1.                  Glaser CA, Honarmand S, Anderson LJ, Schnurr DP, Forghani B, Cossen CK, Schuster FL, Christie LJ, Tureen JH.  Beyond viruses: clinical profiles and etiologies associated with encephalitis. Clin Infect Dis. 2006 Dec 15;43(12):1565-77.

Viral and Rickettsial Disease Laboratory, California Department of Health Services, Richmond, CA 94804, USA. cglaser@dhs.ca.gov

BACKGROUND: Encephalitis is a complex syndrome, and its etiology is often not identified. The California Encephalitis Project was initiated in 1998 to identify the causes and further describe the clinical and epidemiologic characteristics of encephalitis. METHODS: A standardized report form was used to collect demographic and clinical data. Serum, cerebrospinal fluid, and respiratory specimens were obtained prospectively and were tested for the presence of herpesviruses, arboviruses, enteroviruses, measles, respiratory viruses, Chlamydia species, and Mycoplasma pneumoniae. The association between an identified infection and encephalitis was defined using predetermined, organism-specific criteria for confirmed, probable, or possible causes. RESULTS: From 1998 through 2005, a total of 1570 patients were enrolled. Given the large number of patients, subgroups of patients with similar clinical characteristics and laboratory findings were identified. Ten clinical profiles were described. A confirmed or probable etiologic agent was identified for 16% of cases of encephalitis: 69% of these agents were viral; 20%, bacterial; 7%, prion; 3%, parasitic; and 1%, fungal. An additional 13% of cases had a possible etiology identified. Many of the agents classified as possible causes are suspected but have not yet been definitively demonstrated to cause encephalitis; these agents include M. pneumoniae (n=96), influenza virus (n=22), adenovirus (n=14), Chlamydia species (n=10), and human metapneumovirus (n=4). A noninfectious etiology was identified for 8% of cases, and no etiology was found for 63% of cases. CONCLUSIONS: Although the etiology of encephalitis remains unknown in most cases, the recognition of discrete clinical profiles among patients with encephalitis should help focus our efforts toward understanding the etiology, pathogenesis, course, and management of this complex syndrome.

2.                  Majoie HJ, de Baets M, Renier W, Lang B, Vincent A.  Antibodies to voltage-gated potassium and calcium channels in epilepsy. Epilepsy Res. 2006 Oct;71(2-3):135-41.

Epilepsy Centre Kempenhaeghe, Heeze, The Netherlands. majoiem@kempenhaeghe.nl

OBJECTIVE: To determine the prevalence of antibodies to ion channels in patients with long standing epilepsy. BACKGROUND: Although the CNS is thought to be protected from circulating antibodies by the blood brain barrier, glutamate receptor antibodies have been reported in Rasmussen's encephalitis, glutamic acid decarboxylase (GAD) antibodies have been found in a few patients with epilepsy, and antibodies to voltage-gated potassium channels (VGKC) have been found in a non-paraneoplastic form of limbic encephalitis (with amnesia and seizures) that responds to immunosuppressive therapy. METHODS: We retrospectively screened sera from female epilepsy patients (n=106) for autoantibodies to VGKC (Kv 1.1, 1.2 or 1.6), voltage-gated calcium channels (VGCC) (P/Q-type), and GAD. All positive results, based on the values of control data [McKnight, K., Jiang, Y., et al. (2005). Serum antibodies in epilepsy and seizure-associated disorders. Neurology 65, 1730-1735], were retested at lower serum concentrations, and results compared with previously published control data. Demographics, medical history, and epilepsy related information was gathered. RESULTS: The studied group consisted predominantly of patients with long standing drug resistant epilepsy. VGKC antibodies were raised (>100 pM) in six patients. VGCC antibodies (>45 pM) were slightly raised in only one patient. GAD antibodies were <3 U/ml in all patients. The clinical features of the patients with VGKC antibodies differed from previously described patients with limbic encephalitis-like syndrome, and were not different with respect to seizure type, age at first seizure, duration of epilepsy, or use of anti-epileptic drugs from the VGKC antibody negative patients. CONCLUSION: The results demonstrate that antibodies to VGKC are present in 6% of patients with typical long-standing epilepsy, but whether these antibodies are pathogenic or secondary to the primary disease process needs to be determined.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

15342.  Fujikawa A, Tsuchiya K, Honya K, Nitatori T.  Comparison of MRI sequences to detect ventriculitis. AJR Am J Roentgenol. 2006 Oct;187(4):1048-53. 

15343.  Otaigbe BE, Brown T, Esu R.  Confirmed congenital rubella syndrome--A case report. Niger J Med. 2006 Oct-Dec;15(4):448-50. 

Pathogenesis:

15342.  Hamzaoui K, Hamzaoui A, Ghorbel I, Khanfir M, Houman H. Levels of IL-15 in serum and cerebrospinal fluid of patients with Behcet's disease. Scand J Immunol. 2006 Dec;64(6):655-60. 

Therapy:

15343.  Caramello P, Canta F, Balbiano R, Lipani F, Ariaudo S, De Agostini M, Calleri G, Boglione L, Di Caro A.   Role of intravenous immunoglobulin administration in Japanese encephalitis. Clin Infect Dis. 2006 Dec 15;43(12):1620-1.

15344.  Shuper A, Michovitz S, Amir J, Kornreich L, Boikov O, Yaniv Y, Rorke-Adams LB. Idiopathic granulomatous encephalitis mimicking malignant brain tumor. Pediatr Neurol. 2006 Oct;35(4):280-3. 

15345.  Vinas JM, Gonzalez MJ, Ribes AG, Exposito RG, Bragado FG.  Postencephalitic chronic granulomatous disease. Pediatr Neurol. 2006 Oct;35(4):297-9.