2. William John Little (1810-1894
In 1860s, known as
"Cerebral Paralysis” or
“Little’s Disease”
After an English surgeon
wrote the 1st medical
descriptions
Introduction
3. Cerebral“- Latin Cerebrum;
Affected part of brain
“Palsy " -Gr. para- beyond,
lysis – loosening
Lack of muscle control
Introduction
4. A motor function disorder
caused by permanent, non-progressive brain lesion
present at birth or shortly thereafter. (Mosby, 2006)
Non-curable, life-long condition
Damage doesn’t worsen
May be congenital or acquired
Definition
9. An insult or injury to the brain
–Fixed, static lesion(s)
–In single or multiple
areas of the motor
centers of the brain
–Early in CNS dev’t
10. CAUSES
Development Malformations
The brain fails to develop correctly.
Neurological damage
Can occur before, during or after delivery
Rh incompatibility, illness, severe lack of oxygen
* Unknown in many instances
11. CHIEF CAUSE
Severe deprivation of oxygen or
blood flow to the brain
–Hypoxic-ischemic
encephalopathy
or intrapartum
asphyxia
CHIEF CAUSE
12. RISK FACTORS
Prenatal factors
Before birth
Maternal characteristics
Perinatal factors
at the time of birth to 1mo
Postnatal factors
In the first 5 mos of life
14. Maternal Characteristics
Age
Difficulty in conceiving or
holding a baby to term
Multiple births
History of fetal
deaths/miscarriages
Cigarette smoking >30 sticks per day
Alcoholism and drug addiction
Mother’s medical condition
15. Perinatal Factors
High or low BP
Umbilical cord coil
Breech delivery
Over sedation of drugs
Trauma i.e. forceps or vacuum
delivery
Complications of birth
25. Spastic CP
Increased muscle tone,
tense and contracted muscles
Have stiff and jerky or
awkward movements.
limbs are usually underdeveloped
increased deep tendon reflexes
most common form
70-80% of all affected
26. Types of Spastic CP
According to affected limbs:
* plegia or paresis - meaning paralyzed or weak:
Paraplegia
Diplegia
Hemiplegia
Quadriplegia
Monoplegia –one limb (extremely rare)
Triplegia –three limbs (extremely rare)
28. Athetoid/ Dyskinetic CP
involves abnormal involuntary movements
that disappear during sleep and increase with stress.
Athetoid-Wormlike movements
Slow, uncontrolled motion, twisting in character, in the face, extremities, and
torso.
Dyskinesia -Dyskinetic movement of mouth
drooling and dysarthria.
Dystonia - when held as a prolonged posture
20% of the CP cases,
29. Ataxic CP
Poor balance and lack of coordination
Wide-based gait
Depth perception usually affected.
Tendency to fall and stumble
Inability to walk straight line.
Least common 5-10% of cases
30. MIXED CP
A common combination is
spastic and athetoid
Spastic muscle tone and involuntary movements.
25% of CP cases, fairly common
42. CRITERIA
P osturing / Poor muscle control and strength
O ropharyngeal problems
S trabismus/ Squint
T onia: hyper- hypo
E volutional maldevelopment
R eflexes e.g Increased deep tendon
*Abnormalities 4/6 strongly point to CP
44. To rule out other causes:
Thyroid function studies: Abnormal thyroid function may be
related to abnormalities in muscle tone or deep tendon reflexes
or to movement disorders
Lactate and pyruvate levels: Abnormalities may indicate an
abnormality of energy metabolism (ie, mitochondrial cytopathy)
Ammonia levels: Elevated ammonia levels may indicate liver
dysfunction or urea cycle defect
Organic and amino acids: may reveal inherited metabolic
disorders
Chromosomal analysis: if dysmorphic features or abnormalities
Cerebrospinal protein: levels may assist in determining asphyxia in
the neonatal period
45. Imaging studies
Cranial ultrasonography: evidence of
hemorrhage or hypoxic-ischemic injury
CT of brain: congenital malformations,
intracranial hemorrhage, and periventricular
leukomalacia or early craniosynostosis.
MRI of the brain: The diagnostic neuroimaging
study of choice
defines cortical and white matter structures and
abnormalities more clearly than does any other
method
determination of whether appropriate myelination is
present for a given age
46. Others:
Electroencephalography: Important in the diagnosis
of seizure disorders
Electromyography and nerve conduction studies:
Helpful when a muscle or nerve disorder is
suspected
48. - No treatment to cure cerebral palsy.
- Brain damage cannot be corrected.
Crucial for children with CP:
Early Identification;
Multidisciplinary Care; and
Support
49. “The earlier we start,
the more improvement can be made”
-Health worker
I. NONPHYSICAL THERAPY
50. A. General management
- Proper nutrition and personal care
B. Pharmacologic
Botulinum toxin : for children with cerebral palsy with spasticity
antiparkinsonian drugs (eg, anticholinergic and dopaminergic drugs)
antispasticity agents (eg, baclofen) have primarily been used in the
management of dystonia, anticonvulsants,
antidopaminergic drugs, and antidepressants have also been tried
51. C. Surgery
-Intrathecal baclofen pump
insertion: To treat spasticity and/or
dystonia
-Selective dorsal rhizotomy: To treat
velocity-dependent spasticity
- Orthopedic surgical intervention: To
treat scoliosis, joint contractures or
dislocation
53. D. Physical Aids
Orthosis, braces and splints
Positioning devices
Walkers, special scooters, wheelchairs
E. Special Education
F. Rehabilitation Services- Speech and
occupational therapies
G. Family Services -Professional support
54. H. Other Treatment
- Therapeutic electrical stimulation,
- Acupuncture,
- Hyperbaric therapy
- Massage Therapymight help
55. 'The ultimate long-term goal is realistic independence.
To get there we have to have some short-term goals.
Those being a working communication system, education to his potential,
computer skills and, above all, friends'.
- Parent of boy with CP
II. PHYSICAL THERAPY
56. A. Sitting
-Vertical head control and
control of head and trunk .
B. Standing and walking
-Establish an equal distribution of
weight on each foot, train to
use steps or inclines
