cerebral palsy Flashcards
cerebral palsy
an injury to the developing brain
a persistent disorder of movement and posture due to a static lesion in the developing brain
can happen before, during , or several years (3- 4 years) after birth
lesion donsnt change but brain does so clinical features can develop with time
brain facts
white matter= nerve fibres
grey matter = nerve bodies
movement controlled by corrticopinal tract and basal ganglia
facts about developing brain
insult to brain at diff stages of development can produce different signs
up to 20 weeks cerebral cortex starts as neurone lining ventricles
neurons increase in number , migrate and organise
25-32 weeks
growth and perfusion of preventricual disease
white matter development
susceptible to ischameic and energy failure damage
onwards from 30 weeks
Myelination starts-not complete until after birth
Grey matter development
classification of cp
anatomical classification
Hemiplegic- one sided
Unilateral
Diplegic- 2 limbs
Bilateral
Tetraplegic- 4 limbs
4 limb
Monoplegia/Triplegia
clinical classification
Spastic
Stiff
Dyskinetic
Athetoid, Choreiform, Dystonic
Mixed
“Ataxic”
commonest cp
spastic
Commonest
Increased muscle tone
Associated weakness
Damage is to motor cortex or corticospinal tract
Often associated features
Visual probs, epilepsy
what is spastic hemiplegia
One side
Arm and leg
May have unequal tone and strength
Can present with early hand preference
Usually normal IQ
Middle cerebral artery or cortical vessel
Associated features common
Focal epilepsy, visual field defects, sensory impairments
spastic diplegia
Both legs
May have mild arm involvement
Lower limbs stiff and hyperreflexic
Internal rotation of hips and adduction-scissoring
Associated features
Squint
Normal IQ
Particularly problem of prematurity
Damage to periventricular area
spastic quadriplegia
All 4 limbs affected
Upper limbs often > lower limbs
Generalised spasticity and wasting
Associated features common
Learning disability, generalised epilepsy
Feeding difficulties
Speech problems
End result of global insult
e.g. massive IVH or bleed, major brain malformation, CNS infection/trauma
dyskinetic cp
Involuntary movements and abnormal tone affecting whole body
Dystonia- involuntary increase in extensor tone
Athetosis- writhing movements distally
Chorea- rapid jerky movements
Damage to extrapyramidal tissue/basal ganglia
Associated features
Speech problems, feeding problems
IQ usually normal
Historically kernicterus commonest cause
Hypoxic damage to basal ganglia
causes of cp
Main cause is NOT hypoxic birth injury
Majority of cases due to antenatal causes
Often unable to identify cause
thought to be sequence of events in most cases
More common in premature babies
but most prems don’t have CP
Anything that can damage neurons can cause CP
ataxia cp
Ataxia, intention tremor, discoordination, late walking
Present at 1-2 yrs, but floppy from start
Usually a genetic or metabolic cause
so investigate
Prenatal cause
Due to cerebellar injury
Associated with high tone deafness
50% have normal IQ
prenatal causes
Brain malformations
e.g. migration disorders
Ischaemia
Congenital infections
TORCH
Genetic syndromes
Metabolic
Toxic
perinatal causes
Obstetric Emergencies
e.g. APH, cord prolapse
Neonatal Problems
e.g. hypoglycaemia, kernicterus, infection, hypothermia
postnatal causes
Infection
e.g. meningitis, encephalitis
Trauma
e.g. RTA, NAI, near drowning
Vascular
e.g. ischamic, bleed
Metabolic
CP AND PREMATURITY
Significant association
Babies born <33 weeks have rate of CP 30 times that of term babes
Can be a complication of their prematurity
e.g. IVH
Can have occurred in utero
Particularly susceptible at 28-34 weeks
Ischaemic process in watershed zone
Periventricular leucomalacia=spastic diplegia
Signs of cp
Abnormal tone
Abnormal posture
Abnormal reflexes
Abnormal movements
assessment of cp
History
What is problem parent has noted?
Careful antenatal/perinatal history
Developmental history
Trauma, infection, ALTEs
Functional-eating, secretions, self cares, mobility etc
Examination
Full normal examination
Full neuro examination
Investigations
Referrals to other specialists/therapists
investigation of cp
Very dependent on type of CP
May not need many Ix
Investigations looking for cause
Neuroimaging
Genetic Ix
Metabolic Ix
Clever neurological Ix
Investigations looking for consequences
EEG
Neuroimaging
Hearing tests
Reflux Ix
management of health problems
Respiratory/ENT
Recurrent aspiration, pneumonia
Secretions
GI/Nutrition
Feeding issues
GORD
Constipation/Urinary problems
Neurological
Seizures
Hydrocephalus
Orthopaedic
Contractures
Scoliosis
Spasticity
specficial medical therapies
Spasticity management
Baclofen, Diazepam
Botox
Intrathecal baclofen
Tendotomy
Movement disorder drugs
Trihexphenidyl
Benztropine
