CEREBRAL PALSY BSPT 2-B-2

CEREBRAL PALSY

 “a group of disorders of the o Delayed onset of

development of movement menstruation
and posture, causing activity o irregular menstruation or
limitations that are attributed long intermenstrual
to nonprogressive disturbances intervals
that occurred in the o Parity of three or more
developing fetal or infant
o Maternal medical
brain”
conditions: intellectual
 Three major criteria for
diagnosis of cerebral palsy: disability, seizures,
o a neuromotor control thyroid disease
deficit that alters  Paternal and sibling factors
movement or posture o Motor deficit in a sibling
o a static brain lesion
Prenatal
o acquisition of the brain
injury either before birth  Prematurity (gestational age
or in the first years of life less than 32 weeks)
 Low birth weight (less than 2500
EPIDEMIOLOGY
g)
 2.0 to 2.5 per 1000 live births  Maternal epilepsy
 Asian national origin subgroups  Hyperthyroidism
have a lower rate of CP than  Maternal Infections (STORCH)
whites o S-Syphilis
o TO-Toxoplasmosis
TIME OF BRAIN INJURY
o R-Rubella
PRENATAL Conception to o C-Cytomegalovirus
PERIOD the onset of o H-Herpes
labor  Bleeding in the third trimester
PERINATAL 28 weeks  Incompetent cervix
PERIOD intrauterine to 7  Severe toxemia, eclampsia
days postnatal  Hyperthyroidism
POSTNATAL First two years of  Drug abuse
PERIOD life  Trauma
 from fetal or neonatal period -  Multiple pregnancies
3 years  Low socioeconomic status
 Dx may not be made until 5 yrs.  Placental insufficiency
or later
Perinatal
RISK FACTORS
 Prolonged and difficult labor
Before pregnancy  Premature rupture of
 Maternal factors membranes
  Presentation anomalies PATHOPHYSIOLOGY
 Vaginal bleeding at the time of
 Arterial oxygen decrease by 10
admission for labor
to 15%.
 Bradycardia
 ~17% of CO goes to the brain
 Hypoxia

Postnatal (0-2 years)

 CNS infection (encephalitis,

meningitis)
 Hypoxia
 Seizures
 Coagulopathies
 Neonatal hyperbilirubinemia*
 Head trauma

CLASSIFICATION

2 Major Classification:

 Type of movement Disorder Various Pathological condition:

 Anatomical Distribution
 Periventricular
Physiological Classification Leukomalacia
 Parasagittal Cerebral
 Pyramidal (Hypertonia)
Injury
 Extrapyramidal (Hyperkinesia)
 Focal/Multifocal
CEREBRAL PALSY Ischemic Cerebral
SPASTIC DYSKINETIC ATAXIC MIXED Necrosis
MONOPLEGIA CHOREA
DIPLEGIA ATHETHOSIS
 Selective Neuronal
QUADRIPLEGIA CHOREATHETHOSIS Necrosis
TRIPLEGIA DYSTONIC  Status Marmoratus
TETRAPLEGIA
DOUBLE
HEMIPLEGIA

Neurodevelopmental Delay or Arrest

Periventricular Leukomalacia

 Main Ischemic lesion of

premature infants with
impaired cerebral perfusion
 Affected:
o Posterior white matter
o Anterior white matter
around the foramen of
Monro.

Parasagittal Cerebral Injury

 Full-term Infants involves the

watershed areas
 Mainly affects: Cerebral
cortices and Subcortical white
matter
 Spastic Quadriplegia,
intellectual deficits
 UE are more involved

GRADES OF INTRAVENTICULAR
HEMORRHAGE IN THE PREMATURE BRAIN

GRADE HEMORRHAGE
1 ISOLATED TO THE
GERMINAL
MATRIX
2 WITH NORMAL
VENTRICULAR
SIZE
3 WITH
VENTRICULAR Focal and/or Multifocal ischemic
DILATION cerebral necrosis
4 WITH
PARENCHYMAL  Selected area of necrotic
HEMORRHAGE lesion in the distribution of
major vessels
 Spastic Hemiparesis
 Typically related to middle
cerebral artery strokes.
 Associated with Seizures
 SUBTYPES OF HYPOXIC ISCHEMIC
ENCEPHALOPATHY

Lesion Location
Parasagittal Bilateral in
cerebral injury superior medial
and posterior
Selective Neuronal Necrosis portions of the
cortex
 Among full-term neonates
 Cortical areas with loss neurons
Periventricular Bilateral white
with astrocytosis leukomalacia matter necrosis
 Intellectual deficits, seizures, near lateral
ataxia, attention deficits ventricles
descending
Status Marmoratus
fibers of the
 Neuronal loss; gliosis; motor, optic and
hypermyelination of basal acoustic
ganglia (marbled radiations
appearance), thalamus and
Focal and Infarction in a
some cortical areas
multifocal specific vascular
 Movement disorders; Spastic
ischemic brain distribution
Quadriplegia
necrosis
 Athetoid CP following a
diagnosis of kernicterus, due to Status Neuronal injury in
concentrated damage to the Marmoratus the basal
basal ganglia with bilirubin ganglia
encephalopathy Selective Lateral
neuronal geniculate,
necrosis thalamus and the
basal ganglia
Clinical Finding
Upper extremities more severely
affected than lowers
Spastic diplegia and quadriplegia
visual and cognitive deficits
Hemiplegia and seizures
Choreoathetosis or mixed
Mental retardation, seizures
CLASSIFICATION
1. Physiology (the nature of the
motor abnormality) – pre-, peri,
postnatal or untraceable
2. Topography – body parts
affected
3. Etiology – congenital or
acquired
4. Clinical/ Neuroanatomic
features – brain parts affected
5. Functional capacity (severity)
& Therapeutic requirements –
mild, moderate, severe
NEUROLOGIC CLASSIFICATION
 SPASTIC CP – 50-60%
 DYSKINETIC CP – 25-30%
 ATAXIC CP – 5%
 MIXED CP – rare
NEUROLOGICAL AFFECTATION
 CORTEX: The cortex controls
thought, movement and
sensation. Damage can result
in spastic cerebral palsy.
 BASAL GANGLIA: The basal
ganglia help movement
become organized, graceful
and economical. Damage
can result in Athetoid cerebral
palsy.
 CEREBELLUM: The cerebellum
co-ordinates movement,
posture and balance. Damage
can result in ataxic cerebral
palsy
PHYSIOLOGIC CLASSIFICATION
 Pyramidal
o Spastic types
o neuromotor findings that
are consistent and
persistent
o Spasticity: “clasp knife”
resistance that is followed
by a sudden “give”
 Extrapyramidal
o Chorea, Athetosis,
Dystonia, Ataxia
o increased tone persisting
throughout slow passive
flexion and extension of an
extremity
o “lead pipe” rigidity
o 4-limb involvement: LE>UE
DYSKINETIC CEREBRAL PALSY
 Caused by damage to the
middle area of the brain
known as the basal ganglia.
 Muscles rapidly change from
floppy to tense with many
unwanted movements.
 Speech may be hard to
understand because of
difficulty controlling the tongue
and vocal cords.
 May have Athetosis, choleric,
dystonic, or hemiballismus
 Athetosis – most common CP
due to Rh incompatibility or
kernicterus
 TYPES OF DYSKINETIC CP 5. Ataxic
 Unsteadiness w/
1. Athetosis
uncoordinated movement
 Slow, writhing involuntary
 Nystagmus
movements of distal
 Dysmetria
extremities
 Wide-based gait
 Active agonist &
antagonist mm.
 Intensity may increase w/
emotions & purposeful
activities

ATAXIC CEREBRAL PALSY

2. Chorea
 Caused by damage to the
 Abrupt, irregular, jerky
cerebellum, which is at the
movement
base of the brain.
 Occurs in head, neck &
 Ataxic CP appears clumsy,
extremities
lack balance and often have
3. Choreoathetosis
an unsteady gait, shaky hand,
 Combination of Athetosis
movements and jerky speech.
& choreiform movement
 Large amplitude
1. Physiologic Classification
involuntary movement
 Mixed Type CP
 Athetosis is dominant
o Description includes both
4. Dystonia
spastic & Dyskinetic
 Slow, rhythmic movement
classification
w/ tone changes
2. Topographic Classification
 Found in trunk &
 Monoplegia
extremities
o Only one limb is involved.
 AbN posture
 Paraplegia
o Both the legs are involved
 Hemiplegia
o Both upper and lower
limbs are involved on one
side
 Triplegia
o Three limbs are involved
  Quadriplegia
o all the four limbs are
involved (UE>LE)
 Diplegia
 The lower limbs are more
involved than the upper limbs
3. Etiologic Classification
 Prenatal causes
o Infection, metabolic
disorders, anoxia, toxins,
genetic disorder and
LOCATION DESCRIPTION
infarction
 Perinatal causes Hemiplegia Upper and lower
o Anoxia extremity on one
 Postnatal causes side of the body
o Toxins, trauma and
infection Diplegia Four extremities,
4. Neuroanatomic Classification legs more
 Periventricular leukomalacia affected than
with prematurity the arms
o MC abnormality
o Results to spastic diparesis Tetraplegia Four extremities
 Basal ganglia injury with term plus the trunk,
neck, and face
asphyxia
o Results to dystonic CP
Triplegia Both lower
TONUS LESION SITE extremities and
one upper
Spastic Cortex extremity

Dyskinetic Basal ganglia – Monoplegia One extremity

extrapyramidal (rare)
system
Hypotonic/Ataxic Cerebellum Double Four extremities,
hemiplegia arms more
Mixed Diffuse affected than
the legs

BASED ON INVOLVED BODY PARTS

 Monoplegia
o One area affected. Either
UE or LE
o Least Common type
o Mild clinical presentation

 Diplegia
o LE>UE
o LE: UMNL (Spasticity); UE:
Mild
o coordination problem
o Diplegic Gait Pattern
 Spastic adductors,
gastrocnemius & hip
flexor
o Eye Problem
o Seizure
o Cognitive Impairment
 Hemiplegia
o One side of the body
involve (B) Arm and Leg
o UE>LE
o Etiology:
 Congenital (70-90%)
 Acquired (10-30%)
o MRI Unilateral Lesion
o R>L
o UMNL Sign on the
Affected Area
o (+) Sensory, visual & motor
deficits
o Cognitive impairments
(28%)
o Seizure (33%)
 Triplegia
o 3 extremities involve,
usually (B) LE and one UE
o UMNL: Spasticity – involved
limbs and mild
coordination problem in
noninvolved limb
o Gait Pattern: Toe Walking
and Scissoring
(simultaneous adduction,
knee hyperextension and
PF of the LE)
 Quadriplegia
o All four extremities and
truck re-affected (trunk:
hypotonia with
appendicular hypertonia
or total body hypertonia)
o UE>LE
 o UMNL; Spasticity & GROSS MOTOR CLASSIFICATION
persistence of primitive SYSTEM (GMCS)
reflexes
o (+) Opisthotonic Posturing
o ^ risk of aspiration
o High incidence of
cognitive & visual
impairments
o Seizure (50%)

CASE ANALYSIS:

A pediatric physical therapist,

is examining a patient with a
diagnosis of cerebral palsy. He notes
that all of the extremities and the
trunk are involved. Further
assessment also reveals that the THE GROSS MOTOR FUNCTION
lower extremities are more involved CLASSIFICATION SYSTEM (GMFCS)
than the upper extremities. The
patient most likely has which Before 2 years 2-4 years
classification of cerebral palsy? Level Manipulate Gets up
I objects with from sitting
hands and without
5. Functional Classification
walk holding
 Class I: No limitation of activity independently onto
 Class II: Slight to moderate something
limitation
 Class III: Moderate to great Level Belly crawls, Can
limitation II pull to stand assume
 Class IV: No useful physical on furniture sitting
activity and cruise position
without
assistance,
walk with
assistive
device
 minimal hand mobility using
Level Can roll and ‘w’ sit and function assistive device
III creep forward require
on stomach adult All areas of Functional
assistance motor functions limitations in
to are limited. sitting and
assume standing are not
sitting fully
compensated
Level Can roll Able to roll for through the
IV independently and creep, use of assistive
can sit device.
when
placed, 6. Therapeutic Classification
but need  Class A: no treatment required
both  Class B: minimal bracing and
hands on habilitation
the floor.  Class C: extensive bracing or
other apparatus;
Level Limited Requires
multidisciplinary team required
V voluntary adult
for long-term habilitation
movements, assistance
no head to roll  Class D: long-term care
control required

EARLIEST INDICATION OF CP

 Delay in disappearance of
4-6 years 6-12 years primitive reflexes
 Moro reflex
Can climb stairs Walk indoors
 Palmar grasp reflex
and outdoors,
 Asymmetric tonic neck reflex
climb stairs.
 Tonic labyrinthe reflex
Sitting with both Walk indoors or
hands free, walk outdoors on
short distances level surface
without assistive only
device

Walk with Walk indoors or

assistive device outdoors on
level surface
with an assistive
mobility device.

Sit Rely on wheeled

independently in mobility, may
a chair but achieve self
 Signs suggestive of CP in an infant:

 Abnormal behavior
o Excessive irritability
o Poor eye contact
o Poor sleep
 Oromotor problems
o Frequent vomiting
o Poor sucking
o Tongue retraction
o Persistent bite
o Grimacing
 Poor mobility
o Poor head control
o Hand preference before 2
years of age
 Abnormal tone

NORMAL DEVELOPMENTAL MILESTONES

SENSORY IMPAIRMENT

 Deficits
o Two-point discrimination
o Proprioception
o Stereognosis
 MC→ hemiparetic CP

VISUAL IMPAIRMENTS

 Strabismus
o MC visual disorder
 high myopia
 absence of binocular fusion
 dyskinetic strabismus
 severe gaze dysfunction
 optic neuropathy or cortical
visual impairment
 HEARING IMPAIRMENTS RESPIRATORY DISORDERS

 Sensorineural hearing loss  Impaired control of respiratory

o Associated with muscles
congenital TORCH  Ineffective cough
 Toxoplasmosis  Aspiration
 Rubella
MUSCULOSKELETAL DISORDERS
 Cytomegalovirus
 Herpes  Foot/ankle
 Equinus deformity→ MC
COGNITIVE IMPAIRMENTS
o Equinovarus
 Severe NM impairments >  hemiparetic CP
cognitive impairments o Equinovalgus
 Athetoid CP→ Normal  Spastic diparesis &
cognition quadriparesis
 Knee
PSYCHOLOGICAL IMPAIRMENTS
o Knee flexion contracture
 Attention-deficit disorder o Genu valgus
 Passivity  Hip
 Immaturity o Acquired hip dysplasia
 Anger o Windswept deformity
 Sadness  Adduction deformity
 Impulsivity of the elevated hip
 Emotional lability and an abduction
 Low self-esteem deformity
 Anxiety

EPILEPSY

 15-55% in CP
 MC→ severe CP (quadriparesis
& hemiparesis)

OROMOTOR IMPAIRMENTS

 Feeding difficulties
o weak suck
o poor coordination of the
swallowing mechanism
o tongue thrusting  Spine
o tonic bite reflex o Kyphosis
 Speech disorders o Lordosis
 mild articulation disorders to o Scoliosis
anarthria  Upper extremity
o Spasticity and muscle
imbalances
 GAIT IMPAIRMENTS
Varus Increased
Location Impairment Potential ankle
Effects supination in
stance or
Hip Increased Scissoring; swing
adductor difficulty
tone advancing Valgus Increased
leg in swing pronation in
phase stance or
swing;
Increased Anterior midfoot
iliopsoas pelvic tilt; break
tone increased
lumbar CP is likely if there is no:
lordosis;
crouched Head control 3 months
gait
Sitting 6 months
Increased Intoeing;
femoral false
anteversion genuvalgus; Rolling over 6 months
compensato
ry external Walking 18 months
tibial torsion
WHAT BEHAVIORAL SYMPTOMS
Abductor Trendelenburg DURING THE FIRST YEAR SHOULD
weakness gait
AROUSE SUSPICION ABOUT THE
Knee Decreased Crouched POSSIBILITY OF CP?
hamstring gait
range of  Excessive irritability, constant
motion crying, and sleeping difficulties.
 Early feeding difficulties with
Hamstring/ Stiff-kneed difficulties in coordinating suck
quadriceps gait and swallow, frequent spitting
co-
up, and poor weight gain
contraction
 “Jittery” or “jumpy” behavior
Ankle Increased Toe walking;  Easily startled behavior
gastrocsoleus genu  Stiffness when handled
tone or recurvatum;
contracture
 Paradoxically “precocious”
difficulty development
clearing foot
during swing WHAT GROSS MOTOR DELAYS ARE
DIAGNOSTICALLY IMPORTANT IN THE
Internal tibial In-toeing;
torsion ineffective INFANT WITH POSSIBLE CP?
push-off
 Inability to bring the hands
External Out-toeing;
together in midline while in a
tibial torsion ineffective supine position by the age of 4
push-off months
  Head lag persisting beyond 6 PROGNOSIS
months
 Molnar’s Prognostication Index
 No volitional rolling by 6 months
(for ambulation)
 Inability to independently sit
 2 y/o and above
straight by 8 months
 Based in the type of CP
 No hands-and-knees crawling
 Best prognosis – spastic
by 12 months
hemiplegia or ataxic
LAB/NEUROIMAGING STUDIES  Poor prognosis – quadriplegic;
flaccid/rigid
 Clinical Hx or findings from
neuroimaging do not indicate
a specific structural
abnormality
 Additional & atypical features
are present in the Hx or clinical
examination
 A brain malformation is
BLECK’S AMUBLATION STATUS (2YRS
detected in a child with CP
AND ABOVE)
 Lactate and pyruvate values
 Thyroid function studies
 Ammonia level
 Serum quantitative amino acid
and urine quantitative organic
acid values
 Chromosomal analysis
 Cranial ultrasonography
 CT scan
 MRI EXAMINATION OUTLINE
 EEG  Neurological examination
 EMG o Skull, head circumference
LEVINE (POSTER) CRITERIA o Spine
o Mental status
1. Posturing/abnormal movements o Cranial nerves
2. Oropharyngeal problems o Vision - hearing - speech
3. Strabismus o Motor system
4. Tone o Muscle tone
5. Evolutional maldevelopment o Muscle power
6. Reflexes o Muscle bulk
o Degree of voluntary
*Abnormalities in four of these six
control
categories strongly point to the
o Reflexes
diagnosis of CP
o Involuntary movements
o Sensory examination
o Sphincters
 o Developmental milestones
 Musculoskeletal examination
o Range of motion
o Deformities, contractures
o Posture
 Functional examination
o Sitting
o Balance
o Gait
ANTI-SPASTICITY DRUGS
 Benzodiazepines
 Dantrolen Sodium
 Baclofen
 Clonidine
 Tizanidine
 Intrathecal Baclofen
 Intramuscular Neurolysis
 Botox Injection
SURGERY
 Goals:
o Improve function &
appearance
o Prevent or correct
deformities
o Reflect a functional
approach to problems of
alignment
 Hip Surgery
o Varus Derotational
Osteotomy
 Knee Surgery
o Hamstring Tenotomy,
transfer or lengthening
 Foot Surgery
o Tendon lengthening or
transfer
o Arthrodesis
o Osteotomy
W.M. PHELPS
 Movement patterns & inhibition
of abnormal tone
 15 modalities
 Extensive bracing
TEMPLE FAY
 Ontogenetic development of
man is believed to be a
recapitulation of phylogenetic
development.
 Building up of motion from
reptilian squirming, amphibian
creeping thru mammalian
reciprocal motion on all fours
to primate’s erect walking
DOMAN-DELECATO
 Recommends patients to
inhale CO2, restriction of fluid
intake & development of
cerebral hemisphere
dominance
 Children are “hanged” upside
down & whirled around to
stimulate vestibular apparatus
 Hang & walk with their hands
on horizontal ladder as
observed in apes
VACLAV VOJTA
 Emphasis on activation of
postural development &
equilibrium reactions to guide
normal development
 Based of reflex locomotion
pattern (reflex creeping &
rolling)
PETO
 Conductive education
 Ability to function
independently w/o aids
 Group therapy
 SIGNE BRUNNSTROM  Partial Body Weight Support
Treadmill Training (PBWSTT)
 Synergistic Movement Pattern
 Constraint-Induced Movement
 Use of reflexes & associated
Therapy (CIMT)
reactions to facilitate
movement ALTERNATIVE THERAPY

KARL & BERTA BOBATH  Hyperbaric Oxygen Therapy

(HBOT)
 Neurodevelopmental
 Adeli Suit Therapy (ASS)
Treatment (NDT) w/ reflex
inhibition & facilitation
 To normalize tone
 Inhibit AbN primitive reflexes
 Facilitates automatic reactions
& subsequent movement

MARGARET ROODS

 Sensory stimulation for

activation & inhibition
 To activate movement &
postural responses at
automatic level while following
development sequence
HERMAN KABAT
 Proprioceptive Neuromuscular
Facilitation (PNF)
FUNCTIONAL TRAINING
 ROM Exercises
 Strengthening Exercises
 Postural & Motor Control
Training
 Skill Performance Training
EMERGING TECHNIQUES
ORTHOSES
 Prevent contractures
 Provide optimal alignment
 Provide selective motion
 Protect weak mm.
 Control AbN tone & related
deviations
 Enhance function
 Protects tissue postoperatively
MANAGEMENT OF SPASTICITY
 ROM Exercises
 Therapeutic Exercises
 Modalities (heat & cold)
 Casting & splinting
 Biofeedback