A 30-year-old housewife presented with a one-week history of progressive painless bilateral ptosis. Initially the ptosis affected the left eye and was followed five days later by ptosis of the right eye. She also noticed gradual-onset malaise and fatigability upon doing her regular activities progressing to decreasing dexterity in both upper limbs and fatigability on walking. She denied any preceding history of flu-like symptoms or gastrointestinal infection and no diurnal fluctuation in her symptoms were present. Her medical history was otherwise unremarkable.
Neurological examination revealed normal mental status. There was bilateral ptosis (Figure 1) with inability to open the lids volitionally. Upward gaze produced mild lid elevation. The pupils were equal and reactive to light, and there was no restriction in horizontal and vertical eye movement, and Bell's phenomenon was preserved. Neurological examination of the cranial nerves was otherwise normal. Sensory examination was normal. Muscle strength, tone, coordination, and gait were normal. Deep tendon reflexes were absent. 
Complete blood cell count and biochemical laboratory screening (renal, liver and thyroid function, electrolyte, and glucose) were normal. Since ocular myasthenia gravis needed to be ruled out, an edrophonium test was performed but was negative, and repetitive supramaximal stimulation (SRS) testing on day 9 of the illness with recording from the right abductor digiti minimi (ADM) and the both biceps did not show a decremental response. Cerebrospinal fluid (CSF) analysis yielded albuminocytological dissociation with a protein of 0.6 gm/L (normal 0.15-0.45 gm/L) and less than 5 white blood cells/uL (normal < 5/ul). CSF glucose was normal. CSF viral serology and gram stain and culture as well as tuberculosis smear and culture were negative. Serum anti-GQ1B, antiganglioside and antiacetylcholine receptor antibodies sent on day 12 of the illness (before initiating treatment) were negative. 
Magnetic resonance imaging (MRI) of the brain was normal. Nerve conduction study (NCS) (Tables 1 and 2) performed on day 10 of the illness revealed significant reduction in the compound motor action potentials (CMAP) with conduction blocks in the median and ulnar nerves and reduced motor conduction velocity (MCV) in the lower limbs with reduced CMAP amplitudes. The F wave was preserved but dispersed in the upper limbs and absent in the lower limbs. Electromyography (EMG) showed diffuse signs of denervation in all myotomes of the face, upper limbs, and lower limbs. In addition, significant polyphasia was noted in the muscles of the face. These findings were consistent with acute predominantly axonal inflammatory polyradiculoneuropathy.
 By that time (day 10 of the illness), the patient started developing a gradual increase in lower limb weakness and had increasing difficulty in walking. The patient was started on intravenous immunoglobulin (IVIG) therapy (0.4 g/kg/day IV for 5 days) with rapid and complete resolution of her neurological findings (Figure 2).