This report describes the demographic, cognitive, and clinical features of 104 SPD subjects in order to systematically examine the phenomenology and social/occupational aspects of this disorder. While the number of participants does not approach the size of large epidemiological studies, it is, to our knowledge, the largest cohort of neuroleptic-naive SPD subjects recruited directly from the community. As such, the findings provide important insights into the effect this disorder has on its sufferers both in terms of their professional status, as well as their social standing and personal situations. For both genders, SPD individuals tended to have lower socio-economic status, more difficulty with unemployment, to be single and living with their family of origin, or alone. The disorder was also associated with fewer years of education and, perhaps related, lower Vocabulary scores. Furthermore, true to their clinical characterization as belonging to schizophrenia spectrum disorders, SPD persons manifested more suspiciousness and paranoid ideation, qualities which in conjunction with other features made effective and satisfactory social functioning difficult. Thus, these findings corroborate, and expand upon, existing reports in the literature.
Poor occupational functioning in these subjects was evident. Despite their above average to above average IQ and college experience, the SPD subjects failed to reach the occupational standing predicted by that of their parents compared with controls (SES corrected), similar to what others have shown (Kunkel et al., 1998
), and analogous to what has been described in the schizophrenia literature as “downward drift” (Loffler and Hafner, 1999). Moreover, they more frequently had a period of time during which they were unable to work or attend school, although if they had an appropriate job, they were able to maintain it. Poor occupational and social achievement are mediated by a complex constellation of factors, some of which are delineated below.
For example, cognitively, the SPD subjects scored lower than comparison subjects on Vocabulary age-scaled scores, regardless of whether WAIS-III or WAIS-R was used. This effect remained even after correcting for the effect of parental SES. The literature has been inconsistent concerning whether the SPD condition affects IQ scores, with some groups finding a trend level difference (Cadenhead et al., 1999
). However, in Trestman et al. (1995)
, subjects were matched on education and there was no difference on WAIS-R Block Design or Vocabulary. Similar conclusions were reached for WAIS Vocabulary scores (Mitropoulou et al., 2002
). However, education and vocabulary scores often correlated in the literature, as in this sample, complicating the interpretation. Another potential explanation for the difference between this study and the previous negative reports is that IQ scores here are higher for SPD subjects than any other studies’ control group. This current recruitment strategy reached higher IQ subjects in general, and at higher IQ, it may have been possible to demonstrate more deficits in SPD subjects (Diaz-Asper et al., 2004
Another cognitive function that was somewhat compromised in this SPD sample was performance on Block Design, which reflects impaired spatial attention. Although this group difference did not quite reach statistical significance, there was a trend level difference with SPD subjects scoring lower. The difference between groups was not likely due to the history of major depression in the SPD subjects as Kohler et al. demonstrated that co-morbid depression in schizophrenic patients had no effect on WAIS-R Block Design scores (Kohler et al., 1998
). In terms of gender differences in cognitive function, male compared with female SPD subjects had more cognitive deficits and more non-clinically significant learning problems, similar to what has been shown in schizophrenia (Goldstein et al., 1998
). Finally, a paired comparison between Vocabulary and Block Design scores revealed that SPD subjects, but not control subjects, had a selective deficit in Vocabulary, similar to what has been shown in schizophrenia.
Another area of impairment in this SPD sample was social functioning. Half of the SPD subjects had no close friends and they were unlikely to live with partners/spouses. The significance of this finding goes beyond a sense of loneliness, as poor social relations increases mortality in normals (Avlund et al., 1998
SPD symptomatology could also contribute to SPD social isolation. Within our SPD group, positive symptoms of SPD predominated. Illusions/unusual perceptual experiences, suspiciousness/paranoid ideation, and magical thinking/odd beliefs were the three most commonly reported symptoms (78% of subjects). This is consistent with a report of positive symptoms occurring more frequently in SPD subjects without a family history of schizophrenia (Torgersen et al., 2002
) as was the case in the current sample. The presumed low genetic loading of schizophrenia in this sample may have led to disproportionately high rates of positive symptoms in these SPD subjects compared with the entire population of SPD subjects. This may be further underscored by the relatively low frequency of odd speech in our sample (46%) which is more common in SPD subjects with a schizophrenic relative (Torgersen et al., 2002
; Kendler et al., 1995
). Therefore, this large current sample of SPD subjects may represent a subpopulation of SPD subjects with more positive symptoms and less genetic vulnerability. This hypothesis, however, can not be tested due to the recruitment methods.
The functional anatomy subserving these clinical symptoms is unclear, although some suggestive evidence has emerged. In SPD, illusions and magical thinking impairment correlated with the right fusiform gyrus volumes (Dickey et al., 2003a
); odd speech with left superior temporal gyrus volumes in females (Dickey et al., 2003b
); and in non-psychiatric subjects a fMRI experiment designed to simulate low level paranoia/delusions, selectively activated the left inferior frontal gyrus (Brodmann area 44) (Blackwood et al., 2000
), a region shown to have metabolic rates in SPD subjects intermediate between control and schizophrenic subjects (Buchsbaum et al., 2002
). Although tentative, these findings, taken together, suggest that at least some of the dominate symptoms of SPD may be attributable to abnormalities in the frontotemporal cortices, again, not unlike what has been shown in schizophrenia (Niznikiewicz et al., 1999
; Weinberger et al., 1992
Gender comparisons in terms of SPD clinical symptoms suggest that male SPD subjects compared with female SPD subjects had a constellation of scores demonstrating more significant impairment, including higher SANS scores, more disability due to odd thinking/speech, more recreational drug and alcohol use and fewer friends. Males also more frequently suffered from paranoid and narcissistic personality disorders. The only measure on which female SPD subjects were more impaired was the SPQ disorganization sub-scale. This self-administered scale tapped subjects’ unusual appearance and vague, rambling speech. It was the only measure of the SPQ that relied on the opinions of others (“other people see me as slightly eccentric (odd)”) and was the only factor of the SPQ in which there was no correlation with SCID interviewers’ observations. Thus, it may in fact suggest that female SPD subjects may not have fully recognized or appreciated how others viewed them. Again, gender differences in clinical features have been shown to be important in schizophrenic patients (Goldstein, 1996
In addition to presenting with the constellation of clinical symptoms characteristic of SPD, the prevalence of co-morbid Axis I and Axis II disorders in this SPD sample exceeded that expected in the general population, which is consistent with other reports (Cadenhead et al., 1999
; Mikhailova et al., 1996
; Mitropoulou et al., 2002
, and also likely contributes to the impairment in the personal and occupational lives experienced by this group of SPD subjects. Indeed, the potential confounding effects of co-morbid Axis I and Axis II disorders for the SPD subjects may have elevated their social and occupational impairment relative to the controls. However, given the frequency of co-morbidity in the SPD population, potential SPD subjects were not ruled-out due to additional Axis I and II disorders. This led to a heterogeneous sample of SPD subjects. Note that comparison subjects, while recruited similarly to SPD subjects, were specifically selected for having no history of Axis I or Axis II disorder in themselves or in a first-degree relative. One possibility for future studies would be to recruit comparison subjects who had depression or anxiety. In that way, the effects of disturbed mood on social or occupational impairment would be balanced between the SPD and comparison subjects so that the additive effect on occupational and social impairment due to having a diagnosis of SPD could be parceled out.
Despite co-morbidity none of the SPD subjects have ever received a neuroleptic and none were on psychoactive medications during the study. Possible explanations for lack of health care include potential difficulties SPD subjects experience in obtaining appropriate healthcare given their social anxiety or, in spite of their difficulties, did not recognize themselves as ill enough to require treatment.
As enumerated above, the SPD subjects demonstrated several aspects of normal functioning, which may have been key to their ability to live independently without many social supports. They were bright and this may have allowed them to develop compensatory strategies for managing their symptoms. This may have also allowed them to maintain their jobs, once obtained. Additionally, they had children at rates similar to the comparison subjects, attesting to some degree of ability on the part of the SPD subjects to form social relationships at some point in their lives.
Limitations of this study included potential ascertainment bias in several ways. First, the advertisements for research may have solicited brighter subjects than in the entire population of SPD subjects. Additionally, advertisements focused on positive symptoms and social anxiety and, therefore, may have attracted SPD subjects with predominately those symptoms. For example, as the advertisement specifically solicited subjects with few close friends, the ad may have attracted more SPD subjects without friends than generally exist in the SPD population. However, only approximately half of the subjects met that criteria. Furthermore, as it is difficult to script an advertisement for some of the criteria, such as odd and peculiar behavior, inappropriate affect, or odd speech, it is possible that subjects impaired by those clinical features may have been under-represented in this population. Of note here, only approximately half the SPD subjects met those three criteria. Nonetheless, it is difficult to know the true incidence of each of these criteria in the SPD population given the social isolation of these subjects and the scant literature on this issue. Indeed, an attempt to quantify the relative frequency of the criteria was one of the goals of this study. Two additional potential limitations of this study include the cross-sectional nature and the lack of Bonferroni correction. Specifically, as this was a cross-sectional study, and not a longitudinal study, an argument could be made that some of the younger subjects will go on to develop schizophrenia. The average age for both genders, however, was older than is typical for the development of schizophrenic symptoms (average age 22.0 years) (Goldstein et al., 1998
), lessening the potential of this being a prodromal cohort. Finally, these data were not Bonferroni corrected and many of the findings would not have remained significant if a strict correction had been applied. Nonetheless, the findings parallel those in the schizophrenia literature.
Finally, Kety et al. (1967)
described SPD as being along the same spectrum as schizophrenia and coined the term “schizophrenia spectrum” suggesting a similar genetic predisposition and clinical presentation. Siever and Davis (2004) have documented the biological similarities between schizophrenia and SPD, and here we have documented cognitive and functional deficits in SPD which are also seen in schizophrenia. This raises the issue as to whether SPD would be better termed schizophrenia II, not unlike the nomenclature of bipolar II, in which the symptoms follow those in bipolar disorder, but are less extreme. The importance of this exceeds a semantic argument. By viewing SPD as a disease, closely allied with schizophrenia, research into the pathogenesis and potential treatment approaches may be strengthened.