Seronegative Morvan Syndrome Presenting With Agrypnia Excitata and Peripheral Nerve Hyperexcitability: A Phenotype-Supported Diagnostic and Therapeutic Approach in a Resource-Limited Setting.

We report a 63-year-old Palestinian man with seronegative Morvan syndrome presenting with the complete clinical triad: continuous neuromyotonia with visible myokymia, severe insomnia consistent with agrypnia excitata phenotype (2-3 h/night; Insomnia Severity Index [ISI] 24/28, validated Arabic version), tachycardia (118 bpm), profuse diaphoresis, and 13-kg weight loss. Electromyography (EMG) demonstrated characteristic myokymic (40-150 Hz) and neuromyotonic (> 150 Hz) discharges across 12 muscles without denervation. Brain MRI, CSF analysis, and comprehensive malignancy screening were unremarkable. Validated cell-based assays confirmed seronegativity for CASPR2 and LGI1 in both serum and CSF. A phenotype-supported diagnosis was pursued integrating the clinical triad, electrophysiological confirmation, and systematic exclusion of mimics. Combined immunotherapy (intravenous methylprednisolone, prednisone taper, azathioprine) and symptomatic treatment (carbamazepine, melatonin) resulted in marked clinical improvement at 6 months: Medical Research Council (MRC) sum score 48 → 58/60, creatine kinase (CK) 928 → 185 U/L, ISI 24 → 4, and sleep restored to 7-8 h/night, with no significant adverse effects. This case illustrates a phenotype-supported diagnostic approach applicable in resource-limited settings where first-line biological therapies are unavailable.