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 NEURAL TUBE
DEFECTS

DK5690_FM.indd 1 12/19/06 2:06:47 PM

 PEDIATRIC HABILITATION

Series Editor

ALFRED L. SCHERZER
Cornell University Medical Center
New York, New York

1. Prevention of Mental Retardation and Other Developmental

Disabilities, edited by Michael K. McCormack
2. Developmental Disabilities: Management Through Nutrition
and Medication, Eric Denhoff and Steven Feldman
3. Early Diagnosis and Therapy in Cerebral Palsy,
Alfred L. Scherzer and Ingrid Tscharnuter
4. Parenting Children with Disabilities: A Professional Source
for Physicians and Guide for Parents, Peggy Muller Miezio
5. Visual Disorders in the Handicapped Child, John L. Goble
6. Early Diagnosis and Therapy in Cerebral Palsy: A Primer
on Infant Developmental Problems, Second Edition, Revised
and Expanded, Alfred L. Scherzer and Ingrid Tscharnuter
7. Attention Deficit Disorders and Hyperactivity in Children:
Early Diagnosis and Intervention, edited by
Pasquale J. Accardo, Thomas A. Blondis,
and Barbara Y. Whitman
8. Medical Care in Down Syndrome: A Preventive Medicine
Approach, Paul T. Rogers and Mary Coleman
9. Manual of Developmental and Behavioral Problems
in Children, Vidya Bhushan Gupta
10. Attention Deficits and Hyperactivity in Children and Adults:
Diagnosis • Treatment • Management, Second Edition,
Revised and Expanded, edited by Pasquale J. Accardo,
Thomas A. Blondis, Barbara Y. Whitman, and Mark A. Stein
11. Early Diagnosis and Interventional Therapy in Cerebral Palsy:
An Interdisciplinary Approach, Third Edition, edited by
Alfred L. Scherzer
12. Autistic Spectrum Disorders in Children, edited by
Vidya Bhushan Gupta
13. Genetics of Developmental Disabilites, edited by
Merlin Butler and F. John Meaney
14. Neural Tube Defects, edited by Sonya G. Oppenheimer

DK5690_FM.indd 2 12/19/06 2:06:48 PM

 NEURAL TUBE
DEFECTS

EDITED BY
SONYA G. OPPENHEIMER
Cincinnati Children's Hospital Medical Center
Cincinnati, Ohio, U.S.A.

New York London

DK5690_FM.indd 3 12/19/06 2:06:48 PM

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 Preface

Neural tube defects are one of the most complex birth defects and require an
understanding of the interactions of multiple systems: the central nervous
system, the urological system, and the musculoskeletal system. Because of
this, a truly multidisciplinary team of specialists, including neurosurgeons, ortho-
pedists, urologists, nephrologists, physiatrists, orthotists, pediatricians, physical
therapists, occupational therapists, nurse coordinators, advanced practice
nurses, geneticists, genetic counselors, and now perinatologists, fetal surgeons,
and ethicists, are required to provide comprehensive treatment.
Before the 1960s, a complicated team was not needed because the majority
of infants born with this defect died from infection and/or hydrocephalus. Once
surgical techniques were improved and survival increased, there was a realization
that helping these children required many different disciplines communicating
with each other and the family. Interdisciplinary teams were established in
many medical centers. All team members soon recognized that each member
had to have knowledge about all areas.
My intent in editing this book is to provide information that will allow all
the different disciplines to gain understanding of how the problems of each
system relate to the other systems. The therapists need to know what the
reason is for a child to develop progressive orthopedic deformities and to question
whether it is due to possible tethering of the spinal cord, not a failure of therapy.
Development of poor handwriting and progressive hypotonia may be caused by a
syrinx of the cord. Development of decubitus may be due to a change in ortho-
pedic status, including progressive scoliosis. Deterioration of schoolwork may
be due to a subtle shunt malfunction.
Though there are separate chapters written by authors in different disci-
plines, the subjects interdigitate with each other. Not only is the knowledge
within individual disciplines important, but it is necessary to recognize that

iii
iv Preface

communication with all team and family members is essential so the child and
young adult can reach their potential.
This book represents my commitment of 35 years of experience with
people with spina bifida but, most important, shares what I have learned from
the families, children, and young adults with this most complex birth disorder.
I want to thank my own family: my husband, Frank, and sons, Michael and
Peter, who over the years not only allowed me to spend time with families of
children with spina bifida, but also developed an understanding of people with
special needs.

Sonya G. Oppenheimer
 Acknowledgment

As faculty in the Division of Developmental and Behavioral Pediatrics at Cincin-

nati Children’s Hospital Medical Center, this project was supported by Grant No.
T73MC00032-16 awarded by the Maternal and Child Health Bureau, Health
Resources and Service Administration, DHHS, and Grant No. 90DD0546/05,
awarded by Administration on Developmental Disabilities, Administration for
Children and Families, DHHS.
I would like to thank Nancy Ice, Administrative Assistant, for all of
her help.

v
 Contents

Preface . . . . iii
Acknowledgment . . . . v
Contributors . . . . ix

1. History of Spina Bifida . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Sonya G. Oppenheimer

2. The Global Epidemic of Folic Acid – Preventable Spina Bifida . . . 9

Godfrey P. Oakley, Jr.

3. Multidisciplinary Management Including Prenatal Care . . . . . . 21

Catherine M. Shaer

4. School-Age Child: Academic Issues . . . . . . . . . . . . . . . . . . . . . . . 37

James W. Loomis

5. Psychological Functioning in Children and Adolescents

with Spina Bifida . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Robert T. Ammerman, Marsha J. Nortz, M. Douglas Ris,
and Nicolay C. Walz

6. Teenage Emphasis Achieving Independence . . . . . . . . . . . . . . . . 79

Donna Cheek Zahra

7. Adolescent Health-Care Transition . . . . . . . . . . . . . . . . . . . . . . . 95

Thomas S. Webb and Tena Benson

8. Adults Who Have Spina Bifida: Work and Mental Health . . . 117
Gregory S. Liptak

vii
viii Contents

9. Review of Current Neurosurgical Issues . . . . . . . . . . . . . . . . . . 137

Kerry R. Crone and Benjamin Ling

10. New Orthopedic Trends . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151

Junichi Tamai, Jose Herrera-Soto, and Alvin H. Crawford

11. New Urological Trends . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199

Kazuyuki Nishinaka and Curtis A. Sheldon

12. Families that Have Children with Spina Bifida . . . . . . . . . . . . . 243

Marlene L. Lutkenhoff

13. Ethical Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255

Linda S. Lazar
Index . . . . 269
 Contributors

Robert T. Ammerman Division of Behavioral Medicine and Clinical

Psychology, Cincinnati Children’s Hospital Medical Center, Cincinnati,
Ohio, U.S.A.
Tena Benson Division of Developmental and Behavioral Pediatrics,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Alvin H. Crawford Division of Pediatric Orthopedic Surgery, Cincinnati
Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Kerry R. Crone Department of Neurosurgery, Cincinnati Children’s
Hospital Medical Center, University of Cincinnati College of Medicine,
Cincinnati, Ohio, U.S.A.
Jose Herrera-Soto Arnold Palmer Hospital for Children, Orlando,
Florida, U.S.A.
Linda S. Lazar Division of Developmental and Behavioral Pediatrics,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Benjamin Ling Department of Neurosurgery, Cincinnati Children’s
Hospital Medical Center, University of Cincinnati College of Medicine,
Cincinnati, Ohio, U.S.A.
Gregory S. Liptak Department of Pediatrics, Upstate Medical University,
Syracuse, New York, U.S.A.
James W. Loomis Center for Children with Special Needs, Glastonbury,
Connecticut, U.S.A.
Marlene L. Lutkenhoff Division of Developmental and Behavioral Pedi-
atrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.

ix
x Contributors

Kazuyuki Nishinaka Division of Urology, Cincinnati Children’s Hospital

Medical Center, Cincinnati, Ohio, U.S.A.
Marsha J. Nortz Division of Behavioral Medicine and Clinical Psychology,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Godfrey P. Oakley, Jr. Department of Epidemiology, Rollins School of
Public Health of Emory University, Atlanta, Georgia, U.S.A.
Sonya G. Oppenheimer Division of Developmental and Behavioral Pedi-
atrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
M. Douglas Ris Division of Behavioral Medicine and Clinical Psychology,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Catherine M. Shaer The George Washington University Biostatistics
Center, Rockville, Maryland, U.S.A.
Curtis A. Sheldon Division of Urology, Cincinnati Children’s Hospital
Medical Center, Cincinnati, Ohio, U.S.A.
Junichi Tamai Division of Pediatric Orthopedic Surgery, Cincinnati
Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Nicolay C. Walz Division of Behavioral Medicine and Clinical Psychology,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Thomas S. Webb Division of Developmental and Behavioral Pediatrics,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.
Donna Cheek Zahra Nemours Children’s Clinic, Jacksonville,
Florida, U.S.A.
 1
History of Spina Bifida

Sonya G. Oppenheimer
Division of Developmental and Behavioral Pediatrics,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, U.S.A.

EARLY DESCRIPTION OF SPINA BIFIDA, 10,000 B.C. – 1760

The history of neural tube defects begins in prehistoric time with the discovery of
skeletons identified as having pathological findings consistent with spinal boney
abnormalities (1). These skeletons were carbon dated and felt to exist since
10,000 B .C . and were found in a cave of taforalt in Morocco. Both adults and
infant skeletons indicated that this deformity (probably not spina bifida
cystica) was compatible with life (2). Spina bifida occulta was found in 90%
of 10 adult skeletons from a historic American Indian burial site. The anthro-
pological findings raised questions whether spina bifida was caused by a
genetic influence or an environmental influence (3). An article in the Irish
Medical Journal in 1986 reviewed archeological sites in Ireland from the
Bronze Age 2000 B .C . to Medieval Era 1000 A .D . and the 15th to 18th century.
Nonclosure was found in sacral segments. These findings are intriguing in that
there was no information concerning children, possibly indicating that higher
lesions were fatal. The authors concluded that the high risk noted in recent
years, particularly around Dublin, compared with the low risk in the early centu-
ries may indicate the influence of an environmental factor. Detailed data are
available in the tables in the Irish Medical Journal. The controversy regarding
the etiology continues, despite the discovery of the relationship of folic acid
with spina bifida, and continues to allow us to use the term polygenetic multifac-
tored causation.

1
2 Oppenheimer

Descriptions of spina bifida have been suggested in the writings of

Hippocrates. Other historical references are seen in the writings of Pieter Van
Forest in 1587 and Casper Bauhan in 1964 (4). The most historical connection
is the Rembrandt painting “The Anatomy Lesson of Dr. Tulp” in 1632 (5). In
it, he described patients with spina bifida as did Ruysch (6), also in a painting
by Johan R. Van Neck in 1683. In 1760, Mark Gagne, who is considered the
founder of modern pathological anatomy, recognized the link between spina
bifida and hydrocephalus. Medical literature continued to describe various
aspects of spina bifida including Van Recklinghaus’ description of all forms of
the condition.

PARAPLEGIA AND INCONTINENCE

A fascinating description from a papyrus in the 17th century B .C . highlighted
quadriplegia and its association with incontinence with urine and sexual function
(6). Paraplegia was considered in Edwin Smith’s surgical papyrus in the second
millennium B .C . as an ailment not to be treated (7). Of interest, bracing and
splints, however, have been used since 2400 B .C . Incontinence was also described
in the writings of Hippocrates. Galen (8) understood the relationship between
disease, spinal cord, and bladder problems. The concept of catheters to achieve
continence is not new but has been used since the 17th century, and even catheters
made of bronze and lead were used to bypass urinary obstruction. Surgical diver-
sions for continence were attempted in 1852 by developing an ileo conduit with
ureters draining into a bowel loop and were refined by Dr. Brickers in 1950.
Surgical repairs of these abnormalities were attempted from 1641 to 1892.
Despite the numerous varieties of treatments, they all resulted in death until
Dr. Bayer in 1892 recommended using muscular flaps for closure (9). Previous
treatments had varied from using excision of the sac to sclerosing the sac with
items such as silver nitrate.

HYDROCEPHALUS
Dr. David Shurtleff, a leader in modern treatment for patients with
myelomeningocele, summarizes in his presidential address for the Society of
Research in Hydrocephalus and Spina Bifida the history of treatment of spina
bifida to the recognition of the associated hydrocephalus and subsequent develop-
ment of the Holter cerebral shunt which controlled progressive hydrocephalus (10).
In the 17th century, the possible link between hydrocephalus, paraplegia,
and incontinence was identified. The Arnold Chiari phenomenon though still
not totally understood was recognized in 1894 as a contributing factor to the
production of the hydrocephalus (11). The production of cerebral spinal fluid
and the circulation of the fluid were further described in 1827 through 1872
and later confirmed by Dandy (12).
History of Spina Bifida 3

AGGRESSIVE TREATMENT
The treatment for hydrocephalus included trephining, compression, and even
continuous drainage (12). Procedures that were done in the time of the ancient
Greeks and continued in to the 1880s included injection of sclerosing
substances into the ventricles to stop the production of the spinal fluid. Other
techniques were used to drain the fluid. The first modern shunt was developed
by Nelson, Spitz, and John Holter, an engineer whose son had hydrocephalus
in 1952 (1). This led to the beginning of aggressive treatment for infants born
with spina bifida.

OUTCOMES OF TREATMENT
Based on the improvement of all these early techniques, studies analyzing out-
comes of treatment began to appear in the literature. Laurence and Tew (13)
reviewed 425 cases of children born with spina bifida between 1956 and 1962.
Very few had been operated on. Sixteen percent in 1964 were still alive, 111
had been stillborn, 59 died in the first week, 184 died between one week and
one year of age, and 5 died over the age of 12 months. The survival rate, there-
fore, of untreated children with myelomeningocele was 11% or 47 out of 408. Of
those 47, 11 had moderate to severe involvement with limited walking ability and
impaired bladder control. Twenty-four were wheelchair-bound and incontinent,
two-thirds had obvious hydrocephalus; however, the mean intelligence quotient
was 86 and more than half were mentally retarded. This would be interpreted
that out of every 100 affected children, 25 would be born dead and 5 would
die within 24 hours. This would be a group that is considered irreducible
minimum mortality. Of the remaining 70, 25 will die in the first month, 20
between two and six months, 10 between 6 and 12 months, another 5 more
before school age. Ten children would then be alive at the age of five indicating
that one in seven might reach school age but only one in 70 is likely to attend
school (14).
The literature then began to cite different examples of various outcomes
with treatment. However, overall natural mortality without surgical treatment
has been reported by others to be approximately 85%. Of those not treated,
only 4% would be considered to have IQs above 85. Once aggressive treatment
for all children with spina bifida was undertaken, the question of quality of life
began to surface. After aggressive treatment in the early 1950s and 1960s,
several large multidisciplinary treatment centers began to review their treatment
results. Measures of successful treatment were considered on today’s terms.
Outcomes were mortality, degrees of morbidity including shunt complications
and intelligence (less mental retardation), ambulation, and achievement of
continence. The Children’s Division of the Institute of the Rehabilitation
Medicine at New York University formed an interdisciplinary study group in
1961. This group published a monograph edited by Chester A. Swyniard,
4 Oppenheimer

Comprehensive Care of the Child with Spina Bifida Manifesta (15). They studied
165 active patients. Care of the patients in the institute primarily consisted of
inpatient admissions of approximately 34 days and was followed by periodic
outpatient visits. The overall goal of treatment was maximum self-
sufficiency, independent living, appropriate educational experiences, and
pursuit of vocational endeavors. The premise was that the management of hydro-
cephalus accounted not only for mortality but also for morbidity of intellect. Of
interest, of 75 patients in their nontreated hydrocephalus group, 62% went on to
develop hydrocephalus. The natural history of this group became known as non-
progressive hydrocephalus. This group would provide information on the natural
history of nonpressured hydrocephalus with rapid head growth. These children
scored lower in the full scale IQ of the WISC and there were highly significant
differences in the untreated group, particularly with lower verbal scores, lower
performance scores, and average verbal ability (currently referred to as nonverbal
learning disabilities). The group without hydrocephalus was considered to have
findings similar to people with spinal cord pathology, whereas those with hydro-
cephalus presented a group of children with brain damage. Urinary incontinence
was achieved by the Crede method which meant pushing on the bladder to empty
it. Survival depended on preservation of renal function, elimination of residual
urine, and control of the urinary infection. The major form of control of inconti-
nence was a Bricker ureterostomy to prevent renal failure. Eighty-six patients
from 7 months to 26 years of age had a measured rehabilitation potential
related to the initial degree of neurological deficit. This, however, was influenced
by complicating factors including skeletal deformities, bowel and bladder
management, decubiti, obesity, IQ, social problems, and parental attitude.
Overall, mortality within the first 21 years of life was between 80% and
85%. The conclusion of Swinyard’s report in 1965 stated that the maximum
obstacles for those children without hydrocephalus are the lack of community,
social, educational, and vocational resources. The second major impact of
morbidity was stool incontinence. Despite heroic efforts of parents and interdisci-
plinary teams, the management of bowel planning remained frustrating. Multiple
techniques including suppositories, stool softeners, extra fiber, and enemas did
not establish continence. Because of these problems with uncontrollable bowel
movements, some patients eventually resorted to a colostomy that, although a
major operative procedure, allowed them to have better control of the bowel
movements at work, school, and society.

TREATMENT AMBULATION
The pendulum of aggressively treating ambulation as part of the overall care of
children with spina bifida has gone from multiple surgical methods that
allowed what was interpreted as normal ambulation to using mobility tools
that allow for movement. The concept of paraplegia was known in the middle
ages and efforts to heal it have been attempted since the 12th century (16). The
History of Spina Bifida 5

use of bracing has been identified in Egyptian tools of the fifth dynasty in 2400
B .C . More advanced splinting was in use since the 17th century. With the advent
of lighter plastics, bracing was encouraged. However, to appropriately brace the
child, multiple orthopedic surgeries including hip releases and tendon transfers
and releases were required. Again, many children who were able to ambulate
prior to entrance to school or the beginning of teenage years gradually began
to use wheelchairs because they recognized that they could move faster and
the fatigue of walking and splints was not there. Surgical techniques were per-
formed by John Sharrard who is best known for his transfer of the psoas
tendon and ileac muscles and restoring abductor power to the hips (16).
A major deformity, however, that was frequently ignored was the spinal
deformity. Harrington (17) developed spinal implementation for surgical correc-
tion by using the Harrington rods. Luque and Cardoso (18) developed techniques
by incorporating sublaminar wiring of each vertebral body. This subsequently
prevented the complication of pulmonary hypertension and progressive spinal
deformity. A major more recent orthopedic problem has been the treatment of
the kyphotic deformity. A review article by Banta (19) summarizes other ortho-
pedic techniques and wisely questions a better understanding of the importance of
long-term outcome and comprehension of evaluation of the motor dynamics
involved in paraplegia (1). The years of treatment controversies including
surgical techniques and ethical issues raised by the treatment and nontreatment
of people born with spina bifida persist until current times and are reviewed in
the chapter on bioethical treatment of children with spina bifida.

FETAL SURGERY
Probably, the newest treatment for infants born with spina bifida is the
recommendation of fetal surgery (20). This approach again raises parental
and professional hope that in utero surgery will result in the prevention of
complications of spina bifida. An NIH study entitled MOMS (Management
of Myelomeningocele Study) is in process to determine whether the claims
of this surgery (decreased hydrocephalus, changes in the Chiari malformation,
and improved ambulation) can be documented by a vigorous research
protocol (21).

ETIOLOGY AND PREVENTION

The history of various hypotheses of possible causes of spina bifida culminated in
recognition by Professor Richard Smithells of a possible form of nutrition, par-
ticularly folic acid metabolism (22). Folate relationship with this disorder is
believed to be related to a genetic predisposition to the metabolism and the
MPHFR gene, which is more prevalent in families with neural tube defects
and, of interest, is also found in higher incidence in the Irish population. This
relates to the prior epidemiological studies that spina bifida was more common
6 Oppenheimer

in people of Irish/English ancestry. Folic acid used preconceptionally is expected

to reduce the incidence of spina bifida by 70%. However, it will not totally
eliminate this disorder, just as early prenatal detection by amniocentesis with
subsequent choice of pregnancy termination did not eliminate the birth of
infants with spina bifida.
A recent issue of the American Journal of Genetics is devoted entirely to
causation, better understanding of various aspects of neural tube defects includ-
ing embryology, epidemiology, genetic causes, and environmental contributions
to their etiology (23). Interested readers’ attention is brought to this seminar
publication and is not summarized in this history.

PERSONAL EXPERIENCE
As a personal note, the Spina Bifida clinic at the Cincinnati Children’s Hospital
Medical Center, Division of Developmental Disabilities setting which serves the
Southwest area of Ohio and Northern Kentucky (started in 1965) averaged
approximately 24 to 25 new children born with spina bifida a year. Despite the
folic acid usage, the clinic currently still has 10 to 12 new infants with spina
bifida, most of whom are from families who did not take the extra folic acid.
This does not include the number of infants that were possibly terminated
during this period. The newest phase in the history of spina bifida is the recog-
nition that there are many people who are over 21 and were treated aggressively
in the 50s, 60s, and 70s. These people are now adults and present a new continu-
ing challenge for professionals interested in this area. This topic is discussed
throughout the book but is also discussed in the chapter on transition.

REFERENCES
1. Smith GK. The history of spina bifida, hydrocephalus, paraplegia, and incontinence.
Pediatr Surg Int 2001; 17:424–432.
2. Kuttner RE. Prehistoric spina bifida occulta. JAMA 1978; 240(24):2631.
3. Saluja PG. Evidence of spina bifida in skeletal remains from Ireland. Irish Med J 1986;
79(6):145–149.
4. (Bauhan) Morgagni JB. The Seats and Causes of Diseases Investigated By Anatomy in
5 Books, Bk. 1, Letter 12. Translated from Latin by Benjamin Alexander. Vol. 1 NY:
Hofner, 1960:244– 474.
5. Tulip N. Observations medicarum. Ludavics Elzevirius. Vol. 63. Amsterdam: Tulp N.
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tibus). Ann Med Hist 1917; 1:367.
History of Spina Bifida 7

9. Bayer C. Zur Techoukdu Operation der spina bifida and encephalocoel. Prager Med
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Spina Bifida Manifesta. Rehabilitation Monograph XXXI. New York, NY:
New York University Spina Bifida Study Group, 1966.
16. Sharrard WJW, Grossfield I. The management of deformity and paralysis of the foot in
myelomeningocele. J Bone Joint Surg Br 1968; 50(3):456–465.
17. Harrington P. Treatment of scoliosis. Correction and internal fixation by spine instru-
mentalation. J Bone Joint Surg Am 1962; 44-A:591–610.
18. Luque E, Cardoso A. Segmental correction of scoliosis with rigid internal fixation.
Orthop Trans 1977; 1:136 –137.
19. Banta JV. The orthopaedic history of spinal dysraphism. I: The early history. Dev Med
Child Neurol 1996; 38:848– 854.
20. Tulipan N, Bruner JP, Hernanz-Schulman M, Love LH, Walsh WF, Nickolaus D,
Oakes WJ. The effect of intrauterine myelomeningocal repair on the central nervous
system structure and neurosurgical function. Pediatr Neurosurg 1999; 31:183–188.
21. Mitchell LE, Adzick S, Melchionne J, Pasquariello PS, Sutton LN, Whitehead AS.
Spina bifida. Lancet 2004; 364:1885–1895.
22. Eskes TKB. From anemia to spina bifida—the story of folic acid. A tribute to
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23. Seminar Med Genet. Am J Med Genet C Semin Med Genet 2005; 135(1).
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