We present two cases of focal neuromyotonia (FN) occurring in the context of β‑adrenergic inhaler therapy. Both patients exhibited isolated cramping and involuntary posturing of the fingers, with sustained overactivity of the finger flexors—unilateral in one case and bilateral in the other. Electromyography (EMG) of flexor digitorum superficialis (FDS) demonstrated high‑frequency decrementing neuromyotonic discharges accompanied by complex repetitive discharges (CRDs). Voluntary activation produced normal motor unit potentials, and EMG of all other sampled muscles showed normal patterns, confirming the strictly focal nature of the disorder.
Focal neuromyotonia is a rare hyperexcitability syndrome presenting with isolated finger‑flexion deformities and neuromyotonic EMG discharges, without evidence of generalised peripheral nerve hyperexcitability. In reviewing the literature, we identified four previously reported cases associated with COPD and chronic β‑adrenergic therapy, notably those described by Modarres et al., who reported two COPD patients on long‑term salbutamol therapy developing progressive finger‑flexion FN, and by Dhanapalaratnam et al., who highlighted a similar clinical pattern in older patients with chronic airway disease treated with inhaled β₂‑agonists.
Beyond COPD‑associated cases, several single case reports describe FN occurring in other contexts, including Isaacs’ syndrome, C9ORF72 expansion, focal demyelinating neuropathy, and compressive neuropathies, indicating that focal neuromyotonia represents a heterogeneous clinical endpoint triggered by diverse peripheral nerve insults.
Clinically, focal neuromyotonia may be misinterpreted as Dupuytren’s contracture, focal dystonia, or compressive mononeuropathy. Misdiagnosis can lead to delayed or inappropriate interventions, including unnecessary surgical procedures. Recognising the pattern of persistent involuntary flexor overactivity with neuromyotonic EMG discharges, particularly in patients receiving chronic β‑adrenergic agents, is therefore essential. When medication‑related hyperexcitability is suspected, management typically focuses on review and rationalisation of inhaled β‑agonists, alongside targeted neurological treatment. Case literature supports the use of carbamazepine and, in selected focal cases, botulinum toxin injection, both of which have demonstrated symptomatic benefit in reported patients.
Finally, although many cases in this subgroup appear medication‑related, clinicians should remain alert to the broader differential diagnosis. Associations with autoimmune peripheral nerve hyperexcitability (e.g., Isaacs’ syndrome), neurodegenerative disease, and structural focal neuropathies underscore the importance of comprehensive evaluation, including autoimmune serology, nerve conduction studies, and targeted imaging when appropriate.
