Title : When fatigability misleads: Acute cerebellar stroke masquerading as myasthenia gravis exacerbation
Abstract:
Background: Exacerbations of Myasthenia Gravis (MG) commonly present with fluctuating weakness and fatigability, often triggered by infection. However, reliance on this pattern may obscure alternative neurologic diagnoses. Distinguishing MG exacerbation from central nervous system pathology is critical, particularly when atypical features are present.
Case Presentation: A 64-year-old man with seropositive MG (on pyridostigmine, prednisone, and azathioprine), type 2 diabetes mellitus, hyperlipidemia, and chronic oropharyngeal dysphagia presented with 12 hours of generalized weakness and vomiting. On admission, his extremity weakness was consistent with prior documented MG baseline. Initial evaluation, including head CT, was unremarkable. Chest imaging revealed a left lower lobe opacity concerning for pneumonia, and he was started on broad-spectrum antibiotics. Respiratory parameters, including negative inspiratory force (-60 cm H?O) and single breath count, were within normal limits.
Despite appropriate therapy, the patient reported progressive right upper extremity weakness and difficulty maintaining head posture. Neurologic examination revealed bilateral fatigability but also asymmetric weakness (left greater than right) and hyperreflexia with clonus in the left lower extremity—findings atypical for MG. Cranial nerve examination was largely unchanged from baseline, without new ptosis or bulbar compromise.
Given concern for a central process, brain MRI was obtained and demonstrated a large left cerebellar lesion with mass effect on the fourth ventricle and brainstem, along with a small acute/subacute left parieto-occipital infarct. Initial differential included posterior fossa mass versus subacute hemorrhagic stroke. After multidisciplinary review, findings were determined to be most consistent with an acute ischemic stroke with hemorrhagic conversion. The patient was managed conservatively with corticosteroids and close neurologic monitoring in the intensive care unit. No neurosurgical intervention was required. He was discharged with outpatient neurology follow-up.
Discussion: This case highlights a diagnostic pitfall in patients with known MG, where baseline weakness and infection-triggered symptoms may anchor clinicians toward exacerbation. The presence of asymmetric weakness, upper motor neuron signs (hyperreflexia, clonus), and preserved respiratory function should prompt evaluation for alternative diagnoses. Posterior fossa strokes, particularly those with hemorrhagic conversion, may present subtly but carry significant risk due to mass effect and brainstem compression.
Conclusion: In patients with MG presenting with worsening weakness, clinicians must maintain a broad differential and remain vigilant for red flag features inconsistent with neuromuscular junction pathology. Early neuroimaging is essential when focal or upper motor neuron signs are present, as timely recognition of stroke can significantly alter management and outcomes.
