Encephalitis with thalamic and basal ganglia abnormalities: etiologies, neuroimaging, and potential role of respiratory viruses.

BACKGROUND: Encephalitis is a severe neurological syndrome with devastating consequences. Despite extensive testing, the etiology often remains unknown. Involvement of the thalamus or basal ganglia (T/BG) occurs in a subset of patients with encephalitis and may be an important etiological clue. In order to improve diagnosis of T/BG patients, we reviewed this subgroup within the California Encephalitis Project (CEP). METHODS: Data from T/BG cases enrolled in CEP were retrospectively reviewed. Cases were stratified by age and grouped by etiological classification: infectious, postinfectious, and noninfectious. Neuroimaging reports were examined and compared between etiologies. RESULTS: T/BG neuroimaging abnormalities were reported in 6% of 3236 CEP cases. An etiology was found in 76%: 37% infectious, 16% postinfectious, and 23% noninfectious. The most frequently identified infectious agents were respiratory viruses, accounting for 31%, predominantly in children. Other infections more common in the T/BG group included Creutzfeldt-Jakob disease, arbovirus, and Mycobacterium tuberculosis. Infectious and postinfectious cases had higher median cerebrospinal fluid white blood cell count than noninfectious etiologies. Notably, T/BG neuroimaging characteristics were associated with distinct etiologies. In particular, symmetric hemorrhagic abnormalities involving the thalamus were most frequently found within the respiratory virus group. CONCLUSIONS: T/BG involvement in patients with suspected encephalitis was associated with specific etiologies. In addition to agents with established predilection for the T/BG such as M. tuberculosis and arboviruses, a surprisingly high number of cases were associated with respiratory viruses, especially in children. Neuroimaging abnormalities in such patients can aid clinicians in narrowing the etiological scope and in guiding testing.

Effects of (D-Ala2)methionine enkephalinamide in PMA-induced mouse ear edema.

The synthetic opioid peptide (D-Ala2) methionine enkephalinamide (DAMEA) was reported to be an extremely potent inhibitor of the "respiratory burst" of polymorphonuclear neutrophils (PMNs). In the present paper the activity of DAMEA was investigated in the PMA-induced mouse ear edema since there is strong evidence that reactive oxygen species (ROS) are involved in the pathogenesis of this inflammatory reaction. DAMEA inhibited PMA-induced mouse ear edema in a dose-dependent manner between 10(-6) and 10(-9) mol/ear. The well-known anti-inflammatory activity of narcotic analgesics could be explained partly by an inhibition of ROS production.