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Pedia: Neuro

Pedia: Neuro

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Introduction to Pediatric Neurology
Dr. de Sagun
July 27, 2006

Outline:
Approach to a Neurologic Disease
Congenital CNS Malformation
Increase intracranial pressure
Paroxysmal Disorders
Psychomotor Retardation

Pediatric Neuro History

Chief complaint
HPI
System Review
Past Personal History

\ue000Gestational history
\ue000Birth history: asphyxia
\ue000Immunization
\ue000Developmental history
\ue000Past medical history
\ue000Family history

General PE
Diagnostic Approach to a Neurologic
Disease
Questions to answer
1. Does the child have a neurologic
disorder?

2. If so, where is the site of the lesion, or
does it involve all part of the brain to
an equal degree? Lateralize, if
possible.

3. What is the lesion? Check course of
the illness (acute, subacute, static or
remitting)

Nature of the Illness
1.Congenital: must have started early
on in the age
2.Infectious: acute or accompanied by
fever, dramatic onset
3.Developmental: developmental delays
come in
4.Neoplastic: gradual but progressive
manifestation of symptoms
5.Vascular: acute, reach the peak of
symptoms immediately

6. Immunologic
7. Degenerative
8. Nutritional
9. Metabolic

10. Paroxysmal
Neurodiagnostic tests
1. Lumbar puncture & CSF analysis
a. Indicated in CNS infections

b. Normal values in newborn
differ from infants and older
child

c. ICP can be determined

d. Bacteriologic tests on the fluid
would help in management
e. C/I in cases with lesions at the

site of lumbar puncture

CSF Analysis
Character of fluid: clear, colorless
Cell count: RBC, WBC, differential
count (neutrophils, lymphocytes,
blast cells)
Protein level
Sugar level and ratio to blood
sugar
Gram stain, culture and antibiotic
sensitivity
IgG values
Viral studies

2. EEGa. Indicated in seizures and
paroxysmal disorders
b. Determination of brain death
3. Electrodiagnostic tests
a. EMG
\ue000A concentric needles is

electrode inserted into
the muscle records the
action potentials
generated by muscle
activity

\ue000Indicated in lower motor
neuron disease
b. NCV
\ue000Determines the

conduction rate of motor
nerves by stimulating the
nerve at 2 points and
recording the latency
between each stimulus
and muscle contraction

\ue000Distinguishes between
demyelination and axonal
degeneration
4. Evoked potentials
a. Visual evoked potential
(VEP/VER)
\ue000Useful to establish

vision in children who are
thought to be visually
handicapped or blind

b. Brainstem evoked potentials
(BAER)
\ue000Checks the integrity of
the auditory system
5. Neuroimaging
a. Cranial ultrasound
\ue000Least invasive, uses
fontanels and opened
sutures as windows
\ue000Helpful in perinatal
asphyxia, monitoring
ventricular size
b. CT Scan
\ue000Very useful in

delineation of intracranial
structures; utilizes
radiation

\ue000Procedure of choice in

acute encephalopathy,
trauma, subarachnoid
bleed, intracranial
calcifications

c. MRI
\ue000Does not use radiation;
delineates intracranial
structures
\ue000Gray-white matter

delineation is excellent
hence it is useful in
degenerative diseases,
intractable seizures and
unexplained
developmental disabilities

\ue000Helpful in spinal cord
lesions
\ue000Inferior to CT scan in
intracranial calcifications
and acute hemorrhage
6. Other tests

a. Muscle or Nerve biopsy: for
accurate diagnosis of type of
muscle disorders and nerve
disorders

b. Cerebral angiography: for
vascular disorders
c. Neuropsychological testing
d. Metabolic tests in the urine
and blood
e. Antiepileptic drug assay
f. Muscle enzymes
Congenital Disorders of the Nervous
System
\ue000Malformations of the brain and spinal
cord form during the NS development
\ue000Intrinsic and extrinsic factors play a role
\ue000Etiology of malformations is not known
in 60% of cases
\ue000Understanding the normal embryonic

embryonic development is vital for the
understanding and classification of
abnormalities

Common Causes of CNS Malformations
\ue000Teratogens
o
Physical agents: trauma,
hyperthermia, radiation
o

Infectious agents: rubella, HSV,
CMV, mumps, varicella,
treponema, toxoplasma

o
Maternal illnesses
o
Maternal toxin and drug
exposure
\ue000Genetic Conditions
Congenital Defects and the Embryonic
Stages
I. Neural tube formation
Chiari syndrome

Cranioschisis (anterior neuropore)
Anencephaly
Encephalocoele
Meningocoele

Raschischis (posterior neuropore)
Meningocoele
Myelomeningocoele
Spina bifida

II. Segmentation and Cleavage
Basilar impression
Holoprosencephaly

III. Sulcation, Proliferation, Neural Migration,

Organization
Callosal agenesis
Heterotopias
Macrogyria/Microgyria
Neuronal migration defects
Cerebral anomalies
Lissencephaly
Schizencephaly

IV. Myelination
White matter hypoplasia

V. Mesodermal Development
Craniosynostosis
Fibrous dysplasia

NEURAL TUBE DEFECTS (DYSRAPHISMS)
Spina bifida occulta
\ue000Midline defect of the vertebral bodies
without protrusion of the spinal cord or
meninges

\ue000Usually asymptomatic
\ue000Usually at level L5 and S1
\ue000No abnormality of the spinal cord,

meninges or nerve roots
\ue000Occasionally with other developmental
disabilities such as syringomyelia,
tethered cord
\ue000A dermal sinus tract or opening may be
a cause of recurrent meningitis
Meningocele
\ue000Meninges herniate through a defect in
the posterior vertebral arches

\ue000Spinal cord usually normal
\ue000Fluctuant mass seen in the midline
\ue000Surgery if with leaking CSF or if only

thin skin covering
\ue000CT scan or MRI prior to surgery
Myelomeningocele
\ue000Most severe form of dysraphism
\ue000Spinal cord and meninges protrude into
the defect
\ue000Etiology: unknown
o
Drugs, nutritional, genetics
have been implicated
\ue000Clinical manifestation
o

Dysfunction of many organs as
skin, gut, skeleton, peripheral
nervous system

\ue000May be associated with hydrocephalus
(Chiari Type 2)
\ue000Management: multidisciplinary
Encephaloceles
\ue000Affect the skull through a midline bony
defect (cranium bifidum)
\ue000Cranial meningocele
\ue000Cranial encephalocele may be

associated with other defects as
aqueductal stenosis, Dandy-Walker
malformation, or Chiari malformation

Anencephaly
\ue000Primitive brain with connective tissues,
hypoplastic pituitary, absent cerebrum &
cerebellum
\ue000Death in several days
DISORDERS OF NEURONAL MIGRATION
Lissencephaly or Agyria
\ue000Absence of cerebral convolutions and
poorly formed sylvian fissure with
appearance of a 3-4 month fetal brain
\ue000With a 4-layered cortex instead of 6
\ue000Clinical manifestations
o

Failure to thrive, MR, seizure
disorder, chromosomal
features (Miller-Dieker
Syndrome)

o
CT and MRI: smooth brain
Schizencephaly
\ue000Unilateral or bilateral clefts with the
cerebral hemispheres due to an
abnormality in morphogenesis
\ue000Clinical manifestations
o
MR, seizures, microcephaly,
spastic paresis
Porencephaly
\ue000Presence of cyst or cavities within the
brain
\ue000Clinical manifestations
o
Often associated with other

brain malformations as
microcephaly, MR, optic
atrophy, seizures

\ue000Cysts usually unilateral; usually do not
communicate with a fluid-filled cavity
Holoprosencephaly
\ue000Results from defective cleavage
\ue000Patients may have a single ventricle,
other malformations
\ue000Mortality is high
Microcephaly
\ue000Head size > 3SD below the mean for
age and sex
\ue000Typeso
Primary: genetic
o
Secondary: non-genetic
Hydrocephalus
\ue000Results from conditions with impaired

circulation and absorption of the CSF or
increased production by a choroid plexus
papilloma

\ue000Typeso
Obstructive or non-
communicating
o
Non-obstructive or
communicating
\ue000Clinical manifestations
o
Enlarging head with big

fontanel, wide sutures,
prominent scalp veins and
setting sun signs

o
Long tract signs
o
Irritability, lethargy, vomiting
o

Gradual change in personality;
deterioration in academic
performance

\ue000Diagnosis
o
Complete PE and NE
o
Ultrasound

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