Israel Medical Association Journal

Background: Only a small proportion of schizophrenia patients present with catatonic symptoms. Imaging studies suggest that brain motor circuits are involved in the underlying pathology of catatonia. However, data about diffusivity dysregulation of these circuits in catatonic schizophrenia are scarce.

Objectives: To assess the involvement of brain motor circuits in schizophrenia patients with catatonia.

Methods: Diffusion tensor imaging (DTI) was used to measure white matter signals in selected brain regions linked to motor circuits. Relevant DTI data of seven catatonic schizophrenia patients were compared to those of seven non-catatonic schizophrenia patients, matched for sex, age, and education level.

Results: Significantly elevated fractional anisotropy values were found in the splenium of the corpus callosum, the right peduncle of the cerebellum, and the right internal capsule of the schizophrenia patients with catatonia compared to those without catatonia. This finding showed altered diffusivity in selected motor-related brain areas.

Conclusions: Catatonic schizophrenia is associated with dysregulation of the connectivity in specific motoric brain regions and corresponding circuits. Future DTI studies are needed to address the neural correlates of motor abnormalities in schizophrenia-related catatonia during the acute and remitted state of the illness to identify the specific pathophysiology of this disorder.

Background: West Nile virus, the etiologic agent of West Nile fever, is an emerging mosquito-borne disease. WNV[1] was recognized as a cause of severe human meningo-encephalitis in elderly patients during outbreaks in various parts of the world.

Objectives: To analyze WNV encephalitis therapy and its outcome after prescribing hyperimmune gammaglobulin therapy.

Methods: Eight subjects with WNV encephalitis were treated with supportive therapy and 5 days of IVIG[2] 0.4 g/kg/day containing high WNV antibodies obtained from healthy blood donors.

Results: Patients who were treated with IVIG as soon as possible exhibited an improvement in their symptoms. All subjects presented with high fever, progressive confusion and headaches, nausea and vomining. The Glasgow Coma Screen for six patients ranged between 8 and 13 and all were discharged with a score of 15. The remaining two subjects died during their hospitalization.

Conclusions: In severe WNV infection, where the disease affects the central and/or peripheral nervous system, early intervention with IVIG together with supportive treatment is recommended.