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ORGANIC DISORDERS  
 
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Introduction 
This protocol includes three sections with information about the following topics: 
 Organic 
disorders 
 Head 
injuries 
  Cognitive impairment due to prescribed medication. 
The common theme that links these conditions is the presence of impaired cognitive 
function. 
This is of particular relevance for disability analysts, as much of what we do involves 
making an assessment of what a person can or cannot do. 
Cognitive function enables all the various mental activities that allow us, in a 
practical sense, to interact with our environment.  In short, it determines to a large 
extent, what we can, or cannot do day to day. 
The information in this protocol, although comprehensive, has focused mainly on 
those conditions which are likely to be encountered frequently in the disability 
analysis setting, or where it is felt that specific guidance would be helpful. 
 
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1. Organic 
Disorders 
As a group, these conditions share the feature that they are due to some 
demonstrable abnormality of brain structure or function. 
Cognition is frequently affected, but they may present clinically as a behavioural or 
emotional disturbance.  The boundaries of these conditions are somewhat blurred, 
but they can be broadly divided into three categories: 
 Delirium 
 Dementia 
  Specific neuro-psychiatric syndromes. 
Many of these conditions are rarities, even in the specialist clinical setting.  It is 
beyond the scope of this protocol to include detail of these.  Where a condition is 
likely to be encountered more frequently, or where there are specific points that 
merit emphasis, more information is provided. 
1.1 Delirium 
A short section on delirium is included for completeness.  In the past, delirium was 
often referred to as an acute confusional state.  It must be stressed that in the 
context of disability analysis, these conditions are unlikely to be encountered, apart 
from after the acute illness, perhaps when the individual is recuperating.  These are 
acute medical conditions, and hospital admission and investigation will usually be 
necessary to elucidate the cause. 
1.1.1 Aetiology 
The list of possible causes of delirium is lengthy but can be grouped into the 
following categories: 
  Drugs and alcohol 
 Intracranial 
causes 
  Metabolic and endocrine causes 
 Systemic 
infections 
 Postoperative 
states. 
Delirium is more common in the elderly, and those who for some reason have 
reduced cerebral reserve.  The latter is commonly due to pre-existing dementia, but 
other causes include head injury, and cerebrovascular accidents.  A significant 
history of substance abuse also puts individuals at risk. 
Amongst elderly people admitted to hospital, the prevalence of delirium is 30%.  In 
general medical or surgical wards, 5 to 15% of patients present with, or develop 
delirium.  In surgical intensive care units, the number rises to 20 to 30%. 
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1.1.2 Clinical 

features 
The onset of delirium is acute in nature.  The clinical course fluctuates with lucid 
intervals periodically.  Relevant clinical features may include the following: 
  Drowsiness and disorientation in time and place 
 Perceptual 
abnormalities 
 Anxiety 
  Poor concentration and impaired memory 
 Delusions/paranoid 
ideas. 
For a diagnosis of delirium to be made the following four features should be present: 
  Time course as described above 
 Altered 
consciousness 
  Change of cognition 
  Evidence of a medical cause. 
1.1.3 Treatment 
Treatment will be of the underlying cause.  Good, supportive nursing care is 
essential in the short term. 
Anti-psychotic medication to control extreme anxiety or agitation may be required. 
1.1.4 Prognosis 
This is again largely dependent on the underlying cause of the delirium.  Delirium is 
associated with a high mortality.  Prompt recognition and treatment of the underlying 
cause increases the chance of survival.   
The acute episode is likely to last something in the order of a week, but longer 
periods of delirium, up to a month in duration, can occur. 
1.2 Dementia 
Dementia is a chronic syndrome characterised by cognitive impairment without 
altered consciousness.  Some specific types of dementia, which are likely to be 
more commonly encountered, or which have particular features are detailed at 1.2.6 
onwards. 
The importance of making a specific diagnosis when a patient has dementia has 
been recognised in recent years, due to the increasing availability of treatment 
options.  Making a diagnosis is still largely dependent on the application of clinical 
tests, rather than laboratory or other investigations.1 
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For the diagnosis of dementia to be made, two or more of the following cognitive 
functions must be affected: 
 Memory 
 Language 
  Abstract thinking and judgement 
  Praxis (complex movement) 
 Visuoperceptual 
skills 
 Personality 
 Social 
conduct. 
The impairment will have reached a level that is starting to have an impact socially, 
or on the ability to function in the workplace. 
1.2.1 Aetiology 
There are many causes of dementia.  Amongst the elderly, by far the commonest 
are vascular and degenerative disorders.  Pre-senile dementia refers to those 
individuals aged less than 65 years.  In younger age groups, a much wider range of 
possible causes needs to be considered, so that those that are treatable can be 
excluded.  A list of possible causes of dementia is contained in Appendix A. 
1.2.2 Prevalence 
The prevalence of dementia increases with ageing.  As the ageing population in the 
developed world increases, we can expect the number of people with dementia to 
show a significant rise.  It is estimated that 5% of those aged over 65 have 
dementia.  In those over 80, figures range from 10 to 20%. 
Looking at where people live once they are over 65 shows a marked difference.  In 
the community, 5% of those over 65 have dementia, whilst in residential or nursing 
homes more than 80% of over 65s have dementia. 
1.2.3 Clinical 
features 
The usual mode of presentation is poor memory, but altered personality or 
behaviour can also feature in the early stages.  Pre-morbid personality has a large 
influence on the clinical features.  Those with good social skills may retain 
comparatively good function in spite of intellectual impairment.  The elderly, socially 
isolated and hearing impaired are less able to compensate for intellectual 
impairment. 
The onset is often slow and insidious.  Early symptoms may not be recognised by 
others, or may be difficult to detect.  Impaired attention span or reduced 
concentration are common, non-specific features. 
As dementia progresses, difficulty in new learning becomes more conspicuous and 
recent memory loss more noticeable.  Patients become inflexible and less able to 
adapt to new situations. 
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When the restricted abilities become stretched beyond their capacity, the person 
may experience a ‘catastrophic reaction’ comprising an explosive outburst of grief or 
rage. 
Two major behavioural syndromes are recognised, having the following features: 
  Apathy, inertia and loss of interest in work and hobbies 
  Restlessness, disinhibition, distractibility, and loss of empathy and social skills. 
These two pictures may overlap. 
Inability to self-care, and disorientation are later features.  Behaviour may become 
stereotypical or feature mannerisms.  Irritability, anxiety, aggression and depression 
are all common features.  Insight may be retained to some degree early on.  This 
can cause the person great distress. 
Eventually, speech and thought processes become incoherent, to the point where 
the person can become mute. 
Certain sub-types or syndromes have been described.  Although there may be 
overlap clinically and pathologically, these are useful as clinical descriptions. 
Subcortical dementia 
This is characterised by: 
  Slowness of thought 
  Difficulty with complex, sequential intellectual tasks 
  Impoverishment of affect and personality 
  Retention of learning, calculation and language skills. 
Cortical dementia 
This is characterised by: 
  Early and prominent impairment of memory 
  Reduced visuospatial abilities 
  Difficulty with word finding. 
Semantic dementia 
This variant can prove particularly disabling.  There is selective, progressive loss of 
meaning for verbal and non-verbal material.  Comprehension is impaired, and the 
person has great difficulty with naming and categorising.  Autobiographical memory 
is not usually affected.  Semantic dementia is associated with temporal lobe atrophy. 
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Differentiating between early dementia (particularly Alzheimer’s disease) and age 
related cognitive change still relies mainly on clinical judgement.  In normal ageing 
the following remain unaffected: 
  Accuracy of responses 
 New 
learning 
 Verbal 
abilities. 
What may be seen is a gradual slowing of the speed of cognition.  Serial 
neuropsychometric assessments, such as the Mini Mental State Examination 
(MMSE) or magnetic resonance imaging may be helpful in doubtful cases.  The 
MMSE is described in Appendix B. 
In recent years, there has been a move away from looking at human cognitive 
neurology in terms of topographical location.  A network approach is now followed.  
This is described in Appendix C. 
1.2.4 Treatment 
Dementia is an incurable condition.  In recent years, drug treatment has become 
available which may improve certain aspects of the condition, such as memory.  The 
drugs currently licensed for use in the UK are acetylcholinesterase inhibitors.  Other 
drugs, such anti-psychotics may be used to control symptoms such as anxiety or 
agitation.  However, evidence to support the continued use of drugs such as 
thioridazine is lacking, and the incidence of adverse side effects high.2  Concern 
has also been expressed that anti-psychotics may in fact accelerate cognitive 
decline.3  Worthwhile functional gain may result from antidepressant medication, in 
depressed patients.   
Any medication should be prescribed with caution, and in the knowledge that 
cognitive impairment may be aggravated rather than helped.   
1.2.5 Prognosis 
Dementia is an irreversibly declining condition.  In the USA, it is reported as being 
the fourth commonest cause of death. 
1.2.6 Alzheimer’s 
disease 
The commonest cause of dementia in the elderly, it accounts for half of all cases.4  
The condition is slightly more common in women.  In the UK, research studies have 
estimated that there are 400,000 sufferers.5  This may be an underestimate, as The 
Alzheimer’s Society quotes a significantly higher  figure of 700,000.6  Prevalence is 
expected to double over the next 50 years.5  Currently, the point prevalence in over 
65’s is 2% - 7% (in those moderately or severely affected). 
Aetiological factors have yet to be fully clarified.  In recent years, research has 
identified both causative genes and genetic risk factors (the latter can increase the 
risk of developing the condition by up to eightfold).7  Other known risk factors include 
previous moderate or severe head injury as a young adult, and Down’s syndrome.8 
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Pathologically, changes in the brain include marked shrinkage of tissue, with 
widening of the sulci and enlargement of the ventricles.  Senile plaques containing 
amyloid, and neurofibrillary tangles form.9  The amount of neuropathological change 
correlates directly with the degree of cognitive impairment. 
The onset of Alzheimer’s disease is often insidious, and pre-morbid personality may 
modify the clinical features early on.  As the illness progresses, both cognitive and 
non-cognitive impairments will become more evident.  From the time of diagnosis, 
the mean life expectancy is 7 years.   
Once the diagnosis of Alzheimer’s disease has been made, management of the 
patient should focus on a number of issues.  Both patient and family will require long 
term support from a multidisciplinary team.  At some point, residential nursing care is 
likely to be a requirement.  The trigger for this is more likely to be a behavioural 
aspect rather than cognitive decline.3  For relatives, the commonest ‘management’ 
difficulties being severely disrupted sleep pattern or aggressive behaviour. 
The management of this condition has changed in recent years with the recognition 
that the rate of deterioration can be slowed by the use of medication.  The drugs 
used are acetylcholinesterase inhibitors, which delay the breakdown of acetylcholine 
released into synaptic clefts. 
Rivastigminegalantamine and donepezil are more efficacious, and have a better 
side effect profile than earlier drugs used.10,11,12  Both cognitive function and 
activities of daily living show measurable improvement on treatment with 
rivastigmine.10 
All three drugs have been approved by the National Institute for Clinical Excellence, 
for treatment of mild and moderate Alzheimer’s disease, where the mini mental state 
examination (MMSE) score is over 12.  Other conditions are stipulated, for example 
certain baseline tests must be carried out and treatment should only be initiated by a 
specialist physician.13 
The potential role of statins in lowering the risk of developing Alzheimer’s disease 
has yet to be supported by any valid research trials.14 
Specific therapy such as Reality Orientation has been shown to benefit both 
behaviour and cognition, where it forms part of long term management.  It can be 
presented continuously by a carer, or in a ‘classroom’ setting (using an information 
display board).15 
1.2.7 Vascular 
dementia 
In the past, this was referred to as multi-infarct dementia.  The pathological changes 
include enlarged ventricles and multiple areas of infarction in the brain.  It is more 
common in men and there is a strong association with hypertension.   
The progression in this type of dementia is usually stepwise, with focal motor signs a 
common feature.  In contrast with Alzheimer’s disease, the cognitive impairment is 
not due to reduced cholinergic function. 
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Vascular dementia has a shorter life expectancy after diagnosis, compared to 
Alzheimer’s disease, of 4 to 5 years.  Many patients with this type of dementia are 
treated with aspirin.  There is no research evidence to indicate that this has any 
therapeutic impact on the dementia.16 
1.2.8 
Dementia with Lewy bodies 
It is thought that this type of dementia accounts for about 20% of cases.17  The 
condition has been recognised in patients aged between 50 and 83 years, with a 
mean age at onset of 75 years.  It is slightly more common in men. 
The distinctive Lewy bodies were first seen in the substantia nigra of patients with 
Parkinson’s disease.  In patients with this type of dementia, they are found in the 
cerebral cortex. 
This type of dementia differs from Alzheimer’s disease in that cognitive impairment 
shows a fluctuating course clinically.  Other characteristic features include marked, 
vivid visual hallucinations and Parkinsonism.  Patients may have frequent falls and 
syncopal episodes. 
Anti-psychotic drugs should be avoided as these patients are extremely prone to 
extra-pyramidal side effects.  A few studies have shown cholinesterase inhibitors to 
be effective in treating dementia with Lewy bodies.17  As evidence accumulates they 
may become first line treatments. 
1.2.9 Pick’s 
disease 
This rare form of dementia usually presents earlier, between the ages of 50 and 60 
years.  It is slightly more common in women, and some cases are due to an 
autosomal dominant gene transmission. 
Pathologically, the features include atrophy of the frontal and temporal lobes.  
Microscopic examination of the abnormal neurones reveals the characteristic Pick 
bodies.  These are intracellular inclusion bodies that can be stained with silver. 
The clinical picture with this condition is of personality change and social 
disinhibition.  Apathy is often a prominent feature, and as the disease progresses, 
speech abnormalities are likely to feature. 
1.2.10  AIDS dementia complex 
Minor cognitive impairment is relatively common in HIV infection which can produce 
a wide range of neuropsychiatric disorders.  It can result in neurological symptoms 
and dementia, both in the presence and the absence of AIDS. 
The virus can directly infect brain tissue, causing AIDS dementia complex. This is 
usually a later feature of the illness, and occurs in around 30% of patients. 
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Characteristic symptoms are decreased memory and concentration, or low mood 
and apathy.  It may be difficult to differentiate in the early stages from a depressive 
illness.  The dementia progresses to cause global intellectual impairment with major 
neurological signs such as ataxia. 
As might be expected with a late feature, the prognosis of AIDS dementia complex 
is very poor. 
1.2.11 Prion 
diseases 
There has been particular interest in these conditions in recent years, culminating in 
the description of Variant Creutzfeldt-Jakob disease (vCJD) in 1996.18  All the prion 
diseases remain extremely rare in the UK. 
The cases described who were eventually diagnosed as having vCJD were all 
unusually young in age, and their illnesses tended to be of longer duration compared 
with other prion diseases, with 50% living longer than a year.  The clinical 
presentation was of mood or behavioural change, with cognitive impairment 
occurring as a late feature, along with severe cerebellar and extra-pyramidal signs. 
Creutzfeldt-Jakob disease affects an older age group of 50 to 70 years, and causes 
a rapidly progressive dementia usually fatal a few months from onset. 
1.2.12 Huntington’s 
disease 
This is an autosomal dominant condition affecting men and women in equal 
numbers.  Onset is usually when the person is in his or her thirties, and is likely to 
comprise involuntary choreiform movements initially.  Psychiatric features such as 
depression or paranoid symptoms are common.  Progressive cognitive impairment 
appears later on in the illness.  The rate at which the dementia progresses varies 
between individuals, but the prognosis for this incurable condition is always poor, 
with death the expected outcome within 15 years of onset. 
1.2.13  Mild Cognitive Impairment (MCI) 
In recent years, a separate clinical entity termed mild cognitive impairment (MCI) 
has been recognised.  This comprises measurable memory loss that falls 
somewhere between normal ageing and mild dementia.  Research evidence has 
shown that patients with MCI have an increased risk of developing Alzheimer’s 
disease.  There is no evidence to date to support the use of medication in individuals 
who may have MCI.19 
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1.3 
Specific Neuro-psychiatric Syndromes 
This section describes some other organic disorders, which differ in that they do not 
present with cognitive impairment as a global picture. 
1.3.1 
Focal cerebral syndromes 
Shared features of these conditions are that they: 
  Show more selective impairment of cerebral function 
  May have specific or localised brain pathology demonstrable. 
Frontal lobe   
The patient may present with altered personality or inappropriate behaviour due to 
disinhibition.  Judgement and the ability to think abstractly may be affected.  They 
may demonstrate ‘perseveration’, which is difficulty in switching between tasks.  
Concentration and attention span will be reduced, but tests of intelligence are 
usually normal.  The patient may have urinary incontinence. 
Lack of insight is likely to be a major feature. 
Parietal lobe 
If the non-dominant lobe is affected there will be visuo-spatial difficulties.  Difficulty 
with daily tasks such as dressing may be apparent.  Features of dominant lobe 
involvement include receptive aphasia, body image disorders and right–left 
disorientation.  Patients may deny that there is anything wrong with them, or claim 
that affected limbs do not belong to them. 
Temporal lobe 
A complex clinical picture may present.  Along with specific cognitive deficits and 
neurological signs, there may be personality change and psychotic features.  
Memory impairment or language difficulties may form part of the picture. 
Occipital lobe 
Lesions here may present with cortical blindness, homonymous hemianopia, visual 
disorientation or with complex visual hallucinations. 
Corpus callosum 
The picture here is of acute and severe intellectual impairment. 
Thalamus, basal ganglia and brainstem 
Lesions here may present in a variety of ways.  Personality, intellect, memory or 
language can all be affected. 
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1.3.2 

Secondary psychiatric syndromes 
Cerebral or systemic disease can result in a number of different secondary 
psychiatric syndromes.  Clinical presentation may be in the form of one of the 
following: 
 Psychosis 
 Mood 
disorder 
 Anxiety 
disorder 
 Personality 
disorder 
 Delusional 
disorder 
  Organic hallucinosis – usually visual or auditory 
  Obsessive compulsive disorder. 
There are many possible underlying causes.  More common ones include substance 
misuse disorders, dementias and epilepsy. 
1.3.3 Memory 
disorders 
There are thought to be multiple memory systems in the human brain. 
Immediate memory – this can be tested by telling the patient a name and address 
(previously not known to them).  After five minutes, they are asked to recall the 
name and address. 
Recent memory – a typical day history is a good method of testing this. 
Long term memory – enquiry about events prior to the presumed onset of the 
memory disorder will test this. 
Recall  is not the same as recognition  and  needs to be differentiated.  Some 
patients may retain the ability to recognise information although that they cannot 
recall information. 
Organic disorders usually affect the recall of recent rather than distant events.  The 
loss is usually partial. 
Another way of looking at memory, which can help in understanding memory 
disorders, is by dividing memory function into: 
Implicit (procedural) memory 
  This involves motor skills, conditional behaviours and repetition priming. 
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Explicit (declarative) memory 
  Short term consciously accessed material.  This ‘store’ is used for example when 
dialling an unfamiliar telephone number. 
  Long term consciously accessed material.  This ‘store’ is split into episodic 
functions for autobiographical events, and semantic functions for knowledge of 
the world.  Episodic memory is concerned with both past events and new 
learning. 
Causes of amnesia, or memory failure can be divided into: 
Transient 
  Transient global amnesia 
  Transient epileptic amnesia 
 Head 
injury 
 Alcoholic 
blackout 
 Post-electroconvulsive 
therapy 
  Post traumatic stress disorder 
 Psychogenic 
fugue 
  Amnesia for criminal event. 
Persistent 
 Amnestic 
syndrome 
 Herpetic 
encephalitis 
 Vascular 
disorder 
 Head 
injury. 
Amnestic syndrome (amnesic/ Korsakov’s) 
This is a specific impairment of episodic memory.  The ability to learn new 
information and to recall past events are both affected.  Intellectual dysfunction is 
not a feature of amnestic syndrome.  Social and occupational functioning are likely 
to be significantly affected by this condition. 
A cardinal feature is that there will be evidence of a general medical condition 
causing the memory impairment. 
A marked degree of this type of memory impairment occurs in the Wernicke-
Korsakov syndrome (see protocol on alcohol).  Gaps in memory may be filled by 
confabulation, though this is more commonly seen in delirium or frontal lobe 
syndrome. 
The prognosis is poor if the cause is encephalitis or irreversible brain damage. 
Of those with Wernicke-Korsakov syndrome, roughly half will never improve, and a 
quarter recover fully, with thiamine treatment.   
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Transient global amnesia 
This syndrome needs to be excluded in those patients who present with episodic 
neurological and psychiatric disturbance.  Memory is disturbed for a short period 
(less than 24 hours).  Onset is sudden, and the patient may present as an 
emergency.   
The patient remains alert and neurologically intact.  Personal identity is retained 
(unlike in psychogenic fugue) and they may retain the ability to undertake tasks such 
as driving competently.   
Complete recovery is usual, and further episodes do not usually occur.  Transient 
changes in blood flow in the brain as demonstrated by functional imaging studies, 
are thought to be a possible underlying cause. 
1.4 
Main Disabling Effects 
In the majority of cases, the disabling effects of cognitive impairment are significant, 
and there is often a huge impact on the daily life of both patient and family.  Once 
cognitive impairment reaches a certain level, the ability to self care is affected, and 
increasing levels of supervision may be needed to ensure personal safety of the 
individual, if behavioural difficulties such as wandering develop.   
The concept of mild cognitive impairment (MCI) is also of relevance for disability 
analysts.  A recent longitudinal study comparing patients with MCI with normal 
subjects, demonstrated that more than 30% had difficulty with tasks of daily living 
such as toileting and using the telephone.  In the past, MCI was thought not to be 
associated with any change in the ability to cope with activities of daily living.20   
1.4.1 
Assessing the Claimant  
The typical day history will provide much of the evidence needed, with regard to the 
level of cognitive impairment.  Information about memory, attention span and 
concentration can be gleaned from a description of the usual activities of daily living, 
focusing on what the person can or cannot do. 
Clinicians frequently use special tests of cognitive function to assist them in reaching 
a diagnosis.  In the context of disability analysis the use of such tests is not 
appropriate.  A specific diagnosis is not required, and many of the tests could not be 
applied properly in the available time.  A further consideration is that an individual 
who is cognitively impaired may be unduly distressed by the effort of completing the 
test, or when confronted by their shortcomings in undertaking the test. 
Selected parts of the Mini Mental State Examination (see Appendix B) may in some 
instances provide useful supporting evidence for the Decision Maker, perhaps in 
situations where it would seem that the level of disability is less than that claimed.  
Such situations are likely to occur infrequently, and in most instances ample 
evidence will be available from the history and observations. 
 
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1.4.2 

The IB-PCA  
Many of those affected by these conditions will be past retirement age, and not in a 
position to apply for an income replacement state benefit. 
Younger individuals may apply for Incapacity Benefit.  Social security legislation 
recognises the severe disabling effects of dementia, in allowing a Decision Maker to 
determine exemption if documentary evidence of dementia is received.  Advice from 
an approved medical adviser does not have to be sought by the Decision Maker in 
these circumstances.  A significant number of cases will be accepted at the scrutiny 
stage, where the available evidence indicates that physical functional impairment is 
likely to be above the threshold. 
As such, where a claimant’s main medical diagnosis is a type of dementia, it is 
highly unlikely that they will present for medical examination during the PCA 
process. 
If a claimant does present for examination, there may be scope for advising 
exemption under one of the following exempt categories: 
  Multiple effects of the impairments of the function of the brain or nervous system 
causing severe and irreversible motor, sensory and intellectual deficits. 
  Severe and progressive immune deficiency states characterised by the 
occurrence of severe constitutional disease or opportunistic infections or tumour 
formation.
 
  Involving the presence of mental disease, which severely and adversely affects 
a person’s mood or behaviour, and which severely restricts his social 
functioning, or his awareness of his immediate environment.
 
If it is clear that a claimant has a medical condition likely to give rise to severe 
disability, then early consideration should be given to exemption advice. 
If the examining doctor does not feel that the claimant’s condition is severe enough 
to warrant exemption, the mental health assessment should be applied in the usual 
way. 
All 4 areas of mental health functioning are likely to be affected, but the area of 
‘completion of tasks’ particularly so.  If the opportunity arises to obtain information 
from a third party, this can provide invaluable corroborative evidence, as the 
claimant may have limited insight into their condition. 
 
 
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2. Head 
Injury 
2.1 Introduction 
Although head injury is an acute problem dealt with in the Accident and Emergency 
setting, the after-effects and residual disability can be significant and the resultant 
functional impairment can at times be devastating.   
Head injury may occur in isolation, but is usually seen in combination with other 
injuries.  Head injuries can be fatal, but it must be borne in mind that the 
consequences of other injuries in a poly-trauma situation can be equally disastrous. 
The long-term effects may include epilepsy, neurological deficits, dizzy spells, 
headaches, poor concentration, impaired cognition, psychiatric syndromes and 
hydrocephalus.21 
The extent of medical and nursing care required over the long-term depends upon 
the severity of the initial head injury, the extent of recovery and the nature and 
severity of the residual problems. 
2.2 Description 
2.2.1 Aetiology 
The commonest cause of head injury is road traffic accidents.  Vehicular failure 
accounts for only 10% of the accidents, the majority being due to human failure (e.g. 
influence of alcohol and drugs, false judgement, tiredness and carelessness).   
Falls and accidents around the home are a more common cause in children and 
elderly people. 
Head injury is not a commonly reported industrial injury. 
2.2.2 Prevalence 
About 10% of the cases in an Accident and Emergency Unit will be head injuries.22  
A majority of these head injuries are minor and do not require any major medical 
intervention.  Only about 20% of all head injuries will need admission to the hospital 
and 2-3% of those admitted will prove fatal.22  
Of the deaths associated with head injury, 33 to 50% occur before admission to the 
hospital and about 33% occur within 24hours of admission to the hospital.22  It must 
be stressed that death may be a consequence of other related injuries or 
complications thereof.   
Over 50% of those affected are less than 30 years old and there is a male 
preponderance.21 
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2.2.3 Classification 

Head injuries may be classified as closed  or  open.  There is no communication 
between the outside environment and the intradural contents in closed injuries 
whereas there is leak of cerebro-spinal fluid (CSF) in open injuries.   
There may or may not be an associated skull fracture.  Skull fractures signify high 
velocity injuries and there is a higher likelihood of primary brain injury in the 
presence of skull fracture.  The skull fracture may be linear or stellate, depressed, 
open or involving the base of the skull. 
2.2.4 
Pathology of Internal Injury 
Primary Brain Injury 
These are further classified into three types: 
  Concussion: This is associated with transient alteration in level of 
consciousness and very minor cognitive disturbance, which is also transient.  
There is no residual neurological deficit. 
  Diffuse Axonal Injury: Higher cortical functions are affected and they take a 
very long time to recover, if at all.  There is organic and psychological 
dysfunction including amnesia, memory disturbance, change in personality with 
either depression or disinhibition. 
  Focal Brain Injury: Includes injuries to sharply demarcated areas of brain in the 
region of injured blood vessels or bony prominence.  Other causes include 
depressed skull fractures.  There may be contusion, laceration, haemorrhage 
and haematoma at the injured site.  It may lead to secondary brain injury. 
Secondary Brain Injury 
Further insult to the brain tissue following primary injury constitutes secondary injury 
and is a direct consequence of the primary injury.  It is further classified into the 
following types: 
  Cerebral Hypoxia: It results from reduced cerebral perfusion and reduced 
oxygen in the blood.  Cerebral oedema and haematoma cause raised 
intracranial pressure thereby reducing cerebral perfusion.  This causes cellular 
hypoxia, which potentiates the cellular oedema, and a vicious cycle is set up with 
rapid worsening of the condition.  In addition, in cases where there is co-existent 
chest injury, blocked airway, respiratory depression, drug or alcohol ingestion 
and inhalation pneumonia, the level of oxygenation is reduced further. 
 
Hypotension due to shock further reduces perfusion. 
  Intracranial Bleeding: This can be extradural, subdural or intracerebral.  A 
haematoma has the potential to cause detrimental effects by direct pressure 
effects on the underlying brain tissue.  There is also a generalised rise in the 
intracranial pressure with reduction in cerebral perfusion and danger of 
herniation or “coning” of the brain stem.  About 10% of severe head injuries 
develop an extradural haematoma.  It usually results from rupture of the middle 
meningeal artery and requires urgent surgical intervention.   
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Subdural haematoma is more common and occurs in 30% of severe head 
injuries.  In contrast to extradural bleed, there is usually underlying brain injury 
and mortality is up to 50%.  Intracerebral bleed results from primary brain injury 
and there is associated diffuse axonal injury. 
  Infection: Meningeal infection following undetected fractures may cause 
secondary brain injury.  Prophylactic antibiotics for open fractures may help 
prevent this dreaded complication. 
2.3 Diagnosis 
2.3.1 Symptoms 
and 
signs 
History is very important in head injuries.  There may be amnesia for the event.  The 
duration of unconsciousness and amnesia are proportional to the severity of the 
injury.   
Examination must be comprehensive to rule out other injuries.  In case of the poly-
trauma patients, assessment is as per the Advanced Trauma Life Support (ATLS) 
Guidelines. 
The level of consciousness is the most important clinical finding in a person with 
head injury.  The Glasgow Coma Scale is the best objective tool for initial and 
ongoing clinical assessment of people with head injuries and is also a good 
prognostic tool.23  The Glasgow Coma scale is reproduced in Appendix D
Accurate assessment of level of consciousness can be performed only after full 
oxygenation.  Neurological assessment is an extremely important part of 
assessment of head injury.  Any evidence of alcohol or drug misuse must be taken 
in to account.   
Change in pupillary diameter is a very sensitive indicator of intracranial bleed.  A 
developing haematoma can lead to pupillary dilatation and loss of light reflex on the 
same side.  However, in the general population there is a finite incidence of pre-
existing pupillary asymmetry and it is worthwhile establishing if there were any 
ocular abnormalities prior to the injury.  Bilateral pupillary dilatation with loss of light 
reflex is an indicator of brain stem injury. 
A slowing pulse and rising blood pressure with unilateral pupillary dilatation, against 
a background of deteriorating consciousness, are signs indicative of rising 
intracranial pressure. 
Most fractures of the skull may be obvious only on X-rays.  Clinical signs of a 
fracture of the skull base include periorbital haematoma, subconjunctival 
haemorrhage, CSF rhinorrhoea, CSF otorrhoea, and bruising over the mastoid 
(Battle's sign).   
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2.3.2 Investigations 

Important observations in acute setting include: 
 
Consciousness (Glasgow Coma Scale) 
 
Pupil size and response 
 
Respiratory rate and pattern 
 Pulse 
rate 
 Blood 
pressure. 
Observations are recorded on a special head injury chart.  Further investigations 
include special skull X-rays and CT scan.  There are recommended criteria for 
request of skull X-rays after recent head injury and these are tabulated in Appendix 
E
.  Similarly there are criteria for CT scan and/or neurosurgical consultation and 
these are tabulated in Appendix E
2.3.3 Differential 
Diagnosis 
The effects of alcohol, drugs, epilepsy, diabetes, hypoxia, haemorrhagic shock and 
other conditions that affect consciousness may all confound the assessing physician 
faced with a comatose patient with head injury.  These co-existing conditions may 
be wholly, partly or not at all responsible for depression in the level of 
consciousness.  Pre-existing ocular pathology may be responsible for pupillary 
asymmetry and abnormal pupillary reflex response. 
2.4 Treatment 
2.4.1 
Acute Care and Management  
For head injuries the criteria for hospital admission are listed in Appendix E.  Those 
who do not merit hospital admission should be advised to spend the first night with a 
responsible adult and should return to the hospital if there is any deterioration in the 
clinical condition.   
On admission, minor head injuries only need observation.  A special head injury 
chart
 should be used to monitor progress.   
Patients with minor head injuries who are fully alert and show no evidence of 
neurological deficits can be allowed to go home after 24 hours even in the presence 
of a simple skull fracture.  Rest for a week is advised as some cognitive functions 
like concentration take a few days to recover to pre-injury levels.   
All patients with severe multiple injuries are managed as per the ATLS guidelines.   
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The management of severe head injuries is highly specialised.  One or more of the 
following measures may need to be instituted in cases with severe head injury: 
 Intensive 
monitoring 
  Endotracheal intubation and artificial ventilation 
 Nasogastric 
aspiration 
  Maintaining fluid and electrolyte balance 
  Monitoring intracranial pressure and measures to control it (e.g. intravenous 
mannitol or controlled hyperventilation)     
Intracranial haematoma may need to be drained surgically, especially if there is focal 
neurological deficit due to pressure effect from the haematoma or there is a risk of 
impending herniation of the brain stem.   
2.4.2 Rehabilitation 
Recovery from traumatic brain injury is complex and variable and can take a very 
long time.  Initial recovery is very rapid but various functions may recover over 
different time scales making it a very complex problem to assess and manage.21 
Recovery is not only due to anatomical reorganisation but also due to behavioural 
compensation and functional adaptation. 
Rehabilitation is necessarily a team approach and because of the complex recovery 
process it needs to be tailored to individual needs.  It is imperative to involve the 
individual and the family as active members of the team right from the start.21,24 
The team members (physiotherapist, occupational therapist, psychologist etc.) have 
to gain an in-depth knowledge of the individual in context of their pre-morbid level of 
functioning and abilities and this includes their personality and behaviour as well.   
Although there usually is a substantial degree of spontaneous recovery, there is a 
need to learn to adapt to the residual problems and to get back to independent 
existence.  New ways of performing tasks and interacting with others have to be 
learned. 
Psychological support needs to be provided.  Behavioural difficulties, cognitive and 
emotional problems all have to be addressed in a sensitive manner. 
Goals should be set for the short and long term and these goals need to be realistic 
and meaningful for the individual.  The therapist’s goals may be worthless to the 
individual and compliance in such cases may be minimal at the best. 
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Post-concussional syndrome may present after head injury (usually severe enough 
to result in loss of consciousness) and includes symptoms like fatigue, memory loss, 
short attention span, irritability, executive dysfunction, learning problems, lack of 
initiative and poor insight.  Loss of self-esteem and fear of permanent brain damage 
can lead to anxiety or depression.  The aetiology of this syndrome is thought to be 
twofold – organic genesis with psychologically driven persistence.  Some patients 
are hypochondriacal, adopting a permanent sick role and searching for a diagnosis 
and cure.  Compensation motives are not always a feature.  The symptoms may 
vary in severity and can prevent the individual from effectively functioning in their 
previous roles.  Despite recovery, some level of residual functional loss is likely and 
a sensitive readjustment of career goals while addressing these problems is called 
for. 
The ultimate aim of rehabilitation is successful integration of the individual in the 
community. 
Severe residual problems may need life-long care in a small number of cases. 
2.5 
Main Disabling Effects 
The disabling effects of head injury and consequent traumatic brain injury can be 
myriad and variable.  The nature and severity of the problems and their various 
permutations not only depend on the extent of the injury but also on the pre-morbid 
characteristics of the individual. 
Focal neurological deficits may never recover and can cause physical impairment of 
varying severity.  However, this protocol deals only with the psychological aspects of 
brain injury. 
2.5.1 Mild 
disability 
This is usually a consequence of minor brain injury where loss of consciousness has 
been less than 20 minutes and posttraumatic amnesia less than 1 hour.25  
The varying symptoms reported include headache, dizziness, fatigue, reduced 
speed of thought, poor concentration, poor memory, irritability, depression and 
anxiety.  Most individuals with minor brain injury return home within a few days and 
the symptoms subside over days to weeks.  Cognitive deficits resolve within 3 
months in the majority of individuals.25 
A very small minority has some cognitive deficit for several years after the injury.  
Many of the non-specific physical symptoms like headache and fatigue are assumed 
to result from the chronic effort to overcome or cope with the persisting cognitive 
deficits. 
Though apparently normal, it may be difficult for these individuals to hold down jobs 
or maintain relationships.  Ignorance about the cognitive deficits and the problems 
arising therefrom leads to feelings of frustration, guilt and anxiety. 
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It must, however, be reiterated that these long-term residual cognitive deficits are 
minor and present only in a small minority of individuals after minor brain injury.  The 
majority of individuals return back to pre-morbid level of function within a period of 3 
months. 
2.5.2 
Moderate to severe disability 
This is usually a consequence of moderate to severe traumatic brain injury where 
unconsciousness has lasted for more than 20 minutes and post traumatic amnesia 
for over 1 hour.26 
In these cases there are persistent residual cognitive and behavioural problems 
leading to significant functional impairment.  Commonly reported long-term deficits 
include: 
  Attention deficit / reduced concentration  
 Fatigue 
  Learning and memory problems 
  Impaired planning and problem solving 
  Concrete thinking (inability to deal with abstract concepts) 
  Lack of initiative  
 Inflexibility 
  Dissociation between thought and action 
 Impulsivity 
  Irritability and temper outbursts 
 Physical 
aggression 
 Communication 
problems 
  Socially inappropriate behaviour and disinhibition 
  Self-centred behaviour and egocentricity 
  Changes in affect (flat affect, inappropriate emotions and mood) 
  Lack of insight 
A wide range of symptoms may be reported with the resultant functional impairment 
varying in severity.  Innumerable permutations of the above deficits and their 
manifestations are likely in these individuals with moderate to severe disability.   
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2.6 
Assessing the Claimant  
2.6.1 General 
Considerations 
Poor attention and memory may affect the ability to cope with tasks and with 
pressure.  A previously active individual may become inactive and sit for hours doing 
nothing.  There may be a tendency to forget the risks and hazards of daily life.  Poor 
concentration may lead to an inability to pursue previously enjoyed leisure activities.   
Short attention span may be evident, as the claimant would need lots of prompting.  
Short attention span may also affect the ability to read.   
Ability to learn and retain new skills is likely to be affected.  There may be 
impairment in problem solving and planning.  Complex tasks involving strategies, 
long-term planning and error checking may be affected.   
Adapting to new and unfamiliar situations is difficult.  Abstract thinking may be 
impossible.  It may be difficult to generalise from a single example.  The ability to 
understand humour and indirect language may be lost. 
There may be a tendency to rely on rigid routines.  Anxiety and irritability on change 
of routines may be a feature. 
There may be a failure to control, regulate and monitor thoughts and behaviour. 
Lack of initiative may lead to self-neglect and avoidance of routine tasks.   
Fatigue may cause the claimant to feel overwhelmed by multiple tasks and the 
individual tends to leave tasks incomplete. 
Behavioural problems and temper outbursts may lead to interpersonal problems and 
an inability to interact with people.  They may also have a tendency to physical 
aggression.  Frustration may cause irritability and a resultant preference to be left 
alone.  There might also be problems in communication. 
2.6.2 History 
 
A detailed history of the head injury and the functional problems should be obtained.  
The information and evidence on the claimant’s file should be noted.  A careful 
account of the typical day should be noted.  An attempt must be made to establish 
the level of pre-morbid function, abilities and behaviour. 
2.6.3 
Informal Observation  
Physical and psychological deficits may become evident on observation during the 
assessment.  Informal observation of the claimant’s mood, emotions, concentration, 
initiative, ease of communication and insight must be made.  Much valuable 
information may be gained by this method. 
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2.6.4 Physical 

Examination 
This may be appropriate if there are any reported or observed physical functional 
disabilities. 
2.6.5 IB-PCA 
Considerations 
The Mental Health Assessment must always be done in individuals with 
functional impairment following head injury.
 
It must be borne in mind that such individuals may have low tolerance and a very 
small minority may be prone to temper outbursts and very rarely physical 
aggression.  See the CME module “Dealing with Potentially Violent Situations” 
for detailed guidelines. 
Those with severe and irreversible motor, sensory and intellectual deficits arising 
from traumatic injury may be exempt from the PCA if there is enough evidence to 
support such a decision at file scrutiny stage.  However, such individuals may 
sometimes be called for assessment if evidence in the IB55 is lacking.  If the criteria 
for exemption are satisfied then the disability analyst should terminate the 
assessment following the guidelines outlined in the CME module “Exemption 
advice at the examination stage”

 
Answers to the questions in the Mental Health Assessment can be drawn from the 
history, account of the typical day and the informal observations made. 
 
 
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3. 
Cognitive Impairment due to Prescribed 
Medication 

3.1 Introduction 
The range of drugs available for medical practitioners to prescribe is vast, with new 
preparations being added to the list at a steady rate.  The number of serious side 
effects caused by prescribed drugs is very small when consideration is given to the 
number of prescriptions issued to patients. 
The majority of patients being treated for a disabling condition will be prescribed 
some form of medication by their general practitioner, and many will be on more 
than one preparation.  Many patients report side effects which they attribute to their 
medication.  Where the medication is needed short term, and the side effects rated 
as of ‘nuisance value’ only, the patient may be encouraged to persevere with the 
treatment by their doctor.  If the treatment is intended to be longer term then 
consideration of an alternative preparation is likely to be made. 
Side effects are frequently dose related, or can be expected to diminish once the 
patient has been taking the medication for a period of time.  A good example of this 
is the well-documented anti-cholinergic effect exerted by tricyclic anti-depressants, 
which usually disappears after about 3 weeks on treatment. 
Many drugs may cause cognitive side effects but the main purpose of this section of 
the protocol is to highlight the approach that should be taken in the context of 
disability analysis.  Therefore, a detailed description of all individual drugs that can 
cause such side effects will not be included.  Drugs causing specific psychiatric 
symptoms such as depression have been mentioned in the relevant protocol. 
3.2 
Specific Side Effects 
Side effects, which have the potential to affect cognitive function, include the 
following: 
Drowsiness/Fatigue: This is the commonest side effect likely to be reported by the 
claimant.  Prescribed drugs that can cause this include benzodiazepines, opioid 
analgesics, anti-histamines, major tranquillisers and anti-depressants.  It would be 
expected that some of these drugs would only be prescribed in the short term 
(benzodiazepines), or intermittently (anti-histamines).   
Confusion: This is less likely to be reported but is noted as a possible side effect of 
many prescribed drugs.  It can arise as a side effect of all the anti-epileptic drugs in 
common use, benzodiazepines, opioid analgesics, anti-histamines, major 
tranquillisers, corticosteroids, thyroxine and anti-depressants. 
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Impaired memory and/or concentration: Few drugs have been documented as 
causing these side effects.  Lithium is one example where impaired memory is 
reported with long term use.  Other drugs include buserelin, zolpidem and some 
anti-epileptics.   
Irritability:  Though primarily not a direct cognitive effect, it can lead to mild 
impairment of concentration and is not uncommonly reported by claimants.  Drugs 
most likely to cause this are anti-epileptics, anti-depressants, naltrexone, 
acetazolamide, and aminophylline. 
3.3 
Assessing the Claimant 
Enquiry about specific daily activities may be helpful.  For example, it is useful to 
know whether the claimant has been advised by their GP not to drive or operate 
machinery.  It would be highly unusual for medication causing significant cognitive 
impairment to continue to be prescribed without clear therapeutic benefits or 
alternatives being tried.  A detailed recent drug history should be taken. 
In some instances it may be extremely difficult to ascertain whether a claimed side 
effect is due to prescribed medication or the underlying condition.  This is particularly 
so with symptoms which are more difficult to define or quantify, such as fatigue or 
drowsiness.  In a number of instances, both the condition and the treatment can 
make the patient feel tired and lacking in energy.  This should not influence unduly 
the functional assessment made, but may require a brief explanation for the 
decision-maker if the cause of cognitive impairment is unclear. 
3.4 IB-PCA 
Considerations 
In the context of the IB-PCA, significant cognitive impairment due to 
prescribed medication is likely to be encountered very infrequently. 

Enquiry about the side effects of medication is a requirement in all IB-PCA 
assessments.  Where a claimant reports a side effect that may give rise to cognitive 
impairment, the disability analyst should complete a Mental Health Assessment as a 
matter of course.   
The usual approach must be taken when applying the Mental Health Assessment.  
Evidence from all available documents, clinical history, account of a typical day, 
informal observations and examination of the mental state will all contribute to 
descriptor choice.  Careful attention should be paid to variability, when assessing the 
cognitive side effects of symptoms. 
Cognitive impairment can affect all 4 areas of mental functioning, but where 
significant it would be expected that there will be particular impact on the ‘completion 
of tasks’ section. 
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An examining doctor may feel that a claimant’s history of cognitive impairment due 
to medication is implausible.  This may be because there is a strong consensus of 
medical opinion about the possible side effects arising from the particular drug.  If it 
is decided not to proceed with the Mental Health Assessment, the justification 
should include pertinent information about the drug, and relevant features of the 
mental state to support that decision. 
In doubtful cases it is always best to apply the Mental Health Assessment so 
that clear advice can be formulated for the Decision Maker. 

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Appendix A - Causes of Dementia 
There are many possible causes of dementia.  These can be usefully grouped into 
the following categories: 
 Primary 
degenerative 
 Genetically 
determined 
 Vascular 
 Traumatic 
  Inflammatory, autoimmune or infectious 
  Metabolic, endocrine or toxic 
  Vitamin and other nutritional deficiency 
  Neoplastic, post-radiation or post-anoxic. 
 
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Appendix B - Mini Mental State Examination 
This is one of the most widely used tests of cognitive function.  It can be particularly 
helpful in monitoring or following cognitive performance over a period of time when 
applied at intervals to an individual.  It has also been used extensively in the 
research environment as a method of evaluating the effects of specific treatments 
for dementia.  A number of standard questions are asked, with points accrued for 
correct answers up to a maximum of 30.  The NICE guidelines stipulate a MMSE 
score of at least 12 before certain drugs can be prescribed. 
Orientation 
The patient should be asked if they can recall the following facts: 
1. Year 
2. Season 
3. Date 
4. Day 
5. Month 
6.  State (in the UK the country or region might be used) 
7. County 
8.  Town or city 
9.  Hospital (or name of the building in which the interview takes place) 
10. Floor. 
 
Registration 
Tell the patient the name of 3 objects (at one second intervals). 
Ask the patient to repeat them (score one point for each correct answer). Repeating 
the objects until they are learnt. 
 
Attention and calculation 
Serial ‘7’s scoring one point for each correct answer, stopping after 5 answers. 
The patient can, as an alternative be asked to spell WORLD backwards. 
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Recall 
Ask the patient to recall the ‘3’ objects, scoring one for each recalled. 
 
Language 
Ask the patient to name a watch and a pencil as you point to them.  (2 points) 
Ask the patient to repeat the phrase ‘No ifs, ands, or buts’. 
Ask the patient to follow a three-stage command.  For example – ‘Take a paper in 
your right hand.  Fold the paper in half.  Put the paper on the floor.(3 points in total) 
Ask the patient to read and carry out the following instruction.  CLOSE YOUR EYES. 
Ask the patient to write a simple sentence of their choice, containing a subject and 
an object.  The sentence should make sense, but spelling errors can be discounted. 
The last part of the test involves asking the patient to copy a diagram of two 5 sided 
figures overlapping by one corner each.  The figures should have sides of 1.5 cm in 
length, and the intersecting sides should form a quadrangle.  If all sides are 
preserved, and the intersecting sides form a quadrangle, one point is added to the 
score. 
 
                            
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Appendix C - Neurocognitive networks 
Traditionally, cognitive function was mapped topographically.  These days the 
concept of neurocognitive networks within the brain has widespread acceptance.  
The five main networks are as follows:  
  Right hemisphere, posterior parietal cortex and frontal eye fields for spatial 
awareness. 
  Left hemisphere including Broca’s and Wernicke’s areas for language. 
  Hippocampus, amygdala and cingulate cortex for memory and emotion. 
  Prefrontal and posterior parietal cortex for working memory and executive 
function. 
  Temporo-parietal and temporo-occipital cortex for face and object recognition. 
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Appendix D - Glasgow Coma Scale 
 
 
SCORE 
EYE OPENING 
 
Spontaneous 4 
To verbal command 

To pain 

None 

 
 
 
MOTOR RESPONSE 
 
Obeys Commands 

Localises pain 

Flexion withdrawal to pain 

Abnormal flexion (decorticate) 

Extension to pain (decerebrate) 

None 

 
 
 
VERBAL RESPONSE 
 
Orientated 5 
Confused conversation 

Inappropriate words 

Incomprehensible words 

None 

 
 
 
SEVERITY OF INJURY INDICATED BY SCORE AT ASSESSMENT AFTER 
RESUSCITATION 
Severe head injury 
3 - 8 
Moderate head injury 
9 - 12 
Mild head injury 
13 - 15 
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Appendix E - Criteria for Skull X-ray, CT scan and 
hospital admission after head injury 
Criteria for Skull X-ray after head injury (Based on guidelines of the working 
party on head injuries, Royal College of Surgeons of England). 

1.  Loss of consciousness or amnesia at any stage. 
2.  Any neurological symptoms or signs. 
3.  Cerebrospinal fluid or blood emanating from the nose or ear. 
4.  Suspected penetrating injury or marked scalp bruising or swelling (simple scalp 
laceration alone is not a criterion for skull X-ray) 
5. Alcohol 
intoxication. 
6.  Difficulty in assessing the patient (e.g.  young patients or epileptics). 
 
Criteria for CT scan and / or Neurosurgical referral after head injury (Based on 
guidelines of the working party on head injuries, Royal College of Surgeons of 
England). 

1.  Fractured skull in combination with any of the following: 
–  Confusion or depression of conscious level 
–  Focal neurological signs 
–  Fits or seizures. 
2.  Confusion or other neurological disturbance persisting for more than 12 hours, 
even if there is no skull fracture. 
3.  Coma continuing after resuscitation. 
4.  Suspected open fracture of the vault or base of the skull. 
5. Depressed 
skull 
fracture. 
6.  Deterioration of conscious level or other neurological signs. 
 
Criteria for hospital admission after head injury (Based on guidelines of the 
working party on head injuries, Royal College of Surgeons of England). 

1.  Any depression of conscious level or confusion at time of examination (a short 
period of unconsciousness or amnesia by itself is not a criteria for admission). 
2.  Severe headache or vomiting. 
3.  Any neurological abnormality 
4. Skull 
fracture 
5.  Difficulty in assessing the patient (e.g.  alcohol intake, children, epileptics) 
6.  Homeless or those living alone (i.e.  inability to discharge for overnight care by 
responsible adult). 
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4. 
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