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Acute disseminated encephalomyelitis: where does it start and where does it stop?

The paper by Beleza et al. in this issue presents a case of Haemophilus influenzae meningitis in an immunocompromised 17-year-old male. After commencing antibiotic therapy there was a further deterioration with evolution of coma and pyramidal signs. Magnetic resonance (MR) neuroimaging showed asymmetric disseminated white matter lesions typical of acute disseminated encephalomyelitis (ADEM). The case challenges a number of previously defined ‘characteristics’ of ADEM. Firstly, it has generally been considered that the precipitating infectious agent does not gain entry into the central nervous system (CNS).1 Indeed, the conventional hypothesis is that a peripheral (non-CNS) infection stimulates an aberrant host immune response associated with disruption of the blood–brain barrier and auto-aggressive immune attack of the CNS.1 The evidence for a bacterial CNS infection in this case report was convincing: polymorphs were the dominant cerebrospinal fluid (CSF) leucocyte (CSF lymphocytosis is typical of ADEM), CSF glucose was low, and CSF protein abnormally elevated. Haemophilus influenzae was not grown on CSF culture but incriminated using recognized alternative means. The adolescent was immunocompromised and, therefore, vulnerable to encapsulated bacteria. The subsequent clinical deterioration was typical of ADEM, with rapid onset encephalopathy and pyramidal signs. Paradoxically, steroid therapy that had made the adolescent vulnerable in the first instance was successfully used to treat the CNS inflammation. Although the apparent precipitant of this ‘ADEM’ case was atypical, the course and response to steroid therapy was typical of ADEM, supporting the hypothesis that cases such as these should be part of the ADEM spectrum. Of course, disease models already exist of direct infection of the CNS resulting in secondary immune-mediated CNS inflammation, including the animal model Theiler murine encephalomyelitisinduced demyelinating disease and human Lyme neuroborreliosis. These disease models and the report by Beleza et al. challenge the ADEM dogma that the precipitating infection cannot gain entry into the CNS.