Structural abnormalities in the cuneus associated with Herpes Simplex Virus (type 1) infection in people at ultra high risk of developing psychosis.

Schizophr Res. 2012 Mar;135(1-3):175-80. Epub  2012 Jan 12.

Whitford TJ, Wood SJ, Yung A, Cocchi L, Berger G, Shenton ME, Kubicki M, Phillips L, Velakoulis D, Yolken RH, Pantelis C, McGorry P, Amminger GP.

Source

Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne and Melbourne Health, Carlton South, VIC 3053, Australia. wht@unimelb.edu.au

Abstract

It has been suggested that some cases of schizophrenia may be caused by an interaction between physiological risk factors and exposure to certain neurotropic infectious agents such as Herpes Simplex Virus type 1 (HSV1). This study investigated whether HSV1 exposure was associated with structural brain abnormalities in individuals who, because of genetic or other factors, were deemed at ultra high risk (UHR) of developing psychosis. Twenty-five UHR individuals with a history of HSV1 exposure (HSV1+), 33 UHR participants without a history of HSV1 exposure (HSV1-) and 19 healthy controls participated in the study. All participants underwent a T1-weighted structural MRI scan, and HSV1 exposure was determined based on the presence of IgG class antibodies in the blood serum. Voxel based morphometry revealed that the HSV1+ participants exhibited volumetric gray matter reductions in the cuneus, relative to both the HSV1–and healthy control participants (p<0.05, small volume corrected for familywise error). The results of the study suggest that a history of HSV1 infection is associated with volumetric gray matter reductions in individuals at ultra-high risk for developing psychosis, and are consistent with previous studies that have identified structural gray matter abnormalities in HSV1-infected patients with established schizophrenia.

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Psychosis and herpes simplex encephalitis.

South Med J. 1985 Nov;78(11):1347-50.

Schlitt M, Lakeman FD, Whitley RJ.

Abstract

We have reported an unusual presentation of herpes simplex encephalitis in a patient with a 3 1/2-year history of a schizo-affective disorder. In the month immediately before diagnosis, the patient lost contact with reality and became violent. After successful treatment with antipsychotic medication, he had agitation and disorientation, as well as fever and cerebrospinal fluid pleocytosis. There were no focal neurologic findings. When a low-density lesion in the right temporal lobe was defined by computerized axial tomography, brain biopsy and culture isolated herpes simplex virus type 1. After therapy with vidarabine, the patient regained independence in simple daily activities. This case stresses the possibility of herpes simplex encephalitis in patients with an acute mental change.