or GRADE are adapted to evaluate the evidence. The RAND/UCLA Appropriateness Method User Manual provides the methodology to determine the appropriateness of imaging and treatment procedures for specific clinical scenarios. In those instances where peer reviewed literature is lacking or equivocal, experts may be the primary evidentiary source available to formulate a recommendation.

Extravascular infiltration of neuromuscular blocking drugs (NMBDs) is a perioperative complication that may result in delayed and recurrent paralysis due to gradual systemic absorption from subcutaneous tissue. We report the case of a 64-year-old female who experienced inadvertent peripheral intravenous infiltration (PIV) during intraoperative administration of vecuronium and rocuronium. Following routine reversal with sugammadex, she developed recurrent episodes of respiratory compromise and profound weakness in the post-anesthesia care unit, consistent with delayed absorption of the extravasated NMBD. Each episode resolved promptly after repeat intravenous administration of sugammadex. This case highlights the unpredictable clinical course of NMBD extravasation and demonstrates that recurrent paralysis may occur despite initial successful reversal, requiring quantitative neuromuscular monitoring, extended postoperative observation, and administration of repeat doses of sugammadex as delayed systemic absorption occurs.

Necrotizing myopathy typically presents with subacute symmetric proximal weakness and marked creatine kinase elevation. Acute areflexic paraparesis with sensory abnormalities may instead suggest Guillain-Barré syndrome and create uncertainty regarding neuromuscular localization. A man in his 50s presented after collapse with abrupt bilateral lower-extremity paralysis. Examination demonstrated 0/5 strength across proximal and distal lower-extremity muscle groups, marked rigidity and hypercontracture, areflexia, and sensory impairment, with preserved upper-extremity function. Early laboratory abnormalities included serum sodium 164 mmol/L, potassium peaking at 6.5 mmol/L, creatinine 4.96 mg/dL, blood urea nitrogen 194 mg/dL, creatine kinase greater than 60,000 IU/L, and marked aminotransferase elevations. Lumbar puncture on hospital day (HD) 3 showed cerebrospinal fluid protein 70 mg/dL, glucose 66 mg/dL, and fewer than one nucleated cell/mm3. Guillain-Barré syndrome remained an early consideration; intravenous immunoglobulin was administered, and hemodialysis was initiated for severe hyperkalemia in the setting of acute renal failure. Inpatient electromyography and nerve conduction studies were unavailable; therefore, a concurrent neuropathic process could neither be confirmed nor excluded. Bilateral thigh magnetic resonance imaging demonstrated diffuse intramuscular edema, and right-thigh biopsy subsequently established a necrotizing myopathic pattern with frequent necrotic and regenerating myofibers and sparse inflammation. The biopsy pattern was etiologically nonspecific, and the underlying cause remained unresolved. This case illustrates that areflexia and cerebrospinal fluid albuminocytologic dissociation should not override substantial biochemical, radiographic, and histopathologic evidence of muscle injury. In patients with acute paralysis and massive creatine kinase elevation, neuropathic and myopathic processes should be evaluated in parallel.

Guillain-Barré syndrome (GBS) is an acute immune-mediated peripheral neuropathy characterized by rapidly progressive symmetric limb weakness and diminished tendon reflexes, which may be complicated by respiratory muscle paralysis in severe cases. Current first-line treatments primarily consist of intravenous immunoglobulin (IVIg) and plasma exchange (PE), but approximately 20% of patients have an incomplete response to standard therapies. Additionally, issues such as limited supply of blood products, adverse reactions, and contraindications may limit conventional treatments. Efgartigimod alfa is an engineered human IgG1 Fc fragment that targets the neonatal Fc receptor (FcRn) and competitively inhibits FcRn-mediated lgG recycling, thereby promoting the lysosomal degradation of circulating IgG, including pathogenic IgG autoantibodies, and reducing serum IgG levels. Intravenous efgartigimod alfa is approved for AChR antibody-positive generalized myasthenia gravis (gMG), whereas the U.S. approval for chronic inflammatory demyelinating polyneuropathy (CIDP) applies to the subcutaneous efgartigimod alfa/hyaluronidase co-formulation. Neither formulation is currently approved for GBS. Because IgG-mediated autoimmunity contributes to the pathogenesis of a subset of GBS, FcRn blockade provides a biologically plausible therapeutic strategy; however, its relevance may vary according to the underlying immunopathology. This narrative review summarizes the mechanistic rationale, preliminary clinical evidence, and available safety observations regarding efgartigimod in GBS, critically evaluates the limitations of the current evidence, and discusses unresolved questions and priorities for future research.

Thyrotoxic periodic paralysis (TPP) is a reversible but potentially severe complication of thyrotoxicosis characterized by acute muscle weakness and hypokalemia resulting predominantly from intracellular potassium redistribution. Although classically associated with Asian populations, TPP is increasingly recognized in Latin America. We report a 38-year-old Colombian man with recurrent nocturnal proximal quadriparesis, preserved deep tendon reflexes, serum potassium of 2.3 mEq/L, and biochemical thyrotoxicosis secondary to Graves disease. In parallel, we conducted a structured review of published Colombian cases identified through searches of PubMed/MEDLINE, Scopus, Web of Science, SciELO, and Google Scholar from inception through 1 May 2026. Fourteen previously published cases were identified, yielding 15 cases including the index patient. All patients were male, with a mean age of 31.4 ± 7.4 years. Deep tendon reflexes were normal in 4/13 (30.8%) cases in which they were documented, demonstrating that preserved reflexes do not exclude TPP. TSH was suppressed below 0.05 mIU/L in 14/15 (93.3%) patients. Electrocardiographic findings were reported in only 7/15 cases, and antithyroid drug doses in 6/15, highlighting substantial heterogeneity in reporting. All reported patients recovered muscle strength following acute management. TPP should therefore be considered in patients presenting with acute proximal weakness and hypokalemia even when deep tendon reflexes are preserved or overt manifestations of thyrotoxicosis are absent. Standardized reporting of biochemical, electrocardiographic, therapeutic, and follow-up data is needed to improve characterization of TPP in underrepresented populations.

Distal renal tubular acidosis (dRTA) is associated with autoimmune disorders, particularly Sjögren's syndrome. Hypokalemic muscle weakness due to dRTA is an uncommon presentation of Sjögren's syndrome and may mimic primary hypokalemic periodic paralysis, resulting in a diagnostic delay. We present the case of a 35-year-old woman who reported recurrent limb weakness in the presence of hypokalemia (serum potassium: 2.7 mmol/L). She had previously been diagnosed with primary hypokalemic periodic paralysis, but this diagnosis was challenged as she was found to have normal anion gap metabolic acidosis and an alkaline urine pH with significant potassium wasting. The patient reported the presence of subtle sicca symptoms only on direct questioning. Further workup revealed positive serology for Sjögren's syndrome. She was managed with potassium and sodium bicarbonate replacement and given oral steroids and azathioprine for long-term management. Following correction of electrolyte abnormalities, the patient's muscle strength improved significantly, and she regained functional mobility. Her metabolic acidosis also resolved, and she experienced no further episodes of weakness or electrolyte imbalance during 12 months of follow-up. Primary Sjögren's syndrome-associated distal RTA should be considered in patients presenting with recurrent hypokalemic paralysis, particularly in the presence of normal anion gap metabolic acidosis and alkaline urine pH. Early treatment prevents recurrent paralysis and long-term renal complications.

Hypokalemic periodic paralysis (HypoPP) is an inherited skeletal muscle ion channelopathy of CACNA1S or SCN4A characterized by recurrent episodes of weakness, often triggered by rest after exercise or by reduced K+ (carbohydrate ingestion, stress). Here, we describe a multigenerational family in whom a KCNA7 missense variant [c.834A>C (p.Arg278Ser)] co-segregated with susceptibility to recurrent attacks of weakness in association with hypokalemia as low as 1.3 mEq/L and a 40% decrement of the compound muscle action potential after exercise, suggesting an additional HypoPP gene. Arg278 is the outermost positively charged residue (R1) within the S4 transmembrane segment of the voltage-sensor domain of K V 1.7, orthologous to the canonical patten of arginine missense mutations at R1 or R2 in S4 segments for HypoPP-mutant Ca V 1.1 and Na V 1.4 channels. To determine the functional consequences of Arg278Ser, we expressed wild-type and mutant K V 1.7 channels in Xenopus oocytes and HEK293 cells. Arg278Ser, but not wild-type K V 1.7, generated an anomalous inwardly rectifying current at hyperpolarized membrane potentials that was nonselective Na [+] or K [+] , consistent with the anomalous gating pore conductance that causes susceptibility to HypoPP. Other pathogenic variants of KCNA7 have previously been implicated only in inherited cardiac arrhythmias. Collectively, the genetic, structural and electrophysiological findings support KCNA7 Arg278Ser as a pathogenic variant underlying HypoPP and implicate KCNA7 as a disease gene for periodic paralysis, extending the established gating-pore mechanism of HypoPP to K V 1.7.

Parapharyngeal infections may result in a pseudoaneurysm of the internal carotid artery, a rare but potentially fatal condition. Early recognition and multidisciplinary management are crucial to avoid catastrophic outcomes. We present a case of a twenty-two-year-old man with a parapharyngeal abscess complicated by an internal carotid artery pseudoaneurysm. The patient presented with painful left neck swelling, fever, dysphagia, and hoarseness. Examination revealed oropharyngeal asymmetry, ipsilateral vocal cord paralysis, and shoulder weakness findings consistent with jugular foramen syndrome. Imaging demonstrated a parapharyngeal abscess with a surrounding hematoma encasing the distal internal carotid artery, which appeared aneurysmal and was confirmed as pseudoaneurysm. Despite appropriate antibiotic therapy, the patient's neck pain progressively worsened, and repeat imaging demonstrated enlargement of the lesion. Urgent endovascular coil embolization was successfully performed. The patient was discharged on the second postoperative day and remained neurologically stable at six-month follow-up, with radiological improvement. Carotid pseudoaneurysm secondary to deep neck infection is exceedingly rare. Infection may spread from the parapharyngeal space to the carotid sheath, causing progressive arterial wall erosion. Early identification is crucial, as rupture carries high mortality without intervention. Recent evidence supports endovascular management as a safe and effective alternative to open surgery, particularly for lesions involving the skull base or petrous segment, where surgical exposure is hazardous. This case underscores that deep neck infections presenting with cranial neuropathies or opioid-refractory pain warrant prompt vascular imaging, and that endovascular occlusion represents a safe and effective treatment when collateral circulation is sufficient.

Acute otitis media (AOM) is a common infection, whereas peripheral facial nerve palsy is an uncommon extracranial complication in the post-antibiotic era. We report the case of a 53-year-old immunocompetent man who developed acute suppurative otitis media complicated by ipsilateral peripheral facial nerve palsy following an upper respiratory tract infection. The illness began with sore throat and cough during Hajj and progressed to severe right-sided otalgia, followed by complete right lower motor neuron facial weakness despite sequential empirical oral antibiotics. On return to Pakistan, otoscopy demonstrated a bulging, pulsating opaque tympanic membrane. Laboratory investigations revealed neutrophilic leukocytosis with normal glycated hemoglobin. Computed tomography of the temporal bones showed acute right oto-mastoiditis with middle ear opacification, an air-fluid level within the mastoid, and subtle possible erosive change along the lateral facial nerve canal without intracranial extension. The patient was treated conservatively with intravenous ceftriaxone, oral corticosteroids, and early structured facial physiotherapy. Facial nerve function improved by approximately 70% within 10 days and recovered completely by day 25 without surgical intervention. This case highlights the importance of recognizing facial nerve palsy as a rare but potentially reversible complication of AOM. It also emphasizes the increased burden of upper respiratory tract infections during mass gatherings and the need for early otologic and neurological evaluation in pilgrims presenting with persistent otalgia or new facial asymmetry to facilitate timely treatment and favorable outcomes.

A 56-year-old man with a family history of myopathy developed generalized muscle weakness at age 45. At age 52, he was diagnosed with inclusion-body myopathy with Paget disease of bone and frontotemporal dementia (IBMPFD), confirmed by muscle pathology and a pathogenic VCP mutation (c.464G>A, p.R155H). Concurrent testing identified a heterozygous SCN4A variant (c.215C>T, p.P72L), a known modifier in myotonic dystrophy type 2 (DM2). At age 56, neurological examination showed proximal muscle weakness (MMT grade 3), distal lower extremity weakness (grade 4-5), and areflexia. He ambulated independently with knee locking, though squatting was impossible. No myotonia or periodic paralysis was observed. Multimodal imaging captured classic IBMPFD hallmarks: skeletal muscle computed tomography (CT) showed advanced fatty degeneration of paraspinal and limb muscles; brain magnetic resonance imaging (MRI) revealed mild frontal lobe atrophy; and bone scintigraphy showed increased uptake in the lumbar spine and iliums. Although the SCN4A p.P72L variant exacerbates DM2, the patient's three-year progression from independent walking to cane use remained consistent with the natural history of IBMPFD. This case suggests that in the presence of a robustly penetrant VCP phenotype, the SCN4A variant does not necessarily exert a clinical modifying effect.