Aims: Previous family, adoption and twin studies of schizophrenia have shown that genetic factors contribute significantly to the risk of schizophrenia. The aim of the present study was therefore to investigate whether exploratory eye movement (EEM) abnormalities are related to the genetic markers linked to schizophrenia.Methods: Twenty-three probands with schizophrenia, 23 of their healthy siblings (23 proband-sibling pairs), and 43 unrelated normal controls performed EEM tasks. Two parameters were measured: (i) number of eye fixations in responsive search (NEFRS) and (ii) responsive search score (RSS).Results: Abnormalities in NEFRS and RSS were more frequent in schizophrenia probands than in their unaffected siblings and in normal controls, and were also more frequent in the healthy siblings than in normal controls. Thus, the EEM test performances of the healthy siblings were intermediate between those of the probands with schizophrenia and those of normal controls. Conclusion:Abnormalities of the EEM test parameters may be related to the genetic etiology of schizophrenia. The use of EEM parameters as an endophenotype for schizophrenia may facilitate linkage and association studies in schizophrenia.
A genome-wide scan for a locus responsible for exploratory eye movement (EEM), which is quantitative and can be disturbed in association with schizophrenia, was performed. A 10-cM resolution genome-wide linkage analysis of the EEM disturbance with 358 highly polymorphic microsatellite markers in 38 nuclear families with 122 members (38 probands, 47 sibs, and 37 parents) including 58 sib-pairs yielded the suggestive linkage to the GCT10C10 marker on chromosome 22q11.2 (LOD = 2.48). Dense mapping with additional markers around the GCT10C10 marker yielded evidence for significant linkage between EEM disturbance and markers D22S429 and D22S310 on chromosome 22q12.1 (LOD score of 4.63) with suggestive evidence for the chromosome region 22q11.2-q12.1. Our findings suggest that a relatively small number of loci may control the schizophrenia-related quantitative EEM trait. We believe that identifying gene(s) on chromosome 22q associated with the EEM phenotype may forward our understanding of the etiology of schizophrenia.
The present case provides direct evidence of human herpesvirus 6 reactivation in resected lymph node tissue in a patient with drug-induced hypersensitivity syndrome. This case clearly demonstrates that appropriate pathological evaluation of lymphadenopathy for drug-induced hypersensitivity syndrome, which mimics malignant lymphoma in clinical, radiological, and pathological findings, is required. CASE REPORTA 57-year-old woman was referred to our department because of generalized erythema involving mainly her face and upper trunk, with a morbilliform eruption for a week, persistent pyrexia, and a sore throat for the preceding 3 weeks. She had been treated for bipolar disorder and had a history of atopic dermatitis and bronchial asthma in her childhood. She had been on lorazepam, famotidine, and loxoprofen for a decade, and carbamazepine had been started 1 month prior to coming to our department ( Fig. 1, day 1). She was allergic to soybeans, corn, eggs, and rice. She had not been in contact with any sick persons. At her first visit to our department (day 34), physical examination showed mild periorbital edema and expanding erythema from her face to both lower legs, with a morbilliform eruption, but no mucosal ulcers or erosions were noted. Thus, she was tentatively diagnosed as having an adverse cutaneous reaction to carbamazepine; therefore, carbamazepine was stopped, and oral prednisolone therapy was started at a dose of 20 mg/day. One week after starting the prednisolone therapy (Fig. 1, day 43), her sore throat and high-grade fever had almost disappeared, and some aspects of the cutaneous lesions, such as pigment deposition and nonpalpable purpura, had improved. Of note, at this time, she noticed generalized lymphadenopathy and returned to our department.At her 2nd visit to our department (day 43), physical examination showed generalized superficial lymphadenopathy (supraclavicular, cervical, axillary, and inguinal), and each node was 20 mm in size, firm, nonfixed, circumscribed, and rubbery, suggesting lymphoma. Laboratory examination revealed marked elevations of her white blood cell count (37,400/l, with 1% basophils, 7% eosinophils, 25% neutrophils, 44% lymphocytes, 14% atypical lymphocytes, and 3% monocytes), lactate dehydrogenase (1,657 IU/liter), and soluble interleukin 2 receptor (11,600 U/ml). Moderate elevations of serum hepatic biliary enzymes were also noted (aspartate aminotransferase, 81 IU/liter; alanine aminotransferase, 144 IU/liter; alkaline phosphatase, 264 IU/liter; ␥-glutamyl transpeptidase, 371 IU/liter). Two sets of blood cultures were negative, and no evidence of a recent infectious mononucleosis (IM) syndrome (Epstein-Barr virus) or IM-like syndrome (cytomegalovirus, Toxoplasma gondii, human immunodeficiency virus) was detected (Fig.
This study was undertaken to examine whether males develop schizophrenia at a younger age than females, and whether temporal socioeconomic change affects the age at onset of schizophrenia. The subjects were 848 ICD-9 schizophrenics who were admitted to Nihon University Hospital, Tokyo, Japan, during the period of 1955-64 (n = 468 (214 males and 254 females), group A) or during the period of 1982-91 (n = 380 (220 males and 160 females), group B). Schizophrenic males showed an earlier age at onset than schizophrenic females. However, the mean age at onset of schizophrenia did not differ significantly between group A and group B. These results indicate that the gender difference in age at onset of schizophrenia has not been influenced by temporal socioeconomic change.
Objective: To assess whether a difference in psychiatric vulnerability exists between patients with systemic lupus erythematosus (SLE) and those with schizophrenia. Methods: Twenty women with SLE underwent exploratory eye movement analysis, and a responsive search score (RSS) was obtained, two months after the onset of the disease. Fifteen women with schizophrenia in remission also underwent this analysis. Exploratory eye movement was recorded by an eye mark recorder, which detects corneal reflection of infrared light. The number of eye fixations (instance of more than 0.2 seconds of eye fixation time) was recorded, and the RSS was calculated from eye fixation analysis. Results: Mean (SD) RSS differed significantly between patients with SLE and those with schizophrenia (9.85 (1.87) v 7.27 (1.58) points, respectively, p<0.0001), whereas no difference in mean RSS was found between patients with SLE and 19 normal women. No difference in mean RSS was found between patients with active SLE and those with inactive SLE (9.51 (1.87) v 10.0 (1.77) points). Conclusion: The psychiatric vulnerability in patients with SLE, measured by the RSS, differs from that in patients with schizophrenia.
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