Researchers at Chang Gung Children’s and Memorial Hospitals, Taoyuan, Taiwan, investigated the clinical manifestations, laboratory, EEG, and neuroimaging features of M pneumoniae-related encephalitis and its prognosis. Ninety-nine patients seen between Jan 2001 and June 2010 were all positive by serology, and 47 (47.5%) developed postencephalitic epilepsy. Onset ranged from 9 months to 14 years (mean age 6.8 years). Seizures occurred in the acute phase in 53 (53.5%), most commonly focal with secondary generalization (40%). Status epilepticus occurred in 25%, refractory in 15%. Initial symptoms were fever, altered consciousness, and personality or behavior change. Elevated CSF protein was a risk factor for postencephalitic epilepsy. Initial EEG was most commonly focal/diffuse cortical dysfunction (37%) and focal epileptiform discharge (26%). Focal epileptiform EEG in the acute phase increased the risk of developing postencephalitic epilepsy 5-fold. Follow-up ranged from 6-131 months. Significant risk factors for postencephalitic epilepsy include seizures in the acute illness and focal epileptiform discharges in the initial EEG. All children with status epilepticus during hospitalization developed postencephalitic epilepsy. Of the 47 children with postencephalitic epilepsy, 19 (40%) had intractable seizures, and 40% had favorable outcomes. [1]

COMMENT. Previous reports of postencephalitic epilepsy from centers in Taiwan have examined clinical and prognostic factors [2]. Of 44 patients, 20 had a favorable outcome and 24 a poor outcome. Factors indicating a poor prognosis during the acute encephalitis phase were 1) status epilepticus as the first seizure (p<0.005), 2) slow background activity (p<0.001) and multifocal spike discharges on EEGs (p<0.01), and 3) herpes simplex viral encephalitis (p<0.01). Herpes simplex virus type 1 is a major pathogen causing postencephalitic epilepsy. Early identification of the HSV-1 and treatment with antivirals may improve the outcome and prevent the epilepsy complication.

Hippocampal dynorphin and epilepsy. Animal studies at UC-Irvine have investigated the relation of the dynorphin promotor system in the hippocampus to HSV-1 precipitated seizures. Reduced dynorphin expression in the dentate gyrus due to HSV-1 infection leads to an increased propensity to seizures. The loss of dynorphin immunoreactivity in the hippocampus is independent of a direct viral induced cell loss, suggesting a neurochemical basis for viral-induced seizures. Viruses are environmental triggers for seizures. [3]

Influenza vaccination (and/or Mycoplasma pneumoniae) as cause of transverse myelitis [4]. In response to a report of transverse myelitis (TM) in a 27-year-old woman 4 days after vaccination with monovalent A (H1N1) live, nasal attenuated influenza vaccine, Ambrose et al comment that the patient may have had mycoplasma pneumonia 20 days before symptom onset. M pneumonia is a well-established cause of TM, with an interval of 4 to 30 days between respiratory illness and neurologic symptoms. Possible mycoplasma infection and influenza vaccination should be considered as potential etiologies of TM in this patient.