Cerebral palsy

Malathi k MPT( NEUROLOGY)

IInd year
INTRODUCTION
• Cerebral palsy are a group of conditions and not a single clinical or
pathological entity
• Cerebral palsy was identified in the year 1900s as an incident that
occurs shortly before, during or after birth
• It is a non progressive disorder which develops damage to CNS and
occur before during or immediately after birth of child
• The primary disorder is of motor execution but associated dysfunction
include sensory deficits(hearing or vision), epilepsy, learning
disabilities, cognitive deficits, emotional, social and behavioural
problems and speech and language disorders.
Epidemiology
• Incidence:
• 1.5 and 3 per 1000 live birth
• Prevalence
• Approximately 2 per 1000 live birth
History of cerebral palsy
• Formerly known as cerebral paralysis.
• First identified by English surgeon William Little in 1860 on thebasis
of observable characteristics of movement and posture
• Delver and Phelps used bracing and surgery
• In 1950 and 60s redefined the clinical characteristics of cerebral palsy
and orient the Intervention strategiesto the principles of motor
development and learning
• Kabat and Knott introduced Proprioceptive Neuromuscular facilitation
changed the customary pattern of child into more functional
movement pattern in logical sequences
Clinical aspects
• Definition.
• cerebral palsy is defined as a persistent disorder of movement and
posture appearing early in life and due to a development non progressive
disorder of brain
• Cerebral palsy is aterm used to describe e a broad spectrum of motor
disability which is non progressive and is caused by damage to brain at or
around birth
• Motor disorder are often accompanied by disturbance of sensation,
cognition, communication and perception and /or behavior or a seizures
disorder
• Etiology
• antenatal [70 to 80% of cases]
• Perinatal
• postnatal
• Antenatal causes
• Genetic causes
• Intrauterine virus infection
• Hypoglycemia
• Trauma
• Malnourishment of fetus
• Maternal thyroid disorder
• Maternal seizure disortder
• Perinatal causes
• Prematurity: either due to trauma during delivery and later on due to immature
respiratory and cardiovascular system
• Low blood sugar
• Hypoxia
• Low bp
• Jaundice
• Chorioamniotis
• Non vertex and face presentation of fetus
• Birth asphyxia
• Postnatal causes
• Delayed cry
• Severe jaundice
• Trauma
• Infection
• Leds to intracranial hemorrhage, periventricular leukomalacia, hypoxia due to meconium
aspiration, kernicterus

• Cohort studies suggest that an increased risk in children born slightly

preterm[37 to 38 weeks] or post term [42 weeks] compared with
children born at 40 weeks
pathophysiology
• Primary neuralation – 3-4 weeks of gestation
• Prosencephalic development- 2-3 months of gestation
• Neuronal proliferation – 3-4 months of gestation
• Neuronal migration- 3-5 months of gestation
• Organization- 5 months of gestation to years postnatal
• Myelination – birth to years postnatal
• Injury or abnormal development may occur at any time
• Injury before 20 weeks of gestation results in neuronal migration defects
• Injury between 26 &34 weeks of gestation results in periventricular leukomalacia
• Brain injury may occurs due to vascular insufficiency
• Prematurity and cerebral vasculature
• Preterm
• The distribution of fetal circulation to brain results in the tendency for hypoperfusion to the
periventricular white mater
• It results in periventricular leukomalacia which is more susceptible to injury between 26- 34 weeks
of gestation
• As these areas carry fibres responsible for motor control and muscle tone of the legs, injury can
leads to spastic diplegia
• Term
• Cerebral vascular and hypoperfusion injuries resembles adult cerebral circulation
• Vascular injuries at this time often occurs in the MCA leads tp spastic hemiplegia
• Brain susceptible to hypoperfusion mostly targets cortex results in spastic quadriplegia
• Basal gangalia may also be affected resulting in extrapyramidal or dys kinetic cp
Classification
• Based on
• Region affected
• Topographical classification
• Region affected
• Spastic
• Athetoid
• Ataxic
• Mixed
• Hypotonic [ either become a spastic, athetoid or ataxic type]
• Topographical classification
• Quadriplegia
• Diplegia
• triplegia
• Paraplegia
• Hemiplegia
• monoplegia
Spastic cp
• It is the most common type of cp occuring in 70 to 80% of all cases’
• Cerebral cortex is affected
• It also accompanies any of the other types of cp in 30% of all cases
• It can be monoplegic, diplegic, triplegic quadriplegic and hemiplegic
• Main motor characteristics are:
• Hypertonus of clasp knife type
• Increased tendon jerks
• Occasional clonus may also occur
• Abnormal postures; held by tight spastic muscles , whose antagonists are weak or apparently weak in that they cannot
overcome the tight pull of the spastic muscles
• Changes in spasticity may occur with excitement, fear or anxiety and pain which increase the muscle tension.it amy also
change with changes in position and sudden or fast movements
• Voluntary movement
• Voluntary motion is present amnd laboured
• Weakness in the initiation of motion or during movement at different partsof the range
• Co contraction of the agonist with the antagonist instead of the normal
reciprocal pattern persists in the spastic type
• The group of muscle or chain of muscles used in the movement
pattern are different from those used in normal children
• Ex: normal arm pattern for feeding and combing is shoulder flexion,
adduction and some external rotation
• In spastic cp the pattern is usually flexion, adducton and internal rotation and
pronation of elbow
• Lack of isolated or discrete movements and fine motor coordination
are also delayed
• Abnormality of voluntary movement
• Abnormal movement poattern( synergies)
• Lack of isolated movements
• Abnormal co contractions
• Deformities develop due to abmnormal postures
• Abnormal repetition of stereo typed movements
• Associated impairments
• Intelligence varies and usually asssociated with tetraplegia
• Sensory loss occasionally occurs in hemiplegiawith visual field loss and loss sof sensory hand function
• Perceptual problems especially of bodya nd spatial relationship are more common in spastic type.
• Poor respiration with later rib cage abnormalities
• Feeding problems exist
• Epilepsies are morew common in tetraplegia and hemiplkegia
Athetyoid cp
• It is a mixed muscle tone
• Often show involuntary motions
• Damage occurs in extrapyramidal motor syste and pyramidal tract
• It occurs in 10 to 20 % of all cases
In new born infants high bilirubin level if left untreated may rresult in brain da,mage in certain areas( kernictyerus)
• Presence of of involuntary movements are caleed as athetoss
• Bizarre, purposeless movementswhich may be uncontrollable
• It may be slow or fast. They may be writhing, jerky, termor,swiping or rotatory patternor they may be unpatterened
• Increased by excitement, insecurity and the effort to make av oluntary movemebnt or even to tackle a mental problem
• it may get decreased when the child feels fatigue or in prone position or the child is held in very deep attention
• May appaear in hands or feetor in proximal and or in distal joints
• Postural control
• The involuntary movementd or dystonic spasmsmay throw a child off balance
• Voluntary movements
• Posssible but there is an initial delay before the movement is begun
• Lavck of finer movements
• Hypertonia or hypotonia
• Fluctations of tone
• Hyperytonus or dystonia is a lead pipe rigidity or cog wheel rigidity
• Continuous resistance to [passive streetchj throughout hrre full ROM
• It may be particul;arly disabling especially ewhen combined with spasticity
• Arousal of emotions incrtease toine and sleep decrease tone
• Athetoid dance
• Some athetoid are unable to maintain weight on their feet and continually
withdraw their feet or upward and outward
• May take weight on one feet and pawing and scraping the ground in a
withdrawal motion with the othe leg
• Paralysis of gaze movements may occur
• They may be floppy in babyhood and exhibit the involuntary
movement in when they reach 2 to 3 years of age
• Associated impairments
• Intelligence is very good and high
• Hearing loss of a specific high frequency type
• Drive and outgoing personalities are often observed
• Emotional labiality is more frequent
• Articulatory speech difficulties and breathing problems are present
• Feeding difficulties
Ataxic
• It is causec by damage in the cerebellum
• They are least common type of cp occuring only in 10% of cas4e
• Disturbances of balance
• Poor fixation of head, trunk shoulder and pelvic girdle
• Instability is found
• Unsteady gait
• Voluntary movement
• Present but cluymsy and incoordinated
• Dysmetria( overreach or under reach)
• Intention tremor
• Poor fine hand movements
• Hypotonia
• Excessive flexibility of joints and poor muscle power
• Nystagmus may exist
• Associated impairments
• Inteellectual impairments appears
• A pure ataxic is rarely diagonsed except for a group of genetic origin
Hypotonic cp
• Hypotonic cp have musculatiure that is floppy and can move onl;y a
little or niot at all
• Location of damage is widespread in CNS
• Least common types of cp
• Mixed cp
• Signs and symptoms iof spastic cp is seen with any other type of cp
• Mist commonly mixed wwwwith athetoid
Risk babies
Biological risk
Low birth weight (1500 g or less)
Gestational age of 32 weeks or less
Intracranial hemorhage
Musclke tone abnormalities
Recurrent neonatal seizures
Feeding dysfunction
Asphyxia with apgar score less than
4 within 5 minutes
Established risk
hydrocephalus
microcephaly
Chromosomal abnormality
Musculoskeletal abnormalities
( CDH, Limb deficiencies)
Multiple birth more than twins
Inborn error of metabolism
Environmental / social risk
Single parent
Parental age less than 17
Lack of parent and infant
attachment
Maternal drug or alcohol abuse
Behavioural state abnormality
Diagnosis of cp
• Detection of risk babies through screening
• Should start at fetal life and continues into early childhood
• Prenatal screening
• Routine check up for mother during pregnancy is beneficial
• Health education
• Diet advice
• Exercise presxcription
• Sleep and working habits
• Clinical examination
• Height and weight of foetue
• BP, samples of blood and urine
• Special test
• Phenylketonuria
• Glycosuria
• Albuminuria
• RH incompatability
• Congenital syphillis, Rubella, AIDS, neural tuibe defect
• USG from 8 to 12 weeks
• Amniocentesis(16 to 18 weeks of pregnancy) for chromosomal defect
• Postnatal screening
• Starts in the immediate neonatal period and during the first two years
• To find the biochemical defects
• Hearing and visual problems
• Clinical examination
• To assesss weight, height and head circumference
• To find musculoskeletal defects
• Testicular descxent
• Gestational age
• At 6 weeks repeat test
• Blood examination( heel prick at 2 to 5 days of age)
• to find out the respiratory conditions, cardiac pathology, haemoglobinopathies can be detecyted
• Neuromuscular pathologies
• Metabolic disorders
• Gene abnormalities
• The diagnosis of cp depends ypon on the
• Patients history
• Delay in gross motor anmd fine motor development
• Abnormalities in tone and posture
• Movement in neurologic examination
• Investigations
• Ct scan
• Helps to identify congenital malformations
• Intracranial hemorrhage
• Periventricular leukomalacia
• Magnetic resonance imadginmg
• Most useful after 2 to 3 weeks of life
• Defines gthe cortical and whote matter structiures
• Predicts the neurodevelopmental outcomes in preterm infants

• To add image
• Electroencephalography
• Evaluate severe hypoxic ischemic encephalopathy
• Shows marked suppression of amplitude and slowing, followed by a
discontinuous pattern of voltage suppression, with bursts of hoigh voltage
sharp and slow waves at 24 to 48 hours
• Usedc to confirm a diagnosis of epilepsy
• Not indicated if seizures are not suspected
• EMG and NC studies
• Helpful when muscle or nerve disorder is suspected
• Evoked potentials are used to evaluate the anatomic pathways of the auditory
and visual systems
management
• It includes
• Medical management
• Surgical management
• Medical management
• Spasticity and dystonia management
• Botulinum toxin A
• Abobotulinum toxin A( age group 2 to 17 years)
• Onabotulinum toxin A reduce spasticity for 3 to 6 months( 12U / kg)
• Localized and segmental spasticity Botox A is effective
• Generalized spasticity- Diazepam and tizanidine
• Adverse effects asthenia, muscle weakness, dipolopia, dysphonia, dysphagia

• Phenol intramuscular neurolysis

• More painful procedure
• Can treat larger muscle groups
• Antidepressamt and anticonvulsant
• Anticonvulasant( benzodiazepines bsuch as diazepam, valproic acid and barbiturates)
• Treat myoclonus
• Baclofen and benzodiazepines used to treat spasticity
Surgical management
• Intrathecal baclofen pump insertion
• Decrease spasticity in lower extremities, trunk , upper extremities and improve
speech

Selective dorsal rhizotomy

Beneficial in both the short term and long term to treat spasticity
It includes a laminectomy and surgical ablation of 70 to 90% of the dorsal or
sensory nerve root
It decreases spasticity by decreasing reflexive motor neuron activation which is
thought to result from the lack of descending fibre input
Surgical management
• Stereo Tactic Basal Ganglia
It improves rigidity, choreo athetosis and tremor
Orthopedic surgical intervention
Tendon lengthening or transfer can decrease spastic muscle
imbalance and deforming forces
Osteotomy can realign limbs, including the femoral neck, tibia and
calcaneus
Reconstructive surgery to the upper limbs can restore muscle
balance, release contracture and stabilize the joint to improve placement
of the hand in space, voluntary grasp release and pinch function
Surgical management
• Complications
Prognosis
• CP is not a progressive but the symptoms can become more severe
over time
• It depends on the intensity of therapy during early childhood
• Tend to develop arthritis at a younger age than normal because of
pressure placed on joints by excessively toned and stiff muscles
• Intellectual level among people with CP varies from genius to
intellectually impaired
• Can expect to have a normal life expectancy
• Survival is associated with the ability to ambulate, roll and self feed
Assessment
• Subjective Examination
Name
Age
Gender
Address
Chief Complaint
Obtained from parents especially mother or from relatives and
through case sheet
When did the mother first noticed the dysfunctions
Siblings having same type of symptoms
Assessment
• History
Past History
Review of complications of pregnancy and delivery, birth weight, gestation,
any neonatal or perinatal difficulties, feeding problems and other health related
problems
Developmental milestones
Prenatal history
Age of mother
Consanguity marriage
Any drugs taken during pregnancy
Any trauma and dtress
History of TORCH infection
History of previous abortion, still born or death after birth
Multiple pregnancies
Assessment
Perinatal History
Place of delivery
History of pre-term or post-term delivery
Birth asphyxia
History of prolonged labor pain
Type of delivery
Presentation of fetus (breech)
Condition of mother at the time of delivery
Assessment
• Post natal History
Delayed birth cry
History of trauma
Neonatal infection
Micro cephaly
Nutritional habits of the child
Any medical surgical or physiotherapy treatment taken before
Ability level of the child at that time
Apgar seore
Assessment
On observation
Behaviour of the child
Alert, irritable or fearful in the session or during particular activities
Child becomes fatigue easily
Communication of the child
With the parents
Whether child initiates or responds with gestures, sounds, hand or finger pointing, eye pointing or uses words and speech
Other observations
Involuntary movements
Deformities and contracture
Scar and tropic changes
Postural fault
Gait abnormalities
Use of external appliances
Assessment
Attention span
What catches child attention?
How much time child attention is maintain on particular thing?
How does parent assisting to maintain attention?
What distracts the child?
Does child follow suggestions to move or prompting to act?
Assessment
Position of the child
Which position does the child prefer to be in?
Can child get into that position on his own or with help?
With assistance child make any effort to go into that position?
Symmetry of the child
If involuntary movement present, then in which position this movement are
decreased or increased?
Assessment
Postural control and alignment
How much parental support is given?
Check whether a child bears more weight on one side of his body or on one hand or foot
Postural stabilization and counter poising in all postures
Fear of fall in child due to poor balance experience
If the child center of gravity appears to be unusually high, resulting in floating lags and poor
ability to raise head against gravity
Assessment
Use of limb and hand

Limb patterns in changing or going into position as well as using them in position
Attitude of limbs during playing in all positions
Whether one or both hands are used, type of grasp and release
Accuracy of reach and hand action
Any involuntary movement, tremmer or spasm which interfere with action are present
Assessment
Sensory aspects

Observe child vision hearing touch smell and temperature

Does child enjoys particular sensation
Whether child enjoyed moved or having position changed
Form of locomotion
How child is carried?
Any use of wheel chair or walking aids?
Which daily activities motivates child to role creep, crawl, bottom shuffle or walk, running head and other
gaits?
Assessment
Deformatis
In upper limb
Shoulder protraction or retraction, adduction and internal rotation, elbow flexion, fore arm pronation, wrist
and finger flexion
In the lower limb
Hip and semi flexion, internal rotation and adduction, knee semi flexion, ankle plantar flexion, foot
pronation and supination, toes flexion
Athetoid or dystonic posturing usually incorporates extremities of movement such as total flexion or
extension
Wind swept deformative of hip
Assessment
Higher cognitive function
Drowsy and lethargic
Decreasing intellectual function
Mental metadation
Attention deficit
Poor memory
Poor comprehension of speech and language
Assessment
Cranial nerve integrity
Squint (oculomotor)
Visual defects (optic nerve)
Auditory defects (auditory nerve)
Feeding and swallowing problem (lower cranial nerve)
Special senses
Visual and auditory defects
Tactile and vestibular hyposensitivity or hypersensitivity
Assessment
On examination
Sensory assessment
It is difficult to assess sensation in baby’s and young children with severe multiple
impairment
If any hearing or visual are present
Then assessment done by specialist
Assessment
Motor integrity
Abnormalities of tone
Muscular weakness
Loss of voluntary control
Decreased coordination
Assessment
Reflex integrity
Abnormal DTR
Abnormal superficial reflexes
Abnormal primitive reflexes may be persistent (ATNR, extensor thrust, gallant
reflex, etc.)
Assessment
Range of motion and flexibility
Decrease in the range of motion of the involved limbs
Tightness and contracture in hip adductors, hamstrings, calf are very common
Anthropometric measurement
Height or length decreased
Weight decreased or obese
Head circumference
Decreased or increased
Assessment
Growth Parameters
Height until 24 to 36 months of age, length in recumbency is measured using an
infantometer
After the age of 2 years, standing height is recorded by a stadiometer
Head circumference of the child
The tape is used to measure occipito frontal head circumference from external occipital
protuberance to glabella
Assessment
Age Developmental milestones
4 to 6 weeks Social smile
3 months Head holding
6 months Sits with support
7 months Sits without support
5 to 6 monthsReaches out for bright object
6 to 7 monthsTransfer objects
8 to 10 months Crawl
10 to 11 months Creep
9 months Stand holding furniture
12 months Walk
13 months Walks without support, say three words with meaning
15 to 18 months Join 2 or 3words into sentence
15 to 18 months Climb stair
24 months Weaning cloth
3 to 4 years Dressing self, ride tricycle
Joint rom measurement
• Passive joint range of motion
• To demonstrate muscle length,muscle tightness and soft tissue tightness
• Muscle tightness may or may not have full Rom
• Active joint range of motion
• Ability to move and not as equivalent to muscle strength
• Quality of muscle action to be noted
• Different positions may affect joint ROM in some cases. Check in
supine, prone, sitting, sidelying, standing as well
• Goniometer measures ranges provided a standard procedure is used
• Example: hip flexor tightness
bend one knee to chest. The other may flex off bed
overcome hip flexion by downward pressure on the front of thigh
check how far to overcome and how w much pressure is required
Normal: 0-20 degrees for age ( 6-12 )
• Hip adductor and Abductor tightness
• Hip rotator tightness
• Knee flexor and extensor tightness
• Foot plantar flexion ,
• shoulder flexor and adductor tightness
Elbow extensor tightness
Wrist flexion and extension
Finger and thumb adduction and abduction, flexion and extension
• Active range.
• It can also be observed in functions as follows
• head and trunk flexion, extension,rotation observed during head raise
in prone, supine, sitting,standingbdevelopmental channels

shoulder elevation, abduction,rotation, flexion and extension movements

are observed during creeping, reaching and other arm movements
Elbow flexion and extension movements during reaching activities
Wrist and hand during hand function development
• Hip flexion and extension Observed during all function
• Knee flexion and extension observing the child sitting using active
extension to kick your hand or a danglings toy and his knee extension
in standing tall