Statin-associated myopathy represents a well-recognised adverse effect of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, ranging from myalgia to life-threatening rhabdomyolysis. Neurological involvement in the form of peripheral neuropathy mimicking Guillain-Barré syndrome (GBS) is rare and diagnostically challenging. We report a case of a 72-year-old man with diabetes mellitus, hypertension, and single-vessel coronary artery disease who underwent percutaneous transluminal coronary angioplasty (PTCA) and was initiated on atorvastatin 40 mg once daily as secondary prevention. Within two months of initiation, he developed myoglobinuria followed by rapidly evolving bilateral upper and lower limb weakness on admission. Peak creatine kinase (CK) was 48,000 U/L, with urine myoglobin exceeding 12,000 ng/mL. Nerve conduction studies demonstrated a lower-motor-neuron-type demyelinating sensorimotor polyneuropathy, while electromyography revealed a myopathic pattern. Although GBS was a primary diagnostic concern, cerebrospinal fluid analysis did not corroborate due to the absence of albuminocytologic dissociation. The patient was managed with statin discontinuation and aggressive intravenous fluid resuscitation. Myoglobinuria started to resolve by day two. At discharge, upper limb weakness had fully resolved, and lower limb power improved from 1/5 to 3/5, with CK declining to 8060 U/L. This case highlights that severe statin-associated rhabdomyolysis with mixed electrophysiological features of demyelinating polyneuropathy and myopathy can closely mimic GBS. The significant clinical improvement following statin withdrawal without immunomodulatory therapy favours a toxic neuromyopathic process over an immune-mediated aetiology, emphasising early recognition and prompt discontinuation of the offending agent to prevent complications and improve outcomes.

Guillain-Barre syndrome (GBS) is an acute immune-mediated polyneuropathy classically presenting with ascending lower limb weakness; however, rare regional variants may pose diagnostic challenges. We report a case of an unusual upper limb-predominant variant of GBS following a self-limiting diarrhoeal illness, presenting with acute shoulder pain, progressive bilateral hand paraesthesia and upper limb weakness without lower limb, bulbar or cranial nerve involvement. Neurological examination demonstrated proximal and distal upper limb weakness with upper limb hyporeflexia. Cerebrospinal fluid analysis revealed albumin-cytologic dissociation; anti-GM1 antibodies were positive; cervical spine MRI excluded structural pathology and nerve conduction studies confirmed an axonal motor neuropathy consistent with the acute motor axonal neuropathy variant of GBS. The patient was treated with a 5-day course of intravenous immunoglobulin alongside physiotherapy, resulting in gradual neurological recovery and functional improvement. This case emphasises the importance of recognising atypical regional presentations of GBS to facilitate timely diagnosis and prompt initiation of immunomodulatory therapy.

Background: Guillain-Barré syndrome (GBS) is an autoimmune peripheral neuropathy that can lead to paralysis and respiratory failure. In addition to infections, several drugs have been suggested as potential triggers of GBS. This study investigated drug-associated GBS using a spontaneous adverse event reporting database through disproportionality analysis for signal detection and time-to-onset analysis. Methods: The Japanese Adverse Drug Event Report (JADER) database was analyzed to assess more than 4000 drugs for potential associations with GBS. Signal detection was performed using reporting odds ratios, Fisher's exact test, and total report counts. For vaccines and immune checkpoint inhibitors, time-to-onset patterns were further evaluated using Weibull distribution analysis. Results: Disproportionality signals suggesting potential associations with GBS were identified for 45 drugs, including vaccines, immune checkpoint inhibitors, tumor necrosis factor-α inhibitors, other anticancer drugs, antifungal agents, and interferons. Reports following vaccination were most frequently observed within 1-3 weeks after administration of coronavirus disease 2019 (COVID-19), influenza, and pneumococcal vaccines, and within 1-3 months after human papillomavirus 2-valent vaccination, with a gradual decrease thereafter. Reports following immune checkpoint inhibitor use were most frequently observed 1-3 months after nivolumab, ipilimumab, and pembrolizumab administration, whereas atezolizumab showed a peak in reporting within 1-3 weeks. In contrast to vaccine-related reports, no clear temporal trend in reporting was observed. Conclusions: Drugs that modulate immune function, including vaccines and immune checkpoint inhibitors, may be associated with reported GBS events. Vaccine-related reports showed an early concentration in time to onset, whereas immune checkpoint inhibitor-related reports did not demonstrate a clear temporal pattern. These findings should be interpreted as hypothesis-generating and warrant further investigation.

A man in his 50s with poorly controlled diabetes and chronic kidney disease presented with rapidly progressive bilateral facial diplegia 1 week after hospitalisation for pneumonia. Examination demonstrated symmetric lower motor neuron facial weakness without limb involvement; reflexes were 1+ throughout. Brain and internal auditory canal MRI were unremarkable. Cerebrospinal fluid showed albuminocytologic dissociation (protein 151 mg/dL, WBC 3 /mm[3]). Serum antiganglioside antibody testing was positive for GM2 IgG at 72 IV. CSF infectious studies were positive for West Nile virus IgM (3.07) and IgG (2.81), confirming acute neuroinvasive infection during Missouri's 2025 outbreak. The patient was treated with intravenous immunoglobulin and showed progressive improvement in facial strength, eye closure and speech, with continued recovery at 4 weeks. This case emphasises West Nile virus as a potential precipitant of facial diplegic Guillain-Barré syndrome.

Acute immune system-mediated neuropathy, referred to as Guillain-Barré syndrome, is a common etiology of acutely acquired weakness that often presents with proximally spreading initial distal extremity weakness and paralysis. Less common manifestations include delayed facial nerve palsy and weakness, occurring in approximately 15% of patients. This case report highlights a rarer initial presentation of Guillain-Barré syndrome in a 43-year-old man initially presenting with unilateral upper facial weakness whose symptoms progressed to bilateral hand and foot numbness over a 2-week period.