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Paediatrics > The Child with Cerebral Palsy/ Learning Difficulties > Flashcards

The Child with Cerebral Palsy/ Learning Difficulties Flashcards

1
Q

What is the definition of cerebral palsy?

A

An impairment of movement and posture that results primarily from either injury, abnormal development of the cerebral cortex and other components of the brain associated with movement, strength and muscle tone

(doesn’t always present with spasticity)

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2
Q

Which infants are at increased risk of CP?

A
  • Preterm (<25 weeks significant)
  • Low birth rate (<1.5kg significant)
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3
Q

How can CP present?

A
  • Hypertonia (usually spasticity)
  • Hypotonia (or atonia), tends to preceed hypertonia
  • Dystonia (fluctuating tone)
  • Dyskinesia
  • Ataxia (drunken gait, manifestation of midbrain abnormalities)
  • Combination/ mixed pattern
  • Athetosis
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4
Q

What is the chronological progression of gross motor development based on?

A

Cephalo-caudal myelination and maturation, the nervous system is myelinated from the top down therefore gross motor progress descends as the child ages

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5
Q

What is the moro reflex?

A

Holding the child at the back of the neck/ head and lowering them suddenly, arms will abduct then adduct symmetrically

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6
Q

What is the tonic neck reflex?

A

Moving the child’s head to one side leads to ipsilateral arm extension and contralateral arm flexion

(will be asymmetrical in CP)

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7
Q

Where do the UMNs reside?

A

The motor cortex

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8
Q

What are the broad functions of the upper and lower motor neurons?

A
  • UMNs are inhibitory
  • LMNs are excitatory
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9
Q

Where do UMNs derive?

A

Pleuripotential embryonic neuroectoderm, gives rise to the motor cortex, midbrain and brainstem

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10
Q

Where do LMNs derive?

A

Pleuripotential embryonic neuroectoderm, originally primarily in the spinal cord as anterior horn cells

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11
Q

What is volitional movement?

A

The extended execution of an action eg. planned movement

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12
Q

What can alteration of UMN physiology result in?

A
  • Impaired volitional motor function
  • Loss of inhibition of the LMNs (hyperreflexia, weakness, hypertonia)
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13
Q

What are the causes of cerebral palsy?

A
  • All congenital abnormalities
  • CNS malformation/ disruption
  • Intrauterine infection
  • Multiple births
  • Perinatal stroke
  • Intracranial haemorrhage (1/3 due to coagulopathy, thalamic hemorrhage predominantly)
  • Acquired post natal causes (trauma, infection, hyperthermia)
  • Kernicterus
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14
Q

Do intrapartum events that may lead to asphyxia correlate with CP?

A

No

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15
Q

What causes 10-20% of CP cases?

A

Hypoxic-ischaemic encephalopathy

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16
Q

What clinical examinations are essential for suspected CP?

A

Newborn head circumference (diminished)

17
Q

What are the autonomic signs of CP?

A
  • Diaphragmatic dysfunction
  • GORD
  • Velopharyngeal discoordination (dribbling)
  • Alterations in peristalsis
  • Bladder dysfunction (UMN/ spastic bladder)
  • Vasomotor dysfunction
18
Q

When will primitive reflexes disappear?

A

6-9 months

19
Q

When will definitive motor actions develop (plan a movement and carry out smoothly)?

A

5-7 months

(as primative reflexes decline)

20
Q

What are the types of CP?

A
  • Monoplegia (one extremity)
  • Hemiplegia (two ipsilateral extremities)
  • Diplegia (two contralateral extremities of the same type eg. two arms or two legs)
  • Quadriplegia (four extremities)
21
Q

Which type of CP tends to be associated with development of seizures?

A

Hemiplegia

22
Q

Which type of CP will not likely lead to seizure development?

A

Diplegia

23
Q

What are the two most common forms of CP?

A
  • Spastic quadriplegia
  • Spastic hemiplegia
24
Q

What are the priorities for management of cerebral palsy?

A
  • Parental education (most important)
  • Seating, positioning (early developmental milestones)
  • Ambulation (goal is community ambulation)
  • Child’s education (diagnosis does not always mean intellectual impairment)
  • Feeding/ nutrition
  • Social/ emotional wellbeing
25
Q

What is the difference between speech and communication?

A
  • Speech is the coordinated action of the mouth, tongue and diaphragm to produce words
  • Communication is the ability to impart information or indicate a want or need

Children may be impaired in speech but not communication

26
Q

What leads to failure to thrive in children with CP?

A

Lack of neuromuscular function involved in chewing, swallowing etc meaning caloric needs are not met

27
Q

Why are caloric needs increased in children with CP?

A

Due to the constant hypertonia

28
Q

What percentage of children with CP have epilespy?

A

43%

29
Q

What is important to distinguish in children with CP?

A

Developmental delay (DD) and learning disability (LD), DD occurs in most/ all CP patients, LD is a completely separate condition

30
Q

What is the educational health care plan?

A

Special education and classroom accommodations for children based on their disability

31
Q

What are the common surgical interventions for CP?

A
  • Osteotomy
  • Muscle lengthening
  • Tendon lengthening
  • Tendon or muscle resection
  • Arthrodesis or bone fusion
  • Scoliosis repair
  • Selective dorsal rhizotomy (neurofibers cut along the long axis of the spinal cord to reduce sensory input and hypertonia)
32
Q

What is the management of spasticity in CP?

A

Rehabilitative therapies
- OT
- PT
Injectables
- Botox
Oral preparations
- Dantrolene (Ca2+ inhibition)
- Benzodiazapenes (presynaptic receptor inhibition)
- Baclofen (gamma aminiobutyric acid analogue)
- Clonidine (alpha 2-adrenergic agonist)
Surgical treatment
- Orthopedic: bone, soft tissue, tendon
- Neurosurgery: selective dorsal rhizotomy, stereotaxic encephalotomy)
Pump infusion
- Intrathecal medications (baclofen)

33
Q

What is baclofen?

A

Molecularly similar to GABA, acts to inhibit overactive LMNs

Intrathecal - surgically planted using a catheter going into the side of the spinal cord and bathes the neuronal axis in that area to improve the tone

34
Q

What is periventricular leukomalacia?

A

Common in premature babies, the white matter (leuko) surrounding the ventricles (periventricular) is deprived of blood and oxygen leading to softening (malacia)

Can lead to spastic diplegia, form of cerebral palsy secondary to periventricular leukomalacia

35
Q

What is the presentation of periventricular leukomalacia?

A

Necrosis of the area surrounding the lateral ventricles causes upper motor neuron lesions, leading to spasticity in the patient’s lower limbs

36
Q

What form of cerebral palsy would result from upper motor neuron damage in the cerebellum?

A

Ataxic type cerebral palsy

37
Q

How does ataxic cerebral palsy present?

A
  • Motor delay
  • Hypotonia
  • Varying signs of ataxia (dysarthria, dysdiadochokinesia, nystagmus)
  • Impaired balance and coordination
  • Intention tremora
  • Wide-based gait
38
Q
A

Paediatrics (16 decks)

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