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(Solved) Epilepsia, 48(12):2258-2265, 2007 doi:1111/j.1528-1167.01276.x FULL-LENGTH ORIGINAL RESEARCH High risk of reading disability and speech sound...

For this assignment you will review a single scholarly article from the APUS Library and summarize what it says about. You don't need to have an abstract, as is typically required for APA style, for this paper but you must include an APA formatted cover page in addition to the References page. The 2-3page requirement does not include the cover or reference pages.

The introductory paragraph will give a brief description of the topic and the article that you will be reviewing.

The article summary will include the following:

• Discussion of the focus of the research
• Description of the hypothesis of the study
• Description of how the study was conducted including the population that was studied, the methodology used (i.e. naturalistic observation, experiment, case study, survey, etc). How the data was collected and analyzed
• Description of the results of the study

Your review/discussion of the article will include

  • A discussion of the way the research was conducted and potential impact on results (e.g. problems with the study methodology that might have affected its validity and/or generalizability).
  • A description of three ideas inspired in you by the article.
  • A description of the use, impact, or potential the research might have.

You don’t have to be a professional expert to write this section. Think about it this way--if you were someone working with children facing the challenges of the disorder you selected to read about and report on, what would you want future researchers to keep investigating that you believe could prove valuable to sufferers and their families? For example, a medical professional or psychologist might be interested in having researchers continue to study how broad a particular diagnostic classification spectrum needs to be to avoid catching too many and too few kids in the diagnostic net (it goes without saying that we would love to be able to diagnose accurately 100% of the time and cure everyone, but we will leave that off the table since it should be everyone’s goal and anyone reading about a disorder could have that cross his/her mind).

Your paper must be written at a college level. This means a minimum amount (nobody often achieves perfection) of spelling and grammar errors that don’t get in the way of following your points; no use of personal first or second person pronouns (“I” or “you”) in your article summary; no personal story sharing or creative writing style wording (papers that begin with a question or “Imagine for a moment that…” or “Webster’s Dictionary defines _____ as…” style openers are fine for some courses but not for this assignment. Simply start with, “This paper focuses on ________” with the topic of your paper in the blank space, and then move on to summarizing the findings of the publication you cite in the paper and the other required elements).

The 2nd part of your paper will include your review/discussion of the article as outlined previously. This section of your paper may include first person writing. Please be sure that your article summary is clear and distinct from your review of the article. Do not intermingle the two sections of your paper.

I will attach the article. Below is the citation for the reference page. Make sure to cite it in the paper as well.

Clarke, T., Strug, L. J., Murphy, P. L., Bali, B., Carvalho, J., Foster, S.. . Pal, D. K. (2007). High risk of reading disability and speech sound disorder in rolandic epilepsy families: Case–Control study. Epilepsia, 48(12), 2258-2265. doi:10.1111/j.1528-1167.2007.01276.x

Epilepsia, 48(12):2258–2265, 2007
doi: 10.1111/j.1528-1167.2007.01276.x FULL-LENGTH ORIGINAL RESEARCH High risk of reading disability and speech sound disorder
in rolandic epilepsy families:
case–control study
∗ Tara Clarke, †Lisa J. Strug, ∗ Peregrine L. Murphy, ∗ Bhavna Bali, §Janessa Carvalho,
§Suzanne Foster, †Geoffrey Tremont, ¶Bernadine R. Gagnon, ‡Nelson Dorta,
and ∗ †‡Deb K. Pal
∗ Department of Epidemiology and †Division of Statistical Genetics, Mailman School of Public Health, and
‡Department of Psychiatry, Columbia University Medical Center, New York, New York; §Neuropsychology
Program, Rhode Island Hospital, Providence, Rhode Island; ¶Edward D. Mysak Center for Speech and Hearing,
Teacher’s College, Columbia University, New York, New York, U.S.A. SUMMARY
Purpose: Associations between rolandic epilepsy
(RE) with reading disability (RD) and speech sound
disorder (SSD) have not been tested in a controlled
study. We conducted a case–control study to determine whether (1) RD and SSD odds are higher in
RE probands than controls and (2) an RE proband
predicts a family member with RD or SSD, hence
suggesting a shared genetic etiology for RE, RD,
and SSD.
Methods: Unmatched case–control study with 55
stringently defined RE cases, 150 controls in the
same age range lacking a primary brain disorder diagnosis, and their siblings and parents. Odds ratios
(OR) were calculated by multiple logistic regression, adjusted for sex and age, and for relatives,
also adjusted for comorbidity of RD and SSD in the
Results: RD was strongly associated with RE after
adjustment for sex and age: OR 5.78 (95% CI: 2.86– Rolandic epilepsy (RE) is the most common epilepsy
syndrome affecting children (Shinnar et al., 1999). It is a
developmental epilepsy with a complex genetic inheritance
that has yet to be elucidated (Bali et al., 2005). Centrotemporal spikes (CTS) are the electroencephalographic hallAccepted July 25, 2007; Online Early publication September 12, 2007.
Address correspondence and reprint requests to Tara Clarke, Mailman
School of Public Health, 722 West 168th Street, New York, NY 10032,
U.S.A. E-mail: [email protected]
Blackwell Publishing, Inc.

C 2007 International League Against Epilepsy 11.69). An RE proband predicts RD in family members: OR 2.84 (95% CI: 1.38–5.84), but not independently of the RE proband’s RD status: OR 1.30
(95% CI: 0.55–12.79). SSD was also comorbid with
RE: adjusted OR 2.47 (95%CI: 1.22–4.97). An RE
proband predicts SSD in relatives, even after controlling for sex, age and proband SSD comorbidity:
OR 4.44 (95% CI: 1.93–10.22).
Conclusions: RE is strongly comorbid with RD and
SSD. Both RD and SSD are likely to be genetically
influenced and may contribute to the complex genetic etiology of the RE syndrome. Siblings of RE
patients are at high risk of RD and SSD and both
RE patients and their younger siblings should be
screened early.
KEY WORDS: Phonologic disorder—Articulation
disorder—Speech delay—Developmental dysphasia—Developmental
dyslexia—Centrotemporal sharp waves—Complex genetic—Familial aggregation—Comorbidity—Cognitive deficit—
Family study. mark of RE. The association of RE or CTS with reading
disability (RD) and language impairment has often been
suggested (Staden et al., 1998; Vinayan et al., 2005), as has
association with impairment in the development of speech
motor control, also known as speech sound disorder (SSD)
(Bladin, 1987; Doose, 1989; Lundberg et al., 2005; Park
et al., 2005). Neither the association between RE and RD
nor between RE and SSD has been rigorously tested in a
case–control study, and thus association has not been unequivocally established. Furthermore, although cognitive
deficits are widely assumed to be a consequence of the 2258 2259
Speech and Reading in Rolandic Epilepsy
epilepsy disorder (Staden et al., 1998; Deonna, 2000), an
alternative hypothesis is that cognitive deficits are one of
many manifestations of an inherited impairment of brain
maturation (Doose et al., 2000). A prediction of the alternative hypothesis is that RD and SSD would occur in RE
relatives who themselves do not have epilepsy.
We aim to determine whether (1) RD and SSD rates are
higher in RE probands than controls and (2) whether having an RE proband in the family is a significant predictor of
having a family member with RD or SSD. If RD and SSD
are truly comorbid with RE and aggregate in RE families,
then RE, RD, and SSD may share some underlying genetic
risk factors that can be investigated using linkage analysis.
Additionally, if siblings are at high risk of RD or SSD, then
there are implications for early screening and intervention.
Answering both research questions not only advances our
understanding of the RE syndrome, but may also have important public health relevance. M ETHODS
This was an unmatched case–control study with 55 cases
and 150 controls. Fifty-five typical RE cases and their
families were recruited from U.S. pediatric neurology centers in New York, New Jersey, Pennsylvania, Connecticut, Rhode Island and Massachusetts for a genetic linkage study (see Acknowledgements). Referring clinicians
were board certified in clinical neurology and neurophysiology and specialized in child neurology. Ascertainment
was through the proband, with no other family member required to be affected. The families were then telephoned
by a study physician and invited to participate in a study to
find the genetic basis of RE, with no intervention or clinical
Cases were enrolled if they met stringent eligibility criteria, including at least one witnessed seizure with typical features: nocturnal, simple partial seizures affecting
one side of the body, or on alternate sides: oro-facialpharyngeal sensorimotor symptoms, with speech arrest and
hypersalivation, age of onset between 3 and 12 years,
no previous epilepsy type, normal global developmental milestones, normal neurological examination, at least
one interictal EEG with centrotemporal sharp waves and
normal background, and neuroimaging that excluded an alternative structural, inflammatory, or metabolic cause for
the seizures. Thus cases with unwitnessed episodes, or
with only secondary generalized seizures were excluded,
even if the EEG was typical. All of the probands’ charts,
EEGs, and neuroimaging were centrally reviewed for the
eligibility by board-certified experts in epileptology, neurophysiology, and neuroimaging prior to recruitment (see
Acknowledgements). Questionable cases were discussed
with an independent expert, a professor of child neurology specializing in epilepsy. Cases were not required to
be comorbid with any neuropsychiatric disorder, and refer- Table 1. Clinical descriptors of RE probands
Age in years at onset first seizure, median (range)
Usual laterality of seizure, n (%)
Inconsistent 7 (3–11)
17 (30)
19 (35)
19 (35) Lifetime seizure total, n (%)
>10 39 (71)
16 (29) Maximal ever seizure spread, n (%)
Face and arm only
Face and arm and leg
Secondary generalized
Ever treated with AEDs, n (%) 19 (35)
15 (27)
21 (38)
18 (33) ring physicians did not know about the comorbidity study.
Table 1 shows the seizure characteristics of the cases.
Controls were recruited from the same hospitals as the
cases, but not from neurological or psychiatric outpatient
clinics. To be eligible, they had to be in the same age range
as the cases, and not have a neurological or psychiatricrelated primary diagnosis. We refer to the index child as
the control proband. Comparison of age, sex, ethnicity, and
family size by case status is shown in Table 2.
The case families were interviewed in their homes by
one of three pediatric-trained physicians (BB, TC, DKP).
Both parents were interviewed, either together or separately, and the proband and siblings were also interviewed
when age appropriate. The investigator administered a
125-item questionnaire covering perinatal, developmental,
medical, educational details, family history and detailed
seizure semiology and treatment history. The questionnaire Table 2. Comparison of demographic factors of
cases and controls
Cases Controls Number of probands
Median age of probands (range)
Male probands, n (%) 55
10.0 (4–22)
39 (71) 150
10.0 (3–16)
78 (52) Number of siblings
Mean siblings per family
Median age of siblings (range)
Male siblings, n (%) 67
11.0 (0–29)
29 (43) 186
10.0 (0–31)
87 (47) Number of parents
Median age of parents (range)
Mean parental education level∗
College education (%)
Up to high school (%) 108
41.0 (26–56) 296
39.0 (22–62) 56
44 60
40 43 (78)
12 (22) 116 (79)
30 (21) Self reported ethnicity§
Non-white ∗
Fathers’ and mothers’ education levels were very similar.
§Some data missing in controls. Epilepsia, 48(12):2258–2265, 2007
doi: 10.1111/j.1528-1167.2007.01276.x 2260
T. Clarke et al.
was jointly developed by a pediatric neurologist (DKP),
pediatric neuropsychologist (ND), adult neuropsychologist
(GT), and pediatric speech pathologist (BRG). The same
questionnaire items were used, with minor modifications
for age, for the cases, controls, siblings, and parents. Questions that were answered positively were followed up in detail by clinical interview to establish ICD-10 diagnoses and
to distinguish from global learning disability. The questionnaire included 13 items addressing speech articulation
disorder F80.0 (see Appendix). A similar batch of questions was used in a high-risk study of phonological disorder (Tunick and Pennington, 2002). The questionnaire
also contained nine items addressing the ICD-10 definitions of reading disorder F81.0. RD was thus identified by
significant impairment in the development of reading skills
not solely accounted for by mental age, sensory problems,
mother tongue, or inadequate schooling. Operationally, we
asked about difficulties in learning to read in the first year
or two of elementary school, reading remediation, and repeating a grade. We also excluded, by clinical interview,
hearing impairment, social and educational deprivation,
and other factors that were inconsistent with the diagnosis of RD. We checked available school and psychologist’s
reports for confirmation, and all were consistent with our
A subset of 11 probands and 10 siblings underwent
comprehensive neuropsychological evaluation, the details
of which will be reported elsewhere. In brief, the results
of testing strongly supported the validity of our ICD-10
estimation of RD. As part of our battery, we used standard instruments to assess general intelligence: Wechsler
Abbreviated Scale of Intelligence (Wechsler, 2005); academic achievement including spelling: Woodcock-Johnson
III (Woodcock et al., 2001); reading: Gray Oral Reading
Tests 4 (Wiederholt and Bryant, 2001), Test of Word Reading Efficiency (Torgesen et al., 1999); receptive and expressive language: Clinical Evaluation of Language Fundamentals, 4th Edition (Semel et al., 2003), Boston Naming Test, 2nd Edition (Kaplan et al., 2001). All tested subjects had a full scale IQ within or above the normal range.
Using a definition of impairment as a standard score one
standard deviation below normative means in at least two
subtests, we found that ICD-10 classifications had a 100%
positive predictive value and 90% negative predictive value
for reading impairment. At worst, our operational definitions slightly underestimated the actual prevalence of RD.
SSD (OMIM 608445) is defined by developmentally
inappropriate errors (e.g., deletions and substitutions) in
speech production that reduce intelligibility (Shriberg
et al., 1997), and is distinct from stuttering, mutism, or
aphasia. Operationally, we sought a history of delay in the
normal acquisition of speech sound milestones expected
for age, e.g. no single words at 16 months, no two-word
sentences at 2 years of age, age-inappropriate difficulty for
strangers to understand speech, and preschool speech therEpilepsia, 48(12):2258–2265, 2007
doi: 10.1111/j.1528-1167.2007.01276.x apy intervention. We included only families where English
was a first language and excluded from the definition individuals with chronic hearing impairment or recurrent otitis
media. SSD has its highest prevalence in the preschool period, and declines sharply by the age of 5–6 years (Shriberg
et al., 1999). Hence a lifetime history of SSD probably
represents a more accurate estimate of SSD than a speech
pathologist evaluation conducted many years after SSD has
The frequency of RD and SSD in cases, controls, and relatives was calculated within categories of relatedness to the
proband, and sex. Siblings who were below the age range
at risk for diagnosis of SSD or RD were excluded from the
analysis. We assessed the association between RE and RD,
and between RE and SSD in the probands by computing an
odds ratio, with 95% CI, adjusting for both age and sex using logistic regression. Parental education level and ethnicity were comparable between the case and control groups
(Table 2), thus adjustment for these factors was unnecessary. We also used multiple logistic regression to determine
whether having an RE proband in the family was a significant predictor of having RD and SSD in family members.
We adjusted for the RD and SSD status of the proband in
this analysis, because RD and SSD themselves may aggregate in families.
We sought only to assess the increased odds of RD and
SSD in families with an RE proband. We did not assess
familial aggregation or co-aggregation of RE with SSD or
RD because RE infrequently aggregates in families. Analyses were performed using Stata 8.2 for Macintosh OS
X (StataCorp, 2003) and the R statistical package, blind
to subject identity. The study was approved by the institutional review boards of the New York State Psychiatric Institute, Columbia University Medical Center, and
all collaborating centers. Subjects gave written informed
consent. R ESULTS
Twenty-nine RE probands had RD (55%) compared with
24 control probands (16%). There was a male predominance for RD in both case probands (1.57:1) and control
probands (1.52:1). Sixteen siblings, (25%) and 17 parents
(16%) of cases also had RD, compared to 7% of sibling
controls and 6% of parent controls (Table 3).
Table 3. RD and SSD in case and control
probands and relatives
Reading disability Speech sound disorder n (%) Cases Controls Cases Controls Probands
Parents 29 (55)
16 (25)
17 (16) 24 (16)
13 (7)
18 (6) 20 (37)
18 (28)
5 (5) 28 (19)
9 (5)
7 (2) 2261
Speech and Reading in Rolandic Epilepsy
Twenty RE probands had a history of SSD (37%) compared with 28 control probands (19%). Eighteen siblings
(28%) and 5 (5%) of case parents also had a history of
SSD, compared with 5% of sibling controls and 2% of parent controls (Table 3). There was also a male predominance
for SSD in cases (1.95:1) and controls (1.34:1).
Thirteen of the RE + SSD cases (87%) also had RD,
while 72% of RE + RD cases also had SSD. A history of
SSD always preceded a history of RD. A history of SSD
or RD nearly always preceded the onset of the first seizure
in probands. There was a similar pattern among siblings
of cases: 60% of RD siblings also had SSD, while 56%
of SSD siblings also had RD. Interestingly, when the RE
proband did not have RD then no other family member had
The odds of RD in RE cases were 6.29 times higher
than in controls (95% CI: 3.14–12.61). There was minimal
evidence of confounding by age or sex, with the adjusted
odds ratio 5.78 (95% CI: 2.86–11.69). The odds of a parent
or sibling having RD was greater in families of RE cases
than controls, with an odds ratio of 2.84 after adjusting for
age and sex (95% CI: 1.38–5.84). However, when the RE
proband’s RD status was controlled for, there was no significant association of RD in RE families (OR 1.30 95%
CI: 0.55–12.79). This indicates that the risk of RD in family members of RE probands is dependent on the RD status
of the proband.
SSD also showed a strong association with RE: OR 2.54
(95%CI: 1.28–5.06), and after adjusting for age and sex:
OR 2.47 (95% CI: 1.22–4.97). The odds of SSD in parents
and siblings in RE families were 5.36 times the odds of
SSD in parents and siblings of non-RE families (95% CI:
2.40–11.96), adjusted for age and sex (Table 4). The association remained significant even after controlling for the
SSD status of the RE proband: OR 4.44 (95% CI: 1.93–
Considering the siblings separately, the odds of RD in a
sibling were 3.67 times higher than in controls (95% CI:
1.54–8.69) but after adjusting for the proband’s RD status were 1.99 (95% CI: 0.75–5.28). The odds of SSD in a
sibling were 6.39 (95% CI: 2.58–15.8) times higher than
in controls and also remained significant after controlling
Table 4. Association with RD and SSD for
relatives of probands
(95% CI)
a RE Probands Parents and siblings Siblings only 5.78 (2.86–11.69)
2.47 (1.22–4.97)
– 2.84 (1.38–5.84)
1.30 (0.55–12.79)
5.36 (2.40–11.96)
4.44 (1.93–10.22) 3.67 (1.54–8.69)
1.99 (0.75–5.28)
6.39 (2.58–15.8)
5.21 (2.03–13.38) Odds ratio adjusted for age and sex.
Odds ratio adjusted for age, sex and proband comorbidity
b for the proband’s SSD status: OR 5.21 (95% CI: 2.03–
This is the first controlled study to test for an association between RE and RD, and between RE and SSD. We
demonstrate strong evidence of comorbidity between RE
and both RD and SSD, with a twofold to sixfold increased
odds in RE probands. This is also the first family study of
RE and our findings help to disentangle the relationship of
seizures from associated brain traits. The increased odds
of RD and SSD in relatives refute the hypothesis that RD
and SSD are a consequence of the epilepsy itself. Rather,
RD and SSD appear to be independently inherited traits
that segregate in RE families. The fact that the occurrence
of RD in RE families is dependent on the proband’s RD status (there being no RD affected relatives of noncomorbid
RE probands) suggests a genetic (or environmental) risk
factor behind RD may play a part in the causal pathway
of RE. Since not all RE probands are comorbid with RD,
RD+ and RD− forms of RE might represent etiologically
heterogeneous subtypes. In contrast to RD, the association
between RE and SSD in relatives was independent of the
proband’s SSD status. The reason for this is not obvious,
but might be explained by a risk factor shared between SSD
and CTS (i.e., not between SSD and RE per se), which we
discuss below. Before considering the implications for the
disease model of RE and for clinical practice, we discuss
the possible alternative explanations for our findings.
There are a number of possible sources of bias and confounding that must be considered when interpreting the
study. Bias in selecting comorbid cases is the most obvious one, which would serve to inflate estimates of comorbidity. However, most RE cases in the northeastern US are
first diagnosed in pediatric neurology centers (Berg et al.,
1999) and so we believe our ascertainment scheme resulted
in a relatively unbiased community-based sample. Table 1
shows that cases had a distribution of onset age, lifetime
seizures, and treatment history representative of “typical”
RE cases.
As for selection of comorbid RD and SSD cases of RE,
children usually do not first come to the attention of pediatric neurologists with RD or SSD unless global deficits
are present. This does not rule out the possibility that parents of RE cases may self-select for research studies because they sense that their child’s neurological problem is
complicated. However, even if selection bias was operating on cases, this would not explain the increased odds of
RD and SSD in relatives of RE probands, after controlling
for the comorbidity of cases. Conversely, it is possible that
children with RD and SSD, and hence our controls, are
over-represented in pediatric outpatient clinics and serve
to underestimate the true association. The higher prevalence of RD and SSD in control probands compared with
Epilepsia, 48(12):2258–2265, 2007
doi: 10.1111/j.1528-1167.2007.01276.x 2262
T. Clarke et al.
control siblings may reflect differences in age distribution
and recall, or a higher risk of cognitive impairments in hospital attendees. However, the frequency of reported RD and
SSD in our pediatric controls was in the range expected
from previous prevalence studies (Hallgren, 1950; Peckham, 1973; Beitchman et al., 1986; Shaywitz et al., 1990).
Therefore, selection bias, operating either on cases or on
controls, is unlikely to play a large part in the strong associations demonstrated here.
Recall bias for SSDs is another important consideration.
The recall of RD is fairly stable and reliable over time, both
for children and for parents, because RD is often persistent,
even into adulthood. However, speech problems present in
the second year of life and may have resolved or become
less marked by school age. It is also possible that they
may be more accurately recalled and reported when the
child has epilepsy rather than a nonbrain-related diagnosis. Speech problems are particularly liable to recall bias
in parental generations if no grandparental respondents are
available. This may explain the low prevalence of reported
SSD in parents of both cases and controls, and reduces the
statistical power to detect SSD clustering in parents.
The relationship between RE with SSD and RD
SSD has occasionally been noted in RE (Bladin, 1987;
Doose, 1989; Lundberg et al., 2005; Park et al., 2005), but
the neural basis of SSD is unknown in this context. Speech
dyspraxia has been noted in a rare autosomal dominant
form of RE (Scheffer et al., 1995), but there has been no
investigation of speech dyspraxia in the common form of
RE. This lacuna may be due to the relatively short-lived
and mild symptomatic prominence of SSD, often 6 or 7
years preceding the onset of seizures in RE. Genetic factors
do play a substantial role in the etiology of developmental
SSDs (Stromswold, 1998), and some loci for SSDs overlap
those for RD (Stein et al., 2004; Smith et al., 2005). Our
results point to a shared genetic (or environmental) component to SSD in RE families. One possible explanation
for both the RE + SSD comorbidity and increased familial
risk of SSD in RE families is confounding with CTS, which
itself appears to have a genetic basis (Bali et al., 2007), and
anatomically colocalizes to the perisylvian area. The measurement of CTS as a confounder in this study would have
been problematic because demonstrating CTS on EEG is
dependent on sleep state (Kellaway, 1985) and age, rarely
recorded after the age of 16 years or before 3 years. It will
be interesting to investigate whether the shared risk factors for SSD in RE families are genetic, and if so, whether
they are common to SSD in families ascertained through a
proband with SSD rather than a proband with RE.
RD has consistently been found in RE case series from
different language regions of the world (Staden et al., 1998;
Vinayan et al., 2005). The apparent paradox of comorbidity with RE, but lack of independent increased odds in RE
families, may indicate that an RD risk factor (presumably
Epilepsia, 48(12):2258–2265, 2007
doi: 10.1111/j.1528-1167.2007.01276.x genetic, but possibly environmental) is necessary, but not
sufficient, for the manifestation of RE. There is abundant
evidence for the genetic basis of RD, with nine loci and
four identified genes, some overlapping those for SSD (see
Williams and O’Donovan, 2006 for review). The cooccurrence of SSD and RD in individuals and within families is
also seen in our sample ascertained through RE probands.
RD and SSD show a male sex bias in RE, and the same is
true of RD and SSD in the general child population. The
similarities suggest that common neural networks involved
in reading and speech sound production, and possibly common susceptibility factors too, are impaired in RD and SSD
within and without the RE context.
The marked comorbidity of RE with both RD and SSD is
unsurprising given that the clinical and electrographic features of RE reflect disturbance of the perisylvian region.
Speech production, speech perception, auditory processing, and other domains critical to efficient acquisition of
reading skills involve perisylvian networks and their connections. In remarkable contrast, there are few references
in the literature to RD or SSD index cases who are comorbid with epilepsy (Galaburda et al., 1985). One possible
explanation is that such cases might have been excluded
from clinical or genetic epidemiological investigations of
RD or SSD because of the comorbidity with epilepsy. Another explanation is that the etiological factors responsible
for RD or SSD in RE are heterogeneous to those acting on
RD or SSD outside the RE context.
Disease model
Taken with our previous work on the mode of inheritance of CTS (Bali et al., 2007), the value of deconstructing the RE syndrome into component traits becomes clear


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