Meningocele & Spina Bifida

Presented by:
Maya Okta Lestari 2012061057
Haris Cakrasana 2012061058

Anatomy
The spinal cord extends from the foramen magnum where it is
continuous with the medulla to the level of the first or second
lumbar vertebrae.
The spinal cord is 40 to 50 cm long and 1 cm to 1.5 cm in
diameter.
Two consecutive rows of nerve roots emerge on each of its
sides. These nerve roots join distally to form 31 pairs of spinal
nerves.
The spinal cord = cylindrical structure of nervous tissue
composed of white and gray matter, is uniformly organized
and is divided into four regions: cervical (C), thoracic (T),
lumbar (L) and sacral (S)
The spinal nerve contains motor and sensory nerve fibers to
and from all parts of the body. Each spinal cord segment
innervates a dermatome (see below and Figure 3.5).

Development of Neural Tube

By about 16 days after fertilisation, the intraembryonic mesoderm is
formed and the embryo becomes a trilaminar disc is called gastrulation.
One or two days after gastrulation, the notochord can be seen along the
midline of the embryo. The notochord induces a wide strip of ectoderm
overlying it to get thickened to form the neural plate.
Some cells at the junction between the neural plate and the rest of
ectoderm become specialised to form the primordia of the neural crest.
By the 21st day (end of 3rd week), the neural plate gets depressed along
the midline and a groove is formed (neural groove) on the neural plate.
The neural groove gradually deepens; the two edges of the neural plate
come closer and eventually fuse to become the neural tube.
The neural tube initially closes in the middle. The fusion starts around
23rd day and proceeds both cranially and caudally. The anterior neuropore
closes by the 25th day and the posterior neuropore by the 27th day. The
closure of neural tube is completed by the end of 4th week.

Definition
Disgraphism Spinal term group of congenital
anomalies of spinal fusion caused by the failure
of neural tube both bones and skin.
Spina bifida is a congenital abnormality, a defect
in the posterior arch of the spine as a result of
the failure of neural tube closure in the early
embryo

Epidemiology
Approximately 400.000 infants with spina bifida
are born worldwide each year.
The incidence in Europe and North America
ranges between 1-2.5 per 1,000 live births
The incidence in Asian countries, including
Indonesia ranges from 0.1-0.3 per 1,000 live
births

Etiology & Risk Factor

Unknown
Multifactorial
Genetic = single gene mutation (eg. Meckels
syndrome) & chromosomal abnormalities (trisomy
13, trisomy 18)
Nutrition
Intake zinc, folic acid reduce spina bifida incidence

Environmental factor = lower socioeconomic status

Racial
Alcohol consumption
Maternal problems
Use of anti epileptic drugs, maternal diabetes,
hyperthermia, obesity

Types
Spina bifida aperta/mielomeningokel
Spina bifida okulta
Spina bifida cystica

Spina bifida occulta

The most mild, sometimes called hidden spina
bifida
Not discovered until late childhood or adulthood.
Neural defect covered by skin. There is a small gap in
the spine, but no opening or sac on the back. The
spinal cord and the nerves usually are normal.
Prosessus spinous always lost, the laminae may be
lost
Epidemiology = 25% population
Occur in the lumbosacral region (L4-S1)
This type of spina bifida usually does not cause any
disabilities.

Spina bifida aperta/mielomeningokel

The most often, the most serious type

With this condition, a sac of fluid comes through
an opening in the babys back. Part of the spinal
cord and nerves are in this sac and are damaged.
Causes moderate to severe disabilities

Meningocele
With meningocele a sac of fluid comes through
an opening in the babys back may or may not be
covered by skin.But, the spinal cord is not in this
sac.
There is usually little or no nerve damage.
This type of spina bifida can cause minor
disabilities.

Pathophysiology
Neural tube defects are the result of a
teratogenic process that causes failed closure
and abnormal differentiation of the embryonic
neural tube.
Myelomeningocele results when the closure of
caudal neuropore is disrupted during days 26-30
open lesion or sac that contains dysplastic spinal
cord, nerve roots, meninges, vertebra, skin

Clinical Manifestation
Leg weakness and paralysis
Orthopedic abnormalities (i.e., club foot, hip
dislocation, scoliosis)
Bladder and bowel control problems, including
incontinence, urinary tract infections, and poor
renal function
Pressure sores and skin irritations
Abnormal eye movement
Hydrocphalus

 A sac sticking out of the mid to lower back,

dimpling of the sacral area.
Motor, sensory and autonomic deficit related to
the level of the defect.
Symptoms include : loss of bowel and bladder
control, paralysis or weakness of the legs, loss of
sensation.

Diagnosis
Clinical manifestation
USG

Therapy
Surgical closure of the myelomeningocele is
undertaken within 24 to 48 hours of birth to
avoid CNS infection.
The defect covered by moist sterile dressings,and
given prophylactic antibiotics
Skin grafts often are required for large defects.
Ventricular shunts, if indicated, are placed
concurrently with myelomeningocele closure or
at a later

PROGNOSTIC
children with myelomeningocele, 60% to 70%
will ultimately require a shunt insertion,
whereas only 15% to 30%
(24% over a 25-year period), cognitive
development (75% have an IQ higher than 80 if
adequately treated for hydrocephalus),

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