CHILD NEUROPSYCHOLOGY
(2425-PSY3359)
Tasks, practical and lectures
,Inhoud
Task 1 ..................................................................................................................................................... 2
Questions for disucssion ................................................................................................................... 12
Lecture 1 Brain development ............................................................................................................ 17
Task 2 ................................................................................................................................................... 23
Questions for discussion: .............................................................................................................. 28
Lecture 2 Childhood TBI .................................................................................................................... 32
Task 3 ................................................................................................................................................... 35
Questions for discussion: .............................................................................................................. 43
Task 4 ................................................................................................................................................... 50
Questions for discussion: .............................................................................................................. 61
Lecture 3: ADHD: clinical picture, neurocognition and interventions .......................................... 69
Task 5 ................................................................................................................................................... 75
Questions for discussion: .............................................................................................................. 82
Practical................................................................................................................................................ 88
Lecture 4: Autism Spectrum Disorder.............................................................................................. 95
1
,Task 1
Anderson, V., Northam, E., & Wrennall, J. (2018). Developmental neuropsychology: a clinical approach. London:
Routledge. Chapter 9: Childhood traumatic brain injury
Childhood traumatic brain injury (TBI) is a frequent cause of interruption to normal development and may result in residual
impairments in a range of skills information processing, attention, memory, learning and social cognition. The treatment is long-
term and the neuropsychologist is multidimensional (monitoring neurobehavioral recovery, understanding the child’s strengths
and weaknesses in the context of current evidence, liaising with teachers and rehabilitation workers, designing cognitive
interventions and behaviour management programmes, providing counselling with respect to adjustment issues for the child and
family and informing parents and the wider community about the implications of the child’s injuries for daily functioning.
Deficits
May impact on child’s capacity to interact with environment effectively, leading to lags in skill acquisition and increasing
gaps between injured children and their peers.
Also may emerge relating to family stress and adjustment difficulties
Long term consequences depend on a complex interaction of numerous factors (including premorbid child abilities and socio-
emotional function, injury characteristics, environmental context, developmental stage and access to rehabilitation, as well as
factors yet to be identified.
Factors for recovery:
- Injury severity
- Age (some discuss that younger children recover faster, because their brain is more adaptable, but studies now show
that the developing brain may in fact be more vulnerable to early injury because of the potential for such insults to
disrupt neural and cognitive maturation.)
- Developmental level
Risk factors for injury and poor recovery:
- Disadvantaged background
- Pre-existing behavioural and developmental impairments
Additional risk factors:
- Post-injury parent and family stress
- Reduced or limited access to early intervention and support services
Epidemiology:
- Population estimates indicate that there are between 250 and 799 cases per 100000 per year variation across age
groups and sex.
- 80% with mild injuries
- Not seek treatment: 5-10% receive fatal injuries and 5-10% will temporary and/ or permanent neuropsychological
sequelae
Cause of injury:
- 50% of all childhood TBI are transportation- related accidents and falls causes.
- Infants and toddlers: falls and inflicted injuries because of child abuse
- Young children: falls and motor vehicle collisions, either as occupants or pedestrians
- Older children: sports and recreational accidents and pedestrian or bicycle collisions with motor vehicles
- Adolescents: motor vehicle collisions and competitive sports
Demographic characteristics:
- Age at injury:
Mortality and morbidity increase when age decrease (fatality rate 50% for children before 2 and 14% after 14)
- Sex:
Boys are at greater risk than girls, but the ratio changes with age. Under 2 it is almost the same, but school-aged males
are twice as likely as females to get TBI.
o Girls: more likely to sustain their injuries due to falls or as passengers in cars.
o Boys: range of possibilities
- Timing:
It is more likely to occur on weekends, holidays and afternoons (after school in leisure activities) because of reckless
behaviour or inadequate supervision. It is more common in families who are socially disadvantaged, unemployed or
emotionally disturbed (with poor parental neglect and poor supervision) and in children with pre-existing learning and
behavioural deficits.
2
, Neuropathology and pathophysiology:
TBI refers to a traumatic insult to the brain capable of producing damage and functional impairment. These traumatic insults are
usually caused by a physical blow or wound to the head that is sufficient to result in altered consciousness and may lead to
neurologic or neurobehavioral sequelae. TBI is leading to several consequences with specific factors:
- The force of impact
- The intracranial vectors of transmitted force (linear, rotational)
- The thickness of the scalp and skull
- The impact site
- The presence or absence of skull fracture
Closed head injury accounts for about 90% of all TBI. The brain is shaken within the skull cavity, resulting in diffuse axonal
damage and multiple injury sites, but with the skull remaining intact. It is mostly caused by motor vehicle accidents or falls from
height.
Initial pathology results from skull compression and deformation at the point of impact and includes contusion, or bruising, at the
point of the site of the blow and at other cerebral sites. There are areas of the brain that are particularly vulnerable to such
contusions, including basal frontal regions and temporal lobes, where severe surface damage may occur to cortical tissue and
blood vessels. The brain is shaken backwards and forwards and rotated, with the extent of this process driven by the force of the
impact, causing damage to cerebral areas opposite the site of damage (contracoup injuries) and shearing injuries to white matter
as nerve tracts are bent and torn.
The remaining 10% of injuries are made up of penetrating injuries, which involve penetration of the skull by some form of
‘missile’, usually a bullet, rock or knife. Cerebral pathology tends to be localised around the path of the missile, with tissue
destroyed in these areas. There is also risk of cerebral infection (from the alien object entering the brain), swelling, bleeding and
raised intracranial pressure. Neurobehavioral sequelae from penetrating head injury are more likely to include specific features
(e.g., aphasia), reflecting the focal nature of the lesion sustained, than is the case in closed head injury, with the more ‘hallmark’
information processing and executive deficits less pervasive. While these specific impairments may persist, there is an opportunity
to use intact abilities to develop compensatory strategies or ‘alternative routes’ for coping with cognitive demands.
While children are less likely to present with intracranial haematomas, they more frequently experience brain swelling, hypoxic–
ischaemic insult and diffuse injuries. Children have a greater head- to- body ratio, less myelination and greater relative proportion
of water content and cerebral blood volume than do adults.
Classification based on initial injury:
- Primary impact injuries occur as a direct result of the impact of force to the brain and include fractures, contusions
and lacerations and diffuse axonal damage – such injuries are generally permanent and show little response to early
treatment;
- Secondary injuries occur as a consequence of the primary injury. Raised intracranial pressure and brain swelling are
two major secondary complications that are particularly common in children (Kochanek, 2006), while hypoxia and
infection, as well as metabolic changes including hypothermia, electrolyte imbalance and respiratory difficulties, may
also occur.
o Are more predictive for poor outcome, but respond better to appropriate and timely medical intervention.
Cerebral oedema, or brain swelling, refers to an increase in fluid volume within the skull. In the context of TBI, it can occur either
due to a failure of the auto regulatory mechanism of cerebral blood flow due to hypoxia, hypercapnia or obstruction to cerebral
circulation or as a result of increased fluid within the brain associated with a range of possible causal factors, including obstruction
of cerebrospinal fluid flow, accumulation of fluid within cells, increased intravascular pressure or damage to blood vessels. It can
lead to intracranial pressure (surgery may be required)
While relatively uncommon in children, mass effects, caused by vascular interruptions, can lead to increased cerebral volume and
raised intracranial pressure. If not treated quickly, usually via surgical evacuation, these secondary complications may result in
cerebral herniation and ultimately death.
Epidural haematomas refer to bleeds just below the skull surface, above the dura. They do not directly involve brain tissue. They
mostly occur in the context of skull fracture, where vessels in the meninges are damaged. Subdural haematomas refer to blood
3
(2425-PSY3359)
Tasks, practical and lectures
,Inhoud
Task 1 ..................................................................................................................................................... 2
Questions for disucssion ................................................................................................................... 12
Lecture 1 Brain development ............................................................................................................ 17
Task 2 ................................................................................................................................................... 23
Questions for discussion: .............................................................................................................. 28
Lecture 2 Childhood TBI .................................................................................................................... 32
Task 3 ................................................................................................................................................... 35
Questions for discussion: .............................................................................................................. 43
Task 4 ................................................................................................................................................... 50
Questions for discussion: .............................................................................................................. 61
Lecture 3: ADHD: clinical picture, neurocognition and interventions .......................................... 69
Task 5 ................................................................................................................................................... 75
Questions for discussion: .............................................................................................................. 82
Practical................................................................................................................................................ 88
Lecture 4: Autism Spectrum Disorder.............................................................................................. 95
1
,Task 1
Anderson, V., Northam, E., & Wrennall, J. (2018). Developmental neuropsychology: a clinical approach. London:
Routledge. Chapter 9: Childhood traumatic brain injury
Childhood traumatic brain injury (TBI) is a frequent cause of interruption to normal development and may result in residual
impairments in a range of skills information processing, attention, memory, learning and social cognition. The treatment is long-
term and the neuropsychologist is multidimensional (monitoring neurobehavioral recovery, understanding the child’s strengths
and weaknesses in the context of current evidence, liaising with teachers and rehabilitation workers, designing cognitive
interventions and behaviour management programmes, providing counselling with respect to adjustment issues for the child and
family and informing parents and the wider community about the implications of the child’s injuries for daily functioning.
Deficits
May impact on child’s capacity to interact with environment effectively, leading to lags in skill acquisition and increasing
gaps between injured children and their peers.
Also may emerge relating to family stress and adjustment difficulties
Long term consequences depend on a complex interaction of numerous factors (including premorbid child abilities and socio-
emotional function, injury characteristics, environmental context, developmental stage and access to rehabilitation, as well as
factors yet to be identified.
Factors for recovery:
- Injury severity
- Age (some discuss that younger children recover faster, because their brain is more adaptable, but studies now show
that the developing brain may in fact be more vulnerable to early injury because of the potential for such insults to
disrupt neural and cognitive maturation.)
- Developmental level
Risk factors for injury and poor recovery:
- Disadvantaged background
- Pre-existing behavioural and developmental impairments
Additional risk factors:
- Post-injury parent and family stress
- Reduced or limited access to early intervention and support services
Epidemiology:
- Population estimates indicate that there are between 250 and 799 cases per 100000 per year variation across age
groups and sex.
- 80% with mild injuries
- Not seek treatment: 5-10% receive fatal injuries and 5-10% will temporary and/ or permanent neuropsychological
sequelae
Cause of injury:
- 50% of all childhood TBI are transportation- related accidents and falls causes.
- Infants and toddlers: falls and inflicted injuries because of child abuse
- Young children: falls and motor vehicle collisions, either as occupants or pedestrians
- Older children: sports and recreational accidents and pedestrian or bicycle collisions with motor vehicles
- Adolescents: motor vehicle collisions and competitive sports
Demographic characteristics:
- Age at injury:
Mortality and morbidity increase when age decrease (fatality rate 50% for children before 2 and 14% after 14)
- Sex:
Boys are at greater risk than girls, but the ratio changes with age. Under 2 it is almost the same, but school-aged males
are twice as likely as females to get TBI.
o Girls: more likely to sustain their injuries due to falls or as passengers in cars.
o Boys: range of possibilities
- Timing:
It is more likely to occur on weekends, holidays and afternoons (after school in leisure activities) because of reckless
behaviour or inadequate supervision. It is more common in families who are socially disadvantaged, unemployed or
emotionally disturbed (with poor parental neglect and poor supervision) and in children with pre-existing learning and
behavioural deficits.
2
, Neuropathology and pathophysiology:
TBI refers to a traumatic insult to the brain capable of producing damage and functional impairment. These traumatic insults are
usually caused by a physical blow or wound to the head that is sufficient to result in altered consciousness and may lead to
neurologic or neurobehavioral sequelae. TBI is leading to several consequences with specific factors:
- The force of impact
- The intracranial vectors of transmitted force (linear, rotational)
- The thickness of the scalp and skull
- The impact site
- The presence or absence of skull fracture
Closed head injury accounts for about 90% of all TBI. The brain is shaken within the skull cavity, resulting in diffuse axonal
damage and multiple injury sites, but with the skull remaining intact. It is mostly caused by motor vehicle accidents or falls from
height.
Initial pathology results from skull compression and deformation at the point of impact and includes contusion, or bruising, at the
point of the site of the blow and at other cerebral sites. There are areas of the brain that are particularly vulnerable to such
contusions, including basal frontal regions and temporal lobes, where severe surface damage may occur to cortical tissue and
blood vessels. The brain is shaken backwards and forwards and rotated, with the extent of this process driven by the force of the
impact, causing damage to cerebral areas opposite the site of damage (contracoup injuries) and shearing injuries to white matter
as nerve tracts are bent and torn.
The remaining 10% of injuries are made up of penetrating injuries, which involve penetration of the skull by some form of
‘missile’, usually a bullet, rock or knife. Cerebral pathology tends to be localised around the path of the missile, with tissue
destroyed in these areas. There is also risk of cerebral infection (from the alien object entering the brain), swelling, bleeding and
raised intracranial pressure. Neurobehavioral sequelae from penetrating head injury are more likely to include specific features
(e.g., aphasia), reflecting the focal nature of the lesion sustained, than is the case in closed head injury, with the more ‘hallmark’
information processing and executive deficits less pervasive. While these specific impairments may persist, there is an opportunity
to use intact abilities to develop compensatory strategies or ‘alternative routes’ for coping with cognitive demands.
While children are less likely to present with intracranial haematomas, they more frequently experience brain swelling, hypoxic–
ischaemic insult and diffuse injuries. Children have a greater head- to- body ratio, less myelination and greater relative proportion
of water content and cerebral blood volume than do adults.
Classification based on initial injury:
- Primary impact injuries occur as a direct result of the impact of force to the brain and include fractures, contusions
and lacerations and diffuse axonal damage – such injuries are generally permanent and show little response to early
treatment;
- Secondary injuries occur as a consequence of the primary injury. Raised intracranial pressure and brain swelling are
two major secondary complications that are particularly common in children (Kochanek, 2006), while hypoxia and
infection, as well as metabolic changes including hypothermia, electrolyte imbalance and respiratory difficulties, may
also occur.
o Are more predictive for poor outcome, but respond better to appropriate and timely medical intervention.
Cerebral oedema, or brain swelling, refers to an increase in fluid volume within the skull. In the context of TBI, it can occur either
due to a failure of the auto regulatory mechanism of cerebral blood flow due to hypoxia, hypercapnia or obstruction to cerebral
circulation or as a result of increased fluid within the brain associated with a range of possible causal factors, including obstruction
of cerebrospinal fluid flow, accumulation of fluid within cells, increased intravascular pressure or damage to blood vessels. It can
lead to intracranial pressure (surgery may be required)
While relatively uncommon in children, mass effects, caused by vascular interruptions, can lead to increased cerebral volume and
raised intracranial pressure. If not treated quickly, usually via surgical evacuation, these secondary complications may result in
cerebral herniation and ultimately death.
Epidural haematomas refer to bleeds just below the skull surface, above the dura. They do not directly involve brain tissue. They
mostly occur in the context of skull fracture, where vessels in the meninges are damaged. Subdural haematomas refer to blood
3
