Topic 23 cerebral palsy Flashcards
Describe / define cerebral palsy
A group of permanent disorders of the development of movement and posture, causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing foetal 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.
What are the 3 main causes of cerebral palsy
Aetiology
Prenatal risk factors 75%
- Infant
- Maternal
Perinatal risk factors 6 – 8%
(onset of labour – 28th day of life)
Postnatal risk factors10 – 18%
Prenatal risk factors
Prenatal risk factors 75% Infant -prematurity <37 wks gestation -low birth weight <2500g -brain malformations Maternal -infections (cross blood-brain barrier) -eclampsia( high BP) changes blood flow to foetus -lifestyle – alcohol, illicit drugs, poor nutrition -placental bloodflow insufficiency
Perinatal risk factors
Perinatal risk factors (onset of labour – 28th day of life) 6 – 8%
-prolonged / difficult labour
-premature rupture membranes
-breech presentation
-infant bradycardia / hypoxia / birth trauma
◦ <10% intra-partum asphyxia & HIE (Hypoxic-ischaemic encephalopathy)
-sepsis / CNS infection
-intra-cerebral haemorrhage
Postnatal risk factors
Postnatal risk factors10 – 18% CNS infection (encephalitis, meningitis) hypoxia (e.g. near drowning, near SIDS) seizures head trauma (e.g. falls) non-accidental injury (“shaken baby” syndrome) neonatal hyperbilirubinaemia (jaundice) ^ billruben vascular aetiologies
Risk for term infants (1-12 months)
Risk for term infants (1-12 months) Hypoxic ischaemic encephalopathy (HIE) Intracranial haemorrhage Focal ischaemic lesions: ◦ Thrombo-embolic lesions ◦ Basal ganglia lesions Hyperbilirubinaemia (kernicterus)
Hypoxic-ischaemic encephalopathy (HIE) define
Due to perinatal asphyxia
Asphyxia causing hypoxia and acidosis(Often exact timing and underlying cause of
asphyxia are often unknown)
Intraventricular haemorrhage
Hypoxic-ischaemic reperfusion injury of the germinal matrix
Intrinsic vascular fragility of the germinal matrix
Increased risk of the germinal matrix to hypoperfusion injury
(When blood vessels reperfused)
Exposure to biochemical disturbances
Iatrogenic disturbances in intravascular volume
Intrinsic disturbances in coagulation
Periventricular leukomalacia
White matter injury ( softening of white matter around ventricles)
• Mechanism likely ischaemic + infection
Softened tissue dies off and becomes cysts.
Grading:
I. Persisting > 7 days
II. Developing into smallcysts
III. Developing into largercysts, occipital and fronto-parietal
IV.Deep white matter,extensive sub-cortical cysts
Clinical presentation of Cerebral palsy
Damage to the projections to and from the sensorimotor cortex. UMN syndrome are present. \+ve features • flexor / extensor spasm • clasp knife phenomenon • +ve Babinski • exaggerated cutaneous reflexes • autonomic hyperreflexia • dystonia -ve features •reduced strength –weakness •lack of dexterity(fractionation) •reduced endurance – fatigability
• Primary Spacticity
• reduced or insufficient force generation (weakness)
• maximum force occurs early and is reduced
• hypoextensible muscle
O resistance to passive stretch occurs early
O mechanical change in muscle – more stiff
Secondary impairments • skeletal mal-alignment e.g. torsional deformity of the femur / tibia • joint deformity e.g. hip dislocation, kyphoscoliosis • muscle contracture Tonal changes – Dyskinesia • primarily basal ganglia damage and connections to/from prefrontal & premotor cortex • involuntary, uncontrolled, recurring, stereotyped movements and variable muscle tone • inability to: • organise and execute movement • coordinate automatic movement • maintain posture (choreo) Athetosis fluctuating tonal changes primarily low muscle tone extreme, variable involuntary & uncontrolled movements UL, LL & hands > trunk low risk contractures & Deformities
Ataxia(Tonal changes) ~4% cases • primarily cerebellar or extrapyramidal damage • dysmetria, dysdiadocokinesia • loss of balance and coordination • intention tremor • presents as hypotonia in infants • poor postural stability
Hypotonia(Tonal changes)
usually not be related to a particular lesion
more common in infancy, especially those with quadriplegia or ataxia
may be a precursor to spasticity or athetosis
decreased voluntary movement
postural instability
Distribution of tone
element of Classification of cerebral palsy
Hemiplegia~35% cases of spastic CP
• affects arm, face and leg of one side of the body
• may also have:
dysphasia (lesion toWernicke’s or Broca’s)
perceptual dysfunction
Homonymous hemianopia
Diplegia -28% cases of spastic CP (most common in LBW infants) LL and trunk > UL may also have: ◦ asymmetry of severity ◦ facial involvement ◦ difficulty with speech
Quadriplegia ~37% cases with spastic CP UL, LL, trunk and face affected often asymmetrical motor prognosis poor may also have: ◦ visual defect (corticalblindness) ◦ intellectual impairment ◦ seizures