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473623
Cerebral palsy-clinical presentation
Descripción
paeds-community paeds and psychiatry Mapa Mental sobre Cerebral palsy-clinical presentation, creado por v.djabatey el 10/01/2014.
Sin etiquetas
paeds-community paeds and psychiatry
Mapa Mental por
v.djabatey
, actualizado hace más de 1 año
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Creado por
v.djabatey
hace casi 11 años
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Resumen del Recurso
Cerebral palsy-clinical presentation
during neonatal period
babies IDed if at risk
early features
infancy
abnormal limb &/or trunk posture & tone
delayed developmental milestones
+/-slowing of head growth
feeding difficulties w/
oromotor incoordination
slow feeding
gagging
vomiting
abnormal gait once walking achieved
asymmetric hand function before 12 months old
persistence of primitive reflexes (pathological)
normal role of primitive reflexes
aid appearance of normal patterns of movement
to disappear for motor development to progress
diagnosis
by clinical exam w/ attn to
posture & pattern of tone in limbs & trunk
hand function
gait
3 main clinical subtypes
spastic
damage to upper motor neurone pathway
pyramidal/corticospinal tract
persistently increased limb tone (spasticity)
velocity dependent spastic tone
the faster muscle stretched, the greater resistance it'll have
-> dynamic catch
characteristic of spasticity
clasp knife
increased limb tone suddenly gives way under Pa
brisk deep tendon reflexes
extensor plantor responses (upgoing)
unilat or bilat limb involvement
early presentation
even as neonate
3 main types
hemiplegia
unilat arm & leg involvement
arm > leg affected
face spared
present @ 4-12 months old
fisting of affected hand
a flexed arm
asymmetric reaching/hand funcn
subseq tiptoe walk
toe-heel gait on affected side
initially affected limbs flaccid & hypotonic
increased tone then emerges as dominant sign
past med hx
normal
unremarkable birth hx
neontal stroke
can be the cause
hemianopia
ipsilat side as affected limbs
due to larger brain lesions (strokes)
quadriplegia
all 4 limbs affected
often severely
truncal involvement
tendency to opisothonus (extensor posturing)
poor head control
low central tone
more severe CP
assoc
microcephaly
seizures
moderate/severe intellectual impairment
hx of perinatal hypoxic-ischaemic encephalopathy
diplegia
all 4 limbs
legs>arms affected
relatively normal hand funcn
arm motor difficulties most visible on using hands
abnormal walking
assoc
preterm birth
periventricular brain damage
dyskinetic
movements
involuntary
uncontrolled
stereotyped (sometimes)
more evident w/ active movement or stress
variable muscle tone
primitive motor reflex patterns predominate
description
chorea
irreg, sudden & brief non-repetitive movements
athetosis
slow writhing movements occurring distally
e.g. fanning of fingers
dystonia
simultaneous contracn of agonist & antag truncal & prox mm
twisting appearance
relatively unimpaired intellect
presentation
infancy
floppiness
poor trunk control
delayed motor development
abnormal movements can show only toward end of 1st year of life
pathology
damage/dysfunction
basal ganglia
extrapyramidal pathways
cause
kernicterus (hyperbilirubinaemia)
commonest cause in past
due to Rh disease of newborn
hypoxic-ischaemic encephalopathy @ term
current commonest cause
ataxic (hypotonic)
cause
genetically determined
acquired brain injury to cerebellum or its connections
signs ipsilat to lesion
but rel symmetrical
early trunk & limb hypotonia
poor balance
delayed motor developments
features appearing later
incoordinate movements
intention tremor
ataxic gait
description of functional ability
Gross Motor Function Classification
Level I
walks w/o limitations
Level II
walks w/ limitations
Level III
walks using a handheld mobility device
Level IV
self-mobility w/ limitations; may use self-powered mobility
Level V
transported in a manual wheelchair
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