BMJ 2009;338:b701. HERPES SIMPLEX VIRUS–1 ENCEPHALITIS CAN TRIGGER ANTI-NMDA RECEPTOR ENCEPHALITIS:

et al.1 reported an interesting case in which herpes simplex encephalitis (HSE) probably triggered the production of reactive NMDA receptor (NMDAR) antibodies. Within weeks of being treated with acy-clovir for HSE, the patient had what the authors believed was recurrent HSE, yet it later proved to be NMDAR limbic encephalitis. Since the viral encephalitic episode closely resem-bled the autoimmune encephalitic attack, it is difficult to know when the NMDAR limbic encephalitis first manifested. At initial discharge after having 3 weeks of acyclovir therapy, the patient had slow recovery, residual retrograde and anterograde amnesia, and impaired executive function. Some of these residua could have reflected the developing autoimmune encephalitis. The NMDAR immunoglobulin G (IgG) antibody level was 0 at day 1 but 1:800 by day 42. These IgG levels might have become clinically relevant by week 3 of the illness. Following subsequent treat-ment with IV methylprednisolone, it would be interest-ing to know whether the patient’s condition improved beyond initial discharge. Since this is the first case reported, it is unclear how often NMDAR antibodies develop in the con-text of HSE. It is possible that joint use of antiviral and corticosteroid medications may become the stan-dard for the treatment of herpes simplex virus consid-ering the potential for NMDA antibodies to effect prolongation or recurrence of the limbic encephalitis