Ocular onset: intermittent bilateral ptosis and horizontal diplopia fluctuating with fatigue.

Bulbar progression: episodic dysphagia, more pronounced for liquids, associated with nasal regurgitation and fatigable dysarthria.

Figure 1. Bilateral ptosis before initiation of treatment.

Figure 2. Asymmetric eyelid opening with ocular fatigability before treatment.

Figure 3.Resolution of ptosis and improved ocular function after corticosteroid therapy.

Generalization: progressive proximal limb fatigability interfering with daily activities such as climbing stairs and prolonged walking.

The patient denied sensory disturbances, seizures, sphincter dysfunction, toxin exposure, or use of neuromuscular-blocking medications. General health status and lifestyle history were otherwise unremarkable.

Mental status and higher cortical functions were intact. Examination revealed bilateral, fluctuating ptosis worsening during sustained upgaze, with diplopia on prolonged lateral gaze. Mild dysphagia for liquids and fatigable dysarthria were noted. Motor examination showed symmetrical proximal limb weakness with preserved distal strength, normal muscle tone and bulk, and rapid fatigability on repetitive testing. Deep tendon reflexes were symmetric and normal, with no sensory deficits or pyramidal signs. There was no respiratory distress or evidence of impending myasthenic crisis.

Routine laboratory investigations, including complete blood count, renal and hepatic function tests, and thyroid profile, were within normal limits. Due to resource limitations, AChR and MuSK antibody testing and chest computed tomography for thymic evaluation were unavailable.

Electroneuromyography demonstrated a 15% decrement in compound muscle action potential amplitude on low-frequency (3 Hz) repetitive nerve stimulation of the ulnar nerve with recording from the abductor digiti minimi muscle, confirming a postsynaptic neuromuscular junction transmission defect consistent with myasthenia gravis. Single-fiber electromyography, although more sensitive, was not available.

The patient was initiated on oral prednisone at a dose of 1 mg/kg/day. Regular access to pyridostigmine was not possible due to supply limitations, precluding consistent symptomatic therapy. After six weeks of corticosteroid treatment, there was marked improvement in ptosis and bulbar symptoms, followed by substantial recovery of proximal muscle strength by three months. The patient returned to full occupational activities without experiencing respiratory compromise or myasthenic crisis. He remains under regular follow-up, with ongoing efforts focused on minimizing long-term corticosteroid-related adverse effects and evaluating the need for steroid-sparing immunosuppressive therapy should symptoms recur.

The nearly three-year diagnostic delay observed in this case reflects a pattern frequently reported in LMICs and is attributable to limited awareness among frontline healthcare providers, frequent misdiagnosis as primary ocular or functional disorders, and restricted access to electrophysiological testing, immunological assays, and thoracic imaging. Financial barriers and fragmented referral pathways further compound these challenges. Prolonged diagnostic delays increase morbidity and expose patients to the risk of myasthenic crisis, a life-threatening emergency requiring prompt ventilatory support and rescue therapies [14].

Although serological testing enhances diagnostic specificity, particularly in MuSK-positive MG, electrophysiology remains the diagnostic cornerstone in many low-resource environments. A significant decrement in low-frequency RNS, typically greater than 10% - 15%, provides reliable evidence of neuromuscular junction dysfunction [5]. In the present case, the absence of antibody testing, thymic imaging, and SFEMG necessitated reliance on clinical judgment and conventional ENMG, a scenario representative of routine practice in many West African neurology centers [15].

Standard MG management combines symptomatic therapy with immunomodulatory treatment [1][8]. However, therapeutic access in LMICs is highly variable. Pyridostigmine availability is often inconsistent due to supply shortages, while immunosuppressive agents such as azathioprine or mycophenolate mofetil may be limited by cost. Advanced therapies including intravenous immunoglobulin, plasma exchange, and biologic agents remain largely inaccessible because of infrastructure and financial constraints. In this context, corticosteroids frequently serve as first-line therapy despite concerns regarding long-term adverse effects and limited monitoring capacity.

This case highlights the urgent need for strengthened electrophysiological infrastructure, targeted training programs to enhance early recognition of MG, and improved access to essential medications. Locally adapted treatment algorithms emphasizing early corticosteroid initiation with structured monitoring protocols could substantially improve outcomes in resource-constrained settings.