Transcript Types of Cerebral Palsy

Types of Cerebral Palsy
Robyn Smith
Department of Physiotherapy
UFS
2012
1. Spastic Group
Spastic Quadriplegia
Distribution
All four limbs similarly involved
 UL sometimes to a greater degree than
LL
 Distribution of tone may be assymetrical
with one side more involved
 or with one side in flexion and the other
in extension
 Trunk often hypotonic or with increased
extensor tone
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Etiology
Asphyxia
 Anoxia
 Abruptio placenta
 Merconium aspiration
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Usually indicative of severe cortical
damage
Development
Supine
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Asymmetrical ATNR
Uses retraction of
head roll side
No segmental
rotation
Spasticity with IR hip
may lead dislocation
Sitting
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Flexed posture
Strengthens TLR
Grasp weak due IR
pronation arm
Lifts head extension
and retraction
shoulders “chin
poke”
Development
Prone
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Due to TLR battles lift head
STNR with neck flexion and
UL flexion with LL in
extension
Often don’t tolerate prone
Mild – learns to lift head with
extension and may even
creep.
Uses TLR and STNR
constantly
TLR/STNR used to get into
M-sitting in mild cases
Standing & walking
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Very mild cases –seldom
realistic
Uses extension spasticity
LL - ??? No true active
WB
No rotation or
dissociation
AP weight shifts
Shuffling gait
As body weight increases
loose ability to walk
Additional characteristics
Associated with significant associated
problems.
Microcephaly & cerebral atrophy
 Mental retardation
 Cortical blindness
 Epilepsy
 Feeding problems
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Spastic Diplegia
Distribution
All four limbs involved
 UL to a lesser degree than LL
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???? Terminology you will aslo hear
refering to assymetrical diplegia or a
hemiplegia superimposed on diplegia
Etiology
Lesion lies near the para-ventricular
region
Forms part sub-cortical group lesions
Prematurity (PVL/ IVH)
 Hydrocephalus
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Development
Supine
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Far better head and trunk
control than quad
Uses extension of head and
retraction of head to roll
Later as flexion improves
uses arm and upper body to
roll over
No segmental rotation
Kicking may notice
scissoring legs
Sitting
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No segmental rotation
cannot come up into sitting
through side lying
Used STNR to get into Msitting
Pattern hip flexion and
anterior pelvic tilt –becomes
fixed deformity
Often shortening hamstrings,
long sitting difficult with poor
balance and child uses arm
support
Development
Prone
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Creeps using arms to pull
forward
STNR to get into M-sitting
“Bunny hops” or crawls
asymmetrically due to poor
rotation and dissociation
On floor requires arm
support in sitting
Often sitting chair more
comfortable and stable
To get into kneeling pull up
with arms, LL inactive
Standing & walking
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Lumbar lordosis & hip flexion
No segmental rotation or
dissociation
Lateral weight shifts
Often up on toes
High guard and poor balance
Tries get foot flat
Extension LL with scissoring
Walking aid –swing through
gait
Characteristics
Near normal IQ
 Epilepsy
 Feeding problems may occur
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Spastic Hemiplegia
Distribution
Arm and leg on the same side of body
involved
 Arm usually to greater extent than leg
BUT:
 Arm more leg
middle cerebral artery
 Arm =leg
anterior cerebral artery
 “dense”(arm, leg and face)
capsula
interna
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Etiology
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Emboli
Thrombi
Artery
malformations
Prematurity with
anoxia
Development
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Initially may not appear
asymmetric
Start to become evident
6/12
Starts only using
unaffected arm
Orientate themselves
only to unaffected side
Retraction of hemi side
Difficulty in rolling to
unaffected side
Dislikes prone
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Does not crawl
Sitting falls over hemiside to compensate
shifts weight to normal
side
Associated reactions
common
Unable do bilateral
hand activities
Locomotes by bum
shuffling
Development
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Standing no weight
taken on hemi-leg
Pelvis and hip in
retraction, LL flexion
up on toe
Walk by 18/12
Under-development
of hemi leg
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Postural deformities
common e.g.
scoliosis
Characteristics
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Microcephaly
Sensory involvement
Epilepsy
Intelligence varies –left cerebral hemisphere poor
prognosis
Left vs. right hemiplegia:
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Left hemi has speech, language and feeding
problems
Right hemi has visual perceptual problems
Children with spasticity
divided into 2 groups:
Severe
spasticty
Moderate spsticity
Severe spasticity
Features
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In a state of hypertonus
The hypertonia does not change
Little or no movement ability due to tone.
Only small movements are
Contractures tend to be more toward the midposition
Balance reactions are absent
Problems e.g. respiration, feeding and speech
Emotionally child is fearful and cannot adjust to
movement.
Children are often very passive
Moderate spasticity
Features
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Tone moderate at rest increases activity
More able to move due to changeability in tone
Inconsistent performance during execution task
Contractures more dangerous in this group
Associated reactions
Balance reactions present but underdeveloped
Emotionally these children are often frustrated and
insecure
Principles to use when
treating a spastic child
Reducing the spasticity in itself will not
make the child more functional
 Therapist should always have a
functional goal in mind.
 Analyse the patterns of hypertonia and
the way in which it interferes with
postural control and the performance of
functional tasks.
 Asses the degree of compensation
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Principles to use when
treating a spastic child
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Use of tone influencing patterns, postures
and techniques
Facilitate large range movements, free and
rhythmical
Dissociation/ rotation
Mobile weight bearing in elongation
Elongation of muscles
Correct biomechanical alignment
Reciprocal patterns
Shaking and vibrating
Principles to use when
treating a spastic child
Use patterns of activity that lead to
function.
 Facilitate active movements
 Facilitate balance reactions
 Prevent and minimize contracturing
 Grade stimulation
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2. Hypotonic Group
Aetiology
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Most children with
CP start out
hypotonic
Premature babies
are hypotonic
Hypotonia usually
transient
True hypotonia is
rare
Complex differential diagnosis
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The following other possible conditions need
to be excluded:
PNL e.g. GBS
SC lesion
Neuromuscular junction diseases e.g.
Myasthenia Gravis
Muscle diseases e.g. SMA, DMD
UMN = CP
NB:
valuable clinical tool is to test reflexes as
hypotonic CP reflexes will still be present
Long term outcome for intial
hypotonia
45 %
 10%
 45%
?%
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Hypertonic
Diplegia
Dyskinetic
Ataxic
True hypotonia
Features
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Little or no postural control against gravity
Body takes up all the available support
Move with difficulty
Uses limbs as post of postural control i.e. Wide base
Hyper mobility of all joints
Apathetic/ passive. Reduced state of alertness.
Possible lack of motivation due to their inability to
respond . Placid, often describes as “good” baby
Delayed intellectual development
Usually problems with breathing, feeding and drinking
Respiration often shallow with recession of the chest
wall evident. Aspiration common. Children also
usually have a depressed cough reflex with
ineffective cough
Principles to use when treating a
hypotonic child
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Be careful of how stimulate child often hard to arouse
Increase postural tone by stimulation techniques:
– Compression
– Symmetrical patterns
– Static weight bearing
– Rhythmical stabilization
– All forms of tapping
– Movements to be fast and resisted
Work for head and trunk control and alignment
Address associated problems of breathing, eating and drinking
Maximize positioning and handling to ensure the preservation of
joint integrity and to prevent aspiration.
Prevent contractures especially postural deformities
3. Athetoid Group
Athetoid group
Characterised by:
Involuntary movements
 Abnormal or fluctuating postural tone
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Athetoid group
Classified according to type of
involuntary movement into 4 groups
Pure athetosis
 Choreoathetosis
 Athetosis with dystonic spasms
 Athetosis with spasticity
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Distribution tone
Pure athetosis
Tone varies very low
normal
 Distal > proximal
 Slow wreathing movements
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Choreoathetoid
Tone varies very low
high
 Proximal > distal
 Large wreathing movements
 Poor grading of movement
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Athetoid with dystonic spasms
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Hypotonic
OR hypertonic
Athetoid with spasticity
Moderate spasticity
 Proximal > distal
 Poor grading of movement
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Etiology
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Kericterus
hyperbilirubinaemia (severe
jaundice)
Rh incompatability
Prematurity
Asphyxia
Metabolic disorders
Encephalitis/ meningitis
Heavy metal poisoning
Rhumatic fever
Degenerative disorders brain
Management of jaundice
Etiology
= damage to the basal
ganglia
Basal ganglia are NB for:
 Control of movement
 Scale and amplitude determination of
movement
 Important in the control of eye
movements
Characteristics
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High IQ –cortex not involved
However usually severely disabled
Abnormal fluctuating tone
Lack of proximal stability
Poor grading movement
Poor balance
Contracturing usually not a concern
Repetitive assymetrical movement patterns may lead
to deformities
Joint hypermobility
Emotionally volatile
Often frustrated –temper tantrums
Associated problems
Speech
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Vocalization &
speech problem –
speech poor and
indistinct
Hearing loss
Can hear but does
not listen
Feeding
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Difficulty in swallowing
Battle especially with
liquids
Associated problems
Vision
Battle to focus
 May have nystagmus
= rapid, rhythmic, involuntary
eye movements caused by
damage brain
 Eyes unable move
independently head
 Lack of stability of head
affects vision
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Development
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Fluctuating tone present
sometimes birth
Initially seem hypotonic
Develop extension
head, neck, retraction
shoulders
Persistent ATNR
Due to involuntary
movements fail to
develop adequate head
and trunk control
Athetoid very
intelligent and
quickly learn to use
pathological reflexes
for function
Development
Prone
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ATNR get up on one
arm
TLR and STNR to get
into M-sitting
Sitting
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Like to M-sit as is stable
position
Uses ATNR for hand
function
Chair –stabilises using
arm around backrest or
hooks foot around leg
chair
Promotes further
asymmetry
Development
Gait
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Struggle to learn to walk due to
fluctuating tone, poor central control
and involuntary movement
Asymmetry may be noted
Lumbar lordosis and anterior tilt due
to poor central control
Knees locked together
Arm held together or against leg for
stability
Often appears in-coordinated
Principles to use when treating a
child with athetosis
Try stabilizing postural tone
!!!! Remember underlying
muscle tone is LOW
Children with dystonic spasms
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Compression
Tapping
Rhythmical stabilization
Use of small ROM
Weight bearing in good
alignment
Try and promote symmetry
Try and inhibit spasms
Work slowly, small ROM and
in a graded manner
Counteract development of
joint and postural deformities
For the child with spasticity
apply the same principles you
would use for a spastic child
4. ATAXIA
Characterised by:
In-coordinated
movement
Usually noted
proximally
Etiology
Damage to the Cerebellum
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Cerebellar malformations
Cerebellitis
Trauma
Asphyxia
Poisoning/overdose e.g.
Tegretol and epilum toxicity
Metabolic disorders
Neoplastic (tumor)
Infective
Genetic
Importance of Cerebellum
Responsible for
ensuring smooth,
coordinated
movement
Important role in the
execution of the
motor plan
Clinical features
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Generally Low tone.
Spasticity may be present
Intension tremor
absent co-contraction
around joint. Cannot give stability to moving part
Overshoot/ Dysmetria
poor grading of
movement
Use eyes to “fixate” and may have nystagmus
Truncal sway when walking
Uneven stride length and staggering gait, wide
base
Appear to be clumsy. Tend to fall frequently
due inadequate balance reactions
Associated problems
Visual problems
 Speech problems
 Problems with swallowing
 Perceptual and motor planning
problems
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Principles to use when treating a
child with ataxia
Physiotherapy treatment aims to:
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Improve postural control
Improve balance and coordination
Improve their movement possibilities in a safe
environment
Prevent stiffness, deformities and
contractures
Principles to use when treating a
child with ataxia
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Increase postural tone
Work with activities
incorporating rotation to
improve flexion rotation
control
Improve balance and
movement abilities e.g.
obstacle course
Activities requiring limbs
to move separately from
body
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Resisted activities e.g.
walking pushing a
box/chair
Work on placement,
grading, direction and
timing movement
Frenkel
exercises
Address thoracic and
neck stiffness if present
Propriocetive reeducation
Principles to use when treating a
child with vestibular dysfunction
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The vestibular system is the
part of the body responsible
for balance
Located in the inner ear
Important part of the sensory
system as it co-ordinates
information from the
vestibular organ, eyes,
receptors in muscles and
joints, palms and soles of the
feet and the proprioceptors
Results in the adjustment of
muscle tone, limb position,
arousal and balance
Sensory systems
involved in balance:
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Vision
Vestibular system
Somato-sensory
system
Symptoms of a vestibular
dysfunction
Nausea
 Nystagmus
 Developmental delays
 Visual spatial problems
 Poor hand eye and hand foot coordination
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Causes of vestibular
dysfunctions:
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Chronic ear infections
Infarcts and vascular
insufficiencies
Neurological disorders
including cerebellar
degeneration, CP,
hydrocephalus
Head and neck trauma
Immune deficiency
syndromes e.g. HIV
Tumors of the brain
(posterior fossa) and
inner ear (acoustic
neuromas)
Vestibular Rehabilitation
Therapy VRT
Sensory weighting- selection
occurs between visual, vestibular
and somatosensory inputs when
attempting to balance
VRT programme may include:
 Cawthorne-Cooksey exercises
 Balance re-education
 Gaze stabilizing exercises
 Visual dependance exercises
 Somatosensory dependence
exercises
 Otholithic recalibration exercises
Start with eyes open progress to
eyes closed
Can we incorporate
principles in our
Treatment children
with ATAXIA ????
5. Mixed group
Most common
type of Cerebral
Palsy
Etiology
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Asphyxia with diffuse cerebral damage
Most common types mixed CP
are:
Spastic with dystonic movements
 Spastic with ataxia
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References
Brown, E. 2001. NDT basic course
material (unpublished)
 Smith, R. 2009. Paediatric dictate, UFS
(unpublished)
 Smith, R. 2008. role of physiotherapy in
vestibular rehabilitation, PowerPoint
presentation
 Images courtesy of Google images
(2009)
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