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.For instance, in theintrauterine environment twins must compete for nutrients, and they may not beDurand 12-56equally successful.In addition, birth complications, such as the loss of oxygen(anoxia), could affect only one of the twins (Carson & Sanislow, 1993).Obstetricalcomplications appear often in twins with schizophrenia in discordant identical pairsand the more severely affected if both twins have schizophrenia (McNeil, 1987).Different experiences by twins who are already predisposed to the disorder coulddamage the brain and cause the types of symptoms we associate with schizophrenia.The frontal lobes of the brain have also interested people looking for structuralproblems associated with schizophrenia (Gur & Pearlson, 1993).As we described inthe section on neurotransmitters, this area may be less active in people withschizophrenia than in people without the disorder, a phenomenon sometimes knownas hypofrontality (hypo means less active or deficient).Research by Weinberger andother scientists at the National Institute of Mental Health further refined thisobservation, suggesting that deficient activity in a particular area of the frontal lobes,the dorsolateral prefrontal cortex (DLPFC), may be implicated in schizophrenia(Berman & Weinberger, 1990; Weinberger, Berman, & Chase, 1988).When peoplewith and without schizophrenia are given tasks that involve the DLPFC, less activity(measured by cerebral blood flow) is recorded in the brains of those withschizophrenia.Follow-up studies show that some individuals with schizophrenia showhyperfrontality (i.e., too much activity), indicating that the dysfunction is reliable, buthyperfrontality displays itself differently in different people (Callicott et al., 2003).It appears that several brain sites are implicated in the cognitive dysfunctionobserved among people with schizophrenia, especially the prefrontal cortex, variousother related cortical regions, and subcortical circuits including the thalmus and thestratum (Ho et al., 2003).Remember that this dysfunction seems to occur before theonset of schizophrenia.In other words, brain damage may develop progressively,Durand 12-57beginning before the symptoms of the disorder are apparent, perhaps prenatally(Weinberger, 1995).Viral InfectionA curious fact about schizophrenia is that, according to some authors, no adequatedescriptions of people having this disorder appear earlier than about 1800 (e.g.,Gottesman, 1991).If you look at historic records or read ancient literature, you canfind people with such disorders as mental retardation, mania, depression, and seniledementia.Even William Shakespeare, who describes most human conditions,mentions nothing that resembles our current image of schizophrenia.Historically,such an obvious aberration of behavior is puzzlingly absent.One hypothesis is that schizophrenia is a recent phenomenon, appearing onlyduring the past 200 years and that, like AIDS, it may involve some newly introducedvirus (Gottesman, 1991).In other words, a recently occurring schizo-virus couldhave caused some cases of this debilitating disorder (Torrey, 1988b).There is nowsome evidence that at least a few cases of schizophrenia-like disorder may haveexisted as early as the 14th century (Heinrichs, 2003).Whether or not this disorder isa recent phenomenon, there is evidence that a virus-like disease may account for somecases (Kirch, 1993).The higher prevalence of schizophrenia among men living inurban areas (Lewis, David, Andreasson, & Allbeck, 1992) implies that they are morelikely to have been exposed to infectious agents than their peers in less populatedareas.Several studies have shown that schizophrenia may be associated with prenatalexposure to influenza.For example, Sarnoff Mednick and his colleagues followed alarge number of people after a severe Type A2 influenza epidemic in Helsinki,Finland, and found that those whose mothers were exposed to influenza during theDurand 12-58second trimester of pregnancy were much more likely to have schizophrenia thanothers (Cannon, Barr, & Mednick, 1991).This observation has been confirmed bysome researchers (e.g., O Callaghan, Sham, Takei, Glover, & Murray, 1991;Venables, 1996) but not by others (e.g., Torrey, Rawlings, & Waldman, 1988).Evidence that second-trimester developmental problems may be associated withschizophrenia has led researchers to look further into this area.Among the types ofcells that normally migrate to the cortex during this period are the fingertip dermalcells, which are responsible for the number of fingerprint ridges.Although there is nosuch thing as an abnormal number of ridges, identical twins generally have the samenumber.However, if some interruption in second-trimester fetal development resultedin schizophrenia (when, according to the viral theory, a virus may have its effect), itwould also affect the fingertip dermal cells.Researchers compared the fingerprintridges of identical twins who were discordant for schizophrenia with those of identicaltwins without schizophrenia (Bracha, Torrey, Gottesman, Bigelow, & Cunniff, 1992).They found that the number of ridges on the fingertips of the twins withoutschizophrenia differed little from each other; however, they differed a great dealamong about one-third of the twin pairs who were discordant for schizophrenia.Thisstudy suggests that ridge count may be a marker of prenatal brain damage.Althoughthere is no characteristic fingerprint for schizophrenia, this physical sign may add toour understanding of the second-trimester conditions that can trigger the geneticpredisposition for schizophrenia (Weinberger, 1995).The indications that virus-like diseases may cause damage to the fetal brain, whichlater may cause the symptoms of schizophrenia, are suggestive and may help explainwhy some people with schizophrenia behave the way they do (Mednick et al., 1998).However, there is not yet enough evidence to prove the existence of a schizo-virus
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