Case report of a healthy,elderly man with long-term high titers for anti-acetylcholine receptor antibody without myasthenia gravis

Anti-acetylcholine receptor antibodies （AAR） are considered pathognomonic and pathogenetic for myasthenia gravis （MG）. AAR detection confirms clinical diagnosis of MG. However, AAR is rarely detected in patients without MG. The underlying pathophysiological mechanisms in a normal subject without MG have not been adequately addressed in previous studies. The present study reports on a case study of a healthy, elderly man with high AAR titers for 14 years. Pathophysiological mechanisms could be due to AAR heterogeneity in specificity, affinity, and multiform, and to muscle variability in response to AAR.

Central somatosensory conduction slowing in adults with isolated elevated plasma level of homocysteine

Aim:Elevated plasma level of homocysteine(eHcy)is a recognized risk factor for dementia.However,whether the central conduction is affected in patients with an isolated eHcy is unknown.In this study,we addressed whether central conduction is altered in adults with eHcy.Methods:Evoked potential studies including somatosensory(SSEP),visual(VEP)and brainstem auditory evoked potentials(BAEP),were performed to evaluate central conduction in patients with isolated eHcy.Results:Nine SSEP,7 VEP,and 6 BAEP were studied in 9 patients with eHcy(age:63.3±7.5 years old,mean±standard deviation,male/female:4/5).SSEP with median nerve stimulation was delayed in peak latency of N9(5/9/55.6%,abnormal/total subjects/percentage),N13(7/9/77.8%),N20(6/9/66.7%),and/or interpeak latency of N9‑N13(5/9/55.6%),N13-N20(5/9/55.6%),and N9-N20(4/9/44.4%).There was one delayed P100 latency(1/7/14.3%)in 7 VEP.BAEP was within normal limits in all the 6 subjects tested.Conclusion:Our pilot study provided neurophysiologic evidence of central conduction slowness in patients with eHcy,which may be due to a large diameter fiber dysfunction within the somatosensory,but not the visual and auditory,white matter pathway.The central conduction slowing in eHcy may be relevant to the pathophysiologic background for slowing the central processing.