Chronic fatigue syndrome (CFS) is characterized by persistent mental and physical
fatigue for at least 6 months. Its pathophysiology is unknown and there is no proven effective treatment. We describe three cases who fulfill the criteria of CFS, in whom a defect of neuromuscular transmission and
dysautonomia are present and who respond to
acetylcholine-
esterase inhibition. Case 1: 18-year-old female with a 3-year history of CFS. Response of compound-muscle-action potential, recorded using surface recording
electrode, over left abductor pollicis brevis muscle, to repetitive nerve stimulation (RNS) at a rate of 10 Hz showed a 42% incremental response. Composite autonomic scoring system (
CASS) showed mild
cholinergic impairment (cardiovagal score: 1; sudomotor score: 2). Serological tests for Epstein-Barr virus (EBV) revealed positive
antiviral capsid
antigens (anti-VCA)
immunoglobulins G (
IgG). Oral
pyridostigmine therapy (30 mg) resulted in marked improvement in symptoms. Case 2: 28-year-old female with 10-year history of CFS. RNS, using identical protocol, showed a 60% incremental response over the same muscle.
CASS showed mild
cholinergic impairment (cardiovagal score: 1; sudomotor score: 2) and this patient was also positive for EBV. This patient responded dramatically to 10-mg
pyridostigmine. Case 3: 29-year-old female with a history of CFS for longer than 15 years. Repetitive stimulation, using identical paradigm to left abductor pollicis brevis muscle, showed a 42% incremental response.
CASS showed mildly
cholinergic impairment (cardiovagal score: 2; sudomotor score: 1). EBV antibody titers were positive. Patient responded to 30-mg
pyridostigmine with an improvement in her
fatigue. These three cases generate the hypothesis that the
fatigue in some patients with clinical CFS might be due to a combination of mild neuromuscular transmission defect combined with
cholinergic dysautonomia. Support for this thesis derives from the improvement with
cholinesterase inhibition.