short yet comprehensive coverage of the topic of cerebral palsy and management

1. Most Common Permanent
Disability of Childhood

2. CEREBRAL
PALSY
By: Harjot Singh Gurudatta
Moderator: Dr. Rohit Sharma

3. William
John
Little
(18101894)
• In 1860s, known as
"Cerebral Paralysis” or
“Little’s Disease”
• After an English surgeon
wrote the 1st medical
descriptions

4. CEREBRAL PALSY (CP)
• Cerebral“- Latin Cerebrum;
– Affected part of brain
• “Palsy " -Gr. para- beyond,
lysis – loosening
– Lack of muscle control

5. CEREBRAL
PALSY
• A motor function disorder
– caused by permanent, non-progressive brain lesion
– present at birth or shortly thereafter. (Mosby, 2006)
• Non-curable, life-long condition
• According to a recent definition CP “describes a group of permanent
disorders of the development of movement and posture,causing
activity limitation, that are attributed to non-progressive disturbances
• that occurred in the developing fetal or infant brain. The motor
disorders of cerebral palsy are often accompanied by disturbances of
sensation, perception,cognition, communication, and behaviour; by
epilepsy; and by secondary musculoskeletal problems”

6. CEREBRAL PALSY
A Heterogenous Group
of Movement Disorders

7. In CP
• Muscles are unaffected
• Brain is unable to send
the appropriate
signals necessary to
instruct muscles when
to contract and relax

8. CAUSES
OF CEREBRAL PALSY

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 developmentSevere
deprivationon of oxygen or
blood flow to the brain
– Hypoxic-ischemic
encephalopathy
or intrapartal asphyxia

10. Etiology
Prenatal(MC)
• I, iron def.,poor –nut.
• Inf, UTI, high fever
• Chorioamniotis
• HTN, DM
• Teratogens
• Poor ANC
• Rh ?
• Twins
• Fetal vasculopathy
• Maternal
drugs/smoking(>30)
Perinatal
• Birth asphyxia
• Breach/vacuum/forc
• Premature /
LBW(>60/1000)
• IUGR
• Hyperbilirubenemia
• Intraventricular
hemorrrhage
• Sepsis, pneumonia,
meningitis
• Develop.
Malformation,
• abruptio
Postnatal
•CNS
infections
•Head
injuries
•Seizures
•Hypoxic
damage
•Hyperpyrexi
a damage
•Stroke

11. TYPES
OF CEREBRAL PALSY

12. Classification of CP
According to:
1. Neurologic deficits
2. Type of movement involved
3. Area of affected limbs

13. 1. Accdg. to Neurologic Deficits
• Based on the
- extent of the damage
- area of brain damage
• Each type involves the way
a person moves

14. 3 MAIN TYPES
1. PYRAMIDAL
- originates from the motor
areas of the cerebral cortex
2. EXTAPYRAMIDAL
- basal ganglia and cerebellum
3. MIXED

15. 4 MAIN
TYPES(
Movem
ent)

16. 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

17. Types of Spastic CP A/C LIMB
INVOLVED
• Paraplegia
• Diplegia LL>UL , mc, normal iq,walks eventually,though delayed
• Hemiplegia UL>LL, seizures+, sensory changes in ul, limb
length discrepancy
• Quadriplegia only slight H N control loss,low iq, highest hip
subluxation,cognitive deficiency,
• Monoplegia –one limb (extremely rare)
• Whole body with seizure, drooling hn
control loss

18. Diplegia/ Paraplegia
•both legs w/
slight
involvement
Elsewhere
May also have
Contractures
of
hips and knees
and
talipes
equinovarus
(clubfoot).
•both legs

19. Hemiplegia
limbs on only one side

20. • Hemiplegia on right side
– Hip and knee contractures
– Talipes equinus (“tip-toeing”
- sole permanently flexed)
– Asteriognosis may be present.
(inability to identify objects by
touch)

21. Quadriplegia

22. • Spastic
Quadriplegia
Characteristic “scissors”
positions of lower limbs
due to adductor spasms.

23. Athetoid/ Dyskinetic CP
•
Fluctuating tone
– involves abnormal involuntary movements
– that disappear during sleep and increase with
stress.
– Interferes with speaking, feeding, reaching,
grabbing, and any other skills
• 20% of the CP cases, Wormlike
movements
•
Slow, uncontrolled motion, writhing or twisting in
character in the face, extremities, and torso.
•
Dystonia - when held as a prolonged posture
– Grimacing, drooling and dysarthria.
– Adductor spasm

24. Movements may become
choreoid
(rapid, irregular, jerky)
and
dystonic
(disordered muscle tone,
sustained muscle
contractions)
especially when stressed and during
the adolescent years.

25. 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

26. MIXED CP
• A common combination is
spastic and athetoid
• Spastic muscle tone and involuntary
movements.
• 25% of CP cases, fairly common

27. DEGREE OF SEVERITY
1. Mild CP- 20% of
cases
2.
Moderate CP50%
- require self help
for assisting their
impaired
ambulation
capacity.
3.
Severe CP30%;
-totally
incapacited and
bedridden and
they always need
care from others.

28. The Peabody Development
Motor Scales
• In-depth assessment
• 6 Subtests include:
–
–
–
–
–
–
Reflexes
Stationary
Locomotion
Object Manipulation
Grasping,
Visual-Motor
Integration.
– The subtests yield
a gross motor
quotient
– a fine motor
quotient
– a total motor
quotient.
• Ages covered: from birth
through five years of age

29. Denver Test II
• Developmental Screening Test
• Cover 4 general functions:
– personal social (eg. smiling),
– fine motor adaptive (eg. grasping & drawing)
– language (eg. combining words)
– gross motor (eg. walking)
Ages covered: from birth to 6 years

30. Signs and
Symptoms;
Diagnosis
OF CEREBRAL PALSY

31. History + Exam
– Include all that may
predispose an infant to
brain damage or CP
• Risk factors
• Psychosocial
factors
• Family adaptation
•
Often admitted to hospitals for corrective
surgeries and other complications.
–
–
–
–
–
–
Respiratory status
Motor function
Presence of fever
Feeding and weight loss
Any changes in physical state
Medical regimen
P osturing / Poor muscle control and strength
O ropharyngeal problems(drooling?swallowing?feeding?)
S trabismus/ Squint
T one (hyper-, hypotonia)Muscle strength testing
E volutional maldevelopment
R eflexes (e.g. increased deep tendon)
*Abnormalities 4/6 strongly point to CP

32. d.
c.
e.
f.
b.
a.
g.
h.

33. Early Signs
Infancy (0-3 Months)
• Stiff or floppy posture
• Excessive lethargy or
irritability/ High pitched cry
• Poor head control
• Weak suck/ tongue thrust/
tonic bite/ feeding difficulties

34. neonatal reflexes
Moro’s reflex
Startle response; Startle reflex; Embrace reflex
when the infant feels as if it is falling,1st abduct
,2nd adduct,ie embrace
Asymmetric tonic neck reflex
"fencing position“
-- head to one side, arm & leg on that side
extended, opposite limbs flexed
Placing reflex
When the dorsal (back) side of the hand or
foot is placed on the edge of a surface, such
as a table, the infant will lift the extremity
and place it on the flat surface.
Landau reflex
When the infant is held in a horizontal prone
position, the infant will lift head and extend
the neck and trunk. When the neck is
passively flexed, the entire body will flex
3m-2y

35. Parachute Reflex
•
When held around the waist in a horizontal prone position and then lowering
the infant slowly, head first to the surface. By age 6 to 8 months the infant
should respond by extending the arms and hands to break the “fall”. If this
response is asymmetrical it indicates an unilateral motor abnormality.

36. CHILD with CP

37. Late infancy
• Inability to perform motor skills as indicated:
– Control hand grasp by 3 months
– Rolling over by 5 months
– Independent sitting by 7 months
• Abnormal Developmental Patterns:
–
–
–
–
Hand preference by 12 months
Excessive arching of back
Log rolling
Abnormal or prolonged parachute response

38. Abnormal Developmental
Patterns after 1 year of age:
• “W sitting” – knees flexed,
legs extremely rotated
• “Bottom shuffling” Scoots along the floor
• Walking on tip toe or hopping
• Bleck ”not sitting independently @4 yrs,
not walking @ 8 yrs bad”

39. ASSO. CONDITIONS
• Hearing and visual
problems
•
•
•
•
• Bladder and bowel
control problems,
digestive problems
Sensory integration
(gastroesophageal reflux)
problems
Failure-to-thrive, Feeding • Skeletal deformities,
dental problems
problems
• Mental retardation and
Behavioral/emotional
learning disabilities in
difficulties,
some
Communication
• Seizures/ epilepsy
disorders

40. DIAGNOSIS
•
•
•
•
Physical evaluation, Interview
MRI, CT Scan EEG
Laboratory and radiologic work up
Assessment tools
– i.e. Peabody Development Motor Skills,
Denver Test II

41. Treatment
OF CEREBRAL PALSY

42. - No treatment to cure cerebral palsy.
- Brain damage cannot be corrected.
• Crucial for children with CP:
–Early Identification;
–Multidisciplinary Care; and
–Support

43. I. Nonphysical Therapy
“The earlier we start,
the more improvement can be made”
-Health worker

44. A. General management
- Proper nutrition and personal care
B. Pharmacologic
Intrathecal, Baclofen
- control muscle spasms and seizures,
Glycopyrrolate -control drooling
Pamidronate -may help with osteoporosis.

45. Baclofen
• Oral delivery was common but
sedation is more, so Intrathecal
Baclofen Using a pump Delivered
directly to the spinal fluid
• GABA agonist – inhibits release of
excitatory neurotransmitter at
level of spinal cord
• It is commonly used in a starting
dose of 1.25 - 2.5 mg BD orally
To avoid brain effects

46. BOTOLUNIM TOXIN
The toxin is produced by the anaerobic sporeforming bacterium Clostridium
botulinum, of which eight immunologically
distinct serotypes – A, B, C1, C2, D,
E, F, and G – have been identified.
Type A and B are used clinically in
variousconditions like focal tissue spasms,
blepharospam, dystonia, achalia, urology,
cerebral palsy, cosmetic surgeries, toe clawing.
Relief of athetosis and dystonia - is difficult
occasionally levo-dopa for severe athetosis and
carbamezepine for dystonia may be helpful.
Thalamotomy for athetoid CP, stereotactic
dentatomy and chronic cerebellar stimulation via
implanted electrode .
Multiple injection sites to avoid
toxicity. acetylcholine-blocking
chemical denervant
Requires adjunctive therapy like
splints, orthoses, casting, manual
stretch, posturing
The children in CT receive bilateral Botox
injection @12 u/kg with topical anaesthesia
and analgesic cover/ sedation

47. C. Surgery
-To loosen joints,
-Relieve muscle tightness,
- Straightening of different twists or
unusual curvatures of leg muscles
- Improve the ability to sit, stand, and
walk.

48. Selective posterior rhizotomy
• Best for : spastic diplegia, 4-8 yrs, no previous
surgery, no contractures, no extra pyramidal signs
• Not done in hemi/ quadriplegia

49. How it Works
• The Sensory nerve fibers are exposed, then stimulated and the
responses of the leg muscles are observed. Those that have an
abnormal or excessive response are severed. Those with a normal
response are left intact.
• Intensive rehabilitation is required after the surgery, usually up to six
weeks, followed by physical therapy on an ongoing basis

50. Walker cp
D. Physical Aids
Orthosis, braces and
splints
- Keep limbs in correct
alignment
- Prevent deformities.
- Ankle foot orthosis,
knee
ankle
foot
orthoses
Positioning devices
-Enable better posture
Walkers,
special
scooters,
wheelchairs
- make it easier to
move about.
Active exercises
- Passive ROM exercises
- Passive stretching
- Bracing
Spiral thigh brace

51. E. Special Education Rehabilitation
- To meet the child's special needs
- Improve learning.
- Vocational training can help prepare young adults
for jobs
H. Other Treatment
-
Therapeutic electrical stimulation,
Acupuncture,
Hyperbaric therapy
Massage Therapy might help

52. Cerebral palsy
Orthopedic Procedures
Usually multiple deformities at different joints
Knowledge of complex effects each deformity has on
other lower extremity joints
Diiferentiate between
primary deformity : needs treatment
compensatory deformity :
can improve without intervention

53. Cerebral palsy
Prerequisites for effective surgery
• Type : spastic
• Extent : hemiplegics / diplegics : good results
quadriplegics : minimal
improvement
• Age : 3- 12 years
• IQ : good
• Good upper limb function : for walking
• Underlying muscle power : not weak
• Walker / non-walker :walker
surgery hardly changes state but improves
gait, to get him better from current state

54. Cerebral palsy
Timing For Orthop Surgery
• For structural changes : Early
e.g. Hip subluxation , usually <5 years
• To improve function ( gait ) :
defer until walking ( independently / with aids )
until gait pattern develops and could be assessed
walking : 18 – 21 months in hemiplegia
3 – 4 years in spastic diplegia
• Optimum time of lower extremity surgery
5 – 7 years: can analyze and observe gait pattern

55. Avoid birthday surgeries
?ETA
Equinus
? Hams
Crouch
? Psoas
Flexion
? Rectus Femoris
Stiff Knee
Ok

56. Cerebral palsy
Hip Deformities
• Dynamic deformities
• Tight adductors – scissoring
• Tight flexors – with pelvic inclination
compensatory knee / ankle/ trunk deformities
• Hip subluxation / dislocation :
not common in walking patients with diplegia
• Wind-swept deformity : in quadriplegics
• Internal rotation : in spastic hemi & diplegics

57. Adductor Deformity
Superficial layer
-
Pectineus
Adductor longus
gracilis
• Needs to be corrected if gait is disturbed<20 abduction and scissoring.
• Do open Adductor tenotomy of Adductor longus.Gracilis and some add.
Brevis can be released
• Its important not To include much of adductor Brevis and spare post. Obt.
Nerve
• Long leg casts given 3 week

58. Thomas test for ruling out knee ffd
Holts test for hamstring tightness
Adductor and medial hamstring??
Explained later
Ely test for RF Spasm
•
Ilio-psoas
( the main and most powerful )
•
•
•
•
Sartorius
Tensor fascia lata
Rectus femoris
Adductors
FLEXION DEFORMITY
Ascertain the site of primary anomaly
Hip flexion deformity > 20o needs surgery
<30DEG Iliopsoas Recession and Z plasty
In ambul.
>3o Rectus femoris, Sartorius, Glutei ant.
Fibre

59. Cerebral palsy
Hip Problems in
Spastic Quadriplegia
Hip at risk
(valgus, anteverted, acet. Dysplasia,
increased NS angle,flexion
contracture>20, abduction <30)
Femoral Anteversion more than true Valgus

60. • When a hip at risk is identified,a program of aggressive
physical therapy and abduction splinting typically is started,
later soft tissue release of contracted tendons is indicated.
• In Subluxated hip, younger children, soft tissue releases
alone may be sufficient, but most patients with hip
subluxation require osteotomy in addition to soft tissue
release. Operative correction of femoral valgus and
anteversion and acetabular dysplasia is necessary at this
stage to prevent further subluxation and dislocation.
osteotomies
described by Salter,
Pemberton,
Dega, Ganz, and Steel
and salvage-type
osteotomies such as
the Chiari and shelf
may be done

61. Cerebral palsy
Spastic Diplegia – The Knee
• Crouched gait :
- tight hamstrings : needs hamstring release
- could be secondary to weak triceps surae
• Type of surgery :
- - lengthening : best ( medial first , ? then lateral)
Ascertain primary deformityThe
Hamstring Test
Holt’s method
•
•
Hip flexed 90 degrees
Popliteal angle
degrees less than full extension
More hip flextion increases flexion

62. Fractional medial hamstring
lengthening
Lengthening hamstrings :
reduces hip extension power
increases hip flexion
Add hip flexor ( Psoas ) lengthening if
concomitant hip flexion is present
Add distal rectus femoris release (ELY test)
if concomitant cospasticity(stiff knee gait) of
quadricep and hamstrings +nt exacerbates
knee hyperextension
OR transfer RF to Sartorius, smt, iliotibial band

63. Cerebral palsy
Spastic Diplegia – The Foot & Ankle
Toe Walking
• Dynamic :
Treat by :
Bracing
Spasticity reduction
Surgery ( careful ! )
• Fixed :
Treat by :
Serial casting
Surgery
SILVERSKOLD

64. LENGTHENING OF
THE
ACHILLES TENDON
For equinus
Indications :
- fixed deformity
- tight TA
Problems :
over lengthening esp in z
Weak push off
Types :
z -plasty
sliding : - percutaneous
- open

65. Cerebral palsy
Spastic Diplegia – The Foot & Ankle
Equino - varus
• Not very common but more
disabling and Most Imp. Is
Tibialis post contracture or
Tibi. Ant weakness
• Treatment :
- split transfer of tib. post.
tendon
lateral half, posterior to
interosseous memb.,
to peroneus brevis laterally
- elongation of tib. Post.
and split transfer of tib. ant.
Laterally
Dwyer closing wedge
osteotomy of calcaneus for
varus heel.
Full transfer can cause weakness

66. •
•
•
•
•
Equino - valgus
More frequently seen in di/ quadri
Tight TA and Talonavicular subluxation
No perfect muscle balancing procedure
The gastrocnemius-soleus acts as the primary
deforming force and TA lenghthening is must
Treatment :
ETA and subtalar arthrodesis
Osteotomies

67. Intoeing
• Usually caused by
femoral ante-version
• Internal tibial torsion
adds to intoing
• If severe : Derotation
osteotomy
Delay to late
childhood if possible
• Derotation osteotomy of
femur might cause
tightening of medial
hamstrings
( might need
lengthening )
Femur anteversion

68. "Time and gravity
are enemies of very aging body,
especially mine." - Adult with CP
“A disabled child has the right to enjoy a full and
decent life, in conditions which ensure dignity,
promote self-reliance and facilitate the child’s
active participation in the community.”
-UN Convention on the Rights of
the Child. 1989.
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