4. DEFINITION OF CEREBRAL PALSY:
◾ Agroup of disorders of the development of movement and
posture, causing activity limitations
◾ Non progressive disturbances that occurred in the developing fetal or
infant brain
Cerebral palsy is a permanent disorder of movement and posture caused by lesion
in immature brain during fetal or infancy resultingsensory and motor deficit along
with mental retardation, speech impairment and hearing problems (P. Rosenbaum
et al, 2006)
5. MAJOR CRITERIA:
A neuromotor control deficit that alter the movement and posture.
A static brain lesion.
Acquisition of the brain injury either before birth or in the 1st year of life.
6. ETIOLOGY:
Exact cause of cerebral palsy is not clear, the brain damage can occur
during pregnancy, at the time of birth or after the birth.
80% children with cerebral palsy show structural problem in white matter
in their brain (Yarnell, 2013).
Typical causes during the intrauterine life are exposure to radiation,
infections, hypoxia and birth trauma.
Other causes that can lead to cerebral palsy are immaturity, head injury
after birth, genetic factor, maternal infection, periventricular leukoamalcia,
cerebral dysgenesis, intracranial bleeding and asphyxia ( 2013).
Principal cause of death in these is related to circulatory and respiratory
problem (Durufle-Tapin et al., 2014)
7. CAUSES OF CP:
PRENATAL(70%)
Mostly ,
Intrauterine stroke.
Genetic malformation.
Other, infection, anoxic, toxic vascular
NATAL(5_10%)
Anoxia, traumatic delivery, metabolic.
POSTNATAL
Major causes,
CNS infections.
Vascular causes.
Head injury.
Types of brain damage
Bleeding
Brain malformation
Trauma to brain
Lack of oxygen
Infections
Toxins
unkown
8. RISK FACTORS:
Most common risk factors for cerebral palsy are early delivery and
pregnancy disorders (Placental abruption ,prolonged rupture of
membranes, intrauterine growth restriction, pre- eclampsia, multiple births,
placenta previa, bleeding, cervical conization, and congenital
malformation) (Tronnes et al., 2014).
home delivery and infections during pregnancy are important risk factors
(Bangash et al., 2014).
9. Other problems:
Hearing and visual problems
Sensory integration problems
Bowel and bladder control problems
Digestive problems
Behavior and emotional disturbances
Communication disorders
Failure to thrive
Mental retardation and learning difficulties
Seuizers
12. Pyramidal lesion= spastic.
Extrapyramidal= athetoid , ataxic, dystonia,
and hypotonic
Pyramidal
Lesion is usually in the motor cortex, internal capsule and/or cortical
tracts.
Extrapyramidal
Lesion is usually in the basal ganglia, Thalamus, Sub thalamic and
cerebellum.
15. SPASTIC CP:
Spastic CP is the most common type of cerebral palsy ,in which muscles
are stiff and spasticity is striking feature and is due to deficiency of GABA
in spinal cord.
75% of children with cerebral palsy
Associated with UMN syndrome findings,
Inc muscle stretch reflexes.
Babinski response.
Weakness.
Difficulty with coordination.
Can be associated with extensor or flexor posture( decerebrate and
decorticate).
16. Clinical presentation of spastic child:
The spastic child adopts the Following positions:
The child can’t look at you easily
The head of child pushes back
The elbow and wrist are bent
The fingers are clasped tightly closed
The legs are straight and turned in
The feet point down
17. ATHETOID CP:
athetoid also named dyskinetic cerebral palsy results from extra pyramidal
damage (basal ganglia) and characterized by involuntary movements such as
torsion spasm, dystonia, chorea and athethosis (Mei Hou, 2006)
associated with bilirubin encephalopathy and hypoxic brain injury (Mei Hou,
2006).
Slow involuntary movements of hands, arms and face, involuntary facial
grimaces and drooling, difficulty in sitting and straight walking, difficulty in
holding objects are striking features of athetoid cerebral palsy
(Brainspinalcord.org)
18. ATHETOID CP
A dyskinetic tone abnormality
With alternating tone or cocontrctioan in the antagonist and agonist muscle groups
Causing varied abnormal postures and often fluctuating tone.
Other dyskinetic forms:
Athethosis
Choreiform
Choreoathethoid
Athetosis- slow writhing, wormlike
Chorea- quick, jerky movements
Choreoathetosis- mixed
Hypotonia- floppy, low muscle tone, little movement
19. Clinical presentation of ATHETOID
child
The child is Initially floppy when try to move & speak they become tight
The child can’t sit or balance as they keep getting thrown off balance
by sudden movement
The child is unable to stand up as their legs are constantly moving
They are slow to use their hands because the jerky movement get worse
with effort
20. ATAXIC CP:
In ataxic cerebral palsy there is a problem in coordination and damage is in
cerebellum.
It account for 5% to 10% and least frequent form of cerebral palsy (McHale,
2000)
Rare
Must be differentiated from degenerative processes of the cerebellum.
Results from damage to the cerebellum
Ataxia- tremor & drunken- like gait
Wide base gait
Tendency to fall and stumble
Inability to walk straight line
21. HYPOTONIC CP:
needs to be differentiated from those with identifiable causes of
neonatal hypotonia.
Muscle disease.
Metabolic disorders.
Genetic syndromes.
22. Clinical presentation of hypotonic
child
the child arm and legs feel heavy loose and flopppy
The child feel heavy and muscles are underdevelop
Poor head trunk and limb control
The child have poor balance
28. ASSESSMENT
Focus on child abilities.
What the child can do rather what he cannot dosture o.
Abnormal posture reflex activity.
Abnormal posture tone.
Eye ball observation.
DTRs.
Communication.
Goal setting.
Management is life long, assessment and reassessment.
Child with CP does not born with disability but they have deformity producing
tendencies.
29. Possible Indications of cerebral palsy:
After 2 months:
poor head control
stiffness in the legs that cross or scissors when picked- up
pushing away, arching pack
failure to smile by 3 months
After six months:
Continued difficulty controlling head when picked up
Floppy or limp posture.
Feeding difficulties - persistent gagging or choking
30. To be Continued:
After 10 months:
Crawl by pushing off with one hand and leg while dragging opposite hand and
leg.
Inability to sit unsupported
After 12 months:
Inability to crawl.
Inability to stand without support.
After 24 months:
Inability to walk.
Inability to push toys with wheels.
32. Management of spastic CP child:
Medical treatment
• Baclofen and intratecal Baclofen
• Botulinum toxins A
• Selective dorsal rhizothomy
33. Children with spastic quadriplegia:
ENCOURAGE THE HEAD CONTROL
Children must always have pillow under the head, to bring the head and his eyes forward.
We must keep straightening head and putting back in the midline.
Once child learnt how to hold head in the midline, she need to learn to move from side to side.
SITTING ASTRID
By sitting Astrid, her legs are then bent and opened. This will break the pattern and reduce the tightness.
KNEELING
We could work kneeling in front of a box or chair, can hold his arms on top of box and even keep the
hands open flat on box.
ENCOURAGE HAND CONTROL
We want to try to get his hands open so that the palms and fingers can come in contact with
different things.
34. CHILDREN WITH SPASTIC
HEMIPLEGIA:
Sitting at a table
Walking.
Reduce the tightness.
Lying on his back
Lying on his side
Rotate the sides
Helping the child to
eat and drink
35. HYPOTONIC CHILDREN:
Stimulating floppy muscles:
Don’t pick the child up by the arms hold her around the chest to pick him up and
put him down. this will leave arms free to move and take part in balance. To work
head control , roll a towel and put it under his arms, this will strengthen neck and
back.
Hips strapped back so that hips are at 90 degree.
Feet on the ground.
Hands and arms supported on table.
36. NEURODEVELOPMENTAL
THEARPY(NDT):
Moving through normal movement patterns to experience normal
movement
Major components : reflex-inhibiting posture, inhibition of abnormal
reflexes, normalization of muscle tone, and adherence to normal
developmental sequence of motor progression
37. ⚫ Inhibiting abnormal movement patterns.
⚫ Facilitating normal movement patterns.
Strong evidence that supports the effectiveness of NDT for children with
CP with respect to normalizingmuscle tone , increasing rate of attaining
motor skills,and improving functional motor skills
38. SENSORY INTEGRATION THERAPY:
Principle: a neurobiological process organizes
sensation from one’s own body and from environment and makes it
possible to use the body effectively within environment
Emphasis on importance of three body centered sensory systems : tactile ,
proprioceptive & vestibular
39. CONSTRAINED INDUCED MOVEMENT
THERAPY(CMIT):
child’s brain is plastic and can respond to intense training
⚫ Constraining the non affected arms to encouraged performance of
therapeutic tasks with the affect arm ,which children normally tend to
disagree.
⚫ Child brain is plastic and can respond to intense training AFO.
⚫ Systemic review has found the effectiveness of CIMT for children with
hemiplegic CP.
40.
41. SERIAL CASTING:
⚫ Serial casting may serve to reduce spasticity in muscles
by decreasing the strength of abnormally strong tonic
foot reflexes.
⚫ Serial casting in the CP population has been shown to
improve ROM.
⚫ Casting provides stability and prolonged stretch of a
muscle which is immobilized in a lengthened position.
⚫ At least 6 hrs of prolonged stretch is needed for
effectiveness.
42. STRENGTHENING EXERCISES:
Progressive resisted exercise improves muscle performance & functional
outcomes in CP children
Research had supported effectiveness on increasing force production in CP
43. Electrotherapy:
NMES
Multiple studies have demonstrated the effectiveness of
NMES,
• Reduce spasticity.
• Increase ROM & strength.
• Increase force production.
• Promote initial learning of selective motor control.
44. ORTHOTICS DEVICES, SPLINTS:
Goals :
Maintenance or increase ROM
Protection or stabilization of a joint
Promotion of joint alignment
Promotion of function
45. ANKLE FOOT ORTHOSIS(AFOs):
⚫ Compared with barefoot gait, AFO’s
enhanced gait function in diplegic
subjects. Benefits resulted from
elimination of premature PF and improved
progression of foot contact during stance.
