Topic 23 cerebral palsy Flashcards

1
Q

Describe / define cerebral palsy

A

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.

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2
Q

What are the 3 main causes of cerebral palsy

Aetiology

A

Prenatal risk factors 75%

  • Infant
  • Maternal

Perinatal risk factors 6 – 8%
(onset of labour – 28th day of life)

Postnatal risk factors10 – 18%

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3
Q

Prenatal risk factors

A
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
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4
Q

Perinatal risk factors

A

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

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5
Q

Postnatal risk factors

A
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
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6
Q

Risk for term infants (1-12 months)

A
Risk for term infants (1-12 months)
Hypoxic ischaemic encephalopathy (HIE)
Intracranial haemorrhage
Focal ischaemic lesions:
◦ Thrombo-embolic lesions
◦ Basal ganglia lesions
Hyperbilirubinaemia (kernicterus)
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7
Q

Hypoxic-ischaemic encephalopathy (HIE) define

A

Due to perinatal asphyxia
Asphyxia causing hypoxia and acidosis(Often exact timing and underlying cause of
asphyxia are often unknown)

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8
Q

Intraventricular haemorrhage

A

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

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9
Q

Periventricular leukomalacia

A

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

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10
Q

Clinical presentation of Cerebral palsy

A
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 &amp; 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 &amp;
uncontrolled movements
UL, LL &amp; hands > trunk
low risk contractures &amp;
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

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11
Q

Distribution of tone

element of Classification of cerebral palsy

A

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
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