LEVEL III BLOCK VI MODULE 3 – NEONATOLOGY
Torch by Nathalie Anne R. Hernaez, MD
TORCH TOXOPLASMA
Etiology  Toxoplasma gondii –
obligate intracellular
protozoa
 It is acquired:
a. Perorally
b. Transplacentally
c. Parenterally
Incidence/  3-8 infants per 1000 live
Epidemiology births
 Congenital toxoplasmosis
occurs exclusively as a
result of maternal
infection during
pregnancy
 Maternal infection;
asymptomatic or with mild
illness (fatigue, LAD, IM-
like illness)
 General risk of
transmission: 40%
 Risk of transmission
increases with increasing
gestational age BUT the
severity of manifestations
in the fetus is higher with
the earlier the
transmission
Transmission  The organism
disseminates
hematogenously to the
placenta
String`14 – TORCH by Dr. H.A. Hernaez
OTHER (SYPHILIS)
 Treponema pallidum – motile
spirochete transmitted by
sexual contact or
transplacentally
 Associated with:
a. Lack of prenatal care or
limited prenatal care
b. Maternal illicit drug use
 Can occur at any stage of
pregnancy and can occur at
any stage of maternal syphilis
 Transmission rate of nearly
100%
 Early gestational infection can
occur but the manifestations
th
are seen after the 5 month
 Fetal/ perinatal death: 40%
 Transplacental
RUBELLA CMV HERPES SIMPLEX
 RNA togavirus  DNA herpes virus family  HSV types 1 and 2
 Humans are the only natural  Humans are the only known - Double-stranded DNA virus which
host reservoir after viral replication the virus is
 Mild but extremely contagious transported to the dorsal root
disease ganglia
 Incubation period: 14-23 days
 Congenital rubella  Most common intrauterine infection
- Primary maternal
infection  Common in underdeveloped
- Accidental vaccination countries and low socioeconomic
during pregnancy groups
 Gestational age at the time of
maternal infection – most
important determinant of fetal
infection and congenital
defects
1. Fetal loss
2. Stillbirth
3. Placental infection
4. Congenital rubella
syndrome
5. Normal fetus
 Droplet contact  Close contact of contaminated  Respiratory droplet spread or by direct
secretions (blood, semen, contact with active lesions
breastmilk, urine, cervical
secretions, saliva, transplanted  Transmission from mother to infant
organs) may occur by transplacental,
intrapartum, or postnatally
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  Rates of transmission and
outcome depends on:
a. Placental blood flow
b. Virulence
c. Inoculums
d. Immunologic capacity
of the mother to limit
parasitemia
Clinical  May be mild to severe
Manifestations  More than half might be
normal in the perinatal
period but nearly all will
have ocular problems
later
 Triad:
a. Hydrocephalus
b. Chorioretinitis
c. Intracranial
calcifications
 75% are asymptomatic in
early infancy
1. Healthy appearing infant
with subclinical infection
whose symptoms develop
later in childhood
a. CSF abnormalities
b. Late onset seizures
c. Chorioretinitis
d. Mental retardation
e. Developmental delay
f. Hearing loss
2. Healthy appearing infant
whose symptoms develop
in the first few months of
life
String`14 – TORCH by Dr. H.A. Hernaez
Early Congenital Syphilis
1. Presentation before 2 yrs
of age
2. Prematurity and
intrauterine growth
retardation
3. Hepatosplenomegaly
4. Nasal chondritis
(“snuffles”)
5. Skin rash
6. Osteochondritis
7. Neurologic symptoms
and signs including
hydrocephalus and
cranial nerve palsies
Late Congenital Syphilis
1. Presentation after 2 yrs
of age
2. Craniofacial malformation
3. Dental abnormalities
4. Interstitial keratitis
5. Deafness
6. Neurosyphilis
7. Paroxysmal cold
hemoglobinuria
 2/3 asymptomatic at birth
 Transplacental transmission: 1% of  Transplacental
congenital infection - HSV lesions and viremia at birth
and by elevated IgM cord blood
 Perinatal infection: passage levels
throughout the birth canal,
breastmilk, blood transfusion  Intrapartum
- Responsible for 85-90% of
neonatal infection
 Postnatal
- Fomites in the nursery
- Mothers with active lesions
 Maculopapular rash from the Infants  Congenital infection
face to the trunk and  5-10% of congenital infection are a. Skin lesions and scarring
extremities with postauricular, symptomatic b. IUGR
suboccipital, and posterior c. Psychomotor retardation
cervical lymph node  Symptomatic infants: mortality rate d. Intracranial calcifications
enlargement  20-30% e. Microcephaly
f. Eye involvement
 3/4 of infants show no  90% survivors have sequelae g. Hypertonicity
apparent involvement at birth h. Seizures
but experience consequences Maternal Manifestation
years later  Asymptomatic  Manifestations probably result from
 10% present with IM-like illness destruction of normally formed organs
a. IUGR rather than defects in organogenesis
b. Failure to thrive  Asymptomatic congenital illness
c. Thrombocytopenia - 90% are asymptomatic but 10-  Neonatal herpes – usually
d. Hemolytic anemia 15% are at risk for later symptomatic
e. Blueberry muffin spots sequelae
f. Hepatosplenomegaly  30% are caused by HSV-1
g. Jaundice 1. Sensorineural hearing loss a. Disseminated infection (22%)
h. Myocarditis 2. Periventricular lucencies/ b. Encephalitis (34%)
i. Cataracts calcifications c. Localized to the skin, eyes, or
j. Bony lesions 3. Chorioretinitis mouth (40%)
4. Defect in tooth enamel leading
 Best known for: to increased caries  Disseminated infection
1. Deafness - 57% mortality rate
2. Defects of the eyes, CNS,  Symptomatic congenital infection - Involve all organ systems but
and heart - 20-30% mortality rate: DIC, predominantly the liver, lungs,
hepatic failure, or bacterial adrenals
 Sensorineural deafness infection - Signs of sepsis and shock, DIC,
- Usually bilateral respiratory distress
- Develops in 3/4 of infants
- May be the only
manifestation
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 3. Infant with generalized  Skeletal manifestations:
disease at birth a. Metaphyseal
a. Prematurity, IUGR osteochondritis
b. Jaundice, b. Periostitis
hepatomegaly c. Osteitis
c. LAD, cutaneous d. Destruction of the
lesions proximal medial
d. Myocarditis metaphysic (Wimberger
e. Feeding problems sign)
4. Infant with predominantly  Late manifestations are from
neurologic involvement a chronic inflammation of the
birth skeleton, teeth, and CNS
a. Acute a. Frontal bossing
encephalopathy b. Olympian brow
b. Obstructive c. Higoumenakis sign
hydrocephalus d. Saber shins
c. Subtle neurologic e. Hutchinson’s teeth
deficits f. Mulberry molars
g. Notching of the biting
surface
h. Defects in enamel
formation
i. Rhagades
j. Juvenile paresis
Diagnosis Fetal  Should be considered in
 Fetal ultrasound q 2wks infants with:
 PCR amplification of the a. Unexplained prematurity;
Toxoplasma gene 1 from b. Hydrops of unknown
amniotic fluid etiology; or
 Placental examination will c. Placental enlargement
reveal chronic
inflammation and cysts  Neonates should be
evaluated:
Neonatal a. Maternal treatment is
 Following studies should unknown or inadequate
be done: b. Maternal titers does not
a. Neurologic exam decrease
b. Ophtha exam
c. CT scan  PCR of CSF
d. Antibody tests a. Dark field examination of
e. Viral isolation mucous patches,
f. Lumbar puncture umbilical cord, amniotic
fluid, nasal discharges
String`14 – TORCH by Dr. H.A. Hernaez
 Congenital heart disease
- If infection occurs during
st
the 1 8 weeks of
gestation
 PDA
- Most common
- May occur alone or in
conjunction with
pulmonary artery or
valvular stenosis
 Microcephaly and
neuropsychiatric problems
 Ophthalmologic:
a. Cataracts
b. Microphthalmia
c. Glaucoma
*strabismus, nystagmus, iris
dysplasia
 Predisposed to autoimmune
disease
Diagnosis
 Maternal rubella specific IgM
titer determined 7-14 days
after illness and a rise in
serum antibody titers
comparing acute and
convalescent phase
 Evaluation
1. Isolation of the virus from
the newborn
2. Rubella specific IgM in
cord or infant blood
3. Increasing IgG
1. Hepatosplenomegaly  Encephalitis
2. Prematurity - 15% mortality
3. Petechiae, purpura, - Blood-borne seeding in the brain
thrombocytopenia (direct resulting in cortical hemorrhagic
suppression of necrosis
megakaryocytes)
4. Diffuse interstitial or  Skin, Eyes, Mouth Infections
th
peribronchial pneumonitis) - Usually present by the 10 day of
life
 Long-term: - 1/3 develop neurologic sequelae
1. Chorioretinitis a. Keratoconjunctivitis
2. Sensorineural hearing loss b. Chorioretinitis
3. Microcephaly and intellectual c. Microphthalmos
impairment d. Cataracts
4. Neuromuscular disorders
 Virus isolation in the first 2-3 weeks  Viral isolation
of life – most sensitive and specific - Immunofluorescence
test antibody staining
 DNA hybridization and PCR DNA
amplification
 Amniocentesis – most valuable
single antenatal diagnostic test
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  Cultivation of Toxoplasma b. Serologic tests:
in lab mice from placental - Rapid plasma reagin
tissue samples  (RPR) test
Toxoplasma specific IgM, - Venereal Disease
IgA, or IgG antibody Research Lab
(VDRL) test

 Maternal titer increased

fourfold
 Infant’s titer is greater
fourfolds than the mother’s
 If the infant is asymptomatic

 Evaluation
a. PE
b. Quantitative
nontreponemal test of
serum (not cord blood)
c. Routine CSF exam, CSF
VDRL
d. Long bone radiography
e. CBC
f. Others tests like CXR

 Criteria to the diagnosis

1. Physical, lab, or
radiographic evidence of
active infection

2. Placenta or umbilical
cord is positive for
treponemes using dark
field test or specific direct
fluorescent antibody
staining

3. Active CSF VDRL result

4. Infant quantitative serum

nontreponemal STS titer
fourfold or more than that
of the mother’s

String`14 – TORCH by Dr. H.A. Hernaez 4 of 5

Treatment  Pregnancy  Aqueous Penicillin G for 10-14  Isolation of children with  CMV does not produce thymidine  Cesarean section within 4-6 hours
- Reduces the risk by days postnatally acquired rubella kinase after rupture of membranes
60% for 7 days  Immediate isolation and culture
- Pyrimethamine with  Jarisch-Herxheimer reaction  Gancyclovir  CBC, liver functions test
sulfadiazine and 1. Fever  Congenital rubella - Has significant toxicity:  Hold breastfeeding in mothers with
supplemented with 2. Tachypnea - Considered contagious a. Reversible neutropenia breast lesions
folinic acid or 3. Tachycardia for 1 year unless b. Thrombocytopenia
spiramycin 4. Hypotension repeated urine and blood c. Neurologic symptoms  Acyclovir – drug of choice
5. Prominence of cutaneous cultures are negative d. anemia
 Newborn: all should be lesions
treated 6. death  Treatment can be considered for
the symptomatic infant BUT cannot
 Follow-up: serial quantitative be routinely recommended
tests (3, 6,and 12 months)
- Decrease in titer by 3
months of age
- Non-reactive test in 6
months

Prognosis  70% normal outcome in

treated infants

 Poor outcome:
a. Delayed diagnosis
b. Delayed initiation of
treatment
c. Delayed correction of
increased intracranial
pressure
d. With profound visual
impairment
e. Prolonged
concomitant neonatal
hypoglycaemia and
hypoxia

String`14 – TORCH by Dr. H.A. Hernaez 5 of 5

B6M3L2-Retinopathy of Prematurity Linking Oxygen To ROP
Dr. Jefrrey Lim Role of Oxygen:
May 12, 2021 - Amount delivered vs. length of exposure
Uy, J - Timing of exposure
- Arterial oxygen fluctuations
PREMATURE DELIVERY - Precise control of supplemental oxygen can reduce the
- disrupts the programmed development of the fetus incidence of ROP
- most organ systerionms continue to develop
- except the retina RISK FACTORS
- Low birth weight
RETINOPATHY OF PREMATURITY o 1000 – 1250 g – 47% have some form of ROP
- fragile vascular bed of the retina o <750 g – 90% develop ROP
- exposed to hyperoxic extrauterine environment - Low gestational age
- causes cessation of vessel growth leaving much of the o <28 weeks – 84%
retinal tissue avascular o >32 weeks – rare
- later, increased metabolic demand of a developing - Supplemental oxygen
retina causes excessive abnormal vessel growth in o Frequent apnea
response to hypoxia o Sepsis
o Prolonged ventilation
HISTORY o Anemia
- 1940s
o Incubators with free flowing oxygen INTERNATIONAL CLASSIFICATION OF ROP
o ROP appeared - Devised by 23 ophthalmologists from 11 countries
- 1951 - It was published and accepted in 1984 and expanded in
o Dr. Kate Campbell correlated this with oxygen use 1987
o Supplemental O2 used only for cyanosis - Defined the location (zone) of the disease in the retina,
o Blindness dropped from 50% in 1950 to 4% in 1965 and the extent (clock hours) of the developing
o However, increase rate of infant mortality and vasculature involved, severity (stage) of retinopathy,
cerebral palsy and the presence of plus disease
- 1960s - Updated in 2005
o Blood oxygen monitoring became available o changes include:
o Pulse oximetry ! AP-ROP
o ROP on the rise again lately due to survival of ever ! Pre-plus disease
lower gestational ages ! Clarification of zone 1
- Thus, ROP can be considered a disease of modern
medicine

PATHOPHYSIOLOGY
- 16 weeks AOG - fine vessels start growing from the
optic nerve, gradually gorwing to the retinal surface and
reach peripheral at...
- 36-40 weeks AOG - complete vascularization
- So depending on the AOG the baby is born, the growth
of the retinal vessels are somewhere between the optic
nerve and the retinal periphery
- In utero – relative hypoxia
o Fetal hemoglobin does not readily release oxygen Location and extent of disease.
into the tissues.
o
Zone 1 – 30 circle around optic nerve
Phase 1 Phase 2 o
Zone 2 - 60 around the topic nerve
- Sudden hypoxia - Neovascularization Zone 3 – temporal area of the retina not covered by zone 1
- Short and - Hypoxia due to increase and zone 2
immediate metabolic demand of the
- Choroid bathes developing retina
retina in oxygen - Expression of VEGF, IGF-1
- Vessels - Uncontrolled new vessel growth
obliterated due – prethreshold ROP
to oxygen - Vessels grow into vitreous –
exposure threshold ROP
STAGES Stage 4: Partial Retinal Detachment
Stage 1: Demarcation Line - when there is partial retinal detachment from traction
- between vascularized retina and avascularized retina membranes
- considered the frontlines of the wall for vessel growth

Stage 4a (partial retinal detachment, extrafoveal or not involving

the macula)

Stage 2: Ridge Stage 4b: partial retinal detachment, foveal or involving the
- line becomes thicker, forming a ridge macula. Poor visual prognosis even after surgery

Stage 5: Total Retinal Detachment

- carries and extremely poor visual prognosis
- technically blind for life

PLUS DISEASE
- A parameter that helps us recognize eyes that have
Stage 3: Extraretinal Fibrovascular Proliferation
more propensity to progress into advanced stage
- When ridge develops abnormal neovascular vessels
- Characterized by:
- Stage where we need to treat patient
o Dilation and tortuosity of the retinal vessels
o Iris vascular engorgement
o Pupillary rigidity
o Vitreous haze

Mild Stage 3 ROP

PRE-PLUS DISEASE
- Dilation and tortuosity of blood vessels
- More than normal
- Less than plus disease

Severe Stage 3 ROP with some area of hemorrhage. Abnormal

vessels grow into the vitreous rather than on the retinal surface
AGGRESSIVE POSTERIOR ROP (AP-ROP)
- an uncommon, rapidly progressing, severe form of ROP
- posterior location, prominence of plus disease, and ill-
defined nature of retinopathy
- Previously known as “Rush Disease”
Laser Treatment
- Replaced the use of cryotherepay
- Found to be as effective, if not more effective than
cryotherapy for the treatment of ROP

Head mounted laser

with a handheld
focusing lens to deliver
laser treatment into the
eye. Success of laser
THRESHOLD ROP treatment is around 70-
80%
- When treatment is indicated
- Stage 3 disease in zone I or II
- 5 contiguous clock hours
- 8 cumulative clock hours
- Presence of plus disease

white laser marks from recent
treatment.
After a few weeks show scars have
formed and ROP has regressed.
The laser treated areas are non-
viable areas so laser treated eyes
have a significantly narrow field of
vision.

TREATMENT OF ROP Anti-VEGF Treatment

- Multicenter Trial for Cryotherapy for ROP
- 4099 infants weigh <1251 grams were monitored
- 65.8% of the infants developed ROP
- 81.6% of infants <1000 grams
- 6% developed threshold ROP
Screening For ROP
- Recommended schedule for screening
o Infants <30 weeks gestational age
o Infants <1500 grams BW
o Infants <32 weeks of gestational age, receive
intensive care for 4 weeks or longer
- New Recommended schedule for screening by the
Philippine ROP working Group (2019)
o Infants <32 weeks gestational age or birth weight
<1500gm
o Infants between 32-36 weeks AOG with the ff risk
factors:
! Sepsis
! Transfusion within the first 10 days of life
! Oxygen use, esp without oxygen blender
! Prematurity with an unstable clinical course
Follow Up
- After retina has fully vascularised with no plus disease
- Follow up approx. 5-6 months after last retinal exam
- Watch for possible development of myopia and/or
strabismus
- Some retinas may fail to fully vascularize
- Need follow up for life
- Ranibizumab - (Lucentis) Novartis
- Bevacizumab–(Avastin)Roche – off label use
- May be used for primary treatment
- for salvage after failure of laser treatment
- Given as intraocular injection.
- Success rate: 93%
- BEAT-ROP Study
o Bevacizumab Eliminates the Angiogenic
Threat of ROP
o Compared Bevacizumab to conventional
laser treatment
o Used as primary treatment
o AntiVEGF superior to LASER in zone 1 dse
o No significant difference for zone 2 disease
Surgery for Stage 4A ROP
- Typical tractional +/- exudative component – needs
vitrectomy
- Stage 4A ROP may regress spontaneously as a result
of cryo or laser
- 4A may be observed closely for signs of macular
involvement
- Timely intervention will usually result in good visual
outcome
Surgery for Stage 4 ROP
- nearly 50% of stage 4B ROP retinal detachment
responded well anatomically to scleral buckling
- visual results are generally poor once macula is
involved
Surgery for Stage 5 ROP
- seaber et al assessed the effectiveness of vitrectomy
for stage V ROP
- 51 eyes, mean ff up 61 months
- 15 NLP, 11 light localization, 10 able to follow light
- 4 were able to detect form

After ROP regression

- Retinal changes
o temporal or nasal dragging of retinal vessels
o macular ectopia
o dragging of retina over the optic nerve
o late traction retinal detachments/tears
- myopia – 16-50%
o due to increased corneal curve and or scleral
thinning from tx
- strabismus 14-40%
- amblyopia – 6-33%
- visual field defect – decreased by about to degrees in
laser
- Need to be followed closely lifelong

SUMMARY:
- control of oxygen administration and close monitoring of
O2 saturation can decrease the incidence of ROP
- laser ablation is still the gold standard of treatment for
threshold ROP
- Anti VEGF agents are playing an increasing important
role in the management of ROP, especially AP-ROP
- Surgery for ROP yields very poor visual outcomes
when there is macular involvement
- Thus prevention and early detection is the key to
eradication of blindness from ROP
Lecture 7: "The role of Rehabilitation in Improving the Quality - Diffuse brain insults most likely caused by infection and
of Life of the Child with Cerebral Palsy" ischemia → two of the more common causes of
Dr. Cherie Lee Apiag encephalomalacia
May 20, 2021 - May present with SPASTIC QUADRIPARESIS and at
Uy J higher risk of additional medical and cognitive
problems
Outline
1. Definition of cerebral palsy
2. Epidemiology and etiology
3. Risk factors
4. History and PE
a. Classification
b. Clinical findings and patterns
5. Diagnosis
6. Functional prognosis
7. Medical management
8. Therapeutic management
9. Orthopedic management

Cerebral palsy
- A group of permanent disorders of movement and posture
causing activity limitation attributed to non progressive
disturbances in developing fetal or infant brain
Classification of CP
Epidem and Etiology - Movement patterns
- Cerebral palsy - MC and costly form of chronic motor - Spastic
disability that begins in childhood - Dyskinetic (athetoid, choreoathetoid, dystonic)
- More common and more severe in males compared to - Ataxic
females - Mixed
Spasticity Velocity dependent resistance or
Risk Factors increase in muscle tone in response to
passive movement

Athetosis Involuntary alteration in pattern of

muscle activation during voluntary
movement presenting as writhing
movements

Dystonia Involuntary muscle contraction resulting

in twisting movements and abnormal
posture

Chorea Involuntary, brief, irregular contractions

that are neither repetitive nor rhythmic

Pathology
- Periventricular - Anatomic distribution of motor problems
leukomalacia (PVL)
- MC brain
abnormality
- Involves the white
matter near the
lateral ventricles
- More common in
premature infants
- An outcome of
intraventricular
hemorrhage
Imaging
- Often cause
Recommendations:
spastic diparesis
- Cranial ultrasonography
(71%),
- All infants <30 weeks AOG aat between 7 to 14 days of
hemiparesis
age
(34%), quadriparesis (35%)
- Grade 3 or 4 intraventricular hemorrhage, periventricular
- Deep grey matter lesions to the basal ganglia and thalamic
cystic lesions or moderate to severe ventriculomegaly
region are mainly associated with DYSTONIC CP
- MRI vs CT scan
- Kernicterus-damage to basal ganglia → bilirubin
- MRI preferred to CT for evaluation of a child with
encephalopathy resulting in ATHETOID CP
suspected CP if the etiology has not been established
- Focal cortical infarcts of both grey and white matter involving
the MCA → hemiparetic CP
Evaluation and Clinical Findings - Knee
Comprehensive history - Flexion contractures are
- Risk factors common due to spasticity in the
- Family history hamstrings and static
- History of developmental milestones positioning in a seated position
- Significant delay in attaining motor milestones - Severe knee flexion is
- A discrepancy between motor and cognitive milestones associated with limited hip
should always raise suspicion for CP flexion
- Deviation from developmental milestones - Genu valgus may occur
- Ex. early hand preference of asymmetric use of the - Hip
extremities - early sign of hemiparesis - Acquired hip dysplasia is
- Early head control, rolling or rigid standing are all common in CP and often leads
associated with an abnormally increased tone or to progressive subluxation and
exaggerated primitive reflexes dislocation
- Unusual mean of mobility such as bunny hopping, - Can begin as early as 2 year
combat crawling, or bottom scooting - Muscle imbalance from
PE overactive hip adductors and
- Inspection flexors, femoral anteversion and dysplastic acetabulum
- Tone may lead to posterior dislocation
- Severe hypotonia - lay in a frog-leg position with - Spine
their hips abducted, flexed, and externally rotated - Spinal deformities are
with arms positioned lumply on the sides common including kyphosis,
- Persistent fisting or scissoring - observed in lordosis, or scoliosis
increased tone - Likelihood increases with
- ROM - check for range of motion and check for severity
flaccidity/spasticity - Curves greater than 40
- Earliest indication of CP may be a delay in the degrees progress
disappearance of primitive infantile reflexes - Risk of progression is
- Persistence of primitive reflexes past six months of age, greatest for patients with
asymmetry of the response or an obligatory response at quadriparesis increased
any age → highly suspicious for a significant motor spasticity, a larger curve,
impairment younger age
- Compromised pulmonary function in curves more than
60 degrees and above
- Upper extremity
- Positioned in shoulder
adduction and internal
rotation
- Elbow flexion contractures -
results form the spasticity in
the biceps, brachioradialis,
and brachialis
Disorders associated with Cerebral Palsy - MC deformity of the wrist -
Musculoskeletal system wrist flexion with ulnar
- foot/ankle deviation
- Equinovalgus deformity (a in the picture) - MC deformity of the fingers - flexion and swan neck
- Due to spasticity of gastrocsoleus and peroneal deformities
muscles with weakness of the posterior tibialis
muscle
- Common in older children with spastic diparesis
and quadriparesis
- Equinovarus deformity (b in the picture)
- Results from increased tone or contractures of the
gastrocsoleus complex
- Most common deformity
- Primarily due to a combination of spasticity of the
posterior tibialis muscle and gastrocsoleus
- Appear as inversion and supination of the foot and
a tight heel cord
Management of Child with Cerebral Palsy
- Stretching
- Prevention of contractures
- Institution of daily home exercise program
- Sustained stretch is preferable to manual stretching
- Positioning techniques, orthotic devices, splints, and
casting
- Serial casting - technique where a series of successive
casts are applied in the hopes of progressively
increasing the range of motion with each cast
- Strengthening
- Deficits in voluntary muscle contraction in CP are due to
decreased CNS motor unit recruitment leading to
functional deficit in children
- Noted improvement in gross motor function as
measured by the gross motor function measure after 6-8 - Upper and lower orthoses
weeks
- Increased participation and self esteem
- Partial body weight support treadmill training
- Task-specific repetitive practice can improve activities
including walking
- Benefits
- Improvement in standing and walking including
transfers from a sitting to standing position without
the use of the arms, walking, and climbing stairs in
some patients
- Increase in walking speed in those with GMFCS
level III or IV
- Constraint-induced movement therapy (CIMT)
- Restraint of the uninvolved or unaffected limb in
conjunction with at least 3 hours per day of therapy for
at least two consecutive weeks
- Modified CIMT - requires restraining of the unaffected
limb for fewer than 3 hours per day with therapy
- RCT-revealed improved functional use of the affected
extremity
- Cortical reorganization as demonstrated by
functional MRI
- Electrical stimulation
- Neuromuscular electrical stimulation (NMES)
- Functional electrical stimulation (FES)
- Threshold electrical stimulation

Hypertonia management
- Chemical denervation
- Alcohol blocks
- Phenol injections - muscles commonly targeted are
the musculocutaneous and obturator nerves
- Botulinum neurotoxin (BoNT)
- Bind terminals at the NMJ and blocks the
presynaptic release of Ach
- Commonly target muscles: gastrocsoleus,
hamstrings, hip adductors, flexor synergy muscle of - Adaptive equipment
the upper extremity
- Oral Medications
- Baclofen - binds to GABA receptors in the spinal cord to
inhibit reflexes that lead to increased tone
- Diazepam - facilitates postsynaptic binding of gaba to its
receptors in the brainstem, reticular formation, and
spinal cord
- Clonidine - alpha-agonist that acts in both the brain and
spinal cord enhancing presynaptic inhibition of reflexes - Adaptive tools
- Tizanidine - alpha-agonist that acts in both the brain and
spinal cord enhancing presynaptic inhibition of reflexes
- Dantrolene sodium- depresses the
excitation-contraction coupling in skeletal muscle by
binding to the ryanodine receptor I
- Selective dorsal rhizotomy
- A procedure that involves partial deafferentation of the
levels L1 through S2 nerve roots
- Effect: reduction in spasticity in the lower extremities
(which unmasks motor weaknesS)
- Ideal candidates for sdr:
- children between 3 and 8 years of age with GMFCS
level III or IV

- Orthopedic surgery
- Goal: weakness dysphasic muscles and reduce
potential contracture formation and spasticity
- The muscles often targeted:
- Muscles that cross two joints
- Hip adductors
- Hip flexors
- Hamstrings
- Rectus femoris
- Gastrcosoleus complex
- Rotational osteotomies
- Achilles tendon lengthening
- Surgical spinal fusion