Schizophrenia Research 142 (2012) 111

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Schizophrenia Research
journal homepage: www.elsevier.com/locate/schres

Review

The presentation of dermatoglyphic abnormalities in schizophrenia: A

meta-analytic review
Shana Golembo-Smith a, Deborah J. Walder b, Maureen P. Daly c, Vijay A. Mittal d, Emily Kline e,
Gloria Reeves f, Jason Schiffman e,
a

Department of Psychology, University of Hawaii, Manoa, United States

Department of Psychology, Brooklyn College of The City University of New York, United States
The Graduate Center and Queens College of The City University of New York, United States
d
Department of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, United States
e
Department of Psychology, University of Maryland, Baltimore County, United States
f
Department of Psychiatry, University of Maryland School of Medicine, United States
b
c

a r t i c l e

i n f o

Article history:
Received 6 July 2012
Received in revised form 28 September 2012
Accepted 1 October 2012
Available online 29 October 2012
Keywords:
Schizophrenia
Dermatoglyphics
Meta-analysis
Neurodevelopment

a b s t r a c t
Within a neurodevelopmental model of schizophrenia, prenatal developmental deviations are implicated as
early signs of increased risk for future illness. External markers of central nervous system maldevelopment
may provide information regarding the nature and timing of prenatal disruptions among individuals with
schizophrenia. One such marker is dermatoglyphic abnormalities (DAs) or unusual epidermal ridge patterns.
Studies targeting DAs as a potential sign of early developmental disruption have yielded mixed results with
regard to the strength of the association between DAs and schizophrenia. The current study aimed to resolve
these inconsistencies by conducting a meta-analysis examining the six most commonly cited dermatoglyphic
features among individuals with diagnoses of schizophrenia. Twenty-two studies published between 1968
and 2012 were included. Results indicated signicant but small effects for total nger ridge count and total
AB ridge count, with lower counts among individuals with schizophrenia relative to controls. Other DAs examined in the current meta-analysis did not yield signicant effects. Total nger ridge count and total AB
ridge count appear to yield the most reliable dermatoglyphic differences between individuals with and without schizophrenia.
2012 Elsevier B.V. All rights reserved.

1. Introduction
The neurodevelopmental model posits that schizophrenia is caused in
part by disruptions in central nervous system (CNS) development beginning as early as the prenatal period (Weinberger, 1987, 1995). In addition
to genetic factors, prenatal factors such as infection (see Mittal et al.,
2008a; Brown and Derkits, 2010), maternal stress exposure (Khashan
et al., 2008), and obstetric complications (OCs; Lewis and Murray, 1987;
Dalman et al., 1999; McNeil and Cantor-Graae, 2000) have all been linked
with increased risk for schizophrenia (for review see Mittal et al., 2008b;
Walder et al., in press). These prenatal insults are thought to adversely
impact CNS development and can be assessed indirectly in the atypical
presentation of morphologic traits (e.g., Van Erp et al., 2002; Haukvik
et al., 2010; Qiu et al., 2010).
One such class of morphologic traits is dermatoglyphic abnormalities (DAs). Dermatoglyphic features are relatively stable and
Corresponding author at: Department of Psychology, University Of Maryland,
Baltimore County, Baltimore, MD 21250, United States. Tel.: + 1 410 455 1535; fax:
+ 1 410 455 1055.
E-mail address: schiffma@umbc.edu (J. Schiffman).
0920-9964/$ see front matter 2012 Elsevier B.V. All rights reserved.
http://dx.doi.org/10.1016/j.schres.2012.10.002

cosmetically insignicant epidermal ridge patterns that form prints

on the ngers, hands, and soles. DAs are thought to represent, in
part, the impact of prenatal insults, thus providing a window into
the timing and nature of early development (Cummins and Midlo,
1961; Davis and Bracha, 1996; Lobato et al., 2001). The development
of dermatoglyphics overlaps temporally with neuronal migration
(Bracha et al., 1991). Although the precise origins of DAs remain
unclear, their presence may suggest prenatal disruption relevant to
the formation of neural structures implicated in future development
of schizophrenia.
Several indices have been used to capture DAs. Measures typically
rely on epidermal ridge counting, which makes use of the triradius, or
meeting point of three opposing ridge systems. Commonly used indices
include 1) nger ridge counts (the number of ridges between the core
of the nger pattern and its corresponding triradius), 2) palmar ridge
counts (the number of ridges crossing a line superimposed on the
palm print connecting two triradii), 3) ngertip patterns (shapes created by the patterns of nger ridges characterized as whorls, ulnar/radial
loops, and arches), 4) ATD angle (the angle formed by lines drawn from
triradius t, the most distal axial triradius near the base of the palm, to
triradii a and d, located proximal to the index and little ngers,

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

respectively), and 5) uctuating asymmetries (differences in ridge

counts or pattern types between parallel structures on the left and
right hands) (Cummins and Midlo, 1961; Palmer, 1994).
DAs such as ridge counts and ngertip patterns may reect different
developmental responses to a range of specic insults rather than a unitary construct indicating generic developmental disruption (Compton
and Walker, 2009). Some DAs appear to be more inuenced by environmental causes, with others closely linked to genetic factors (e.g., Holt,
1968; Bracha et al., 1991, 1992; van Oel et al., 2001; Bramon et al.,
2005). For example, from an environmental perspective, mild prenatal
stress is associated with greater dermatoglyphic asymmetry among macaque offspring (Newell-Morris et al., 1989). Similarly, among humans,
prenatal maternal stress during the period of nger ridge development
(weeks 1422) is associated with more DAs among offspring (King
et al., 2009). Evidence indicating a link between chromosomal anomalies
and alterations in dermatoglyphic and palmar exion creases suggests
genetic inuences on the formation of DAs as well (Reed, 1981). Deviant
ATD angles have been associated with chromosomal syndromes; namely, in 22q Deletion Syndrome patients, those with mental retardation had
greater ATD angles than those with psychotic symptoms, who both
had greater angles than healthy controls (Martn et al., 2004). More
specically pertaining to schizophrenia, a family study of people
with a schizophrenia spectrum disorder and their rst-degree relatives found associations between both genetically-inuenced ectodermal derivate abnormalities (e.g., ridge dissociation, abnormal
palmar exion creases) and environmentally-inuenced abnormalities such as total a-b ridge count and schizophrenia vulnerability
(Fatj-Vilas et al., 2008).
Although the noted studies have suggested that specic DAs share
some etiology with schizophrenia, the overall association between DAs
and schizophrenia remains unclear. Bramon et al. (2005) meta-analytic
review of nine studies (published between 1983 and 2003) examining
palmar ab ridge count in individuals with schizophrenia compared to
controls yielded a pooled standardized effect size of 0.39 (p=.03).
There is, however, substantial variability in effect sizes across published
DA studies. For example, Bramon and colleagues found signicant heterogeneity in effect sizes (pb .0001) ranging from 0.05 to 1.15, indicating between-group differences ranging from negligible to substantive.
To date, research on dermatoglyphics has been relatively limited,
and the available literature has been complicated by methodological inconsistencies (for a review see Compton and Walker, 2009). For example, variation in techniques for quantifying DAs has likely contributed to
discrepancies in the literature, rendering cross-study comparisons challenging. Further, modest sample sizes typically used in this line of research may limit statistical power to detect group differences. Efforts
to clarify dermatoglyphic differences between people with schizophrenia and controls using systematic review approaches have been limited.
Bramon and colleagues' meta-analysis, for example, included only nine
studies and limited examination to a single dermatoglyphic measure
(2005). Understanding DAs in the context of a more comprehensive
meta-analysis stands to correct for the limited power problem in the
dermatoglyphic literature and enable comparison between multiple
dermatoglyphic markers. The current study aims to ll this gap in the
literature by conducting an updated (including studies from 1968 to
2012) and comprehensive (examining the six most cited dermatoglyphic features) meta-analytic review of dermatoglyphic abnormalities in schizophrenia patients relative to nonclinical (healthy) controls.
2. Methods
2.1. Literature search and selection
This meta-analysis included peer-reviewed articles examining a
range of dermatoglyphic measures in individuals with schizophrenia
and controls. Relevant articles were identied using the electronic databases PubMed and PsycINFO, using search terms schizophrenia

and dermatoglyphic* and psychosis and dermatoglyphic* between

January 1968 and June 2012. Reference lists of identied articles were
explored for additional articles. Inclusion criteria were modeled after
Weinberg et al. (2007) meta-analysis of minor physical anomalies,
which similarly reect neurodevelopmental disruption (Compton and
Walker, 2009). Inclusion criteria were 1) casecontrol design, 2) available published means and standard deviations, 3) participants with specic diagnoses of schizophrenia obtained using established diagnostic
procedures, 4) data not overlapping between published studies, and
5) availability in English. Studies that included unique dermatoglyphic
features that were only represented in one publication, and did not
appear in any other published research, were excluded. In total, 22 studies were included and 43 were excluded (see Table 1 for a list of studies
excluded from current analyses).
2.2. Dermatoglyphic measures
Six dermatoglyphic indices were examined: total nger ridge count,
total ab palmar ridge count, ngertip pattern asymmetry, ATD angle,
uctuating asymmetry of nger ridge count, and palmar ab uctuating
asymmetry.
2.2.1. Ridge counts
Ridge counting uses the triradius, or the meeting point of three
opposing ridge systems (see Fig. 1). Total nger ridge count (TFRC;
number of ridge counts between the core of the nger pattern and
its corresponding triradius; arch patterns do not have triradii and receive a ridge count of zero) and total ab palmar ridge count (TABRC;
number of palmar ridges crossing a line superimposed on a palm
print that connects triradius a, located proximal to the index nger,
and triradius b, located proximal to the middle nger) are two such
types of epidermal ridge counts (Green et al., 1994).
2.2.2. Fingertip patterns
Fingertip patterns are typically identied as whorls, loops, or
arches, depending on the number of triradii, namely two, one, and
zero, respectively (Mellor, 1968). Whorls are purported to be more
complex than loops, which are in turn more complex than loops
and arches; individuals with more arches than whorls are theorized
to have simplied ngertip ridge patterns (Cummins and Midlo,
1961). As whorls by denition have higher ridge counts than loops
and arches, the same mechanisms leading to lower ridge count
may account for pattern simplication. Fig. 1 shows an example of
the nger ridge count technique of an ulnar loop pattern and the
identication of the corresponding triradius. Fig. 2 shows an illustration of the landmarks used to quantify ab palmar ridge counts.
2.2.3. ATD angle
The ATD angle is a dermatoglyphic feature that compares the length of
the hand to the width by measuring the angle created by superimposing
lines on the palm print from the axial triradius (t) at the base of the
palm to the a and d triradii of the palm located proximal to the 2nd
and 5th digits, respectively (Elizarrars-Rivas et al., 2002).
2.2.4. Fluctuating asymmetry (FA)
FA refers to random differences between parallel structures on the left
and right sides of the body (Mellor, 1992). Greater rightleft (RL) differences indicate greater FA (van Valen, 1962; Palmer and Strobeck, 1986;
Mellor, 1992; Palmer, 1994). Palmar AB uctuating asymmetry (or uctuating TABRC; FABRC) is determined by subtracting right TABRC from
left TABRC, and dividing that number by right TABRC plus left TABRC.
Similarly, TFRC uctuating asymmetry (or uctuating asymmetry of
total nger ridge count; FAFRC) is determined by subtracting right
TFRC from left TFRC and dividing that number by the sum of TFRC
from both hands (Green et al., 1994; van Oel et al., 2001).

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

2.3. Statistical analysis

MIX 2.0 (Bax, 2011) meta-analysis software was used for all analyses. Each dermatoglyphic feature was analyzed separately. Thus,
data from an individual study can be used in multiple sub-analyses.
Hedges' g effect sizes, 95% condence intervals, and z-scores were calculated separately for each study subset. Hedges' g provides a measure of effect size while correcting for biases due to small sample
sizes. As with Cohen's d, a Hedges' g effect size of 0.2 is considered
small, 0.5 moderate, and 0.8 large (Cohen, 1992). The direction of
the effect was positive when scores for the schizophrenia group
were larger than scores for the control group. A Q statistic was then
calculated to examine variance across effect sizes within each data
subset. The Q statistic tests the null hypothesis that the studies' effect
sizes are homogeneous (Cochran, 1954). Data subsets were analyzed
using xed-effects models when the Q statistic test demonstrated
that the effect size of the population did not demonstrate signicant
heterogeneity; those whose Q statistic suggested signicant heterogeneity among studies were analyzed using a random-effects model
(Becker, 1996; Hunter and Schmidt, 2000; Field, 2003).
To determine the potential effects of the le-drawer problem
(i.e., negative or non-signicant ndings tend to go unpublished),
Rosenthal's fail-safe N statistic was calculated for each data subset
(Rosenthal, 1979). The fail-safe N provides an assessment of sampling
bias in that it estimates how many hypothetical studies with an effect
size of zero would need to be incorporated into the analysis to render
the found p-value non-signicant. In addition, Begg and Mazumdar's
adjusted rank correlation test was employed to test for publication
bias (1994).
3. Results
The results of each individual meta-analysis are summarized in
Table 2.
3.1. Total nger ridge count
Table 3 provides raw data, effect sizes, and z-values for the 18 studies reporting TFRC data. Absolute effect sizes for the three TFRC datasets
were signicantly heterogeneous (Q = 56.96, p b .001) and ranged from
g = 0.01 (small) to g = 0.71 (moderate) (Cohen, 1988). Begg's test
Table 1
Studies excluded from current analyses.
Primary reason for
exclusiona

Studies

Not casecontrol design

Zavala and Nez (1970); Balgir et al. (1980); Markow

and Gottesman (1989); Bracha et al. (1992); Green et
al. (1994); Davis and Bracha (1996); Faans et al.
(1996b); van Os et al. (1997); Rosa et al. (2000a),
2000b, 2002; Kelly et al. (2004); Rosa et al. (2005); Daly
et al. (2008)
Raw data or mean scores Rosner and Steinberg (1968); Sank (1968); Stowens et
not available
al. (1970); Polednak (1972); Srinivasa Murthy and Wig
(1977); Mellor (1992); Varma et al. (1995); Chary et al.
(1996); Arboleda-Flrez et al. (1998); Sivkov and
Akavaliev (1998); Ponnudurai (1999); Sivkov et al.
(2007)
Not purely schizophrenia Weinstein et al. (1999); Barrantes-Vidal et al. (2003);
diagnoses
Chok and Kwapil (2005); Chok et al. (2005); Fatj-Vilas
et al. (2008)
Faans et al. (1996a) (CSM sample); Mellor (1968);
Published elsewhere/
Hilbun (1970); Jelovac et al. (1995); Jelovac et al.
Used previously
(1999); Rosa et al. (2003); Johnstone et al. (2005)
published data
Not available in English Nmstek and Hronek (1974); Perkovic (1977);
Dvokov and Zvolsk (1979); Tnyi et al. (2000)
Unique dermatoglyphic Shakibaei et al. (2011)
measure
a

Some studies were excluded for multiple reasons.

Fig. 1. Ulnar loop with corresponding nger ridge line and triradius. The nger print
pattern is taken from the left second nger (L2). In the rst picture, a red box outlines
the triradius of the ulnar loop. The triradius is formed by the convergence of 3 ridges
(colored black). In the second picture, a yellow line from the triradius to the core of
the ngerprint shows that the ulnar loop has a ridge count of 8. A ridge count is
obtained by counting the ridges between the triradius and the core (not counting the
ridges the make up the triradii or the core).

indicated that there was no evidence of a signicant publication bias

(z = 0.95, p = .34). The tests performed on TFRC studies resulted in a
signicant effect size (g = 0.20, 95% C.I. =0.270.13, p b .05), with
lower TFRC among patients with schizophrenia relative to controls.
Fig. 3 presents a forest plot of TFRC effect sizes.
3.2. Total AB ridge count
Table 4 provides raw data, effect sizes, and z-values for 18 studies
reporting TABRC data (including 9 studies not included in the Bramon
et al. (2005) meta-analysis). Absolute effect sizes for TABRC were signicantly heterogeneous (Q = 151.00, p b .001) and ranged from g =
0.03 (small) to g = 1.11 (large). Begg's test indicated that there
was no evidence of a signicant publication bias (z = 0.27, p = .79).
Analyses of TABRC across all studies resulted in a signicant effect size
(g = 0.31, 95% C.I.= 0.380.24, p b .01), with lower TABRC among
patients with schizophrenia. Fig. 4 presents a forest plot of all TABRC
effect sizes.
3.3. ATD angle
Table 5 provides raw data, effect sizes, and z-values for 10 studies
reporting total ATD angle data. ATD angle absolute effect sizes were signicantly heterogeneous (Q =44.49, p b .001) and ranged from g = 0.01

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Fig. 2. AB ridge count example. AB Ridge count: The handprint shows an example of an AB ridge count. The AB ridge count is obtained by counting the ridges (colored black)
between the triradii found below the second and third nger. The triradii are outlined in red boxes, and a yellow line drawn from one triradius (a) to the other (b) allows one to
count the number of ridges between the triradii. Only the ridges that fully cross the line are counted. The AB ridge count is 34 in this example.

(small) to g = 0.84 (large). The meta-analysis was non-signicant

(g =0.10, 95% C.I.= 0.200.01). Begg's test indicated that there
was no evidence of a signicant publication bias (z = 0.26, p = .79).
Fig. 5 presents a forest plot of ATD angle effect sizes.

3.4. Fingertip pattern asymmetrythree-pattern classication

Table 6 provides raw data, effect sizes, and z-values for four studies
reporting three-pattern classication (i.e., whorl, loop, or arch) ngertip
pattern asymmetry data. Overall, there was a non-signicant effect size
of g =0.25 (95% C.I.= 0.080.59) and signicant between-study heterogeneity (Q = 11.75, p b .05). Begg's test indicated that there was no
evidence of a signicant publication bias (z = 0.25, p = .81).

3.5. Fluctuating asymmetry nger ridge count (FAFRC)

Table 7 provides raw data, effect sizes, and z-values for three
studies reporting FAFRC data. The effect size for all datasets combined
was not signicant (g = 0.31, 95% C.I. = 0.501.12); there was signicant heterogeneity across studies (Q = 54.17, p b .001). Begg's
test indicated that there was no evidence of a signicant publication
bias (z = 0.68, p = .50).

3.6. Fluctuating asymmetry AB ridge count (FABRC)

Table 8 provides raw data, effect sizes, and z-values for three studies
reporting FABRC data. The absolute effect size was moderate (g = 0.75)
and non-signicant; there was signicant heterogeneity among studies
(Q = 146.89, p b .001). Begg's test indicated that there was no evidence
of a signicant publication bias (z = 1.36, p = .17).
4. Discussion
4.1. General conclusions
This meta-analysis in part supports a neural diathesis-stress model
of schizophrenia (see Bracha et al., 1991; Walker and Diforio, 1997),
demonstrating small effect size differences between individuals with
schizophrenia and controls across DAs that likely reect early developmental deviation. The two DAs analyzed using the largest overall sample sizes revealed the most reliable and robust (albeit small) effect
sizes; namely, TFRC (g = 0.20, p b .05; fail-safe N = 83) and TABRC
(g = 0.31, p b .01; fail-safe N= 238). These ndings are consistent
with a prior meta-analysis that included approximately half the number
of studies and focused on palmar ridge count in schizophrenia (Bramon
et al., 2005). Among DA measures, TFRC and TABRC appear to most reliably differentiate people with and without schizophrenia and thus,

Table 2
Summary of meta-analyses results.
DA feature

n SZ

n Control

Effect size (g)

95% LL

95% UL

z-score

Fail-safe N

TFRC
TABRC
ATD angle
Fingertip asymmetry (three-pattern)
FAFRC
FABRC

1626
1699
819
249
233
241

1690
1736
687
227
298
298

0.20
0.31
0.10
0.25
0.31
0.75

0.27
0.38
0.20
0.08
0.50
0.65

0.13
0.24
0.01
0.59
1.12
2.13

5.48
8.71
1.81
1.490
0.75
1.05

56.96
151.00
44.49
11.75
54.17
146.89

83
238
43
4
15
14

p b 0.05.
p b 0.01.
p b 0.001.

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Table 3
Total nger ridge count (TFRC).
Study

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect Size (g)

95% LL

95% UL

Arunpongpaisal et al. (2011)

Avila et al. (2003)
Cantor-Graae et al. (1998)b
Elizarrars-Rivas et al. (2002)
Faans et al. (1990)b
Faans et al. (1996b)
Fearon et al. (2001)
Gabalda and Compton (2010)
Jhingan and Munjal (1989)
Kemali et al. (1972)
Kemali et al. (1976)
Pez et al. (2001)a
Reilly et al. (2001)a
Rothhammer et al. (1971)b
Saha et al. (2003)b
Turek (1990)b
van Oel et al. (2001)
Youse-Nooraie and Mortaz-Hedjri (2008)a

68
86
60
20
139
29
126
62
50
55
217
72
19
80
181
310
19
33

135.50
114.17
143.44
161.1
122.03
131.7
126.4
131.84
145.5
142.78
134.9
130.6
131.07
133.78
137.65
116.26
139.74
154.2

68
46
75
20
72
55
82
47
50
54
105
72
37
176
228
400
70
33

139.10
140
146.09
153.2
143.31
128
126.9
115.6
144.06
146.89
142.06
163.9
146.78
131.26
139.57
137.21
125.39
150.4

0.1
0.57
0.05
0.21
0.46
0.07
0.01
0.29
0.04
0.09
0.16
0.71
0.32
0.06
0.04
0.50

0.43
0.93
0.4
0.41
0.75
0.38
0.29
0.09
0.35
0.46
0.39
1.04
0.87
0.21
0.23
0.65
0.19
0.41

0.24
0.2
0.29
0.83
0.17
0.52
0.27
0.68
0.43
0.29
0.07
0.37
0.24
0.32
0.16
0.35
0.82
0.55

2.33
3.059
0.31
0.67
3.11
0.32
0.076
2.76
0.196
0.451
1.35
4.1
1.12
0.42
0.39
6.53
1.21
0.29

(33.92)
(42.24)
(52.51)
(47.39)
(43.86)
(47.2)
(44.4)
(56.15)
(33.9)
(45.36)
(42.23)
(46.87)
(40.71)
(39.80)
(47.12)
(36.96)
(43.88)
(53.87)

(40.12)
(50.09)
(45.54)
(21.12)
(50.89)
(51.6)
(49)
(52.65)
(38.87)
(48.99)
(48.82)
(46.90)
(52.95)
(46.15)
(51.51)
(45.07)
(45.52)
(51.70)

0.31
0.07

Means and standard deviations pooled from left- and right-hand data.
Means and standard deviations pooled from male and female data.
p b 0.05.
p b 0.01.
p b 0.001.
b

appropriately, are the DAs most often reported in the schizophrenia research literature. It is notable, however, that these two features are also
the most widely studied, resulting in sample sizes far greater than
other dermatoglyphic features. Although this disparity should be
taken into account when considering the current results, the
present state of the literature precludes a denitive answer as to
whether this robustness is due to true population differences or
subject to change if future research were to further investigate the
less-studied dermatoglyphic features.
4.2. Timing of prenatal disruptions
Some dermatoglyphic features have been tied to specic stages of
prenatal development. This information can be used to make assumptions about the timing of neurodevelopmental disruptions inuencing
schizophrenia vulnerability. For example, TFRC is thought to reect the
speed of fetal growth, with more ridges indicating faster cell division during the rst and second trimester of gestation (Cohen-Bendahan et al.,
2005). In contrast, TABRC is largely believed to reect later fetal development and to be more inuenced by non-shared environmental factors
(Bracha et al., 1991, 1992; van Oel et al., 2001; Bramon et al., 2005).
More specically, although the AB ridges are among the rst to appear
(i.e., interdigital area II), they develop over a longer period of time, and
thus may be more sensitive to a variety of developmental disturbances
relative to nger ridge formation (Rose, 1987; Faans et al., 1996a).
That TFRC and TABRC yielded signicant effects across studies suggests
that schizophrenia may be more inuenced by disruptions occurring at
multiple stages across prenatal development.

1992; Green et al., 1994; Cantor-Graae et al., 1998). In other words, distinct prenatal events differentially impact specic dermatoglyphic features, all of which may be etiologically related to schizophrenia. For
example, disrupted neurodevelopment due to intrauterine growth restriction may result in abnormal decreases (simplication) of nger
and palmar ridges. Further, prenatal edema results in abnormal increases in ridges (Bracha et al., 1992, 1995). In addition, both human
and animal research suggests that prenatal maternal stress during the
period of ngerprint development (weeks 1422) results in greater
dermatoglyphic asymmetry among offspring (Newell-Morris et al.,
1989; King et al., 2009). In contrast, ectodermal derivate abnormalities
(e.g., ridge dissociation; abnormal palmar exion creases) appear to reect primarily genetically inuence (Fatj-Vilas et al., 2008). It is also
important to note that prenatal insults do not necessary reect a purely
environmental contribution, as an emerging literature suggests that
genes can adversely affect the prenatal environment or lead to additional
obstetric complications as well (Katila et al., 1999; Boin et al., 2001;
Engel et al., 2005). For example, polymorphisms associated with abnormalities in immune function (e.g., an exaggerated inammatory response to infection) may render a mother and fetus more susceptible
to the deleterious effects of prenatal events and lead to fetal neuronal
injury (see Ellman and Cannon, 2008 for a review). Any of these potential causes of developmental disruption may also vary locally between
populations. Thus the heterogeneity of insults may differentially inuence specic DAs among groups of people with schizophrenia,
obscuring potential differences between patients and controls. In
some cases it may be more fruitful to identify individuals who fall
outside (above or below) the expected normative range of DAs,
as reected by relatively increased or decreased ridge counts.

4.3. DA variability
4.4. Limitations
Despite TFRC and TABRC yielding signicant group differences between individuals with schizophrenia and controls, there was considerable variability across studies. For instance, some studies reported
lower TFRC in people with schizophrenia, while others reported
higher TFRC count in people with schizophrenia. Nonetheless, all statistically signicant ndings were in the direction of reduced TFRC
among people with schizophrenia.
Due to local differences, samples may contain individuals with varying mean levels and types of prenatal disruptions, leading to mean differences in DA patterns and confounding omnibus results (Bracha et al.,

There are a number of important limitations in this meta-analysis.

First, we excluded studies of individuals with schizophrenia spectrum
disorders or those at-risk for schizophrenia. In light of evidence of DAs
in at-risk groups (Chok et al., 2005; Langsley et al., 2005; Daly et al.,
2008), future reviews across a broader range of diagnostic groups is
warranted to see if patterns hold along a continuum of psychotic symptom manifestation. Second, the overall number of studies was relatively
small, limiting power to detect statistical signicance. Third, utilizing
xed-effects models in meta-analyses has the potential of increasing

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

TFRC Forest Plot

Arunpongpaisal et al.,
2011
Avila et al., 2003
Cantor-Graae et al., 1998
Elizarrars-Rivas et al.,
2002
Faans et al., 1990
Faans, van Os, and
Hoyos et al., 1996
Fearon et al., 2001
Gabalda & Compton,
2010
Jhingan and Munjal,
1989
Kemali et al., 1972
Kemali et al., 1976
Pez et al., 2001
Reilly et al., 2001
Rothhammer et al., 1971
Saha et al., 2003
Turek, 1990
van Oel et al., 2001
Yousefi-Nooraie &
Mortaz-Hedjri, 2008

-1.5

-1

-0.5

0.5

hg
Fig. 3. Forest plot of TFRC meta-analysis.

Type I error rates. This is particularly problematic when analyses include more than 20 studies and when authors assume homogeneous
population parameters. Nevertheless, alternative strategies are lacking
with respect to analyses that include fewer studies. In the current
study, we aimed to utilize the most accurate effects models by analyzing
population heterogeneity (Field, 2003). Fourth, methodological and demographic variability across studies may have impeded accurate effect
size estimates and contributed to the sizable heterogeneity in means
and effect sizes. The anthropology literature cites longstanding evidence of racial/ethnic group differences (e.g., Cummins and Midlo,
1961; Rosner and Steinberg, 1968; Jantz, 1987), and more recently geographic region of origin differences (e.g., Arrieta et al., 2003; Karmakar
et al., 2005; Karmarkar and Kobyliansky, 2009; Zhang et al., 2010). For
example, northern and southern Chinese populations can be differentiated based on dermatoglyphic analysis (Zhang et al., 2010). Not all studies included in the current meta-analysis matched cases and controls on

ethnicity or region of origin. This collapsing (or lack of matching) across

ethnically or geographically diverse samples may have masked true diagnostic group differences. Likewise, few studies reported data separately by sex, restricting examination of sex effects.
It is noteworthy, however, that in a series of studies, Karmakar,
Kobyliansky and colleagues consistently and accurately classied
males and females across various ethnic groups by applying discriminant analyses to several derived qualitative and quantitative
dermatoglyphic traits (Micle and Kobyliansky, 1986; Kobyliansky
and Micle, 1988; Micle and Kobyliansky, 1991; Karmarkar and
Kobyliansky, 2009). The authors posit that these sex differences indicate common genetic components within the two major classes of
dermatoglyphic traits that are at least in part sexually dimorphic.
The degree to which this carries across diagnostic groups is as yet
unclear. As with any meta-analysis, results are only as reliable as
the studies included.

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Table 4
Total AB ridge count (TABRC).
Study

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect size (g)

95% LL

95% UL

Arunpongpaisal et al. (2011)

Bramon et al. (2005)
Cantor-Graae et al. (1998)
Elizarrars-Rivas et al. (2002)
Faans et al. (1990)
Faans et al. (1996a)
Fearon et al. (2001)
Kemali et al. (1972)
Kemali et al. (1976)
Markow and Wandler (1986)a
Pez et al. (2001)a
Reilly et al. (2001)a
Rothhammer et al. (1971)b
Saha et al. (2003)b
Turek (1990)b
van Oel et al. (2001)
van Os et al. (2000)
Youse-Nooraie and Mortaz-Hedjri (2008)a

68
125
60
20
139
38
140
55
217
81
72
27
86
181
310
19
28
33

76.31 (9.49)
79.1 (10.6)
79.94 (9.32)
89.1 (13.04)
76.6 (9.78)
76.2 (11.1)
78 (16.1)
81.38 (10.49)
82.94 (10.92)
83.44 (13.89)
80.8 (11.52)
79.19 (15.08)
78.00 (10.67)
84.31 (9.85)
71.63 (10.14)
78.41 (12.19)
74.4 (11.5)
84.8 (10.60)

68
98
75
20
72
44
85
54
105
69
72
37
187
228
400
70
19
33

76.68
81.1
80.24
83.7
81.53
81.4
82.6
81.89
81
84.26
86.7
84.17
82.46
83.83
84.14
80.73
77.7
82.3

0.04
0.18
0.03
0.51
0.50
0.46
0.29

0.38
0.45
0.37
0.12
0.79
0.9
0.56
0.42
0.06
0.39
0.76
0.88
0.46
0.15
1.27
0.72
0.86
0.25

0.29
0.08
0.31
1.14
0.21
0.02
0.02
0.33
0.41
0.26
0.1
0.12
0.06
0.24
0.95
0.3
0.31
0.72

0.09
1.33
0.18
1.58
3.41
2.04
2.13
0.25
1.48
0.4
2.56
1.48
1.53
0.47
13.64
0.81
0.93
0.96

(7.92)
(11.6)
(9.47)
(6.75)
(9.8)
(11.4)
(14.7)
(10.56)
(11.09)
(10.80)
(15.42)
(11.23)
(12.96)
(10.89)
(12.09)
(10.59)
(12)
(10.21)

0.05
0.18
0.06
0.43
0.38
0.20
0.05
1.11
0.21
0.28
0.24

Means and standard deviations pooled from left- and right-hand data.
Means and standard deviations pooled from male and female data.
p b 0.05.
p b 0.01.
p b 0.001.
b

TABRC Forest Plot

Arunpongpaisal et al., 2011
Bramon et al., 2005
Cantor-Graae et al., 1998
Elizarrars-Rivas et al., 2002
Faans et al., 1990
Faans, van Os, and Hoyos et
al., 1996
Fearon et al., 2001
Kemali et al., 1972
Kemali et al., 1976
Markow and Wandler, 1986
Pez et al., 2001
Reilly et al., 2001
Rothhammer et al., 1971
Saha et al., 2003
Turek, 1990
van Oel et al., 2001
Van Os et al., 2000
Yousefi-Nooraie and MortazHedjri, 2008

-1.5

-1

-0.5

0.5

hg
Fig. 4. Forest plot of TABRC meta-analysis.

1.5

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Table 5
ATD angle.
Study

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect size (g)

95% LL

95% UL

Avila et al. (2003)

Elizarrars-Rivas et al. (2002)
Pez et al. (2001)a
Jhingan and Munjal (1989)
Rothhammer et al. (1971)b
Turek (1990)b
Jhingan and Munjal (1990)a
Kemali et al. (1976)
Kemali et al. (1972)
Youse-Nooraie and Mortaz-Hedjri (2008)a

86
20
72
50
140
97
50
217
54
33

84 (11.77)
85.84 (18.02)
89.1 (18.84)
84.16 (14.79)
86.39 (13.67)
78.56 (10.28)
74.48 (8.37)
92.54 (19.59)
90.2 (16.27)
93 (18.70)

46
20
72
50
100
157
50
105
54
33

82.53
85.16
89.5
79.46
86.74
86.35
82.55
90.96
90.33
85.6

0.14
0.05
0.02
0.32
0.03
0.66
0.84

0.22
0.57
0.35
0.07
0.28
0.92
1.25
.15
0.39
0.06

0.50
0.67
0.31
0.72
0.23
0.40
0.43
.32
0.37
0.91

0.75
0.16
0.12
1.60
0.21
5.01
4.01
.718
0.04
1.70

(8.25)
(5.46)
(21.80)
(14.18)
(11.87)
(12.50)
(10.6)
(15.88)
(14.24)
(15.72)

0.09
0.008
0.42

Means and standard deviations pooled from left- and right-hand data.
Means and standard deviations pooled from male and female data.
p b 0.05.
p b 0.01.
p b 0.001.
b

anomalies (e.g., Weinstein et al., 1999; Schiffman et al., 2002; Compton

et al., 2007; Mittal et al., 2008b; Mittal and Walker, 2011; Golembo
et al., 2012), structural and functional neuroanatomical abnormalities
(Niznikiewicz et al., 2003; Karlsgodt et al., 2010; Shepherd et al., 2012),

4.5. Conclusions
Findings support DAs as one among other indicators of
neurodevelopmental disruption, including other types of minor physical

ATD Angle Forest Plot

Avila et al., 2003

Elizarrars -Rivas et
al., 2002
Jhingan and
Munjal, 1989
Jhingan and
Munjal, 1990

Kemali et al, 1976

Kemali et al., 1972

Pez et al., 2001

Rothhammer et
al., 1971

Turek, 1990
Yousefi-Nooraie
and MortazHedjri, 2008

-1.5

-1

-0.5

hg
Fig. 5. ATD angle meta-analysis.

0.5

1.5

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Table 6
Fingertip pattern asymmetrythree-pattern classication.
Study

Sample composition

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect size (g)

95% LL

95% UL

Avila et al. (2003)

Markow and Wandler (1986)
Reilly et al. (2001)
Cantor-Graae et al. (1998)
Cantor-Graae et al. (1998)

Male + Female
Male + Female
Male + Female
Females
Male

86
81
22
16
44

1.27
1.54
1.63
1.56
1.09

46
69
37
16
59

0.95
1.13
1.14
0.94
1.46

0.33
0.40*
0.46
0.60
0.36

0.03
0.07
0.08
0.11
0.75

0.69
0.72
0.99
1.31
0.03

1.82
2.41
1.68
1.66
1.79

(0.96)
(1.14)
(0.95)
(1.1)
(0.9)

neuromotor abnormalities (Walker et al., 1994; Schiffman et al., 2004),

cortisol abnormalities (Walker and Walder, 2002; Walder et al., 2012),
immune alterations (DeLisi, 1996; Mller et al., 2000), and neurocognitive
decits (Walder et al., 2008) that may serve as biomarkers of schizophrenia risk. Future research examining the combined effects of these
markers may lead to signicant strides in the etiological understanding
of schizophrenia.
Additionally, conceptual strategies such as viewing schizophrenia
within the context of equinality (Cicchetti and Rogosch, 1996) or as
a series of subtypes, each the product of partially distinct and/or somewhat overlapping etiologies (Walsh et al., 2008; Gay et al., in press),
may help to explain the heterogeneous ndings noted in the present review. Individuals with schizophrenia with more DAs may represent a
subtype characterized by a more adverse prenatal environment. Studies
examining minor physical anomalies and dermatoglyphics within an
equinality framework hold promise for elucidating our understanding
of this theoretical point of view. Further research might also seek to resolve inconsistencies in DA ndings attributable to poorly standardized
methods. Consistency in types of dermatoglyphics measures, techniques for obtaining dermatoglyphic features, diagnostic ascertainment, and sample recruitment may yield more reliable and easily
comparable results. In addition, reporting raw data for male participants separate from female participants may shed light on potential
sex differences. Despite these methodological issues, the current
study detected modest but signicant evidence for differences in
DAs between diagnostic groups, thus lending further support to the
neurodevelopmental model of schizophrenia.
Role of funding source
This work was supported in part by grant R03MH076846 to Jason Schiffman; funding
from the Maryland Department of Health and Mental Hygiene, Mental Hygiene Administration, and Baltimore Mental Health Systems; a Research Seed Funding Initiative (RSFI) grant
from the University of Maryland, Baltimore County; and by the Division of Child and
Adolescent Psychiatry within the University of Maryland.
NIMH; the Maryland Department of Health and Mental Hygiene, Mental Hygiene
Administration, and Baltimore Mental Health Systems; RSFI administrators; and the
Division of Child and Adolescent Psychiatry had no further role in study design; in
the collection, analysis and interpretation of data; in the writing of the report; and in
the decision to submit the paper for publication.

Contributors
Shana Golembo-Smith, Deborah Walder, Jason Schiffman, and Vijay Mittal contributed to all stages of design, implementation, analysis, writing, and editing. Maureen
Daly, Emily Kline, and Gloria Reeves contributed to analyses, writing, and editing. All
authors have approved the nal version of this manuscript.

(0.94)
(0.85)
(1.11)
(0.9)
(1.1)

Conict of interest
The authors have no actual or potential conicts of interest to report.

Acknowledgments
None.

References
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Table 7
Fluctuating asymmetry nger ridge count (FAFRC).
Study

Sample composition

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect size (g)

95% LL

95% UL

Reilly et al. (2001)

Saha et al. (2003)
Saha et al. (2003)
Youse-Nooraie and Mortaz-Hedjri (2008)

Male+ Female
Female
Male
Male

19
63
118
33

0.09
0.17
0.15
0.08

37
106
122
33

0.06
0.17
0.13
0.09

0.44
0
1.25
0.49

0.12
0.31
0.98
0.98

1.00
0.31
1.53
0

1.54
0
8.870
1.98

p b 0.05.
p b 0.01.
p b 0.001.

(0.08)
(0.03)
(0.01)
(0.02)

(0.06)
(0.03)
(0.02)
(0.02)

10

S. Golembo-Smith et al. / Schizophrenia Research 142 (2012) 111

Table 8
Fluctuating asymmetry AB ridge count (FABRC).
Study

Sample composition

n SZ

SZ mean (SD)

n Control

Control mean (SD)

Effect size (g)

95% LL

95% UL

Reilly et al. (2001)

Saha et al. (2003)
Saha et al. (2003)
Youse-Nooraie and Mortaz-Hedjri (2008)

Male + Female
Female
Male
Male

27
63
118
33

0.05
0.07
0.07
0.05

37
106
122
33

0.03
0.06
0.08
0.04

0.57
1.00
1.00
2.47

0.07
0.67
1.26
1.83

1.08
1.32
0.73
3.11

2.21
5.92
7.28
7.46

(0.04)
(0.01)
(0.01)
(0.004)

(0.03)
(0.01)
(0.01)
(0.004)

p b 0.05.
p b 0.01.
p b 0.001.

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