Acquired Brain Injury in Children Flashcards

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1
Q

what is an acquired brain injury?

A

damage to the brain that a child was not born with, instead resulting from an accident/event that happens later on

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2
Q

what is a traumatic brain injury?

A

caused by something happening outside of the body i.e. a head injury

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3
Q

what is a non-traumatic brain injury?

A

caused by something going on inside the body i.e. a stroke

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4
Q

what type of brain injury is a stroke?

A

non-traumatic

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5
Q

what is a stroke?

A

when blood flow to an area of brain is cut of. when blood flow is restricted, brain cells are deprived of oxygen, leading to cell death

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6
Q

what are two subtypes of stroke?

A
  • ischemic
  • haemorrhagic
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7
Q

what is an ischemic stroke?

A

when arteries to brain become blocked/narrowed, causing severely reduced blood flow.

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8
Q

what is a haemorrhagic stroke?

A

when blood vessel in brain leaks/ruptures.

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9
Q

what is the prevalence of strokes in children compared to adults?

A
  • Stroke in children is rare compared to adults
    ▪ 1.2 to 13 cases per 100,000 children under 18 years of age
  • But our estimates are likely to be underestimates -> stroke is often not suspected by those interacting with a child.
  • Time-delay from symptoms to seeing health-care professions, then further delay in the diagnosis of stroke/cause of stroke
  • Compared to adults, delay to diagnosis/misdiagnosis more likely
  • Reported incidence of paediatric stroke rising – probably due to better survival rates for children with congenital heart disease/sickle cell disease, and improved awareness (Tsze & Valente, 2011)
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10
Q

what is the % of ischemic strokes for adults and the main reason?

A

80-85% of strokes are ischemic.

Main risk factors for adult stroke are hypertension, diabetes, atherosclerosis (plaque in the arteries)

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11
Q

what are the most common form of strokes in children?

A

ischemic

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12
Q

what are the causes of strokes in children?

A
  • Cardiac problems, especially congenital heart disease, or following surgery to the heart
  • Sickle Cell Disease - inherited condition which affects the development of red blood cells
  • Serious infections
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13
Q

what are the main causes of strokes in adults?

A
  • hardening of the arteries
  • diabetes
  • high blood pressure
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14
Q

what are the signs of strokes in young people?

A

newborns/infants:
* seizures
* extreme sleepiness
* tendency to only use one side of body

children/teens:
* severe headaches
* vomiting
* sleepiness
* dizziness
* loss of balance/coordination

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15
Q

long-term outcomes/consequences of strokes? [Christerson & Stromberg (2010) – follow up study of 51 children who had strokes]

A
  • 4 had died
  • Majority considered to have neurological deficit and school activity deficit
  • Hemiparesis (weakness in one side of the body) was common

Looked at whether children whose stroke occurred at age 0–6 years, 7–12 years and 13–17 years differed in terms of outcome - did not find significant differences when looking at the various different outcomes in terms of school support, neurological deficit etc.
* issue with statistical power because of how small the sample group is

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16
Q

Schryver et al (2000) followed up 33/35 patients who’d suffered ischemic strokes. Mean age at the time of stroke was 4.6 years (3 months -14 years). Mean follow-up time was 7.1 years (3 months - 20 years) They found that…

A
  • 4 had died, 9 developed seizures, 8 had TIA 2 had further ischemic strokes
  • 15 showed hemiparesis - weakness in one side of the body (mild to severe)
  • Most children needed extra support in school, and there was a shift towards poorer cognitive functioning…
  • But none of the children remained severely disabled, and almost all of the children considered themselves to be as happy as other children
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17
Q

What is TIA?

A

transient ischemic attacks
* essentially mini strokes which have similar symptoms, the different is that it doesn’t do any long-term damage to the brain because only restricts blood flow for a short amount of time)
-> BUT this is a risk factor for proper ischemic strokes

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18
Q

the effect of a stroke on social abilities

A
  • Anderson et al (2013) – compared social competence of children who’d had arterial ischemic stroke (AIS), vs healthy controls and children with asthma
  • Children with AIS had more social problems than controls
  • Lesion volume (side of brain damage) not related to social outcomes
  • Younger age at stroke predicted better social interaction and higher self-esteem (not something other studies found…)
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19
Q

Is Foetal (fetal) alcohol syndrome an ABI?

A

not technically

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20
Q

what is FAS?

A

“Foetal Alcohol Spectrum Disorder” (FASD also includes partial FAS, alcohol-related birth disorders, and alcohol-related neurodevelopmental disorder)
-> Caused by effect of alcohol on developing foetus

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21
Q

what are the physical characteristics of FAS?

A
  • poor growth
  • distinctive facial features
  • health problems related to organs
  • microencephaly
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22
Q

what are cognitive characteristics of FAS?

A
  • microencephaly
  • epilepsy/seizures
  • abnormal development of corpus callosum
  • learning difficulties
  • attention and behavioural problems
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23
Q

For a diagnosis of FAS, the presence of all three symptoms are required. What are these?

A
  1. All three facial abnormalities
    * smooth philtrum (the vertical groove between the upper lip and the nose)
    * thin vermillion border (the border between the lip and the adjacent normal skin)
    * small palpebral fissures (the space between the corners of the eye opening)
  2. Growth Deficits
  3. Central Nervous System Abnormalities (structural, neurological or functional)
    *confirmed prenatal alcohol exposure is not necessary in the presence of all these symptoms, however confirmed absence of alcohol exposure would rule out FAS diagnosis.
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24
Q

What are other FASD conditions?

A
  1. Partial Foetal Alcohol Syndrome (pFAS)
  2. Neurobehavioral Disorder associated with Prenatal Alcohol Exposure (ND-PAE)
  3. Neurobehavioural disorder associated with prenatal alcohol exposure <- similar to other conditions, but does not require any atypicality in face or growth
25
Q

What are the symptoms of partial foetal alcohol syndrome (pFAS):

A
  1. A confirmed history of prenatal alcohol exposure;
  2. Central nervous system abnormalities at the same level as FAS.
    * Individuals with pFAS might not have growth deficiency or one or more of the facial abnormalities associated with FAS.
    * Individuals with pFAS have the same functional disabilities but “look” less like an individual with FAS.
26
Q

what is FAS prevalence rates?

A

UK has one of the highest prevalence rates of FAS, an estimated 61.3 cases per 10,000 births – significantly higher than the global average of 15 per 10,000

27
Q

Why might you argue that FAS is an example of acquired brain injury?

A

Because if alcohol exposure hadn’t had happened, FAS wouldn’t have been acquired

28
Q

Why might you argue that FAS is not an example of acquired brain injury?

A

happens prebirth whereas an acquired brain injury is something that is defined to have happened after birth.

29
Q

what are the neurobiological consequences of FAS?

A
  • Alcohol consumed during pregnancy can pass through the placenta to developing baby
  • Foetus cannot process alcohol the same way the mother can – alcohol exposure leads to abnormal central nervous system development
  • Several mechanisms by which alcohol disrupts CNS development including:
    ▪ Cell death
    ▪ Problems with neural migration (cortical brain layers of cortex- form little protein ladders but alcohol messes with that process so you end up with messed up cortical layers and they tend to look quite smooth - more smooth then you’d expect
    ▪ Disruption of gene expression
  • In some cases high alcohol intake leads to non-viability and foetuses do not survive
30
Q

Cognitive problems of FAS?

A
  • Learning disabilities are common in FAS
    ▪ And even children exposed to alcohol during pregnancy who do not meet criteria have reduced cognitive function
  • Problems with executive function
  • Children whose difficulties are more subtle may receive a diagnosis of ADHD
31
Q

Social problems of FAS?

A
  • Children with FAS sometimes described as “excessively friendly” (dangerous because they don’t discriminate between familiar and unfamiliar individuals- stranger danger)
  • Pre-schoolers with FAS do not discriminate between familiar and unfamiliar people (Streissguth & Giunta, 1988)
  • Social behaviours seem problematic, even when IQ is taken into account- social difficulties not simply due to intellectual problems, and not simply “delayed (Thomas et al., 1988)
  • Even into adolescence, social behaviours towards strangers may be inappropriate, and they are at increased risk of exploitation and abuse
32
Q

Describe a trumatic brain injury.

A

Caused by something happening outside the body e.g. a head injury
* Can include a number of different causes, including:
▪ Damage sustained during a motor accident
▪ A fall
▪ An inflicted injury during a fight
▪ A penetrating head wound (e.g. gunshot wound)

Injuries can be categorised as “closed” or “penetrating”

33
Q

What is a closed injury?

A

when the dura layer has not been damaged (e.g. rapid deceleration) - aka. nothing has gone through the skull

34
Q

what is a penetrating injury?

A

damage to the dura (e.g. gunshot wound)

35
Q

Brain damage due to TBI can be separated into primary and secondary injuries. What is a primary injury?

A

occur at the moment of damage. Could be due to rapid acceleration/deceleration (such as in a car accident), this could be the damage caused by a penetrating injury.

36
Q

Brain damage due to TBI can be separated into primary and secondary injuries. What is a secondary injury?

A

result from altered blood flow or inflammation of the brain. A key concern for medics will be preventing secondary injuries (you want to prevent the development of secondary injuries).

37
Q

TBIs can be categorised as ‘mild’, ‘moderate’ and ‘severe’.

A
  • Mild TBI is what we might consider concussion (the majority of TBIs are “mild”)
    **Terminology also includes focal versus diffuse (quite wide brain injuries which are affecting many different brain areas) damage (though many patients will have a combo of focal and diffuse injuries)
38
Q

Prevalence of TBI in children can be tricky, why is this?

A

estimates vary partly due to variation in how TBI is defined:
* many studies rely on hospital admission/discharge info – but the majority of TBIs are mild and may not be admitted to hospital…
* mckinlay et al. (2008) -> did a prospective study using a birth cohort of 1265 people. Overall prevalence of 30%!

39
Q

what is the most common cause of a TBI in young people?

A

Children aged 0-14 years most common cause of TBI is falls, for 15-25 its contact sports and motor vehicle accidents (you see a bimodal pattern - children under 5 and children over 15ish are most at risk because risk-taking behaviours are more apparent in these age ranges (i.e. young or drunk)

40
Q

Who is at most risk of a TBI?

A

Children <5 years and adolescents aged 15 – 19 years at risk for sustaining a TBI (Langlois et al., 2006)

An incident of TBI increases the individuals’ risk for future TBI

41
Q

What are the cognitive effects (executive function) of traumatic brain injuries?

A
  • Levin et al (2002): using N-back task, found working memory was impaired in children ~4 years post severe TBI compared to mild TBI and TD children
  • Schachar et al (2004) impaired inhibition in some children 2 years post TBI, but only those who had developed secondary ADHD
  • Mangeot et al (2002) examined broader executive function ~ 5 years post-injury for severe TBI, moderate TBI and orthopaedic (control) injuries. TBI groups showed long-term problems in executive functions
  • Executive function problems associated with psychosocial outcomes and also family functioning (children with a higher need, will feed into family life in some extent)
42
Q

What are the cognitive effects (social) of traumatic brain injuries?

A

Childhood TBI associated with social impairment especially if:
* Young at age of injury
* Frontal regions and corpus callosum are affected
* Environmental factors: social disadvantage and family dysfunction

Hanten et al (2011) – used virtual reality to test adolescents’ social problem solving:
* Manipulated cognitive load of scenarios- multiple speakers, irrelevant information
* TBI group showed significant social problem solving difficulties, including describing the problem, generating solutions, selecting appropriate response and evaluating outcomes – these problems were particularly apparent as cognitive load increased.

43
Q

What is the common problem of TBI and ADHD?

A

which one came first?
* Higher incidence of ADHD with a head injury
* But also having ADHD, leads you to sometimes be more impulsive

44
Q

what is shaken baby syndrome?

A
  • “Shaken baby syndrome”, sometimes called abusive head injury, describes cases where infants have been violently shaken
  • Violent shaking of infants results in TBI, but there might not be visible signs of external impact
  • Infants are more likely to have diffuse TBI because of the open fontanelle (more likely to affect/encompass multiple brain regions)… and they are more likely than older children to sustain a TBI due to abuse…
45
Q

Shaken Baby Syndrome in Courts…

A

Research has tried to disentage telling apart inflicted vs. non-inflicted (i.e. accidental) head injury in infants (Hymel et al., 2007)

However, has been debate about how much medical expertise is able to tell apart abusive head injury from ABI from other causes

46
Q

What is the ‘Triad’ Classification of Shaken Baby Syndrome?

A
  1. Subdural haematoma (bleed of brain): where blood collects between the skull and the surface of the brain. It’s usually caused by a head injury
  2. Retinal haemorrhages (bleed of the brain): bleeding from the blood vessels in the retina, inside your eye.
  3. encephalopathy – put forward in 1970s to be indicative of an infant having being shaken: “disease of the brain” so might seem quite vague here, but it is essentially signs of altered state/consciousness/confusion
    * However (understandably) very difficult to gather reliable data on this syndrome
    Best evidence comes from (very few) studies where individuals have admitted to having shaken their baby (where we know the shaking event must have happened)
47
Q

What are the predictors of shaken baby syndrome? How does it come to be?

A
  • Crying may act as a particular trigger for shaking
  • “Normal crying curve” describes the observation that crying behaviour peaks around 5 weeks… (when crying peaks, the number of cases also tends to peak - while indirect, we can assume)
48
Q

How can we prevent shaken baby syndrome?

A

Barr et al. (2006) argue that prevention programs need to consider education about how crying may frustrate parents, and how to recognise this

  • Previous rules “Never shake your baby” do not recognise the emotional toll crying can have on a parent
  • Education about the frustrating properties of crying, and that infants do have periods of crying that are un-soothable may help
    ALL ABOUT PREVENTING THE SHAKING INCIDENTS
49
Q

The Period of Purple Crying program is an eveidence based prevention program with arms to support caregivers in their understanding of early increased infant crying and to reduce incidences of SBS. It allows parents to learn about the crying characteristics. What does PURPLE stand for?

A

P: Peak of Crying
U: Unexpected crying
R: Resists Soothing
P: Pain-like Face
L: Long Lasting
E: Evening

50
Q

Do children recover better from ABIs?

A

Two key theories about why recovery can occur:
* Restitution - injured system heals itself
* Substitution – neural function is transmitted from the injured to a non-injured site (and the new part of the brain starts to take up that function - transmission of neural role)

Researchers have wondered whether a younger brain, being more “plastic”, might be able to recover function better than an adult brain (i.e. substitution will be easier…)

51
Q

Ties into the “Kennard” Principle:

A
  • Margaret Kennard (1899-1975) was a neurologist who investigated effects of neurological damage on primates.
  • Kennard Principle -> concept that immature brain is more resilient to injury compared to more mature brain. A younger brain can reorganise better to preserve function (young an individual/brain was, the better recovery of the brain.
  • Therefore there should be a negative linear relation between age at brain injury and functional outcome
  • Related concept -> “equipotentiality” that any part of the brain can theoretically do any job
52
Q

Dennis & Whitaker (1976): 3 children aged 9-10 years who’d had entire hemispheres removed [for medical reasons i.e. tumours] (~5 months). Language typically is the domain of the left hemisphere. They found no big problems in terms of their hemispherical engagement

A

MW: no right hemisphere à managed to maintain grade level at school, cognitive functions are at a normal level (Verbal IQ 96, Performance IQ 92, Full Scale IQ 93).

SM: no left hemisphere -> maintaining good standing at school, intellectual abilities are normal (Verbal IQ 94, Performance IQ 87, Full Scale IQ 90).

CA: no left hemisphere -> hemiplegic. Age-appropriate level at school. Intellectual abilities are normal (Verbal IQ 91, Performance IQ 108, Full Scale IQ 99).

53
Q

Dennis & Whitaker (1976) conducted very thorough language assessment of these children. They further found that:

A
  • Argued that the children with the left hemisphere removed showed some problems especially in terms of syntax
  • But semantics and phonology were fine
  • Suggests at least some plasticity, but some language functions more able to be supported by the right hemisphere than others?
  • This argues the idea of Interhemispheric transfer (another hemisphere has traditionally taken up the role)
54
Q

Neural Plasticity vs. functional plasticity

A
  • Substitution – neural function is transmitted from the injured to a non-injured site
  • However just because another brain area has taken over a function, does that necessarily mean that the you see functional recovery?
  • Anderson et al (2002): 8 year-old child with tumour in Broca’s area (which got removed- no broca’s area), underwent serial fMRI during language generation task. Increasing activation of other areas suggests that other brain regions were starting to take up language functions à but behaviourally language skills decreased…
  • Even when other brain regions take on functions, they might do so suboptimally…
  • Can see evidence of language problems behaviourally
55
Q

Does age at injury predict better recovery?

A

FASDs -> injury is acquired pre-birth. The outcome of alcohol exposure in this spectrum of disorders seems very variable – we have a “spectrum” of outcomes

Stroke -> Christerson & Stromberg (2010) found no effect of age at stroke, Anderson et al (2013) found younger children showed better improvement in their social outcomes

Shaken Baby Syndrome -> younger age at hospitalization predicted poorer outcome

TBI -> Anderson et al (2000): 124 children examined acutely and 12 months post injury on standardised IQ measures. Aged 3-12 years at injury.
▪ Greater injury predicted poorer IQ.
▪ Age at injury was not predictive for mild/moderate TBI
▪ For severe TBI, younger age at injury was associated with poorer IQ recovery
* Yeates et al (2002): age at injury had little effect on outcomes in their study, but all participants were aged 6+ years at injury…
* Kuhtz-Buschbeck et al (2003) – looked at sensorimotor recovery after TBI. Certainly some functions were regained, but younger age did not predict better outcomes

56
Q

Neither early plasticity nor early vulnerability can fully explain the pattern of data across, or within, the different clinical groups. What does Anderson et al. (2011) suggest:

A

viewing plasticity vs vulnerability as a continuum rather than dichotomously opposing theories

57
Q

Hidden deficits/full impact of early brain injuries may emerge over a period of time

A

As toddlers become children become adolescents, the demands made by their environment increase:
* Expected to manage own work
* Social lives become increasingly complex

58
Q

Westmacott et al (2009) studied 26 neonatal arterial ischemic stroke patients in terms of IQ finding that:

A
  • Preschoolers patients’ performance did not differ from the normative sample for Full Scale IQ, Verbal IQ, or Performance IQ
  • Middle-late childhood: significant decline in Full Scale IQ, which reflected emerging deficits in nonverbal reasoning, working memory, and processing speed (IQ is platoing as their peers begin to get smarter and smarter - starting to hit their limits relative to the control group - we have to take into account when we are looking at those outcomes).