Fluctuating dermatoglyphic asymmetries in youth at ultrahigh-risk for psychotic disorders

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Abstract

Fluctuating dermatoglyphic asymmetry represents one specific class of minor physical anomaly that has been proposed to reflect prenatal insult and vulnerability to psychosis. However, very little is known about fluctuating dermatoglyphic asymmetry in youth showing symptoms of ultrahigh risk (UHR) for psychosis. Using high-resolution photographs of fingerprints and clinical interviews, the UHR group in this study showed greater fluctuating dermatoglyphic asymmetry compared to controls; however, this was not further linked to symptomatology. The results of this study provide an important perspective on potential biomarkers and support neurodevelopmental conceptions of psychosis.

Introduction

A large body of research indicates that genetics and prenatal insult are both significant contributors to vulnerability for psychosis (Mittal et al., 2008a). One proposed measure that taps into both processes is dermatoglyphics; the patterns of ridge folds on the fingers, palms and soles of feet that form during the second trimester (Bramon et al., 2005). As finger and handprints are formed from the same germinal layer as the brain, asymmetries in the fingers may also reflect insult to early prenatal brain development (Compton and Walker, 2009).

Fluctuating dermatoglyphic asymmetry, characterized by different ridge patterns or counts between homologous fingers, may be linked to hereditable factors (Golembo-Smith et al., 2012). Cross sectional studies of family members with a relative or twin with schizophrenia and young adults with schizotypal personality disorder provide substantial evidence for fluctuating asymmetry in those at risk for psychosis (Gabalda and Compton, 2010, Markow and Gottesman, 1989, Mittal et al., 2012, Rosa et al., 2005). Given that dermatoglyphics represent an intersection between the intrauterine environment and genetic factors, these features hold significant promise for biomarker development. Indeed, one notable prospective investigation observed that high-risk family members of persons with schizophrenia, who also go on to develop a psychotic disorder, have simpler fingerprint patterns when compared to healthy persons and high risk persons who do not develop psychosis (Langsley et al., 2005).

Despite a large body of research pointing to fluctuating dermatoglyphic asymmetry as an etiological marker of risk for psychosis, very little is known about whether fluctuating asymmetry is present in individuals at imminent risk for psychosis such as those with ultrahigh-risk (UHR) syndromes. Finding reliable risk factors for this population is particular important as a significant proportion will go on develop psychosis in a short period (Cannon et al., 2008). Indeed, phenotypic markers that allow for early identification of individuals at UHR can help to reduce the duration of untreated psychosis and inform decisions about targeted intervention implementation. While altered dermatoglyphics do not pinpoint a specific prenatal event or genetic contribution; this line of research holds several advantages that may be useful in risk-calculator development (Cannon, 2010). Specifically, dermatoglyphics are readily quantifiable in non-invasive and inexpensive fashion, they provide continuous data, and they also are not affected by rater bias or retrospective bias in comparison to methods of self-report for evaluating the prenatal environment (McIntosh et al., 2002). Further, innovations in print scanning provide a way to clearly examine dermatoglyphics without the complications of ink or colorless ink methods.

In this study, clinical symptoms and dermatoglyphic asymmetries were evaluated in UHR participants and healthy controls. We predicted that the UHR group would exhibit greater fluctuating dermatoglyphic asymmetry when compared with controls and that these asymmetries would be associated with elevated symptoms.

Section snippets

Participants

Participants (n = 51 UHR, n = 45 Control) between the ages of 12 and 21 (Mean age = 18.20, SD = 2.39) were recruited by Internet advertising, email postings, newspaper ads, and community professional referrals. Exclusion criteria included history of head injury, the presence of a neurological disorder, and lifetime substance dependence. The presence of an Axis I psychotic disorder was an exclusion criterion for UHR participants. The presence of a psychotic disorder in a first-degree relative or meeting

Participants

No significant differences were found for demographic variables including age, sex, education or parental education. Men and women in this sample did not differ in terms of fluctuating dermatoglyphic asymmetries, z =  1.837, p  .1. As expected, UHR participants were rated significantly higher than controls on positive and negative symptom domains (see Table 1).

Group differences in fluctuating dermatoglyphic asymmetries and relationship to symptoms

A Kolmogorov-Smirnoff test revealed that the distribution of total asymmetry scores were not normal, D = .13, p  .001, with skewness of 1.004

Discussion

A neural diathesis-stress model of psychosis suggests that early vulnerability may, in part, reflect genetic or epigenetic alterations and prenatal insult (Walker et al., 2008). Evidence suggests that objective signs of prenatal insult such as minor physical anomalies and fluctuating dermatoglyphic asymmetry may be related to an underlying vulnerability that later interacts with neurodevelopmental and environmental factors, ultimately contributing to psychosis (Golembo-Smith et al., 2012,

Conflict of interest

None.

Contributors

Authors O.D.F.R, V.A.M and D.J.D developed the study concept. V.A.M. obtained funding for the study. All authors contributed to the study design. Testing, data collection as well as data analysis and interpretation were performed by O.D.F.R and L.I under the supervision of V.A.M and D.J.D. O.D.F.R drafted the paper under the supervision of D.J.D. L.I and V.A.M provided the critical revisions. All authors approved the final version of the paper for submission.

Acknowledgment

This work was supported by National Institutes of Health Grants R01MH094650 and R21/R33MH103231 to V.A.M.

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