1. Towards a Better Understanding
of
Early Atraumatic Brain Injury and its Treatment
Alan Challoner MA MChS

2. Towards a Better Understanding of Early Atraumatic Brain Injury
and its Treatment
OUTLINE
A General Introduction to Early Brain Injury 4
ATRAUMATIC OR NON-TRAUMATIC BRAIN INJURY 5
THE AFTERMATH OF CONVULSIONS 6
The Nature of Brain Injury 6
‘FIRST AID’ FOR BRAIN INJURIES 6
FOCAL IDENTITY IN THE FUNCTIONAL BRAIN 11
ASSESSMENT AND THE MORE RECENT CHANGES 11
DISORDERS OF THE HORMONE AND METABOLIC SYSTEMS 18
THE HORMONAL PROCESS 19
EFFECTS OF STRESS ON THE BRAIN 20
THE RESPONSE OF THE BODY'S REACTION TO STRESS 20
HOMEOSTASIS 21
PARASYMPATHETIC AND SYMPATHETIC NERVOUS SYSTEM 21
THE EMOTIONAL BRAIN: THE LIMBIC SYSTEM 22
Distress Signals from the Brain 22
Getting Back to Normal 22
Not All Stress is Bad 22
Stress Compromises the Blood-Brain Barrier 22
STRESS AND NOISE 23
Stress and Memory 23
CORTISOL AFFECTS MEMORY FORMATION AND RETRIEVAL 23
CORTISOL AND TEMPORARY MEMORY LOSS-STUDY 23
CORTISOL AND THE DEGENERATIVE CASCADE 24
CORTISOL AND BRAIN DEGENERATION 24
NUTRITION AND METABOLIC DISTURBANCES 24
Sleep and dreaming following Brain Injury 26
Information Processing 30
Executive Functioning 32
Memory 39
Direct effect of brain injury on emotion 46
Page 2 of 116

3. Ego Functions 54
Abnormal Brain Structure & Autism 56
INTRODUCTION 56
AETIOLOGY OF AUTISM SPECTRUM DISORDERS 57
AUTISM AND ITS TREATMENT 64
Management Following Early Brain Injury 68
EARLY MANAGEMENT 68
LONG-TERM MANAGEMENT 68
COGNITIVE PROBLEMS 69
PSYCHIATRIC INTERVENTION FOLLOWING EARLY BRAIN INJURY 72
Some of the Physical and Cognitive Difficulties Encountered
following Atraumatic Brain Damage 74
FEEDING AND SWALLOWING DIFFICULTIES 74
DYSPRAXIA AND NON-FLUENCY 75
PRAGMATIC SKILLS 76
LANGUAGE IN CHILDREN WITH EARLY BRAIN DAMAGE 76
PROBLEMS OF GAIT AND MOVEMENT 80
Types of Emotional, Behavioural, Psychiatric and Social
Problems Seen After Brain Injury in Children 84
Post-traumatic stress disorder 88
PTSD AND EMOTIONAL RESPONSES 91
Rational Drug Interventions 96
DIAGNOSIS AND TREATMENT 96
DRUG INTERVENTIONS 98
Possible Effects of Specific Cognitive Deficits on Behaviour
and Social Functioning 103
BEHAVIOUR MANAGEMENT 108
SPECIAL PROVISION 111
INTERVENTIONS WITH PARENTS 112
EDUCATION OF THE FAMILY AND OF THE CARERS 113
FAMILY COUNSELLING AND FAMILY THERAPY 113
Summary and Conclusions 113
Page 3 of 116

4. Towards a Better Understanding
of
Early atraumatic brain injury and its treatment
___________
A General Introduction to Early Brain Injury
Acquired brain injury is common and may follow traumatic and non- or atraumatic
insults. It has major individual patient and public health implications. Although
head trauma is the leading cause of an acquired brain injury, non-traumatic
injuries are also common. Importantly, the survival rate of children who have
suffered both types of brain injury continues to increase, in part reflecting the
improved (and still improving), acute and resuscitative medical and surgical
treatment given at the time of, and immediately following, the injury.
However, the survival of these children is clearly at some cost — to both the child
and their family — and this includes a corresponding increase in the morbidity rate,
in which children are often left with significant difficulties. These difficulties will
obviously range from mild to severe and may be transient or permanent. In
addition, children may have difficulties that are limited to just one area, or more
typically, the difficulties and their problems are multiple and complex and there will
be major implications for physical and educational (and, subsequently, career)
achievements and social interaction.
Paediatric traumatic brain injury is a major cause for concern when considering
both the number of children sustaining injuries and the large number of children
incurring life-long difficulties that impact on quality of life. Research is continuing to
investigate outcomes and predictors of recovery in both cognitive and
behavioural domains. Findings have contributed to better identification of children
at high risk for neurobehavioral difficulties. The challenge is to develop new
intervention programs to prevent or lessen the impact of such difficulties. 1
Some brain injuries have been caused by vaccines and generally that is the result
of the toxins in the vaccine passing the blood/brain barrier and causing sporadic
1
Catroppa, C. & Anderson, V.
‌ Neuro-developmental outcomes of
‌(2009)
pediatric traumatic brain injury. Future Neurology November 2009, Vol. 4, No. 6,
Pages 811-821.
Page 4 of 116

5. damage to the nerve cells of the brain. This process and some of its results have
been dealt with elsewhere.2
ATRAUMATIC OR NON-TRAUMATIC BRAIN INJURY
It is important to realize that brain damage can be caused by non-traumatic or
atraumatic brain injury (ABI). This may be almost as common as TBI.3 These injuries
may be caused by a number of different disorders and of those the ones that are
significant are:
• as a complication of meningitis or encephalitis;
• prolonged convulsive status epilepticus (when an epileptic convulsion
lasts more than 60 minutes)
• as a complication of some other toxic (e.g. alcohol, drug), metabolic or
biochemical impairment
These non-traumatic brain injuries are relatively common
When a nerve cell is injured or diseased, it may stop functioning and the circuits to
which it contributed will then be disrupted. Some circuits may eventually reac-
tivate as damaged cells resume functioning or alternative patterns involving
different cell populations take over. When a circuit loses a sufficiently great
number of neurons, the broken circuit can neither be reactivated nor replaced. In
general, when a human neuron dies, it is not replaced, except in the capacity of
the dentate gyrus of the human hippocampus to generate new neurons (Eriksson
et aI, 1998)4. Evidence of the generation of new neurons in response to injury or
disease is still lacking.
The experience at Alder Hey Hospital suggests that when one considers all causes
of atraumatic brain injury together, the incidence and prevalence of significant ABI
may be as high, or even higher, than TBI. This pattern seems to have been
emerging over the past couple of years. 5
A great deal of the research into early brain injury has been involved with TBI. Most
cases of ABI occur very early in a child’s life and therefore it is less easy to assess
what changes have taken place as a result of the injury, particularly as there will be
little or no pre-morbid history to take into consideration. That said, the results of
insults to the brain tissue will often have the same implications whether the origins of
the damage are ABI or TBI. The summary that follows will therefore include the
research into TBI and will use that similarity as a means to try and identify what the
2
Challoner, A. 2009. Brain Damage caused by Vaccination.
(http://www.scribd.com/oakwoodbank)
3
Appleton, R. & Baldwin, T. Management of Brain Injured Children. 2nd Ed.
OUP,2006.
4
Eriksson, P.S., Perfilieva, E., Bjork-Eriksson, T., et al. (1998). Neurogenesis in the
adult human hippocampus. Nature Medicine, 4, 1313-1317.
5
Appleton, R. et al. 2006 idem
Page 5 of 116

6. outcomes will be for those who suffer ABI. Where the research involved ABI
subjects then that can be seen to support this method of analysis.
THE AFTERMATH OF CONVULSIONS 6
There is an increased incidence of convulsions following head injury. Convulsions
can cause a rise in inter-cranial pressure (ICP) which may adversely affect cerebral
blood flow (CBF) and contribute to further neuronal damage.
Acute brain injury results in death of a variable number of brain cells, both neurons
and neural connective tissue. At this time, cellular energy metabolism can be
restored over a period as short as 30 minutes but cell swelling still occurs. In the
'latent' phase which follows, magnetic resonance spectroscopy may indicate
oxidative cerebral energy metabolism similar to normal, but the
electroencephalography (EEG) is depressed and CBF reduced.
It is believed that cellular ionic changes begin in the 'latent' phase and progress to
apoptosis (programmed cell death). The latent phase is followed by 'secondary'
deterioration after the acute event and manifests as delayed convulsions,
cytotoxic oedema, extracellular accumulation of potential cytotoxins such as
excitatory neurotransmitters, failure of oxidative metabolism and neuronal death.
There is damage to the blood-brain barrier with escape of water and plasma as
components of the oedema. This may already have been damaged in the first
phase of vaccine damage to the brain when the toxins pass into the brain.
Acute cell necrosis may result in the release of cellular ions, such as calcium, which
may induce vascular spasm of cerebrovascular smooth muscle. These ions may
damage other cells which were unaffected by the primary acute brain insult.
There are physical effects related to sluggish flow of blood in small blood vessels,
such as capillary sludging and platelet aggregation that may progress to critical
and irreversible ischaemia and cerebral infarction. The acute changes in this late
phase may take several days to resolve.
_______
The Nature of Brain Injury
Would that we could simply describe the results of brain
damage and say, "this is how it is.” But what we see, and
how we talk about it, is never based on pure, naive, veridical
perception; rather, it is inextricably bound to what we
already know, what we're looking for, what we're trying to
prove. Just as a proper appreciation of contemporary art
demands familiarity with the fashions and approaches of
earlier eras, so the study of brain damage is inseparable from
consideration of the hypotheses of earlier clinicians, the
categories and syndromes they devised and, lamentably, the
facts they distorted or overlooked. 7
‘FIRST AID’ FOR BRAIN INJURIES
6
Appleton, R. et al. 2006 idem
7
Gardner, H. The Shattered Mind: The person after brain damage. Routledge
& Kegan Paul, London, 1974.
Page 6 of 116

7. When brain cells die, whether from head trauma, stroke or disease, a substance
called glutamate floods the surrounding areas, overloading the cells in its path and
setting off a chain reaction that damages whole swathes of tissue. Glutamate is
always present in the brain, where it carries nerve impulses across the gaps
between cells; but when this chemical is released by damaged or dying brain cells,
the result is a flood that overexcites nearby cells and kills them.
A new method for ridding the brain of excess glutamate has been developed at
the Weizmann Institute of Science. This method takes a completely new approach
to the problem, compared with previous attempts based on drugs that must enter
the brain to prevent the deleterious action of glutamate. Many drugs, however,
can’t cross the blood-brain barrier into the brain, while other promising treatments
have proved ineffective in clinical trials.
Prof. Vivian Teichberg, of the Institute’s Neurobiology Department, working
together with Prof. Yoram Shapira and Dr. Alexander Zlotnik of the Soroka Medical
Center and Ben Gurion University of the Negev, has shown that in rats, an enzyme
in the blood can be activated to “mop up” toxic glutamate spills in the brain and
prevent much of the damage. This method may soon be entering clinical trials to
see if it can do the same for humans.
In the majority of cases, the extent of a learning difficulty resulting from a head or
other brain injury is related to the severity and nature of the head injury 8. For
instance, in a child whose brain injury has been complicated by severe cerebral
oedema (brain swelling) then blood and oxygen supply to the brain may be
severely compromised. This is often termed an 'hypoxic-ischaemic
encephalopathy', resulting in diffuse cerebral damage and on recovery, general
cognitive functioning can be impaired.
The mention of injury to the head or brain strikes a note of apprehension in most
people. Similarly, reports of any injury or debilitating tragedy to children arouse
widespread sympathy and feelings of indignation that the young should suffer in
any way. For the head-injured child, however, such public sympathy appears to
be rather short lived, despite persisting and long-term difficulties stemming from the
injuries. Head injury is never an all-or-nothing phenomenon, irrespective of the
cause; rather, it is a matter of degree, producing relative changes in brain structure
and function. Johnson et al make it evident that the notion of greater plasticity
and recovery of children who suffer head injury is not generally supported. 9
There is little age differentiation in the published reports on children's head injury: a
paediatric population may range from birth to 19 years of age 10 . This has
generated much confusion, especially in relation to evaluating outcome. Age
demarcates stages or periods of development which reflect the underlying
neurological substrate, although age alone is not a sufficient index 11 .
8
Levin, H. S., Benton, A. L., & Grossman R. G. (1982). Neurobehavioural
Consequences of a Closed Head Injury. Oxford: Oxford University Press.
9
Johnson, DA.; Uttley, D. & Wyke, M. (1989) Children’s Head Injury: Who
Cares? Taylor & Francis.
10
Ward, J.D. & Alberico, A.M. (1987) 'Paediatric head injuries', Brain Injury, 1, pp.
21-25
11
Jeffery, R. (1980) 'The developing brain and child development', in
WITTROCK, M.C. (ed.) The Brain and Psychology, New York, Academic Press.
Page 7 of 116

8. Consequently, head-injured children as a population may reasonably be expected
to show quite different, within-group responses to trauma, relative to their stage of
development 12.
Much of the early literature, especially neurosurgical and psychological, implies
that the younger child is less vulnerable and shows a greater recovery from head
injury than those who are older. There have been extensive methodological
criticisms of such work, however, which suggest that given adequate evaluations,
particularly of cognitive function, the young head-injured child does not show a
preferential recovery rate.
Relatively greater impairment appears in children younger than 8 years at the time
of injury, but there has been a general failure to institute longitudinal studies of
infants and toddlers with sufficiently sensitive outcome measures, and parallel
neuro-radiological confirmation. It appears that younger children may also be
more vulnerable to a wide range of secondary factors, including nutrition and
environmental stimulation.
Head injury to the child occurs in the context of development and incomplete
neurological maturation. Consequently, the general concepts of critical periods
and vulnerability are most pertinent to the younger child sustaining head-injury. It
remains speculative as to what extent normal development proceeds after head
injury but, given the greater vulnerability of immature neurones to insult and their
tendency for more rapid degeneration, it seems reasonable that normal
maturation must be at high risk in terms of either the sequence or rate of
development, or both. 13
The age at which a head injury occurs is therefore an important factor to be taken
into consideration. Infants may appear to recover but if the child has been very
severely brain-injured, then they may always require a great deal of intensive
support. Many assessment tools are not appropriate for very young children and
yet subtle deficits can be acquired in the informative years that may affect the
long-term potential.
Clearly, the question, 'does an early injury have a more serious effect on overall
mental development than a later one?', cannot be answered easily, as many
factors including the type of injury and size, extent and location of damage must
be considered, as well as the specific mental activity involved and its cognitive
complexity. It is within this context that complex skills may not be expected of
children in their formative years, and therefore deficits acquired early on may not
become apparent until much later in their lives.
It is very likely that aberrant development may result from secondary factors in the
recovery process, or from subsequent atrophy of damaged tissue. Secondary
neural degeneration in the head-injured child, for example, has not been widely
12
Luerssen, T.G., Klauber, M.R. & Marshall, L.F. (1988) 'Outcome from head
injury related to patient's age', Journal of Neurosurgery, 68, pp. 409-416.
13
Johnson, DA.; Uttley, D. & Wyke, M. (1989) Children’s Head Injury: Who
Cares? Taylor & Francis.
Page 8 of 116

9. reported 14, 15, 16, 17, , but this often arises even in the presence of relatively good
physical ability and appearance.
The Central Nervous System (CNS) possesses a finite adaptive capacity to
withstand the effects of any cerebral insult. Head injury reduces that capacity
and, with increasing severity of trauma and subsequent atrophy, the remaining
capacity of the CNS to adapt to any further neurological insult becomes relatively
limited. With a decline in capacity, new signs and symptoms may appear as
critical thresholds are reached.
As brain development results from complex interactions between genetic and
environmental factors, it seems reasonable to suggest that the young head-injured
child may be in greater need of early rehabilitation than his adult counterpart.
Rehabilitation must aim to facilitate as normal a pattern of development as
possible, hence the need for follow-ups throughout the period of the child's
remaining development.18 Similarly, there must be a development of inter-
disciplinary rehabilitation facilities specifically for the head-injured child, incor-
porating neurological, educational and social factors. Rehabilitation must
become more scientifically based and practised in a coherent and neurologically
meaningful way, rather than the haphazard, inconsistent guesswork which
characterizes rehabilitation in the UK.
When someone is injured it is assumed by both public and doctors that the best
treatment is provided, based on sound knowledge of the patho-physiological
response to trauma 19. Recent reports challenge this complacency 20. The system
of such care would be of far greater practical importance that any of its
constituent parts.
Trauma to the brain exerts perhaps the highest toll among all injuries, simply
because it may dramatically alter the quality of future life for its survivors and their
14
Lange-Cosack, H., Wider, B., Schlfsner, H.J., Frumme, T. & Kubicki, S. (1979)
'Prognosis of brain injuries in young children (1 until 5 years of age)" Neuropaediatrie,
10, pp. 105-127.
15
Cullum, C.M. & Bigler, E.D. (1985) 'Late effects of haematoma on brain
morphology and memory in closed head injury', International Journal of
Neurosdenu, 28, pp. 279-283.
16
Jellinger, K. (1983) 'The neuropathology of paediatric head injury', in
SHAPIRO, K. (ed.) Paediatric Head Traurna, New York, Futura.
17
Mortimer, J.A. & Pirozzolo, F.J. (1985) Remote effects of head trauma,
Developmental Neuropsychology, 1, pp. 215-229.
18
Kaiser, G., Rudeberg, L., Fankhauser, L. & Zumbuhl, C. (1986) 'Rehabilitation
medicine following severe head injury in infants and children', in Raimondi, A.J.,
Choux, M. & DiRocco, C. (eds.) Head Injury in the Newborn and Infant, New York,
Springer.
19
Yates, D.W. (1988) 'Action for accident victims', British Medical Journal, 297,
pp. 1419-1420.
20
Cummins, B. (1987) 'A head injury polemic', British Journal of Neurosurgery, 1, pp. 6-8.
Page 9 of 116

10. families 21, 22, 23 . Nonetheless society continually fails to see the full implications of
disability resulting from head injury in childhood 24 including increased educational
support, lost or diminished careers, poor social and emotional adjustment, and
later demands on mental health services.
The long-term effects of a brain injury on a child can therefore depend upon the
age at which the injury occurs and problems may not always be evident from the
early stages. Unlike adults, children's brains develop rapidly both in size and
complexity through the childhood years and into adolescence.
Neurodevelopment is not uniform through the brain at anyone time, and areas,
particularly those in the frontal lobes, do not become fully operational until
adolescence and early adulthood. Making a positive long-term prognosis from
what may appear a rapidly sound recovery can therefore be misleading. More
subtle deficits, particularly those affecting frontal lobe functioning, may not
become apparent until many years later.
For a substantial number of years, there has been a strong belief that recovery from
head injury is better in children than adults, due to what has been termed 'cerebral
plasticity', that is, damaged skills being compensated for by areas of the brain that
are not affected, and are able to take over the function of the damaged areas, at
least to some degree. However, this is often not the case, and children who have
a very early ABI can often have a poorer prognosis than had they sustained a
somewhat similar injury as an older child or adult. Goodman 25 argued that there
were limits to cerebral plasticity.
Generally, research has indicated that ABI has more significant effect on the
cognitive skills of young children. Typically, it is thought that children younger than
seven or eight years do not improve in intellectual functioning in the same way that
older children and adults do 26, 27 .
Brain functioning and development occur rapidly during a child's life. The period of
most rapid development occurs within the first couple of years of life, but it remains
incomplete well into the teenage years, and final myelinisation 28 does not occur
21
Shapiro, K. (1985) 'Head injury in children', in Becker, D.P. & Povlishock, J.T.
(eds.) Central Nervous System Traurna Status Report, Maryland, NIH.
22
Lezak, M.D. (1988) 'Brain damage is a family affair', Journal of Clinical and
Experimental Neuropsychology, 10, pp. 111-123.
23
Waaland, P.K. & Kreutzer, J.S. (1988) 'Family responses to childhood brain
injury', Journal of Head Trauma Rehabilitation, 3, pp.51-63.
24
Haas, J.F., Cope, D.N. & Hall, K. (1987) 'Premorbid prevalence of poor
academic performance in severe head injury', Journal of Neurology, Neurosurgery
and Psychiatry, 50, pp. 52-56.
25
Goodman, R. (1989). Limits to cerebral plasticity. In: Children's Head Injury:
Who Cares (eds. D. A. Johnson, D. Uttley & M. Wyke). London: Taylor and Francis.
26
Stiles J. (2002). Neural plasticity and cognitive development. Developmental
Neuropsychology, 18,237-72.
27
Stiles, J., Reilly, J., Paul, B., & Moses, P. (2005). Cognitive development
following early brain injury: evidence for neural adaptation. Trends in Cognitive
Sciences. 9, 136-43.
28
Myelinisation. The change or maturation of certain nerve cells whereby a
layer of myelin forms around the axons which allows the nerve impulses to travel
faster.
Page 10 of 116

11. until adolescence.
There is a sequential pattern of myelinisation, with the frontal lobes being the final
areas to mature, usually with the onset of adolescence. The later implications that
early impairment to the frontal lobes can have on the social, behavioural and
cognitive functioning of children in their later years is given in two case studies
reported by Williams and Mateer 29.
In very recent years, neuro-imaging research has yielded important information
concerning the structure, neurochemistry, and function of the amygdala, medial
prefrontal cortex, and hippocampus in posttraumatic stress disorder (PTSD). A
review of neuro-imaging research reveals heightened amygdala responsivity in
PTSD during symptomatic states and during the processing of trauma-unrelated
affective information. Importantly, amygdala responsivity is positively associated
with symptom severity in PTSD. In contrast, medial prefrontal cortex appears to be
volumetrically smaller and is hypo-responsive during symptomatic states and the
performance of emotional cognitive tasks in PTSD. Medial prefrontal cortex
responsivity is inversely associated with PTSD symptom severity. The reviewed
research suggests diminished volumes, neuronal integrity, and functional integrity of
the hippocampus in PTSD. 30 (See PTSD below, p85)
FOCAL IDENTITY IN THE FUNCTIONAL BRAIN
Thought and knowledge about the localization of mental functions in the human
brain have a long and complicated history and are still evolving. There has been
uncertainty about what the concept means, debate about where localization
takes place and even denial that it exists. Ideas about cerebral localization have
been determined primarily by the knowledge of brain anatomy existing at a
particular time and by the availability of techniques for disclosing the presence
and locus of brain lesions. They have also been influenced by concepts of the
nature of disease and the prevailing state of psychological analysis. 31
ASSESSMENT AND THE MORE RECENT CHANGES
It is often only in a neuropsychological assessment that the underlying deficits of
children who have sustained a brain injury become apparent. Deficits in many
cases are not global, especially in the milder cases 32 although subtle deficits do
remain and can affect academic performance 33 where they may be
29
Williams, D. & Mateer, C. (1992). Developmental impact of frontal lobe injury
in middle childhood. Brain and Cognition 20,196-204.
30
Shin, Lisa M.; Rauch, Scott L. & Pitman, Roger K. Amygdala, Medial Prefrontal
Cortex, and Hippocampal Function in PTSD. Ann. N.Y. Acad. Sci. 1071: 67–79; 2006.
31
Benton, A. (2000). Historical aspects of cerebral localization. In Localization
of Brain Lesions and Developmental Functions, D. Riva & A. Benton (eds.); John
Libbey & Company Ltd, pp. 1-14.
32
Bawden, H. N., Knights, R. M., & Winogron, H. W. (1985). Speeded-
performance head injury in children. Journal of Clinical Neuropsychology 7, 39-54.
33
Wrightson, P., McGinn, V., & Gronwall, D. (1995). Mild head injury in pre-
school children - evidence that can be associated with a persisting cognitive
defect. Journal of Neurology Neurosurgery and Psychiatry 59, 375-80.
Page 11 of 116

12. misinterpreted or overlooked. Most neuropsychological assessments have an
intelligence test as their core. However, the concept of intelligence tests
(intelligence quotients [IQ]) is, in many respects, outdated as suggested by Lezak 34
and certainly these tests must be used with caution when making any assumptions
about the brain injured child. Tests of 'intelligence' may be useful as indicators of
levels of functioning and can be used as a basis from which further assessments
can be undertaken, but a screening test in which a broader and more detailed
neuropsychological assessment can take place will be essential and will provide a
better understanding of the injury.
Possibly the best source of general information about neuropsychological
assessments is to be found in Lezak 35, although in recent years, a range of
neuropsychological tests have been developed for use in children. These tend to
be rarely used in their totality and, indeed, concern has been expressed that many
of the sub-tests are not specific in detecting distinct neuropsychological processes,
but rather 'g' or general cognitive ability. In addition, following ABI, sub-tests
requiring more fluid performance tend to be depressed greater than those
comprising what are termed 'crystallized skills', that is, verbal abilities. During the
recovery phase, the discrepancy between these quotients generally decreases,
and although there are a number of reasons why this may occur, it tends to
indicate a general recovery. It can, of course, relate to the heavy practice effects
that are possible from repeated testing, and care therefore needs to be exercised
when gauging improvement through changes in test results. The tests themselves
do not always measure what they intend to measure and may be significantly
affected by other factors.
Lezak comments:
“IQ refers to a derived score used in many test batteries designed to measure a
hypothesized general ability — intelligence. Because of the multiplicity of cognitive
functions assessed in these batteries, IQ scores are not useful in describing cognitive
test performances. IQ scores obtained from such tests represent a composite of
performances on different kinds of items, on different items in the same tests when
administered at different levels of difficulty, on different items in different editions of
test batteries bearing the same name, or on different batteries contributing different
kinds of items. If nothing else, the variability in sources from which the scores are
derived should lead to serious questioning of their meaningfulness.
In neuropsychological assessment in particular, IQ scores are often unreliable
indices of neuropathic deterioration. Specific defects restricted to certain test
modalities, for example, may give a totally erroneous impression of significant
intellectual impairment when actually many cognitive functions may be relatively
intact and lower total scores are a reflection of impairment of specific functional
modalities. Conversely, IQs may obscure selective defects in specific tests .
In fact, any derived score based on a combination of scores from two or more
measures of different abilities results in loss of data. Should the levels of
performance for the combined measures differ, the composite score-which will be
somewhere between the highest and the lowest of the combined measures-will be
misleading. Averaged scores on a Weschler Intelligence Scale battery provide just
34
Lezak, M. D. (1988). IQ. R.I.P. journal of Clinical and Experimental
Neuropsychology 10, 351-61.
35
Lezak, M. D. (2004). Neuropsychological Assessment (4th edn). Oxford:
Oxford University Press.
Page 12 of 116

13. about as much information as do averaged scores on a school report card. In the
same way, it is impossible to predict specific disabilities and areas of competency or
dysfunction from averaged ability test scores (e.g., "IQ" scores). Thus composite
scores of any kind have no place in neuropsychological assessment.
In sum, "IQ", as a score, is inherently meaningless and not infrequently misleading as
well. "IQ" — whether concept, score, or catchword-has outlived whatever
usefulness it may once have had and should be discarded.” (idem)
Both the Weschler Intelligence Scale for Children (WISC) and the Weschler Pre-
School and Primary Scale of Intelligence (WIPPSI) have been replaced by new and
updated versions. The third edition of the WIPPSI provides a much-needed update
of the original WIPPSI which was last revised in 1989. In addition to the material
being updated and made more contemporary and appealing to children, the
tests have been extensively revised. As well as providing the original cognitive
domains of verbal IQ, performance IQ and a full-scale IQ, it now provides further
analysis of the updated and additional sub-tests to provide a global language
score, a processing speed quotient, and a general language composite score, in
addition to the original cognitive domains. It is suitable for children from the age of
two years, six months to seven years, three months.
The WISC Ill-UK has now been superseded by the new WISC IV-UK. This updated
version provides a broadly similar assessment of general ability; however, it also
incorporates significant revisions that include updated normative data, new sub-
tests and an increased emphasis on composite scores which assess more discrete
domains of cognitive functioning. In total, there are now 15 sub-tests available, but
once more, the general test framework evaluates the four original composite
indexes of verbal comprehension, perceptual reasoning, working memory and
processing speed.
The WISC IV is linked to the Wechsler Individual Achievement Test (second edition)
which provides a comprehensive measure of academic achievements in a
number of principal domains. The test can therefore be used to provide a
predictive score and actual score, thereby indicating the extent to which a child
may be under-functioning in a particular attribute. The child's basic educational
attainments and other core attributes can therefore be judged in comparison with
their general level of intellectual ability using the newer versions of Weschler
Objective Numerical Dimensions (WOND) and Weschler Objective Reading
Dimensions (WORD).
The basis of any treatment programme must also take into account the wider
range of neuropsychological deficits in children as these will influence the learning
style and specific learning difficulties. The assessment of brain-injured children may
therefore be more appropriately addressed using a hypothesis testing and problem
solving approach looking at functional deficits. Until recently, there was a very
limited range of neuropsychological tests available for children. These were well
described by Strauss and Spreen 36. Unfortunately, many of the tests had been
devised for adults and although normative data are available for children, they
tended to be derived from very small samples, and the tests themselves may not
hold an inherent interest for children.
36
Strauss, E. & Spreen, O. (1991). A Compendium of Neuropsychological Tests.
Oxford: Oxford University Press.
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14. A number of assessment instruments have become available since 1988. These not
only provide a broader overview of a child's level of functioning, but in many
respects provide very valid and functional assessments for the child, which can
form the basis of an assessment upon which further neuropsychological testing can
be carried out as part of an overall rehabilitation teaching strategy. Although a
child's limitations can be obvious, sometimes they can be more subtle and missed.
A number of general developmental scales have been used in this respect, the
Vineland Social Adaptive Scales being the most notable (Sparrow et al) 37 and
these can provide a detailed overview of a child's functional capabilities in a
number of domains.
The new Adaptive Behaviour Assessment System (ABAS) was published in two
versions in 2000; one questionnaire being completed by the parents, and the other
by the child's teachers. It provides a diagnostic assessment of the child who has
difficulties with daily living skills and is therefore more functionally oriented.
According to the manual, it provides a comprehensive diagnostic assessment for
very young people with a variety of disabilities, disorders and health problems and
also provides a basis upon which a rehabilitation programme can be focused. It is
unfortunate that a number of the questions are American and to date there is no
'anglicized' version.
It does, however, provide a standardized score which can be used in comparison
with other intellectual measures, in addition to providing a profile of 'strengths and
weakness'. The age range is also practical (5-21 years), and can therefore provide
many years of assessment continuity.
During 2004, a number of neuropsychological tests specifically devised for children
became available, with the Developmental Neuropsychological Assessment
('NEPSY') being one example. This test is not often cited in the literature, but is useful
in that it evaluates a range of neuropsychological functioning that provides useful
insight into a child's neuropsychological status.
The NEPSY is most probably the most unique test for children, because it has been
specifically devised for the 3-12 years age range. It provides assessment of six
complex cognitive functions:
• attention;
• executive functioning;
• language;
• sensory motor functioning;
• visual-spatial processing;
• memory and learning.
One of its primary aims is to provide a comprehensive assessment of the
neuropsychological status of children with a range of difficulties. Consequently, it
37
Sparrow, S., Balla, D., & Cichetti, D. V. (1984). Vineland Adaptive Behaviour
Scales. Minnesota: American Guidance Service Inc.
Page 14 of 116

15. is, for example, used for children who have cerebral palsy, epilepsy, hydrocephalus
or traumatic brain injury.
A number of sub-tests in the NEPSY are of particular value when assessing
functional problems that may occur following a head injury. For instance, children
can sometimes be left with an extremely short verbal memory. Simple tests such as
'sentence repetition' can reveal the very real problems a child can have when
they are unable to retain sentences of increasing length and complexity; for
example, asking a child to, 'finish their work, put the book on the table, the pencil in
the drawer and line up by the door', is pointless if the child can only retain one
instruction at a time. It is therefore extremely useful to provide some normalized
information in order to provide an objective assessment.
When considering the effects of an acquired brain injury, it must be acknowledged
that neuropsychological assessments offer only moderate correlations with
everyday functioning, and this is particularly relevant when providing
neuropsychological reports that include comments on prognosis. It is essential that
ecologically valid information is obtained and that very careful consideration is
given with regard to the child's pre-injury status; the level of support that the child
has received following the injury, including educational support; parental
expectations and attitude etc.
These issues are well discussed by Silver 38, who examined the multiple issues that
exist when trying to predict functioning following traumatic brain injury (TBI) in day-
to-day, real-life situations, and especially when having to consider developmental
factors and the intervening variables that may increase or decrease the child's
adaptive functioning over the course of recovery. Ylvisaker and Gioia 39 pointed
out that children with TBI may perform poorly on unfamiliar or unappealing tests,
whereas functioning in the real world with a familiar routine may exceed
expectations suggested by these more formal test results. Cripe 40 emphasized the
necessity for using observations or check-lists and that rating scales are needed in
order to provide some valid appraisal of the child's functioning in the real world.
A further point to consider is the rehabilitation of adults and how well
neuropsychological assessments relate to outcomes. Leahy and Lam 41 examined
the relationship between performance and neuropsychological measures, and the
vocational and independent living functioning of individuals following TBI. They
reported that the correlations were generally poor, with only the intelligence test
and colour and word test scores differentiating individuals who did or did not
require assistance with activities of daily living.
Whereas neuropsychological assessments are extremely important in assessing
38
Silver, C. H. (2000). Ecological validity of neuropsychological assessment in
childhood traumatic brain injury. Journal of Head Trauma Rehabilitation 15,973-88.
39
Ylvisaker, M. & Gioia, G. A. (1998). Cognitive assessment. In: Traumatic Brain
Injury Rehabilitation: Children and Adolescents. 2nd edn. (ed. M. Ylvisaker), pp.
159-79. Boston: Butterworth-Heinemann.
40
Cripe, L. I. (1996). The ecological validity of executive function testing. In:
Ecological Validity of Neuropsychological Testing (eds F. R. Sbordone & C. J. Long),
pp. 171-202. Delray Beach, FL: GR Press/St. Lucie.
41
Leahy, B. J. & Lam, C. S. (1998). Neuropsychological testing and functional
outcome for individuals with traumatic brain injury. Brain Injury 12, 1025-35
Page 15 of 116

16. children's abilities along a number of dimensions and in helping to plan
remediation strategies, the translation between test scores and the skills required in
everyday life in the child's real environment must be made with caution. When
devising therapeutic and rehabilitative packages, great care must be taken
regarding making long-term predictions from test results that, at present, would
appear to be relatively poor predictors of long-term outcome; a much broader
based assessment of a child's functioning, taking all factors into consideration, is
essential before making important statements that may have very long-term
implications to a child's future needs (Rivara et al.) 42.
A broad-based assessment is therefore needed to provide an overall profile of the
child's deficits. Some of this information may be derived from specific tests, but
valuable information can be derived from detailed observation of the child in
normal situations. A comprehensive neuropsychological evaluation should
therefore sample the following range of attributes which may or may not have
been provided by other professionals:
1. A consideration of the child's sensory and motor functioning; this includes
vision and hearing including auditory perception, visual acuity and visual
fields and depth perception. Whereas these will usually have been com-
pleted by the relevant medical personnel, their functional implications are
not always evaluated in the child's normal environment.
2. The child's physical skills need to be considered. At a fine motor level this
includes an assessment of the child's functional living skills including dressing,
feeding and, of course, writing skills - including their speed of writing.
Evaluation of the child's gross motor skills includes the child's functional
mobility within the home and school, and their ability to take part in
recreational sports.
3. An assessment of the child's overall intellectual functioning using a
standardized assessment. This would usually include an assessment to profile
the child's skills, assessing areas of comparative strengths and weaknesses.
4. An evaluation of the child's ability to solve problems in real-life situations and
make reasonable judgements given the information that would be
available to them.
5. An examination of the child's ability to think flexibly, that is, their ability to
cope with changing situations and problems. Problems with mental flexibility
can reveal themselves both in coping with specific academic skills and also
day-to-day living skills.
6. Memory can often be impaired following a brain injury and many tests of
short- and longer-term verbal, auditory and visual memory are available.
However, some formal assessment of the child's functional memory is
needed.
42
Rivara, J. B., Jaffe, K. M., Fay, G. C., Polissar, N. L., Martin, K. M., Shurtleff, H.
A., & Liao, S. (1993). Family functioning and injury severity as predictors of child
functioning one year following traumatic brain injury. Archives of Physical Medicine
and Rehabilitation, 74, 1047-55.
Page 16 of 116

17. 7. In order to organize them in day-today living, it is necessary to assess the
child's ability. Deficits in this skill can often be masked in children because
parents usually fulfil the role for many years. It is only usually following their
transfer to secondary school, that these deficits become manifest.
8. An assessment of the child's basic educational skills is essential; this includes
not only reading accuracy and spelling skills, but also the child's reading
comprehension, as frequently it is their comprehension skills that are
impaired following a brain injury. Mathematical skills are also commonly
impaired, because of difficulties in mental processing.
9. Some assessment is required of the child's ability to process information
efficiently and quickly. The brain-injured child may have difficulties in the
rate at which they can process many tasks. The full extent of these difficul-
ties can be judged at a functional level when comparing their performance
with that of their peers.
10. It is important to make some assessment of the child's ability to learn from
their environment; although testing a child's ability to learn in a structured
setting or teaching situation is important, it must be remembered that a
great deal of information and skills will be learned incidentally from their
day-to-day living.
11. Communication is a crucial skill which can frequently be impaired following
a brain injury. Within the expressive (language) domain, it is necessary to
assess the child's functional communications skills, including intelligibility of
speech, pragmatics and word finding. Within the area of receptive
language, there is a need to evaluate their ability to understand short
instructions and longer, more complex conversation.
12. Some estimation should be made of the child's stamina. Fatigue is a com-
mon problem following a brain injury, particularly in first few weeks and
months, and whereas a child may be capable of several hours of home
tuition, they may not have the ability to cope with the rigours and demands
of a full or even half a school day.
13. Emotional lability is common, and it is necessary to assess the child's ability to
cope with the ups and downs of everyday life, including the frustration often
encountered in the classroom and other learning situations.
14. The child's ability to make valid and appropriate social judgements relating
to the behaviour and intentions of others is often overlooked, and if
impaired can result in behavioural difficulties and a diminished quality of life
for the child. 43
There is no one overall test or method of assessment that can evaluate all these
aspects of functioning. Indeed, in some cases, tests are not appropriate. Given
the rapid progress some children can make, the timing of any formal assessment
can be variable and, in the early stages, assessments may best be done in the
form of structured observations, although some detailed assessments will be
43
Appleton, R.; Baldwin, T. Management of Brain Injured Children. 2nd Ed.
OUP,2006.
Page 17 of 116

18. required at some stage.
With the rapid development of neuropsychological tests that are available for
children, the question arises as to the nature of any assessment, and the
appropriateness of administering battery after battery of test with the aim of
identifying some deficits. This is not only wasting time, but it can put the child
through a stressful experience. 44 It has been assumed that a fixed battery of
assessments provides an assessment of all the relevant neuropsychological
domains (Lezak) 45, but, of course, this is far from true. With the wide variety of tests
that are now available and suitable for children, it is not possible or appropriate to
give serial assessments. It can also add little to our knowledge of the child. Excess
testing can often lead to fatigue and poor test performance (Strauss 46). The
assessment of children's disabilities should therefore follow a hypothesis-testing
approach. 47
This has long been advocated within educational psychology, but more recently
eloquently explained in the book School Neuropsychology (Hale and Fiorello 2004
48
). Clearly, some form of basic assessment is required in the first instance, but a
considerable amount of information should be gathered relating the child's
functioning in the real world from which it is possible to draw inferences about their
neuropsychological functioning and areas of likely deficit. (Appleton, R. et al 2006
idem.)
Using a hypothesis-testing approach, the amount of testing can be limited and
focused on areas where deficits are identified. This obviously needs knowledge of
the tests and an understanding of neuropsychology. Of course, the danger of
such an approach is to risk a confirmation bias, that is, to seek only information that
supports one's hypothesis. It is therefore necessary not to avoid information that
may be contradictory to one's hypothesis, nor indeed to be over-restrictive in the
gathering of information, but to look for supporting evidence from a number of
sources.
It must be recalled that ecological validity should be the main goal of an
assessment, but it is not relevant just to describe a child's neuropsychological
functioning, but rather this should lead on to a positive intervention strategy,
generating a working hypothesis by which a teaching strategy can then evolve.
Changes can then be appropriately assessed, preferably using some form of
objective measure to evaluate whether or not the teaching strategies are
appropriate, as again it is the functional outcome which is especially important.
For these reasons, a hypothesis-testing approach has far more relevance, providing
it follows the cardinal rules of objectivity. A number of tests are now available and
suitable for children, many with well-produced norms, and there may be
considerable overlap in the periods of neuropsychological functioning they are
44
idem
45
Lezak, M. D. (2004). Neuropsychological Assessment (4th edn). Oxford: Oxford
University Press.
46
Strauss, E. & Spreen, O. (1991). A Compendium of Neuropsychological Tests.
Oxford: Oxford University Press.
47
Appleton, R et al 2006 idem.
48
Hale, J. B & Fiorello, C. A. (2004). School Neuropsychology. Guildford: Guildford
Press.
Page 18 of 116

19. assessing. It must be appreciated that in the case of ABI, multiple areas of
functioning may or will have been affected, and a number of hypotheses would
therefore have to be generated and then evaluated. Information should be
sought from a number of different sources and it is often necessary to provide a
preferred hierarchy of intervention, depending upon the particular needs of the
child, so that subsequent stages of action can take place.
It is essential that all members of those working with a child, including the family,
should have a consistent approach to the child. When the child is disoriented, they
should say who they are, and what they are doing, talking them through all
movements, clearly, calmly and positively. If the child is being taught, then they
are told where and why, being careful not to overload them with information
which may be too much for them to process. It is essential to keep all instructions
simple.
DISORDERS OF THE HORMONE AND METABOLIC SYSTEMS
It is important that there is an understanding that those with the type of brain injury
caused by vaccines may be particularly prone to disorders of the hormone and
metabolic systems. They may also have a lack of capacity to rationalise fear and
anxiety whether real or imagined or perhaps as a result of dreams. [See Cortisol
and Dreams below, p27]
If these failings of the system are looked upon as mental illness then there is a grave
risk of causing more harm through inappropriate medication. Such medication will
not only fail to solve the problems but it will exacerbate the original condition by
causing more damage to the system.
The Hormonal Process — Normally, cortisol levels rise during the early
morning hours and are highest about 7 am, so giving the energy that is needed to
begin the day. In the evening and during the early phase of sleep the cortisol level
should drop by approximately 90%. Evening is generally the time when the stresses
of the day are behind you, the time when you can relax and unwind.
For those who are constantly under stress, the cortisol level can remain elevated
over long periods of time. Research now correlates chronically elevated levels of
cortisol with blood sugar problems, fat accumulation, compromised immune
function, exhaustion, bone loss, and even heart disease. Memory loss has also
been associated with high cortisol levels. Continual stress can indeed have a
negative impact on our health.
An additional problem of long-term elevations of cortisol is that the adrenal gland
may wear itself out and no longer be able to produce even normal levels of
cortisol. This is called "adrenal exhaustion" and is associated with many other
health problems.
Besides impacting the immune system, fertility, and bone health, the list of the risks
of high cortisol levels grows longer. New studies demonstrate that elevated cortisol
levels can lead to abdominal weight gain, loss of verbal declarative memory (see
Memory below, p39) words, names, and numbers), insulin resistance, and Type 2
Diabetes.
Page 19 of 116

20. Increasing scientific evidence suggests that prolonged psychological stress takes its
toll on the body, but the exact mechanisms by which stress influences disease
processes have remained elusive. Now, scientists report that psychological stress
may exact its toll, at least in part, by affecting molecules believed to play a key
role in cellular aging and, possibly, disease development.
In this study 49, the UCSF-led team determined that chronic stress, and the
perception of life stress, each had a significant impact on three biological factors
— the length of telomeres, the activity of telomerase, and levels of oxidative stress
— in immune system cells known as peripheral blood mononucleocytes, in healthy
premenopausal women.
Telomeres are DNA-protein complexes that cap the ends of chromosomes and
promote genetic stability. Each time a cell divides, a portion of telomeric DNA
dwindles away, and after many rounds of cell division, so much telomeric DNA has
diminished that the aged cell stops dividing. Thus, telomeres play a critical role in
determining the number of times a cell divides, its health, and its life span. These
factors, in turn, affect the health of the tissues that cells form. Telomerase is an
enzyme that replenishes a portion of telomeres with each round of cell division,
and protects telomeres. Oxidative stress, which causes DNA damage, has been
shown to hasten the shortening of telomeres in cell culture.
"Numerous studies have solidly demonstrated a link between chronic psychological
stress and indices of impaired health, including cardiovascular disease and
weakened immune function," says lead author Elissa Epel, an assistant professor of
psychiatry. "The new findings suggest a cellular mechanism for how chronic stress
may cause premature onset of disease. Anecdotal evidence and scientific
evidence has have suggested that chronic stress can take years off your life; the
implications of this study are that this is true at the cellular level. Chronic stress
appears to have the potential to shorten the life of cells, at least immune cells."
Sweeping changes are needed in the organisation and ethos of the NHS’s
dedicated inpatient facilities and care homes for people with learning disabilities,
the health watchdog for England has said. Care at NHS facilities for people with
learning disabilities falls short of modern safety and quality standards, says the
Healthcare Commission in a new report, and many people live in bleak
accommodation far away from their families. 50
Institutional failings mean that many people are being deprived of their human
rights and dignity and have little access to advocacy services, few choices about
how they live their lives, and limited activities, the report says. Services are too
reliant on drug treatment to control behaviour, it says, when the evidence that this
is a reasonable response is limited.
Effects of Stress on the Brain — there is a need for providers and carers to
understanding about how stress is generated. For everyone, those aggravating
things that go wrong in the day and those irritating things that go bump in the night
49
Blackburn, Elizabeth; Herzstein, Morris & Epel, Elissa. Psychological stress and
disease. Proceedings of the National Academy of Sciences. 30 November 2004.
50
Zosia Kmietowicz. People with learning disabilities are being let down by
NHS. BMJ 2007;335:1177 (8 December)
Page 20 of 116

21. — disrupting routines and interrupting sleep — all have a cumulative effect on the
brain, especially its ability to remember and learn.
As science gains greater insight into the consequences of stress on the brain, the
picture that emerges is not a pretty one. A chronic overreaction to stress overloads
the brain with powerful hormones that are intended only for short-term duty in
emergency situations. Their cumulative effect damages and kills brain cells.
The Response of the Body's Reaction to Stress — This is sometimes
referred to as General Adaptation Syndrome (GAS). When a person experiences
stress, the brain responds by initiating 1,400 different responses including the
transmission of a variety of chemicals to our blood stream. This gives momentary
boost to do whatever needs to be done to survive. Hormones rush to the adrenal
glands to suppress the streaming cortisol on its way to the brain. Other hormones
rush to the brain to round up all the remnants of cortisol that made it to the
hippocampus. These hormones escort the cortisol remnants back to the kidneys
and then on to the bladder. The body at this stage has reached metabolic
equilibrium, also known as homeostasis. (see below p21)
There are three stages to GAS. In the first stage — called alarm reaction, the body
releases adrenaline and a variety of other psychological mechanisms to combat
the stress and to stay in control. This is called fight or flight response. The muscles
tense, the heart beats faster, breathing and perspiration increase, the eyes dilate,
the stomach may clench. This happens as a natural process in order to protect
you in case something bad happens. Once the cause of the stress is removed, the
body will go back to normal. If the cause for the stress is not removed, go to a
second stage called resistance or adaptation. This is the body's response and
provides long term protection. It causes the secretion of more hormones that
increase blood sugar levels to sustain energy and raise blood pressure. The adrenal
cortex (outer covering) produces hormones called corticosteroids for this resistance
reaction.
Overuse by the body's defence mechanism in this phase may eventually lead to
disease. If this adaptation phase continues for a prolonged period of time without
periods of relaxation and rest to counterbalance the stress response, sufferers
become prone to fatigue, concentration lapses, irritability and lethargy as the
effort to sustain arousal slides into negative stress.
The third stage of GPS is called exhaustion. In this stage, the body has run out of its
reserve of body energy and immunity. Mental, physical and emotional resources
suffer heavily. The body experiences "adrenal exhaustion". The blood sugar levels
decrease as the adrenals become depleted, leading to decreased stress
tolerance, progressive mental and physical exhaustion, illness and possibly
collapse.
The hypothalamus-pituitary-adrenal (HPA) chain of command has served humans
well as a means of survival for thousands of years. However, for those suffering from
chronic anxiety and depression this process malfunctions. Continual stress early in
life disrupts the cycle. Instead of shutting off once the crisis is over, the process
continues, with the hypothalamus continuing to signal the adrenals to produce
cortisol.
Page 21 of 116

22. Homeostasis — When a danger finally passes or the perceived
threat is over, the normal brain initiates a reverse course of action that releases a
different type of biochemicals throughout the body. Attempting to bring you back
into balance; the brain seeks the holy grail of "homeostasis," that elusive state of
metabolic equilibrium between the stimulating and the tranquilizing chemical
forces in the body. When either one of the stimulating or tranquilizing chemical
forces dominates the other without relief, then you will experience an on-going
state of internal imbalance. This condition is known as stress; it can have serious
consequences for brain cells.
Parasympathetic and Sympathetic Nervous System — the
sympathetic nervous system (SNS) turns on the fight or flight response. In contrast,
the parasympathetic nervous system (PNS) promotes the relaxation response. Like
two tug-of-war teams skilfully supporting their rope with a minimum of tension, the
SNS and PNS carefully maintain metabolic equilibrium by making adjustments
whenever something disturbs this balance. The vital elements in this process are
the hormones, the chemical messengers produced by endocrine glands. These
hormones travel through the bloodstream to accelerate or suppress metabolic
functions.
The trouble is that some stress hormones are not completely regulated by the
body’s system. They remain active in the brain for too long – injuring and even
killing cells in the hippocampus, the area of the brain needed for memory and
learning. Because of this hierarchical dominance of the SNS over the PNS, it often
requires conscious effort to initiate the relaxation response and re-establish
metabolic equilibrium.
The Emotional Brain: The Limbic System — The primary area of
the brain that deals with stress is its limbic system. Because of its enormous
influence on emotions and memory, the limbic system is often referred to as the
‘emotional brain’. It is also called the mammalian brain, because it emerged
during evolution with our warm-blooded relatives, and marked the beginning of
social cooperation in the animal kingdom.
Whenever a threat is perceived, imminent or imagined, the limbic system
immediately responds via the autonomic nervous system — the complex network
of endocrine glands that automatically regulates metabolism.
The term "stress" is short for distress, a word evolved from Latin that means "to draw
or pull apart.” The Romans even used the term districtia to describe "a being torn
asunder.” When stressed-out, most of us can probably relate to this description.
Distress Signals from the Brain — The sympathetic nervous system
does an excellent job of rapidly preparing to deal with what is perceived as a
threat to one’s safety. Its hormones initiate several metabolic processes that allows
one to cope in the best way with sudden danger.
The adrenal glands release adrenaline (also known as epinephrine) and other
hormones that increase breathing, heart rate, and blood pressure. This moves
more oxygen-rich blood faster to the brain and to the muscles needed for fighting
or fleeing — and, you have plenty of energy to do either, because adrenaline
Page 22 of 116

23. causes a rapid release of glucose and fatty acids into your bloodstream. Also, your
senses become keener, your memory sharper, and you are less sensitive to pain
Other hormones shut down functions unnecessary during the emergency. Growth,
reproduction, and the immune system all go on hold. Blood flow to the skin is
reduced. With the mind and body in this temporary state of metabolic overdrive,
you are now prepared to respond to a life-threatening situation.
Getting Back to Normal — After a perceived danger has
passed, the body then tries to return to normal. But this may not be so easy, and
becomes even more difficult with age. Although the hyper-activating sympathetic
nervous system jumps into action immediately, it is very slow to shut down and
allow the tranquilizing parasympathetic nervous system to calm things down.
Once the stress response has been activated, the (normal) system wisely keeps the
body in a state of readiness.
Not All Stress is Bad — Bear in mind that an appropriate stress
response is a healthy and necessary part of life. One of the things it does is to
release norepinephrine, one of the principal excitatory neurotransmitters.
Norepinephrine is needed to create new memories. It improves mood. Problems
feel more like challenges, which encourages creative thinking that stimulates your
brain to grow new connections within it.
Stress Compromises the Blood-Brain Barrier (BBB) — Stress can
dramatically increase the ability of chemicals to pass through the blood-brain
barrier. During the Gulf War, Israeli soldiers took a drug to protect themselves from
chemical and biological weapons. Normally, it should not have crossed the BBB,
but scientists learned that the stress of war had somehow increased the
permeability of the BBB. Nearly one-quarter of the soldiers complained of
headaches, nausea, and dizziness — symptoms which occur only if the drug
reaches the brain.
Stress and Noise — sudden sound is an urgent wake-up call that
alerts and activates the stress response — a biological alarm that affects the brain
in powerful ways. Because loud noise often heralds bad news, animals and
humans have evolved a rapid response to audio stressors: the roar of a carnivore,
the crack of a falling tree, the scream of a child and more recently; the explosion
of a weapon, the wail of a siren, the crash of the stock market. Sudden and
unexpected noise for those under stress can increase the startle response to noise.
Stress and Memory — chronic over-secretion of stress hormones
adversely affects brain function, especially memory. Too much cortisol can
prevent the brain from laying down a new memory, or from accessing already
existing memories.
The renowned brain researcher, Robert M. Sapolsky, has shown that sustained stress
can damage the hippocampus, the part of the limbic brain which is central to
learning and memory. 51 The ‘culprits’ are "glucocorticoids," a class of steroid
51
Sapolsky, Robert M.; Krey, Lewis C.; & McEwen, Bruce S. Glucocorticoid-
sensitive hippocampal neurons are involved in terminating the adreno-cortical stress
response. Proc. Natl. Acad. Sci. USA. Vol. 81, pp. 6174-6177, October 1984
Page 23 of 116

24. hormones secreted from the adrenal glands during stress. They are more
commonly known as corticosteroids or cortisol.
During a perceived threat, the adrenal glands immediately release adrenalin. If
the threat is severe or still persists after a couple of minutes, the adrenals then
release cortisol. Once in the brain cortisol remains much longer than adrenalin,
where it continues to affect brain cells.
Cortisol Affects Memory Formation and Retrieval — Cortisol also
interferes with the function of neurotransmitters, the chemicals that brain cells use
to communicate with each other. Excessive cortisol can make it difficult to think or
retrieve long-term memories. That's why people get befuddled and confused in a
severe crisis. Their mind goes blank because "the lines are down.” They can't
remember where the fire exit is, for example.
Cortisol and Temporary Memory Loss – a Study — in an animal
study, rats were stressed by an electrical shock, and then made to go through a
maze with which they were already familiar. When the shock was given either four
hours before or two minutes before navigating the maze, the rats had no problem
but, when they were stressed by a shock 30 minutes before, the rats were unable to
remember their way through the maze.
This time-dependent effect on memory performance correlates with the levels of
circulating cortisol, which are highest at 30 minutes. The same thing happened
when non-stressed rats were injected with cortisol. In contrast, when cortisol
production was chemically suppressed, then there were no stress-induced effects
on memory retrieval.
According to James McGaugh, director of the Centre for the Neurobiology of
Learning and Memory at the University of California, Irvine, "This effect only lasts for
a couple of hours, so that the impairing effect in this case is a temporary
impairment of retrieval. The memory is not lost. It is just inaccessible or less
accessible for a period of time."
Cortisol and the Degenerative Cascade — normally, in response
to stress, the brain's hypothalamus secretes a hormone that causes the pituitary
gland to secrete another hormone that causes the adrenals to secrete cortisol.
When levels of cortisol rise to a certain level, several areas of the brain, especially
the hippocampus, tell the hypothalamus to turn off the cortisol-producing
mechanism. This is the proper feedback response.
The hippocampus, however, is the area most damaged by cortisol. In his book
Brain Longevity, Dharma Singh Khalsa, M.D., describes how older people often
have lost 20-25% of the cells in their hippocampus, so it cannot provide proper
feedback to the hypothalamus, so cortisol continues to be secreted.52 This, in turn,
causes more damage to the hippocampus, and even more cortisol production.
Thus, a Catch-22, "degenerative cascade" begins, which can be very difficult to
stop.
Cortisol and Brain Degeneration -— Studies done by Dr. Robert M.
Sapolsky, Professor of Neurology and Neurological Sciences at Stanford University,
52
Khalsa, Dharma Singh; Stauth, Cameron. Brain Longevity. Century, 1997
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25. showed that lots of stress or exposure to cortisol accelerates the degeneration of
the aging hippocampus.53 And, because the hippocampus is part of the
feedback mechanism that signals when to stop cortisol production, a damaged
hippocampus causes cortisol levels to get out of control — further compromising
memory and cognitive function. The cycle of degeneration then continues.
NUTRITION AND METABOLIC DISTURBANCES
Children with head injuries present a number of complex inter-related metabolic
disturbances. The specific requirement for, and effects of nutritional support
cannot be separated from the child's nutritional condition or the pre-injury
environment and must be considered as only part of the total environment for
recovery. Superimposed on the normal requirements for growth and development
are the metabolic problems induced by trauma, the changes in nutrition that may
directly result from focal brain injury, and the effects on neurotransmitter
metabolism which are secondary to tissue damage and nutritional insufficiency. 54
The optimal milieu for recovery after head injury has been poorly investigated, and
the conditions essential for maximizing further development in the head-injured
child remain ill-defined. From a functional viewpoint, the effects on
neurotransmitter metabolism may be considered crucial, but these are unlikely to
persist solely because of dietary factors rather, they may be compounded by post-
traumatic changes in sleep and behaviour, prophylactic drug use, disruption of
social development or on-going social relationships, general levels of home
stimulation and parental management55. A continuum of insufficiency and
impairment of brain growth, development and mental ability may exist for the
head-injured child.
Consistent with a rational approach to rehabilitation, adequate nutritional intake
may be necessary, but not of itself sufficient. Sensory activity may be essential but
nutritional support a necessity in order to obtain it56. Whilst nutritional intervention
may not provide a magic wand for the head-injured child, it might be possible to
increase the probability of positive change by nutritional intervention.
Studies of single amino acids such as tryptophan, tyrosine and choline or lecithin in
relatively large doses may have little meaning in strictly nutritional terms for they are
not representative of how people eat. The effects of ordinary meals on behaviour
are usually smaller than those in studies of single nutrients, so that sizeable numbers
of subjects, adequately sensitive measures and tight methodological controls are
required57. Dose response parameters are largely unknown in this sort of
53
Sapolsky, Robert M.; Uno, Hideo; Rebert, Charles S. & Finch, Caleb E.
Hippocampal Damage Associated with Prolonged Glucocorticoid Exposure in
Primates. The Journal of Neuroscience, September 1990, 10(9): 2897-2902
54
Dickerson, JWT.; Johnson, DA. & Maclean, A. Food for thought: a rôle for
nutrition in recovery. In Johnson, D., Uttley, D., & Wyke, M. A. (1989). Children's Head
Injury: Who Cares? London: Taylor and Francis.
55
Kraemer, G.W. (1985) 'The primate social environment, brain neurochemical
changes and psychopathology', Trends in Neuroscience, 8, pp. 339-340.
56
Ricciuti, H.N. (1981) ‘Adverse environmental and nutritional influences on
mental development: a perspective’, Journal of the American Dietetic Associatian,
79, pp. 115-120.
57
Spreen, O., Tupper, O., Risser, A., Tuokko, H. & Edgell, D. (1984) Human
Developmental Neuropsychology, Oxford, Oxford University Press.
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26. investigation, making it difficult to determine portion sizes for experimental studies.
Whilst less dramatic responses to food than to the pharmacologically pure forms
could be expected, food effects upon brain function may still be of more
significance, at least in longer term maintenance of recovery achieved. It is
important to note that if the specific neurotransmitter receptors are damaged, or
other neuronal populations are also destroyed which contain converting enzymes,
for example, then increasing a particular class of neuro-chemical activity is unlikely
to be uniformly successful, particularly in cases of severe diffuse head injury.
A great deal of research is necessary before nutritional and dietary factors are
implicated in recovery from paediatric head injury. If post-traumatic deficits in
nutritional status persist, compounded by social, cognitive and emotional
difficulties, then dietary evaluation and management may be one avenue to
explore, to help maximize progress and outcome. The effects of dietary stress on
an individual child will not simply be matters of nutritional pathophysiology, but
rather will be moulded and modified by his genetic endowment, stage of
development, home stimulation, social and emotional climates.
With increasing knowledge of neurotransmission and parallel concern about
subclinical nutritional deficiencies, the development of collaborative research
studies in this most complex field would soon help to delineate the validity of
nutritional factors in determining the optimal milieu for recovery in paediatric head-
injury. Head-injured children grow up to become relatively disabled adults, with
the added possibility that, in the presence of structural damage, the normal
ageing process may be exacerbated. Consequently, instilling good dietary habits
in childhood may at the very least be beneficial to long-term mental function.
(Dickerson et al, 1989 idem)
Cohen et al have researched neurological dysfunction caused by traumatic brain
injury and have found that this results in profound changes in net synaptic efficacy,
leading to impaired cognition. Because excitability is directly controlled by the
balance of excitatory and inhibitory activity, underlying mechanisms causing these
changes have been investigated using lateral fluid percussion brain injury in mice.
Although injury-induced shifts in net synaptic efficacy were not accompanied by
changes in hippocampal glutamate and GABA levels, significant reductions were
seen in the concentration of branched chain amino acids58 (BCAAs), which are
key precursors to de novo glutamate synthesis. Dietary consumption of BCAAs
restored hippocampal BCAA concentrations to normal, reversed injury-induced
shifts in net synaptic efficacy, and led to reinstatement of cognitive performance
after concussive brain injury.
All brain-injured mice that consumed BCAAs demonstrated cognitive improvement
with a simultaneous restoration in net synaptic efficacy. Posttraumatic changes in
the expression of cytosolic branched chain aminotransferase, branched chain
ketoacid dehydrogenase, glutamate dehydrogenase, and glutamic acid
decarboxylase support a perturbation of BCAA and neurotransmitter metabolism.
Ex vivo application of BCAAs to hippocampal slices from injured animals restored
58
Branched Chain Amino Acids are Leucine, Isoleucine and Valine. They are
available combined in a powder or as a tablet. Effectiveness of BCAAs can be
increased by consuming 10mg of Vitamin B6 with every 10g of BCAA.
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27. posttraumatic regional shifts in net synaptic efficacy as measured by field
excitatory postsynaptic potentials. These results suggest that dietary BCAA
intervention could promote cognitive improvement by restoring hippocampal
function after a traumatic brain injury.59
_______
Sleep and dreaming following Brain Injury
By measuring electrical activity, we are able to distinguish sleep from its
unconscious imitation by other behaviours. Thus, sleep is an active state of the
brain and its electrical activity continues throughout sleep and differs from that
during waking. Sleep is of the brain.
The research of Payne and Nadel briefly stated is that variations in cortisol (and
other neurotransmitters) determine the functional status of hippocampal ↔
neocortical circuits, thereby influencing the memory consolidation processes that
transpire during sleep. The status of these circuits largely determines the
phenomenology of dreams, providing an explanation for why we dream and of
what. As a corollary, dreams can be thought of as windows onto the inner
workings of our memory systems, at least those of which we can become
conscious.
In addition to exploring these ideas, their paper provides some background
concerning:
(1) the states of sleep and the role of various neurotransmitters in switching
from one sleep state to another,
(2) how the characteristics of dreams vary as a function of sleep state,
(3) the memory content typically associated with dreaming in different
dream states, and
60
(4) the role of sleep in the consolidation of memory.
We know also, that the normal brain controls itself so as to produce sleep. The
clocks that turn sleep on and off are composed of networks of brain cells. These
clocks not only time whether we sleep or wake but also program an elaborate and
orderly sequence of brain events within sleep. In one such event, the continuously
active brain becomes extraordinarily more active every 90 to 100 minutes during
sleep and remains so as long as an hour. It is during such periods that we dream.
59
Cohen, Akiva S.; Cole, Jeffrey T.; Mitala, Christina M.; Kundu, Suhali; Verma,
Ajay; Elkind, Jaclynn A.; & Nissim, Itzhak. Dietary branched chain amino acids
ameliorate injury-induced cognitive impairment. Proceedings of the National
Academy of Sciences. published online before print December 7, 2009,
60
Payne, Jessica D. & Nadell, Lynn. Sleep, dreams, and memory
consolidation: The role of the stress hormone cortisol. Learning and Memory; 2004.
11: 671-678.
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28. 61
Thus, dreaming, like sleep, is of the brain and by the brain.
The brain is the prime beneficiary of sleep, as is made obvious by the progressive
decline in our cerebral capacities when we are deprived of sleep. We first have
difficulty concentrating, attending, and performing coordinated motor acts such
as driving cars. Then we become irritable and suffer an almost painful sleepiness.
After we go five to ten days without sleep, our brain loses its bearings altogether
and madness takes over: the trusting become paranoid; the rational, irrational;
and the sane begin to see and hear things that aren't there. All the dysfunctions
caused by sleep deprivation are rapidly reversed when lost sleep is recovered. We
don't yet know exactly how sleep ensures efficient brain function, but that it does
so is beyond doubt. Thus, sleep is for the brain. Sleep is of the brain, by the brain,
and for the brain. (Hobson, 1989, idem)
Recognizing the connection between the brain and sleep we can better
appreciate why sleep science is so new. It was not until the second quarter of our
own century that a way was found to measure sleep objectively by recording the
brain electrical activity.
There are two combined factors that have helped to produce an observational
sleep science. First, the subjective experience of nightmares and dreams shows
that sleep cannot occur without intense brain activity. Secondly, while animal
sleep appears tranquil, in all mammals — including humans — observable
movements of the eyes, face, and fingers occur periodically during sleep. It seems
inconceivable to us that those who watched sleeping cats' paws twitch, sleeping
puppies' feet scamper, or sleeping babies' faces grimace and smile did not
suspect intense underlying brain activity. We can infer that such outward signs of
motion are related to the inward experience of dreams and therefore a strong
presumptive evidence of brain activation. (Hobson, 1989, idem)
When there is a chronic lack of sleep it seems likely that structures behind the
medulla (see below, this page) might actively contribute to the slowing of non-REM
sleep. Studies by other researchers have implied that an area just next to the hypo-
thalamus, called the basal forebrain, may playa role in controlling non-REM sleep.
The generation of non-REM sleep was shown to be impeded by damaging and
enhanced by stimulating this area of the brain.
Liu et al 62 and Madan et al 63 suggest that conditioned fear causes REMS
alterations, including difficulty in initiating a REMS episode as indicated by the
diminution in the number of seq-REMS episodes. Another finding, the increase in
phasic activity, agrees with the inference from clinical investigations that retrieval
61
Hobson, JA. Sleep. Scientific American Library; 1989; pp3.
62
Liu, Xianling; Tang, Xiangdong & Sanford, L D. Fear-conditioned suppression
of REM sleep: relationship to Fos expression patterns in limbic and brainstem regions
in BALB/cJ mice. Brain Research. Volume 991, Issues 1-2, 21 November 2003, Pages
1-17
63
Madan, Vibha; Brennan, Francis X.;.Mann, Graziella L.; Horbal, Apryle A.;
Dunn, Gregory A.; Ross, Richard J. & Morrison, Adrian R. Long-term Effect of Cued
Fear Conditioning on REM Sleep Micro-architecture in Rats. Sleep. 2008 April 1;
31(4): 497–503.
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29. of fearful memories can be associated with the long-term REMS disturbances
characteristic of posttraumatic stress disorder.
Michel Jouvet is perhaps the world's leading sleep and dream researcher. He
discovered a dream state that he called paradoxical sleep. This third category of
brain activity (distinct from sleeping and waking) is a state of very deep sleep with
some specific motor events, including rapid eye movements (REM). 64
In 1959 Michel Jouvet conducted several experiments on cats regarding muscle
atonia (paralysis) during REM sleep. Jouvet demonstrated that the generation of
REM sleep depends on an intact pontine tegmentum65 and that REM atonia is due
to an inhibition of motor centres in the medulla oblongata. 66 Cats with lesions
around the locus coeruleus67 have less restricted muscle movement during REM
sleep, and show a variety of complex behaviours including motor patterns
suggesting that they are dreaming of attack, defence and exploration.
Jouvet proposed the speculative theory that the purpose of dreaming is a kind of
iterative neurological programming that works to preserve an individual's
psychological heredity, the basis of personality. 68
A different brainstem structure, the pons, has been shown by Jouvet to be critical
for REM sleep generation. He transected the midbrain of a cat, and then
completely removed all the structures above the cut, except the hypothalamus.
The resulting "pontine" cats had a periodically recurrent phase of rapid eye
movements associated with a complete loss of muscle tone. This latter phe-
nomenon (called postural atonia) had been shown also to characterize REM sleep
in normal cats by Jouvet and Francois Michel in 1959 and was later shown to be
true also of human REM sleep (Michel Jouvet et al)69. This experiment pointed to a
timer and trigger for REM sleep in the pons.
64
Jouvet, Michel. The Paradox of Sleep: The Story of Dreaming. MIT
Press 1999.
65
The pontine tegmentum is a part of the pons of the brain involved in the initiation of
REM sleep. It includes the pedunculo-pontine nucleus and the latero-dorsal
tegmental nucleus, among others, and is located near the raphe nucleus and the
locus ceruleus . PET studies seem to indicate that there is a correlation between
blood flow in the pontine tegmentum, REM sleep, and dreaming .
66
The medulla oblongata is the lowest part of the brain, situated at the top of
the spinal cord and controlling activities such as heart beat, blood pressure and
breathing.
67
The Locus coeruleus is a nucleus in a dense cluster of neurons in the dorso
rostral pons of the brain stem involved with physiological responses to stress and
panic. This nucleus gained prominence in the 1960s when new anatomical
approaches revealed it to be the major source of norepinephrine in brain with
projections throughout most central nervous system regions, including the cerebral
cortex, hippocampus, thalamus, midbrain, brainstem, cerebellum, and spinal cord
(Foote et al., 1983; Aston-Jones et al., 1995). These findings stimulated a great deal
of research into this unusual system, resulting in a wealth of knowledge at the
cellular, systems, and behavioural levels.
68
Jouvet, Michel. Paradoxical Sleep - A Study of its Nature and Mechanisms.
Progress In Brain Research Vol. 18 Sleep Mechanisms 1965
69
Jouvet, M., Michel, F., & Courjon, J. (1959). Sur un stade d'activité é]ectrique
cérébrale rapide au cours du sommeil physiologique C.R. Soc. Biol. (Paris), 153,
1024-1028.
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30. Electromyogram (EMG) experiments show that movements are found to be
abolished in REM sleep. Because we do not move our muscles in REM sleep, we
cannot express the motor acts of our dreams. Of course, during their atonic-REM
periods Jouvet's cats could show no cortical EEG changes (because they had no
cortex), but they did have spiking EEG waves in the pons during these periods that
resembled those seen in normal cats. Jouvet proposed that there was both a REM
sleep clock and trigger mechanism in the pons. The clock was reliable because
the episodes occurred in the cat at regular intervals of 30 minutes as in normal
sleep; the trigger was effective because the episodes lasted for the normal
duration of 6 to 8 minutes.
It should be clear therefore that many areas of the complex brainstem are
involved in the control of sleep and waking. Non-REM sleep mechanisms in the
basal forebrain interact with medullary and midbrain reticular systems to produce
EMG slow waves in the cortex; periodically interrupting this process is the REM sleep
generator in the pons, which reactivates the brain. This then leads us to look at
why brain injury can cause sleep disturbance and what parts of the sleep cycle
may be affected.
Glen Johnson, a Clinical Neuropsychologist of the Neuro-Recovery Head Injury
Program, Traverse City, USA writes that, “…all of my head-injured patients have
some form of a sleep disorder.” 70 It is enlightening to read of his experience with
brain injured patients.
“First, let's recognize what happens with a typical sleep disorder caused by a head
injury. Typically, you may go to sleep fairly easily, although sometimes people can’t
stop their thoughts in the evening and have difficulty getting to sleep. Once you
have fallen asleep, you may feel that you’re waking up as often as every hour. By
about 4 or 5 in the morning, you're wide awake, even though you are dead tired. In
addition, many people who have head injuries are easily awakened by small noises.
I've had patients who would sleep though a fire alarm prior to their head injuries, but
who now wake up when a cat walks by.
Sleep is very important to the healing process. If you don't sleep, you're going to be
tired throughout the day. If you're tired throughout the day, your memory will get
worse and you'll be more cranky and irritable. Lack of sleep makes the other head
injury symptoms much worse. Sleep also has an important role in physical healing.”
(idem)
A wide-range study of victims of head injury often reveals disorders that are
neglected by less extensive examinations, and dispels the idea that there is usually
a benign outcome. Following head trauma, there is a marked increase in dreams
of threatening content, despite the fact that, contrary to repression occurring in
many post-traumatic victims, a comatose person with head injury has no
registration of the traumatic event. The loss of self-esteem and self-confidence
creates a permanent state of stress, which can be reflected in the patients’
threatening, frightening and anxiety-provoking dream content. It is reasonable to
assume that dreaming is, in part, an expression of both neurological control and
feedback of intention and action. 71
70
Johnson, Glen. Traumatic Brain Injury: Survival Guide. Online edition at:
www.tbiguide.com
71
Parker, RS. (2000) Concussive brain trauma: neurobehavioral impairment
and maladaptation. Taylor & Francis Ltd.
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31. _______
Information Processing
A common deficit arising from a brain injury, and more commonly from a head
injury, is the inability to process information at the normal rate. Whereas the child
may be able to carry out a variety of mental tasks, the speed at which these are
completed in a brain-injured child may be significantly slower than it would be for
a normal child (Brooks 1984). 72 The deficit may involve the speed at which the
child can understand the task involved, learn the material, retrieve it from memory
and then carry out the mental processes involved.
Deficits in this area can severely limit the ability of the child to function in many
everyday situations and such deficits can arise following even a mild head injury
(Wrightson et al.) 73 In specific detail, the child finds difficulty comprehending
information at the normal rate, formulating their thoughts and then carrying out the
required actions. They may find it difficult to understand if too much information is
presented at any one occasion. They may therefore initially start off understanding
what is going on but rapidly lose their way as the amount of information
accumulates. This is particularly the case if the level of information becomes more
complex and can occur in both the classroom and in social situations.
Borod 74 found brain-injured children to be less competent at comprehending
emotional information. In the teaching situation this often shows itself in the child's
inability to complete written assignments or answer questions in the allotted time,
and therefore never being able to answer a question directed at the class,
because by the time they raise their hand someone else has already answered
before them.
Children who are significantly affected can find themselves severely
disadvantaged at a social level. Whereas adults will give a child a sympathetic
look and the necessary time to collect their thoughts, a more competitive adoles-
cent group will not be so kind or so tolerant. In the playground, the conversation
moves at the pace of the group and for those too slow to respond, they frequently
find themselves left far behind; sometimes it is easier not to even try, and the child
may find themselves becoming increasingly isolated from their peers. 75
The ability to understand, learn and then retrieve information involves a range of
abilities, including attention, short-term memory and the ability to manipulate the
information in order to place it into a more permanent memory system. Essential to
this, is the ability to organize material into a meaningful manner so that it can be
72
Brooks, N. (1984). Cognitive deficits after head injury. In: Closed Head Injury:
Psychosocial Social and Family Consequences (ed. N. Brooks), pp. 44-73. Oxford:
Oxford Community Press.
73
Wrightson, P., McGinn, V., & Gronwall, D. (1995). Mild head injury in pre-
school children - evidence that can be associated with a persisting cognitive
defect. Journal of Neurology Neurosurgery and Psychiatry 59, 375-80.
74
Borod, J. C. (1992). Interhemispheric and intrahemispheric control of
emotion. Journal of Consulting and Clinical Psychology 60, 339-48.
75
Appleton, R et al 2006 idem.
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