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Year 5 - Paediatrics > Cerebral palsy & hypoxic-ischaemic encephalopathy > Flashcards

Cerebral palsy & hypoxic-ischaemic encephalopathy Flashcards

1
Q

Define cerebral palsy and hypoxic-ischaemic encephalopathy.

A

Cerebral palsy - umbrella term for a permanent disorder of movement and/or posture and of motor function due to a non-progressive abnormality in the developing brain (Surveillance of Cerebral Palsy in Europe)

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2
Q

What is the diagnosis if the cerebral palsy occurs after the age of 2 years?

A

Acquired brain injury not CP

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3
Q

Explain the aetiology / risk factors of cerebral palsy and hypoxic-ischaemic encephalopathy.

A

About 80% of CP is antenatal due to:

  1. cerebrovascular haemorrhage or ischaemia,
  2. cortical migration disorders
  3. structural maldevelopment of the brain during gestation.

Other causes:

  • Gene deletions
  • 10% due to hypoxic-ischaemic injury before or during delivery
  • 10% postnatal
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4
Q

Name some postnatal causes of CP.

A
  • meningitis/encephalitis/encephalopathy
  • head trauma
  • hypoglycaemia
  • hydrocephalus
  • hyperbilirubinaemia
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5
Q

Why are preterm infants at risk of CP and what is its aetiology?

A

preterm infants are especially vulnerable to CP from periventricular leukomalacia secondary to ischaemia and/or severe intraventricular haemorrhage and venous infarction.

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6
Q

Summarise the epidemiology of cerebral palsy and hypoxic-ischaemic encephalopathy

A

Most common cause of motor impairment in children, affecting 2 per 1000 live births.

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7
Q

What are the presenting signs of cerebral palsy and hypoxic-ischaemic encephalopathy?

A
  • abnormal limb and/or trunk posture and tone in infancy with delayed motor milestones
  • this may be accompanied by slowing of head growth
  • feeding difficulties, with oromotor incoordination, slow feeding, gagging and vomiting
  • abnormal gait once walking is achieved
  • asymmetric hand function before 12 months of age.
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8
Q

What is the age before which hand preference should not be seen?

A

before 12 months

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9
Q

What may happen to primitive reflexes in CP?

A
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10
Q

List some investigations which are helpful in the diagnosis of CP/HIE.

A

MRI helpful but not essential in making the diagnosis.

Diagnosis made by clinical examination

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11
Q

What should be assessed on clinical examination in CP/HIE?

A
  • Posture
  • Pattern of tone in limbs and trunk
  • Hand function
  • Gait
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12
Q

What is the management of cerebral palsy and hypoxic-ischaemic encephalopathy?

A

MDT management necessary including PT, OT, SALT.

Walking aids/mobility aids

Communication aids - augmentative and alternative communication systems

Hypertonia can be treated with:

  • botulinum toxin IM
  • selective dorsal rhizotomy (cutting some nerve roots to reduce spasticity)
  • intrathecal baclofen (skeletal muscle relaxant)
  • deep brain stimulation of basal ganglia
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13
Q

Describe education and social integration measures in CP.

A

Attending regular classes (mainstreaming); may require full-time helpers

Treatment should be aimed at increasing independence and optimising mobility.

For younger children, activities such as special sport leagues, hippotherapy (horseback riding), wheelchair-adapted swimming pools, and other adapted sport activities are key to social integration.

Later those without an intellectual disability can work in the community, with reasonable accommodations for their physical impairments. People with more intellectual impairment can use sheltered workshops, day programmes, and special transportation considerations are key to avoiding isolation.

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14
Q

Identify the possible complications of cerebral palsy and hypoxic-ischaemic encephalopathy and its management

A
  • Medical
  • Psychological
  • Social
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15
Q

What is the prognosis of CP/HIE?

A

Prognosis is difficult to give to parents as severity and pattern of evolving signs and child’s developmental progress only becomes apparent over months or years.

Likely to have medical, psychological and social problems.

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16
Q

Name 4 causes of a floppy baby (non-neuromuscular).

A
  • Cerebral palsy
  • Down’s syndrome
  • Prader-Willi syndrome
  • Hypothyroidism
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17
Q

Name 4 neuromuscular causes of a floppy baby.

A
  • spinal muscular atrophy
  • spina bifida
  • GBS
  • MG
  • muscular dystrophy
  • myotonic dystrophy
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18
Q

What signs of cerebral palsy are seen here?

A
  • Spastic bilateral (quadriplegia) cerebral palsy
  • Scissoring of legs from excessive adduction of hips
  • Pronated forearms
  • ‘Fisted’ hands
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19
Q

What motor signs suggestive of CP/HIE can be seen in an infant at <9months?

A

Not lifting head, stiff leg on one side and pushing head back - 3 months

Unable to lift head, stiff crossed legs - 6 months

Rounded back, poor use of arms, poor head control, will not take weight on legs - 9 months

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20
Q

What motor signs suggestive of CP/HIE can be seen infants at 9-18 months?

A

No interest in weight bearing, difficulty pulling to standing, pointed toes and stiff legs, cannot crawls on hands and knees - 13 months

Holds arms stiffly, excessive tip toe gait, sitting with weight to one side - 18 months

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21
Q

What is the classification system used for assessing motor development in CP?

A

Gross motor function classification system (GMFCS)

22
Q

What is the classification of CP based on neurological features? Which type is most common?

A
  • Spastic (90%) - bilateral, unilateral or not specified
  • Dyskinetic (6%)
  • Ataxic (4%)
  • Other

NB: in the past it was called based on parts of body affected e.g. diplegia, hemiplegia, quadriplegia.

23
Q

Which part of the CNS/PNS is affected in spastic cerebral palsy?

A

UMN (pyramidal or coticospinal tract) damage

24
Q

Describe the clinical features of spastic cerebral palsy.

A
  • Increased tone (spasticity) - may even be seen in neonatal period but there may be hypotonia in head and trunk initially too
  • Brisk deep tendon reflexes
  • Extensor plantar responses
25
Q

Describe the characteristic features of muscle tone seen in cerebral palsy.

A
  • Velocity dependent - faster the stretch the greater the resistance it will havs, which causes a dynamic catch.
  • ‘Clasp knife’ pattern can also occur when the limb yields under pressure.
26
Q

What are the 3 main types of spastic CP?

A

Unilateral (hemiplegia) - arm usually affected more than leg, face is spared.

Bilateral (quadriplegia) - all four limbs severely affected, trunk also affected with a tendency to opisthotonus (extensor posturing)

Bilateral (diplegia) - all four limbs but legs affected more than arms

27
Q

Which type of spastic CP …

often presents at 4-12 months, with fisting of hand, asymmetric reaching, toe pointing when lifting head and tip-toe walking on one side, initially with hypotonia then spasticity, an unremarkable birth history?

A

Unilateral (hemiplegia) spastic cerebral palsy

28
Q

What is the cause of bilateral (hemiplegic) spastic paralysis in a patients with no history of HIE at birth?

A

Vascular insults such as neonatal stroke (if severe then can also cause hemianopia) of the same side as the limbs.

29
Q

Which type of spastic CP…

is a more severe form of CP associated with seizures, microcephaly, moderate or severe intellectual imapirmnet and possible history of perinatal HIE?

A

Bilateral (quadriplegia) spastic cerebral palsy

= all four limbs affected, extensor posturing of trunk, poor head control and low central tone.

30
Q

Which spastic CP…

is only apparent with functional hand use, abnormal walking and may be associated with preterm birth?

A

Bilateral (diplegia) spastic cerebral palsy

31
Q

What may be seen in bilateral (diplegia) spastic CP on MRI if the infant was born preterm?

A

Diplegia is one of the patterns associated with preterm birth due to periventricular brain damage = MRI brain may show periventricular leukomalacia

32
Q

What are the main features of dyskinetic cerebral palsy? When does it usually present?

A
  • Involuntary, uncontrolled, occasionally stereotyped movements more evident with active movement or stress
  • Tone is variable
  • Intellect may be unimpaired

Presents towards the end of first year of life with floppiness, poor trunk control and delayed motor development in infancy.

33
Q

Describe the tone in 3 ways in dyskinetic cerebral palsy.

A
  1. chorea – irregular, sudden and brief non-repetitive movements
  2. athetosis – slow writhing movements occurring more distally such as fanning of the fingers
  3. dystonia – simultaneous contraction of agonist and antagonist muscles of the trunk and proximal muscles often giving a twisting appearance.
34
Q

What is the pathophysiology/aetiology of dyskinetic cerebral palsy?

A

Damage or dysfunction of the basal ganglia or their associated pathways (extra-pyramidal)

Causes:

  1. Kernicterus due to rhesus haemolytic disease of the newborn
  2. HIE (most common)
35
Q

What does the MRI show in dyskinetic cerebral palsy?

A

Bilateral chages predominantly in the basal ganglia

36
Q

Describe the main features of ataxic(hypotonic) cerebral palsy.

A
  • early trunk and limb hypotonia
  • with poor balance,
  • delayed motor development,
  • incoordinate movements,
  • intention tremor,
  • ataxic gait (evident later)
37
Q

What is the pathophysiology/aetiology of CP?

A

Genetically acquired (most common)

Brain injury (cerebellum or its connections) with signs occurring on same side as the lesion but usually relatively symmetrical

38
Q

Which reflexes and reactions in early infancy that are poor prognostic factors for the development of independent walking in CP?

A
  • Retention of asymmetric and symmetric tonic neck reflexes
  • Retention of Moro (startle) reflex
  • Retention of neck righting reflex
  • Presence of lower-extremity extensor thrust response
  • Lack of parachute reaction
  • Lack of foot placement reaction
39
Q

What is the pathophysiology of hypoxic-ischaemic encephalopathy?

A

Hypoxia/ischaemia can be due to low oxygenation from placenta, umbilicus or postnatal respiratory depression causing cardiorespiratory depression

Compromised cardiac output –>

  1. diminished tissue perfusion –>
  2. hypoxic ischaemic injury to brain and other organs –>
  3. metabolic acidosis –>
  4. capillary lead and oedema

Respiratory depression –> hypoxaemia, hypercarbia, respiratory acidosis

40
Q

How common is HIE?

A

0.5-1/1000 live births

41
Q

When does the hypoxic-ischaemic event usually occur?

A

Immediately before or during labour or delivery

42
Q

List the 5 most common causes of HIE.

A
  1. Placental gas exchange failure - excessive/proloned uterine contractions, placental abruption, ruptured uterus
  2. Umbilical blood flow interruption- cord compression e.g. shoulder dystocia, cord prolapse
  3. Maternal placental perfusion inadequate e.g. from hypotension or hypertension
  4. Fetus compromised e.g. IUGR
  5. Cardiorespiratory adaptation failure at birth i.e. failure to breathe
43
Q

How can you grade the clinical manifestations of hypoxic ischaemic encephalopathy?

A

Mild - irritability, excessive response to stimulation, staring eyes, hyperventilation, hypertonia, impaired feeding

Moderate - marked abnormalities of movement, hypotonia, no feeding and may have seizures

Severe - no normal sponatenous movements or response to pain, varying tone, prolonged seizures refractory to treatment, multi-organ failure present

44
Q

Describe what is meant by primary and secondary neuronal damage in HIE. Which type may be prevented with therapeutic cooling?

A

Primary - immediate neuronal death from HIE

Secondary - delayed neuronal death due to reperfusion injury causing secondary energy failure. This may be prevented with therapeutic hypothermia.

45
Q

What investigation can be used to confirm early encephalopathy?

A

amplitude-integrated electroencephalogram (aEEG, cerebral function monitor) to detect abnormal background brain activity in HIE or seizures

46
Q

What is the immediate management of HIE?

A

Resuscitation and stabilisation with:

  • respiratory support
  • seizures treated with anticonvulsants
  • transient renal impairment with restricting fluids
  • hypotension treated by volume and inotrope support
  • hypoglycaemia and electrolyte imbalance monitored and treated, especially hypocalcaemia
47
Q

What is the evidence for therapeutic cooling?

A

Cooling to rectal temperature of 33-34’C (mild hypothermia using a cooling blanket) for 72 hours in moderate to severe HIE reduces brain damage if started within 6 hours of birth

“For every 8 babies cooled, one extra baby will survive without disability”

Evidence:

Reduction in:

  • death and major disability
  • mortality
  • neurodisability
  • cerebral palsy

No change in:

  • seizures

Increase in:

  • persistent pulmonary hypertension
48
Q

What is the prognosis of HIE?

A

Mild - complete recovery expected

Moderate - if well neurologically and feeding normally by 2 weeks of age then good long term prognosis, but if clinical abnormalities persist then recovery is unlikely.

Severe - mortality of 30-40%, and 80% risk of neurodisability without therapeutic cooling, including CP.

49
Q

What is the prognosis if the MRI at 5-14 days (in a term infant) shows significant abnormalities?

A

High risk of cerebral palsy

50
Q

What are differentials for HIE?

A
  • Inborn errors of metabolism
  • Kernicterus
  • “birth asphyxia” - this has serious medicolegal implications and should only be considered in specific instances
51
Q

When would you consider a diagnosis of birth asphyxia over HIE?

A

When..

  • there is evidence of severe hypoxia antenatally/during labour at delivery
  • resuscitation required at birth
  • features of encephalopathy present
  • hypoxic damage to organs such as liver/kidneys/heart present
  • no other prenatal/postnatal cause identified

Year 5 - Paediatrics (91 decks)

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