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ABCN Clinical Neuropsychology > Cerebral Palsy > Flashcards

Cerebral Palsy Flashcards

1
Q

Cerebral palsy (CP) definition

A

group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain.

  • injury typical occurs prenatal
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2
Q

Age of CP diagnosis

A

No specific upper age limit - generally up to 3 years old.

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3
Q

CP is a clinical diagnosis that generally includes:

A
  • clinical diagnosis = based on observable behavior (not diagnosed in utero)
  • formal neurodevelopmental examination
  • history of activity limitations
  • MRI (frequent findings: white matter damage, cortical or subcortical lesions (particularly involving the basal ganglia), brain malformations, and postnatal injuries (including focal infarction)
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4
Q

Where does CP originate? (Which systems?)

A

In either or both of the two semi-independent motor systems of the brain

pyramidal (70-85%)

extrapyramidal (15-30%)

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5
Q

Pyramidal motor system

A
  • travel through pyramids of medulla
  • responsible for voluntary muscle control

Corticospinal tract:
Cerebral cortex -> internal capsule -> midbrain -> pons -> medulla (75% decussate) -> lower motor neuron (ventral horn)

Injury: spastic CP (upper motor neuron)

Corticobulbar tract (voluntary control of face, head, neck):
Cerebral cortex -> internal capsule -> lower motor neuron (brainstem/CN: 5, 7, 9-12)

Bulbar = medulla, pons, cerebellum

Injury: dysphasia, dysarthria

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6
Q

Extrapyramidal motor system

A
  • do not travel through pyramids of medulla
  • responsible for involuntary control (tone, balance)
  • “fine tunes” movement of pyramidal system by making adjustments to posture and coordination
  • originate in brainstem, cerebellum, and basal ganglia - not cortex (pyramidal)
  • results in non-spastic CP
  • typically involves all extremities (upper>lower)
  • normal IQ
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7
Q

Pyramidal motor system damage results in:

A

Spastic CP

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8
Q

Spastic CP (general definition)

A
  • results from damage to pyramidal system
  • characterized by abnormally high muscle tone (tightness)
  • children born preterm > full-term
  • often associated with underlying periventricular leukomalacia (PVL) and/or intraventricular hemorrhage (IVH)
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9
Q

Spastic CP subtypes

A

Spastic hemiplegic (“half”) CP - arm and leg on one side of body
- arm>leg
- most common in full term children
- cause: perinatal MCA stroke
- can learn to walk and have normal IQ

Spastic diplegic CP - lower extremities, lesser degree of upper extremities
- most common in preterm children
- cause: periventrical leukomalacia (damage to white matter around ventricles)
- cognitive impairment is correlated with severity of motor disability

Spastic quadriplegic CP - ll four extremities and the trunk and neck (i.e., full body)
- caused by a generalized event such as anoxia
- injury to brain occurs prenatally (50%), perinatally (30%), and postnatally (20%)
- most severe subtype; frequently accompanied by epilepsy and cognitive impairments

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10
Q

Spasticity

A

increased muscle tone

Abnormally increased muscle tone or muscle stiffness that can interfere with functional movement and daily activities.

When severe, spasticity is characterized by uncontrollable muscle spasms.

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11
Q

extrapyramidal CP subtypes

A

Dyskinetic CP
- basal ganglia dysfunction
- trouble controlling muscle movement (twisting, abrupt movements)
- difficulty sitting comfortable and coordinating muscles for walking and speaking
- caused by hypoxic-ischemic injury typically in full-term infants

Ataxic CP
- cerebellar dysfunction
- lack of coordination during voluntary gross and fine motor movements
- poor balance, unsteadiness,
a wide-based gait, and shakiness or tremors during activities involving manual dexterity.

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12
Q

Mixed CP

A
  • 20% of cases
  • abnormalities of both the pyramidal and extrapyramidal motor systems.
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13
Q

CP risk factors

A
  • preterm birth (most important - though ~50% of CP are full-term)
  • low birth weight (second)
  • prenatal factors (low SES, maternal infections/toxic exposure, multiple birth, IUGR, brain malformations)
  • perinatal (anoxic damage during delivery (10%), low Apgar at 5 mins)
  • postnatal (infections-e.g., meningitis)

Injury after age 3 = CP diagnosis not accurate, rather should reflect underlying cause (e.g., TBI, stroke)

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14
Q

Physical outcomes in CP

A

1/2 = walk unaided, 1/3 = cannot walk, rest = need assistance

spasticity can result in scoliosis and/or hip dislocation

chronic pain

increased risk of epilepsy

oral motor impairments; if severe can increase aspiration

bladder control

poor sleep d/t positioning issues and discomfort

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15
Q

Cognitive outcomes in CP

A

ID (30-50%) - most common in quadriplegic CP

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16
Q

CP classifications of severity

A

mild (i.e., minimal functional limitations)

moderate (i.e., some assistance is required to accomplish ambulation and daily activities)

severe (i.e., non-ambulatory and extensive assistance is required to accomplish daily activities)

17
Q

Early motor attainment and CP

A

Precocious acquisition of certain motor skills can also be a harbinger of CP:

standing well before the age of 12 months can reflect hypertonia (stiffness and rigidity) in the legs

strong hand preference in the first 12 to 18 months can indicate weakness in the other hand

18
Q

% of children ultimately diagnosed with CP who have unremarkable pre- and perinatal history.

A

50%

19
Q

Most children do not manifest full motor signs of CP until how many years?

A

2 years of age or beyond - a definitive diagnosis usually is made in the second or third year of life

20
Q

Neuropsychological expectations of CP

A

CP is not associated with a prototypical neuropsychological profile, however:

language > visually-based is common

ID to BIF (50%)

SLD (25%)

Attention deficits (d/t periventricular white matter and subcortical damage, and/or epilepsy)

21
Q

Medications for CP reduce …?

A

spasticity

does not do well to address muscle weakness, incoordination, or movement abnormalities.

22
Q

Periventricular leukomalacia (PVL)

A

Cerebral white matter necrosis around the ventricles that interrupts the output of motor tracts.

Periventricular leukomalacia results from interrupted blood flow and oxygen to the area, particularly in preterm babies of less than 32 weeks. In fact, PVL is sometimes referred to as “white matter damage of prematurity.”

23
Q

For a child with cerebral palsy, a favorable prognostic indicator is:

A

Sitting by 24 months

24
Q

The medical history most typical of spastic diplegic cerebral palsy is:

A

premature birth and neuroimaging findings of periventricular leukomalacia

25
Q

The foremost risk factor for cerebral palsy is

A

Premature birth.

26
Q

Most robust neuropsychological findings of CP

A

Average IQ with visuospatial impairment and attention weaknesses

27
Q

Describe typical MRI finding in (1) hemiplegic CP, (2) dyskinetic CP, and (3) spastic diplegic CP

A

(1) MCA stroke,
(2) hypoxic-ischemic injury,
(3) PVL

28
Q

Neuropathology of CP

A

White matter damage, followed bye cortical or subcortical lesions (esp the BG), brain malformations, and postural injuries.

*Neuroimaging has DISPROVEN the belief that birth. asphyxia is the major cause of CP.

29
Q

Key Concepts Related to the Formal Definition of CP

A
30
Q

Classification of CP According to Motor System

A
31
Q

What percentage accounts for mixed CP?

A

20%

Many individual with CP exhibit mixed motor signs but are classified according to the predominant motor impairment.

32
Q

What are the PRENATAL risk factors of CP?

A

Maternal risk factors
- intellectual disabilities
- infection or toxic exposure during pregnancy
- certain diseases during pregnancy (e.g., epilepsy, thyroid disorder, high blood
pressure)

Fetal Risk Factors
- multiple birth gestation
- death in-utero of a co-twin
- male sex of the fetus
- intrauterine growth restriction developmental - brain malformations thrombophilic disorders

33
Q

What are PERINATAL risk factors of CP?

A

Prematurity (MOST risk factor); lower the gestational age = higher the risk.

Full-term infants account for majority of CP cases.

Low birth weight (2nd most important risk factor); lower the birth weight = greater the risk.

Anoxic damage

Low Apgar score at 5 minutes

Abnormal muscle tone (hypotonia)

perinatal stroke

34
Q

What are POSTNATAL risk factors of CP?

A

Infections (e.g., meningitis, encephalitis)
brain injury
*In the case with onset of motor problems consistent with CP due to brain insult that occurred after age 3, then diagnosis of CP is not technically correct. Instead, diagnosis should reflect the underlying cause.

35
Q

Physical Morbidity in CP

A

Walking difficulties (more able to walk than not walk)

musculoskeletal complications (e.g., spasticity - constant extension in limbs, contractions, hip dislocations, scoliosis)

Chronic pain (70%)

Epilepsy (28-50%)

Oral-motor impairments (e.g., chewing, swallowing, control of salvia, respiratory complications due to aspiration, may eventually need a peg tube).

Visual and ocular-motor impairments (e.g., risk of blindness in about 10%).

hearing impairments (10-12%)

Bladder control issues (e.g., urinary incontinence)

Sleep disorders (20-25%) due to positioning

Fatigue

Skin complications (e.g., pressure sores due to reduced mobility)

36
Q

Cognitive Morbidity

A

IQ lower than 70 (30-50%)

Quadriplegia –> more highly associated with ID than any other form of CP.

CP is heterogeneous.

37
Q

Presentation, Course, Recovery of CP

A

Gestation/Newborn (1-28 days)
- Clinical observations; cannot be identified in utero.

Infancy (1-12 months)
- CP detection is difficulty.
- normal development characterized by flux, early motor problems are transient.
- precocious acquisition of certain motor skills can be a harbinger of CP (e.g., standing well before age 12 months could mean hypertonia).

Toddler stage (1-3 years)
- persisting or emerging motor delays.
- Full symptoms manifest ~ 2 years or beyond
- serial examination is important for prognostic information

Childhood (3-18 years)
- in mild case, may not be diagnosed until age 4 to 5 years.
- half may outgrow the disorder by age 7 (esp those with mild, mono paretic, diplegia, or extrapyramdial subtypes)

Adulthood
- not progressive per se, motor symptoms can worsen.
- increased risk of diseases of aging (e.g., osteoporosis, arthritis)..

38
Q

Medication Management of Spasticity

A

ABCN Clinical Neuropsychology (34 decks)

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