Medical students from New York City were integrally involved in the response by health professionals to aid the families of victims of the September 11, 2001, attacks on the World Trade Center. The present study was performed to investigate the emotional impact of this involvement on medical students from the Mount Sinai School of Medicine in New York City. One hundred fifty-seven students responded to a mail survey that explored their personal and professional involvement in the disaster as well as their psychiatric symptoms in the week after the event and at the time of the survey (3.5 months after the event). Findings suggested a differential emotional impact on female students and on students involved in less supervised and more emotionally intense activities. However, involvement in the relief effort, per se, did not contribute to psychiatric symptomatology. It may have been associated with enhanced professional self-esteem among the students. These findings have implications for future planning of psychiatric response to disasters.

Serum antibody titres to herpes-simplex (HSV-1, 2), cytomegalovirus (CMV), and Epstein–Barr virus capsid antigen (EBV-VCA) were determined in 38 unrelated chronic schizophrenic patients, 11 nuclear families with at least 2 schizophrenic members, and 2 control groups. The distributions of antibody titres to herpes simplex and cytomegalovirus were similar among all groups. Patients had higher anti-EBV-VCA titres than non-hospitalized controls; however, hospital staff members in contact with the patients also had significantly higher antibody titres to EBV-VCA. Antibodies to EBV early antigen (EBV-EA) were also determined for 27 unrelated patients and 24 mental hospital employees. The schizophrenic patients had significantly higher antibody titres to EBV-EA than the hospital worker control group. These data do not support the hypothesis that herpes viruses are associated with the aetiology of schizophrenia. Although elevated anti-EBV early antigen titres may suggest persistent active EBV infection, it is unlikely to be related to the aetiology of the disorder, since discordance for EBV seropositivity was present among sibling pairs concordant for schizophrenia.

We investigated linkage between schizophrenia and the loci DXYS14, DXYS17, and MIC2 within the pseudoautosomal region in 85 families with two or more siblings suffering from schizophrenia or schizoaffective disorder. A maximum lod score of 2.44 was reached at MIC2, with a dominant model of inheritance at a recombination fraction of 0.367 in females and 0.046 in males (a F: M sex ratio > 1, i.e. opposite to that expected with a pseudoautosomal locus). Evidence consistent with linkage (P = 0.01) was also obtained with a sibling pair analysis at the MIC2 locus. These data do not support (although they do not definitively exclude) a locus within the pseudoautosomal region; they are consistent with the presence of a gene that predisposes to schizophrenia in the sex-specific regions of the X and Y chromosomes.

The hypothesis that at least a subgroup of familial cases of schizophrenia could be due to a genetic defect on the X chromosome is supported by the observation of an excess of X-chromosome aneuploidies (XXX and XXY) among populations of patients with psychosis. The distal long arm, Xq27–q28, is a candidate region where linkage has been claimed to manic-depressive disorder and a fragile site has been associated with schizophrenia spectrum disorders. The present study excluded linkage to a large part of this region using four polymorphic probes and multipoint lod-score analysis in 10 families with multiple members with schizophrenia.

The hypothesis that the gene for schizophrenia is located in the pseudoautosomal region of the sex chromosomes predicts that same-sex concordance will occur in paternally rather than maternally derived pairs. In 120 families that included at least one sibling pair with schizophrenia, affected members were significantly more likely to be of the same sex when there was a history of illness on the paternal than on the maternal side, the difference remaining significant when parent of origin was assessed by three different methods. The finding is as predicted by the pseudoautosomal hypothesis: therefore a search for the gene should be focused on this small (three megabase) region of the genome. The ratio of same to mixed sex pairs in paternally-derived cases (approximately 3:1) suggests the gene is located in the centromeric one-third of the pseudoautosomal region.

Serum immunoglobulins were quantified in 85 consecutively admitted patients from an acute-care psychiatric in-patient unit. The patients were diagnosed as: major depressive disorder, 53; chronic schizophrenia, 12; schizophreniform psychosis, 4; substance abuse disorder, 12; and miscellaneous other diagnoses, 4. A small sub-group of these patients, which included six with major depression, one with chronic schizophrenia, and one with a personality disorder, were found to have low IgM concentrations. Immunoglobulin levels were not associated with use of medication or length of illness prior to this hospital admission. This study provides further evidence for suppression of humoral immunity in some psychiatric patients (approximately 10%).

An inverse correlation between platelet monoamine oxidase activity and spontaneous eye-blink rate, a putative measure of central dopaminergic activity, was found in medication-free chronic schizophrenic patients without tardive dyskinesia (n = 20, rs = -.47, P <.025). A similar correlation was found when patients with tardive dyskinesia were included but was weaker (n = 27, rs = -.35, P <.05). Normal controls and patients with tardive dyskinesia did not demonstrate this relationship. This report confirms a previous finding of a significant platelet monoamine oxidase-blink rate correlation in chronic schizophrenic patients. Insofar as this relationship is mediated by dopamine, it suggests that dopaminergic relations are more readily demonstrated in schizophrenic subjects than normals. Moreover, tardive dyskinesia appears to obscure this dopaminergic relationship.

Immunoglobulins, IgG, IgA and IgM were quantified in cerebrospinal fluid (CSF) and plasma from chronic schizophrenic patients and controls using an immunofluorescent antibody technique. A generalized reduction in immunoglobulin levels was observed in the schizophrenic patients compared with controls. While this study supports other reports of abnormal immune functioning in schizophrenia, it failed to replicate previous findings of elevations in CSF IgG and elevations in serum IgA. The aetiology and significance of these findings are hypothesized but remain elusive.

A survey of 14 published studies found no consistent association between specific HLA antigens and schizophrenia. Since these studies lacked diagnostic or biological criteria, an investigation was undertaken using recognized diagnostic criteria and CT scan findings. Typing for HLA antigens at loci A, B and C was carried out on 130 patients. Among 92 black schizophrenic patients there was an increase of HLA-A2 which remained significant even after correcting for the number of antigens studied. When the patients for whom CT scans were available were divided according to the presence or absence of evidence of brain atrophy, there was an increase of A2 in the black schizophrenic patients without evidence of atrophy, which remained significant after multiplying by the number of antigens studied. However, there was no significant increase of A2 in those with evidence of atrophy. Similar trends held for the white population but they failed to reach significance. The need for HLA studies on biologically defined groups of schizophrenic patients is stressed.