RCSI Course Book Chapters 22-27 Week 4

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Chapter 22
Neuropsychiatry
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Chapter 22: Neuropsychiatry
Introduction
Neuropsychiatry involves the interface between psychiatry and neurology.
Neuropsychiatry is a specialist medical discipline involving the behavioural or psychological
difficulties associated with known or suspected neurological conditions such as stroke, epilepsy,
head injury, psychogenic non-epileptic seizures, Huntingtons disease, Parkinsons disease,
multiple sclerosis and Wilsons disease.
The neuropsychiatry service in Beaumont Hospital consists of:
o A neuropsychiatry liaison service in which a neuropsychiatrist assesses and manages
psychiatric presentations in inpatients who are admitted under the care of a neurologist with a
suspected or established neurological illness.
o A weekly neuropsychiatry outpatient clinic.
The basic skills required in consultation-liaison psychiatry are similar to those in other psychiatric
settings. In addition however, the psychiatrist has to develop several new skills:
o Learning how to conduct complex psychiatric assessments in the medical or surgical wards.
o Learning how to understand and respond to the needs of the referrer, either physician or
surgeon, even when no psychiatric disorder is present.
o Particular interview skills are required to initiate and complete a psychiatric assessment and
record the appropriate clinical signs in the mental state.
o Assessment of depression in the physically ill.
o Detection of psychological disorders that present with somatic symptoms.
o Assessment of illness behaviour.
o The psychiatrist should be able to assimilate all the relevant facts into a formulation of the
case, including the physical and psychological aspects.
Liaison Psychiatry involves:
o Close communication with medical colleagues in terms of initial communication and ongoing
contact.
o Reading between the lines of a referral and a pro-active approach to problem solving.
o Understanding psychiatric illness and how it influences medical presentations.
o Understanding medical illness and how it influences psychiatric presentations.
o Active consideration of follow-up and integration with community psychiatry and primary
care as appropriate
o Risk assessment skills.

Basic principles
All psychiatric disorders can co-exist with neurological presentations.
Depression is the most common psychiatric co-morbid condition.
Other common psychiatric disorders that occur at an increased rate are psychosis, anxiety disorders
and substance misuse.
These psychiatric disorders can vary over time in relation to the progression of the neurological
disorder and changes in prescribed medications.
There is an increased risk of suicide in people with neuropsychiatric presentations.
Prevalence of the most common psychiatric disorders in neuropsychiatric presentations:
General
population
Epilepsy Acquired
brain
injury
Huntingtons
disease
Parkinsons
disease
Multiple
sclerosis
Wilsons
disease
Depression 6-17% 8-48% 14-40% 20% 20-50% 40-50% 20%
Suicide 1% >5% 3-4% 4-6% 2% 7% Unknown
Psychosis 1% 2-9% 1-17% 3-12% 10-40% 5% 2%
Anxiety
disorders
18% 19-50% 18-60% 34-60% 7-40% Unknown Unknown

Rating scale
Neuropsychological testing may be undertaken to identify specific problem areas such as
comprehension, insight and judgement - see Addenbrookes Cognitive Examination in Appendix
4.
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Biological management of neuropsychiatric presentations
Depression
o Most common psychiatric presentation associated with neurological disease.
o SSRIs are generally considered to be the first-line treatment choice.
o TCAs can be efficacious but may be difficult for patients to tolerate.
o Newer antidepressants (e.g. bupropion, mirtazapine) also may be efficacious.
o ECT is effective for patients with treatment resistant depression.
Psychosis
o Typical antipsychotics are efficacious but can have significant adverse effects in neurological
patients.
o Atypical antipsychotics should be considered the first-line treatment choice.
o Clozapine has the strongest database but is generally considered second- or third-line because
of side effects.
Anxiety, mania, and agitated states
o Anxiety and agitation are common in neurological patients. Mania is much less common.
o First-line treatment choice depends on symptom presentation and aetiology.
For agitated or manic patients, consider anticonvulsants and/or atypical antipsychotics.
For anxious patients, consider SSRIs.
o Benzodiazepines can be effective but can have significant adverse effects in neurological
patients.
o Atypical antipsychotics have been associated with increased mortality in agitated patients with
dementia.
Aggression, impulsivity, and disinhibition
o These states are common in neurological patients and should be carefully distinguished from
anxiety, agitation or mania.
o First-line treatment choice will depend heavily on associated neurological illness, co-
morbidities and acuity.
o For acute agitation, parenteral atypical antipsychotics are the first-line choice. Parenteral
benzodiazepines can be used with caution.
o For prolonged states, consider SSRIs, anticonvulsants and possibly atypical antipsychotics.
Cognitive disturbances
o Acetylcholinesterase inhibitors are the first-line agents for most patients with dementia.
o Memantine may be effective alone or in combination with acetylcholinesterase inhibitors,
especially in patients with moderate to severe dementia.
Important neuropsychiatric conditions
1. Psychiatric consequences of stroke.
2. Psychiatric consequences of temporal lobe epilepsy.
3. Psychiatric consequences of head injury
4. Psychogenic non-epileptic seizures.
5. Huntingtons disease.
6. Parkinsons disease.
7. Multiple sclerosis.
8. Wilsons disease.

1. Psychiatric consequences of stroke
Introduction
Stroke can be either haemorrhagic (15%) or ischaemic (85%).
o Haemorrhagic stroke
Usually results from either a vascular anomaly or a long history of hypertension.
65% of haemorrhages occur in the basal ganglia-thalamus, 15% in the pons.
Haemorrhagic stroke is usually progressive and deadly and can evolve over hours or days.
o Ischaemic stroke
Caused by interruption of the blood supply to the brain.
Atherosclerosis causes narrowing of blood vessels and vascular occlusion can occur by
thrombosis or embolism, which lead to infarcts.
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Psychiatric consequences
1. Cognitive disorders
Vascular dementia
o Not all strokes result in cognitive impairment but when they do, the deficits depend on the
site of the infarct.
o Cognitive deficits tend to be particularly severe with certain midbrain and thalamic
strokes.
o Cognitive deficits may remain fixed or recover, either partially or completely.
o Features that suggest vascular dementia include: sudden onset, stepwise deterioration and
risk factors for cardiovascular disease.
o Emotional and personality changes usually occur early and are followed by cognitive
deficits that are often fluctuating in severity.
o Depression with episodes of affective lability and confusion are common, especially at
night.
o Behavioural slowing, anxiety and occasional episodes of cerebral ischaemia.
o Physical signs include features of arteriovascular disease together with neurological
impairments (e.g. rigidity, akinesia, brisk reflexes and pseudobulbar palsy).
o 10% of people have seizures at some point.
Subcortical dementia
o Gross psychomotor slowing, depressed mood, movement disorders, mild amnesia and
personality changes.
Amnestic disorder
o Anterograde or post-traumatic amnesia (PTA) is prominent with retrograde amnesia
relatively absent.
o Progress is related to the length of PTA. Better prognosis is associated with PTA of less
than one week.
2. Personality changes
Difficulty adjusting to anything different.
Irritability.
Avoiding new experiences and restriction of activities to an unvarying routine.
Previous personality features may become accentuated. A previously withdrawn person may
become suspicious and paranoid.
In more severe cases, with significant damage to the frontal lobes of the brain, disinhibition
can occur with a disregard to social norms.
3. Pathological emotionalism
Difficulty controlling emotional behaviour. People after a stroke may suddenly start crying or,
less commonly, laughing for no apparent reason. This can be distressing for the person and
their carers.
4. Post-stroke depression
Depression is the most common psychiatric consequence of stroke.
Approximately 40-50% of people will present with depression in the first month after a stroke.
Prevalence of depression varies over time with an apparent peak 3-6 months after a stroke.
A higher risk of post-stroke depression has been linked to left-sided cortical and basal ganglia
lesions and to lesions closer to the frontal lobe than to left posterior or right frontal lesions.
5. Post stroke anxiety
Approximately 25% of people after a stroke meet the criteria for generalised anxiety disorder.
6. Psychosis
Manic, hypomanic and paranoid psychosis may result from a stroke, especially with right
hemisphere infarcts.

2. Psychiatric consequences of temporal lobe epilepsy
Introduction
Seizures may be focal or generalised.
o Focal seizures
Simple partial seizures (SPS)
Onset is in a limited area or focus of one cerebral hemisphere.
Consciousness is not impaired.
Complex partial seizures (CPS)
Often occur after a simple partial seizure of temporal lobe origin.
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May progress to a generalised seizure, involving both cerebral hemispheres.
Consciousness is impaired.
o Generalised seizures
Seizures which begin in the temporal lobe but then spread to the whole brain.
These begin with an SPS or CPS phase initially, but then the arms, trunk and legs stiffen
in either a flexed or extended position. After this, coarse jerking of the limbs and trunk
occur.
Types of generalised seizures:
Infantile spasms.
Absence seizures.
Tonic-clonic seizures.
Atonic seizures.
Myoclonic seizures.

Up to 50% of people with epilepsy develop psychiatric disorders, the most common being
depression, anxiety and psychotic disturbances.
Psychiatric syndromes associated with epilepsy are best classified by how they relate in time to the
seizures (i.e. pre-ictal, ictal, post-ictal and inter-ictal).
1. Preictal (aura): the phase prior to the seizure
Vague symptoms during the days and hours leading up to a seizure.
As the seizure onset nears, the intensity of these symptoms may increase.
Derealization and depersonalization.
Cognitive symptoms (dj vu, jamis vu, fugue, twilight states).
Affective symptoms (irritability, lability, anxiety, euphoria).
Perceptual experiences (auditory, visual and olfactory hallucinations or illusions).
Preictal symptoms are relieved by the seizure.
2. Ictal: the phase during the seizure
Ictal anxiety.
Ictal depression
o Occurs less frequently than ictal anxiety.
o Common symptoms are guilt, hopelessness, worthless and suicidal ideation.
Ictal psychosis.
o Visual, gustatory or auditory hallucinations.
Ictal aggression
o Very rare.
Automatisms
o Suggest a focal origin for the seizure such as the medial temporal lobe.
o There is clouding of consciousness and amnesia for the automatism which usually lasts
<5 minutes.
o Lip-smacking and shaking of the hand are examples of automatisms.
3. Post-ictal: the phase after the seizure
Post-ictal confusion
o Disorientation, inattention, variable levels of consciousness and sometimes paranoia.
Post-ictal mood disturbance
o Depression, anxiety or mania.
Post-ictal psychosis
o Usually follows a cluster of seizures or an increase in the frequency of seizures.
o There is usually a period of lucidity (12-72 hours) prior to the onset of psychosis.
o The psychotic symptoms include delusions, hallucinations, thought disorder or mania,
which are usually transient but can last several weeks.
o People with post-ictal psychosis may experience hyper-religiosity.
4. Inter-ictal: the phase between the seizures
Inter-ictal depression
o Depression is the commonest psychiatric disorder seen in epilepsy, affecting
approximately 40% of people.
Inter-ictal bipolar disorder.
Inter-ictal anxiety.
Inter-ictal psychosis
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o A chronic disorder that clinically resembles chronic schizophrenia with symptoms of
delusions, hallucinations and thought disorder.
5. Other psychiatric presentations
Cognitive deterioration
o Common outcome of chronic epilepsy.
Epileptic personality syndrome
o Controversial phenomena traditionally associated with chronic temporal lobe epilepsy.
o The symptoms are: religiosity, hyposexuality, hypergraphia, impulsivity, egocentricity
(overriding concern with the self) and affective viscosity (the tendency to prolong interactions
with others).
Violence
o A controversial issue.
o There does not seem to be an increased risk of violence and aggression in people with
temporal lobe epilepsy or frontal lobe epilepsy.

3. Psychiatric consequences of head injury

Introduction
Brain injury can be classified as:
o Acquired brain injury: all types of brain injury that occur after birth. These impairments
result from either traumatic brain injury (e.g. physical trauma due to accidents, assaults,
neurosurgery, head injury etc) or non-traumatic injury derived from either an internal or
external source (e.g. stroke, brain tumours, infection, poisoning, hypoxia, ischemia,
encephalopathy or substance abuse).
o Traumatic brain injury: an acquired brain injury caused by an external force.
Head injury can be classified as:
o Open (penetrating) injury: a hard blow to the head from striking an object that breaks the
skull and enters the brain.
o Closed injury: a hard blow to the head from striking an object that breaks the skull.
Acceleration/deceleration injury: A closed head injury often sustained in car accidents,
where the brain smashes forwards and then backwards, rebounding against the walls of
the skull, causing damage to both the frontal lobes and the back of the brain.
Injury may be focal (haemorrhage, infarct, contusion) or diffuse (diffuse axonal injury).
Amnesia following a head injury can be classified as:
o Anterograde amnesia (post-traumatic amnesia)
The period following injury until normal memory resumes.
The best measure of head trauma severity, i.e. a good prognostic indicator.
o Retrograde amnesia
The period between the clearly recalled memory prior to the injury and the injury itself.
A poor prognostic indicator.

1. Cognitive impairment
Impairment in memory and thinking
o Difficulty with new learning, attention and concentration, reduced speed and flexibility of
thought processing.
Executive function impairment
o Impaired abstract reasoning, planning, problem-solving and multi-tasking.
Language problems
o Dysphasia, word-finding difficulties, impaired reading and writing skills.
Impaired judgement and safety awareness.
2. Personality and behavioural changes
Impaired social and coping skills, reduced self-esteem.
Impaired emotional control, poor frustration tolerance and anger management, self-
centredness.
Reduced insight, disinhibition and impulsivity.
Apathy, amotivational states.
Perhaps the first reported case of personality change after brain injury was that of the
construction foreman Phineas Gage (1823-1860). In 1848, 25 year old Gage was working on a
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railroad project in Vermont, Canada. He experienced a severe brain injury when a three foot
long, fourteen pound iron bar was violently propelled through his skull. It entered through the
bottom of his left cheekbone and exited through the top of his head, landing almost 100 feet
behind him. Before his accident, Gage had been efficient, capable, kind and polite. After the
accident he was foul-mouthed, rude and easily annoyed.
3. Mood disorders
Following a traumatic brain injury, up to 50% of people have symptoms of depression.
People with a traumatic brain injury have a significantly increased risk of suicide.
Mania can occur in people with a traumatic brain injury but is much less common than
depression and is usually of short duration.
Affective psychosis is associated with right temporal or orbito-frontal injury.
4. Anxiety disorders
Agoraphobia.
Social phobia.
Panic disorder.
Obsessive compulsive disorder.
Generalised anxiety disorder.
Post-traumatic stress disorder.
5. Psychosis
Higher incidence of schizophrenia among people who have experienced a significant head
injury than the general population.
6. Substance misuse
Alcohol or other drugs are directly involved in more than 33% of incidents that cause brain
injury.
20% of people who did not have a substance abuse problem become vulnerable to substance
abuse after a brain injury.
7. Impulse control disorder
Individuals who have had serious head injuries can be at a higher risk for developing impulse
control disorders which represent a failure to resist an impulsive act or behaviour that may be
harmful to oneself or others.
An impulsive behaviour or act is one over which the individual has little or no control.
Affected individuals often feel anxiety or tension in considering these behaviours.
This anxiety or tension is relieved or diminished once the action is performed.
Whether the diagnosis is that of compulsive gambling, stealing, deliberate fire-setting,
compulsive hair-pulling or outbursts of anger/irritability, the affected individual is unable to
voluntarily control, cut back or stop the pathological behaviour.
Specific lobar damage
Frontal lobe damage
Brocas area Expressive (motor) dysphasia
Dosolateral prefrontal cortex Abulia (loss or impairment of the ability to make decisions or act
independently)
Apathy (absence or suppression of emotion)
Executive function impairment (lack of ability to plan or to sequence
actions or tasks)
Personality changes
Orbitofrontal cortex Disinhibition
Emotional lability
Decreased empathy
Poor judgement (e.g. risk taking)
Lack of insight
Precentral gyrus Apraxia (inability to carry out simple tasks, e.g. dressing, eating)
Contralateral monoplegia or hemiplegia
Paracentral gyrus Incontinence
Not well localised Motor perseveration
Primitive reflexes
Inattention

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Parietal lobe damage
Dominant lobe Gerstmanns syndrome
o Acalculi (inability to do mathematical calculations)
o Agraphia (inability to write)
o Alexia (inability to read)
o Finger agnosia (inability to distinguish fingers on the hand)
o Left/right disorientation
Non-dominant lobe Anosognosia (denial of illness)
Constructional apraxia (inability to copy drawings or to manipulate
objects to form patterns or designs)
Dressing apraxia (inability to dress oneself)
Neglect of contralateral limb
Post-central gyrus Postural sensation impairment
Tactile sensation impairment
Two point discrimination impairment
Optic radiation Lower homonymous quadrantanopia

Temporal lobe damage
Wernickes area Receptive dysphasia
Either right or left lobe damage Contralateral superior quadrantanopia
Bilateral lesion Kluver Bucy syndrome (hyperphagia, a tendency to examine objects
by mouth, and hypersexuality)
Medial temporal Amnesia episodic memory
Inferior lateral Semantic amnesia left sided
Amnesia for faces right sided
Insula Cortical deafness
Deju vu
Jamis ju

Occipital lobe damage
Cortical lesion Homonymous hemianopia
Occipito-temporal (non-dominant) Prosopangnosia (amnesia for faces)
Rating scale
Halstead-Reitan Battery
o Neuropsychological test used in people with a suspected brain injury.

Predictors of poor outcome after head injury
Previous head injury.
Older age.
ApoE4 status.
Alcohol dependence.

4. Psychogenic non-epileptic seizures

A 40 year old woman described an episode of dizziness and loss of balance, which caused her to fall to
the floor while she was shopping. She stated that during the episode, she could hear other people
talking to her but she could not respond. She denied tongue biting or bladder incontinence. Her
daughter who witnessed the episode stated that her mothers head and body rolled from side to side.
Introduction
Psychogenic non-epileptic seizures are paroxysmal episodes that resemble and are often
misdiagnosed as epileptic seizures.
During a non-epileptic seizure, marked involvement of the truncal muscles with opisthotonos and
lateral rolling of the head or body occurs. All four limbs may exhibit random thrashing
movements, which may increase in intensity if restraint is applied
Non-epileptic seizures are psychological (i.e. emotional, stress-related) in origin.
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They are usually involuntary and are classified in ICD-10 under dissociative (convulsion)
disorders (see Chapter 21).
They can also result from voluntary feigning as in malingering and factitious disorder.
The website entitled Functional and Dissociative Neurological Symptoms: A Patients Guide,
can be recommended to patients with non-epileptic seizures: www.neurosymptoms.org
Epidemiology
Non-epileptic seizures are common at epilepsy centres, where they are seen in 20-30% of patients
referred for refractory seizures.
Non-epileptic seizures are also common in the general population, with an estimated prevalence of
2-33 cases per 100,000 population.
Females > males.
Comparison between epilepsy and psychogenic non-epileptic seizures
Epilepsy Psychogenic non-epileptic seizures
Origin Neurological Psychological
Emotional precipitant Less common More common
Loss of consciousness Can occur Does not occur
EEG during a seizure EEG changes occur No EEG changes occur
Onset Rapid Gradual
Occur in the presence of other
people
Can occur but is more
typical of non-
epileptic seizures
More common
Occur during sleep More common Less common
Tongue biting during a seizure Severe global tongue
biting and biting the
inside of the mouth
are more common
Tongue biting less common. If
it occurs, only the tip of the
tongue is usually bitten
Incontinence (urine or faeces)
during a seizure
More common Less common
Shutting eyes during the seizure Less common More common
Head moving from side to side
during a seizure
Less common More common
Increase in prolactin level
following a seizure
Present Absent
Treatment Anticonvulsive
medication
Psychoeducation
Cognitive behavioural therapy
Stress management techniques
such as relaxation therapy
Medications may be indicated
for co-morbid psychiatric
conditions

5. Huntingtons disease (HD)

A 40 year old man presented for an assessment of worsening involuntary movements of his limbs and
face. He has also experienced deteriorating gait associated with numerous falls. His wife stated that he
had been suffering from a pervasively low mood over the past year, associated with initial insomnia
and loss of 6kg in weight. On further questioning, it was revealed that the patients father suffered from
involuntary movements in addition to cognitive dysfunction in the last year of his life. Physical
examination revealed additional findings of a Mini Mental State Examination score of 24 out of 30,
hypertonia and muscle rigidity.

Introduction
An autosomal dominant disorder with 100% penetrance.
Caused by the expansion of over 35 repeats of the trinucleotide sequence cytosine adenine guanine
(CAG) within exon one of the HD gene on chromosome 4, that lengthens a glutamine tract in the
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huntingtin protein. The lengthened glutamine tract is thought to confer a novel toxic property on
huntingtin that initiates the eventual demise of neurons, particularly in the caudate and putamen.
The longer the CAG repeats, the earlier the onset and eventual severity of illness.
Conditions with trinucleotide repeats include:
Condition Gene Chromosome Trinucleotide repeat
Huntingtons disease Huntington 4 CAG
Friedreichs ataxia Frataxin (FXN) 9 GAA
Myotonic dystrophy Dystrophia myotonica
protein kinase (DMPK)
19 CTG
Fragile X syndrome Fragile X mental
retardation 1 (FMR1)
X CGG
Spinobulbar muscular
atrophy
Androgen receptor
gene
X CAG
Epidemiology
Caucasians > Asians or Afro-Caribbeans.
Prevalence is similar for males and females.
Adult-onset HD most often begins between ages 35-50 years.
Early onset (juvenile HD): people develop symptoms of HD before age 20 years.

Clinical features
Motor abnormalities, cognitive disturbance and psychiatric symptoms.
Motor abnormalities
o Uncontrolled movement or tics may develop in the fingers, feet, face or trunk. This is the
beginning stage of chorea (involuntary, rapid, ceaseless movement) which can become more
intense when the person is anxious or disturbed.
Cognitive disturbance
o Over time, judgement, memory and other cognitive functions begin to deteriorate into
dementia.
o Cognitive impairment occurs late in the illness.
Psychiatric symptoms
o Depression
Depression is the most common psychiatric symptom of HD. Depressive symptoms increase
during

the initial stages of disease and peak during stage two of the disease, when
independence diminishes. These two critical periods are also associated with an increased
risk of suicide in HD. Depressive

symptoms may slowly diminish during middle and later
stages

of the disease.
o Other reported psychiatric symptoms include hypomania, bipolar affective disorder, anxiety,
obsessive compulsive disorder and psychosis.
Death usually occurs 15-20 years after the onset of symptoms.

Treatment
A diagnostic test allows presymptomatic diagnosis.
No treatment arrests the course of the disease.
Haloperidol (or other antipsychotics) may help reduce abnormal movements.
Tetrabenazine helps reduce abnormal movements.

6. Parkinsons disease

A 64 year old male presents with a gradually progressive resting tremor, stiffness, and slowness when
initiating movement. On examination the following features were noted: an expressionless face and
staring gaze, with limitation of gaze in all directions.
Introduction
Parkinsons disease is a slow, progressive disease of the central nervous system.
Parkinsons disease is caused by the progressive deterioration of neurons in the substantia nigra.
Affected neurons contain lewy bodies. When functioning normally, these neurons produce
dopamine which functions as a chemical messenger allowing communication between the
substantia nigra and the corpus striatum. This communication coordinates smooth and balanced
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muscle movement. A lack of dopamine results in abnormal nerve functioning, causing a loss in the
ability to control body movements.
For every decade of life, there is estimated to be a 9-13% loss of these dopamine-producing
neurons.
Parkinson's disease may arise as a combined consequence of the on-going aging process, coupled
with environmental exposures that accelerate the process of substantia nigra cell death.
Some people may have a predetermined genetic susceptibility to these environmental insults.
A mutation on chromosome 4 for Park 1 (alpha synuclein gene) is associated with the autosomal
dominant form of Parkinsons disease, with early onset.
Epidemiology
Typically begins in a persons 50s or 60s and slowly progresses with age.
Early onset before age 30 years is rare, but up to 10% of cases begin by age 40 years.
Males > females.
Caucasians > Asians and Africans.
Clinical features
Tremor
o Resting tremor, pill rolling.
Rigidity
o Lead pipe or cog wheel rigidity, especially of flexor muscles.
Bradykinesia
o Slowness in initiating and maintaining movement.
Postural instability
o Characteristic bending or flexion of the body, associated with difficulty in balance and
disturbances in gait.
o Depression
The most common psychiatric symptom in Parkinsons disease.
o Anxiety
o Psychosis
Very rare in untreated individuals; however, anti-parkinsonian medications can cause
hallucinations and delusions.
o Dementia in Parkinsons disease
Usually a subcortical dementia with slowing, impaired executive function, personality
change and memory impairment.
o Dopamine dysregulation syndrome
Dopamine dysregulation syndrome has emerged as a recognised complication of
dopamine replacement therapy in the treatment of Parkinsons disease.
Characterised by a compulsive and escalating pattern of dopaminergic medication use
which results in impulse control disorders, including compulsive gambling, compulsive
shopping, compulsive eating, hypersexuality and punding (repetitive and excessive,
aimless behaviour).
Although the first line of symptom management is usually medication reduction, there is a
growing recognition that psychosocial management (including cognitive behavioural
therapy) can be effective

Treatment
Depression: SSRI or TCA.
Levodopa + dopa-decarboxylase inhibitor (e.g. carbidopa) or dopamine agonist or monoamine
oxidase B inhibitor (e.g. selegiline which may be combined with levodopa + dopa-decarboxylase
inhibitor in more advanced disease).

7. Multiple sclerosis

A 34 year old female presents with a six month history of progressive weakness and spasticity in her
right leg, dizziness, fatigue, malaise and blurring of vision in her left eye. She also describes a
pervasive low mood of four months duration, associated with frequent crying spells.

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Introduction
Multiple sclerosis (MS) is predominantly a white matter disease.
There is evidence of an autoimmune mediated inflammatory response

targeted against myelin in
the central nervous system. With

demyelination, nerve conduction becomes impaired, transmission

of nerve impulses is delayed and symptoms ensue.
Periods of relatively good health alternate with episodes of worsening symptoms.
The aetiology is unknown, but both genetic and environmental

influences are considered
important.
Epidemiology
Females > males.
Males have a greater tendency to develop primary progressive MS, while females tend to
experience more relapses.
Caucasians > Asians and Africans.
The average age of onset is between 20-40 years, but the disorder may develop at any age.
Children of parents with MS have a higher rate of incidence (30-50%).
Clinical features
Diplopia, blurred vision, blindness.
Dizziness and vertigo.
Muscle weakness, muscle pain, difficulty with co-ordination and balance.
Fatigue triggered by heat (from weather or exertion) or physical activity.
Paraesthesia.
Bladder and bowel dysfunction.
Heat sensitivity.
Speech difficulties.
o Cognitive deterioration
Problems with attention, concentration, memory, decision making.
o Lability of mood.
o Depression
The most common psychiatric symptom, occurring in up to 50% of people.
Increased risk of suicidal ideation and completed suicide.
Drug-induced low mood is an important differential diagnosis

of depressive disorder in
MS. Steroids, interferon, baclofen,

dantrolene and tizanidine are all drugs that can cause
depression

in their own right.
o Mania
Occurs

more frequently than expected by chance.
May occur as part of the physical disorder or secondary

to drug treatments, e.g. steroids,
baclofen, dantrolene, tizanidine and illicit substances.
o Anxiety.
o Psychosis
Rare.
o Involuntary emotional expression disorder (pseudobulbar affect)
Episodes of laughing or crying that are unrelated to mood or an event.

8. Wilsons disease

A patient was first seen at the age of 10 years with jaundice, hepatomegaly and anaemia. Serum
caeruloplasmin was reduced. At the age of 15 years, a progressive tremor and a disturbance of gait
were detected. Kayser Fleischer rings were noted on slit-lamp examination. At the age of 32 years, she
described a worsening pervasive low mood of six months duration, associated with suicidal ideation.

Introduction
Autosomal recessive inherited disorder of copper metabolism.
Genetic defect localised to chromosome 13, which affects the copper-transporting adenosine
triphosphatase (ATPase) gene in the liver.
Incorporation of copper into caeruloplasmin and the excretion of excess copper into bile are
impaired.
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Copper accumulates initially in the liver.
As liver copper levels increase, copper is released into the circulation and deposited in other
organs, e.g. brain, kidney and cornea.

Epidemiology
Females > males.
Usually presents with liver disease during the first decade of life or with neuropsychiatric illness
during the third decade.

Clinical features
Liver
o Hepatic dysfunction.
Kidneys
o Renal tubular dysfunction.
Eyes
o Pigmented corneal rings (Kayser Fleischer rings).
o Sunflower cataract
Copper deposition in the lens that assumes a sunburst or sunflower appearance, with a
central disc and radiating petal-like spokes.
Nervous system
o Tremor which may be resting, postural or kinetic.
o Dysarthria.
Bone and joint involvement
o Osteoporosis.
o Joint pain.
Haemolytic anaemia
o Presumably due to copper-induced oxidative damage to erythrocytes.
o Cognitive impairment.
o Depression.
o Personality change.
o Psychosis.
Investigations
Increased serum/urine copper.
Decreased serum caeruloplasmin (the copper binding protein).

Treatment
Penicillamine
o Binds to accumulated copper and eliminates copper through the urine.

218

MCQs Chapter 22

Question 1: Which ONE of the following statements is FALSE?
A. Selective serotonin reuptake inhibitors are generally the first line biological treatment for
depression associated with neuropsychiatric presentations.
B. Atypical antipsychotics have been associated with increased mortality in agitated patients with
dementia.
C. Mania is less common than anxiety in neurological patients.
D. Depression is the most common psychiatric presentation associated with neurological disease.
E. Tricyclic antidepressants are usually not efficacious for neuropsychiatric presentations.

Question 2: Which ONE of the following statements regarding stroke is TRUE?
A. The majority of haemorrhagic strokes occur in the pons.
B. Retrograde amnesia is prominent in the amnestic disorder.
C. Approximately 50% of people with present with depression in the first month after a stroke.
D. The majority of strokes are haemorrhagic in nature.
E. Cognitive deficits tend to be more severe with strokes that affect the hindbrain than with those
that affect the midbrain.

Question 3: Which ONE of the following statements regarding stroke is TRUE?
A. Anxiety is the commonest psychiatric consequence of stroke.
B. There is an increased risk of depression after a stroke with left-sided cortical lesions than with
right frontal lesions.
C. Approximately 50% of people after a stroke meet the criteria for generalised anxiety disorder.
D. The peak of depression after a stroke is at 6-8 months after a stroke.
E. There is an increased risk of psychosis after a stroke with left rather than right hemisphere
infarcts.

Question 4: Which ONE of the following statements regarding temporal lobe epilepsy is FALSE?
A. Infantile spasms are a type of generalised seizure.
B. Preictal symptoms are usually intensified during a seizure.
C. Ictal aggression is very rare.
D. Consciousness is not impaired with a focal seizure.
E. Up to 50% of people with epilepsy develop psychiatric disorders.

Question 5: Which ONE of the following statements regarding temporal lobe epilepsy is TRUE?
A. Cognitive deterioration is a rare outcome of chronic epilepsy.
B. There is an increased risk of violence and aggression in people with epilepsy.
C. Hypersexuality and hypographia are symptoms of the epileptic personality syndrome.
D. Automatisms are associated with clouded consciousness.
E. Depression affects 70% of people with epilepsy.

Question 6: Which ONE of the following statements regarding head injury is TRUE?
A. Retrograde amnesia is a poor prognostic indicator.
B. Acquired brain injury occurs prior to birth.
C. Affective psychosis is associated with left rather than right temporal injury.
D. The risk of schizophrenia is not increased following a head injury.
E. There is a decreased risk of suicide in people following a head injury.

219

Question 7: Which ONE of the following is MOST LIKELY to be predictor of a poor outcome
following a head injury?
A. Younger age.
B. Apolipoprotein e4 status.
C. Working in the fishing industry.
D. Married status.
E. Absence of previous head injury.

Question 8: Which ONE of the following statements regarding psychogenic non-epileptic seizures
is TRUE?
A. The onset is rapid.
B. Consciousness is invariably lost.
C. If the tongue is bitten, the area most affected is the base of the tongue.
D. A patient more commonly closes his eyes during a psychogenic non-epileptic seizure than
during a true epileptic seizure.
E. They tend to be neurological in origin.

Question 9: Which ONE of the following associations is FALSE?
A. Myotonic dystrophy - CTG.
B. Spinobulbar muscular atrophy - CAG.
C. Huntingtons disease - CAG.
D. Friedreichs ataxia - GAA.
E. Fragile X syndrome - CCG.

Question 10: Which ONE of the following statements regarding Huntingtons disease is FALSE?
A. Huntingtons disease is an autosomal dominant disorder with 100% penetrance.
B. The longer the affected trinucleotide repeats, the later the onset of the disease.
C. Death usually occurs 15-20 years after the onset of symptoms.
D. No treatment arrests the course of the disease.
E. The prevalence is similar in males and females.

Question 11: Which ONE of the following statements regarding Parkinsons disease is FALSE?
A. The autosomal dominant form of Parkinsons disease is associated with a mutation for Park 1
gene on chromosome 6.
B. Anti-parkinsonian medications can cause hallucinations and delusions.
C. Affected neurons in the substantia nigra contain lewy bodies.
D. The most common form of dementia is subcortical.
E. Up to 10% of cases begin by age 40 years.

Question 12: Which ONE of the following statements regarding multiple sclerosis is FALSE?
A. Periods of relatively good health are interspersed with worsening symptoms.
B. Fatigue triggered by heat is a feature of the condition.
C. The condition is more common in Caucasians than Asians.
D. Multiple sclerosis is predominantly a disease of grey matter.
E. Females are more likely than males to experience relapses.

Question 13: Which ONE of the following statements regarding Wilsons disease is TRUE?
A. Wilsons disease is an autosomal dominant condition.
B. More common in males than females.
C. Serum caeroplasmin is reduced.
D. The condition usually presents with neuropsychiatric disease during the second decade of life.
E. The genetic defect is on chromosome 12.

220

Questions 14-18: Brain injury
A. Dominant parietal lobe
B. Precentral gyrus
C. Bilateral temporal lobe
D. Orbitofrontal cortex
E. Dorsolateral prefrontal cortex
F. Post-central gyrus
G. Unilateral temporal lobe
H. Paracentral gyrus
I. Non-dominant parietal lobe
J. Occipito-temporal region
For each of the presentations below, choose the single most likely area of brain injury from the above
list of options. Each option may be used once, more than once or not at all.
14. Apraxia.
15. Contralateral superior quadrantanopia.
16. Gerstmanns syndrome.
17. Prosopangnosia.
18. Executive function impairment.

221

MCQ answers Chapter 22

1. E
2. C
3. B
4. B
5. D
6. A
7. B
8. D
9. E
10. B
11. A
12. D
13. C
14. B
15. G
16. A
17. J
18. E

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Chapter 23
Psychiatry of the elderly
223

Chapter 23: Psychiatry of the elderly
Introduction
Patients suitable for referral to a Psychiatry of the Elderly Service include:
o Patients aged 65 years and over with a new onset of mental illness.
o Patients suffering from dementia with associated psychological or behavioural problems.
Services include:
o Domiciliary assessment (i.e. an assessment in the home of a patient)
Assessment at home is beneficial as people are most likely

to behave and communicate in
their normal way in familiar surroundings.

It also provides a more accurate picture of a patients needs

and enables learning from the
views of carers.
Professionals can observe

whether patients

can make themselves a hot drink and whether
there are any likely

risks from poor hygiene or fire hazards.
Looking in the fridge and the food cupboards provides

a quick and informative check on
food intake and a patients

ability to monitor when food is no longer safe to eat.
o Day hospital
Provide a very real alternative to acute hospital admission for both dementia sufferers
who have severe behavioural or psychiatric symptoms and people with functional illness
such as depression.
Active psychiatric treatment involving biological, social and psychological approaches
takes place in day hospitals.
o Day centre
Provides socialisation for older people.
Provides carer relief (i.e. a break for carers while the elderly person attends the day
centre).
o Outpatient clinic
Outpatient clinics are particularly useful for follow up of elderly patients with functional
psychiatric disorders such as depression who do not require the intensive treatment
modalities available in the day hospital setting.
o Inpatient care
Acute inpatient beds: required for acute psychiatric illness.
Long-stay inpatient beds: may be required for -
People with dementia who have severe behavioural problems, unamenable to
treatment.
People with dementia who are immobile and may also have severe physical
problems.
People with dementia who are mobile and who do not have severe psychiatric or
physical problems but undertake such activities as wandering. The needs of this
group of people are for care in a safe, supervised environment which allows them to
move around but under supervision and also provides personal care.

Changes associated with normal aging
Brain changes
o Ventricle volume and sulci increase.
o Brain volume and weight decreases
The decrease in brain volume is not uniform.
Occipital cortex is least affected.
o Cellular metabolism decreases.
o Grey matter volume decreases between adulthood and old age.
o White matter volume increases from age 19-40 years and then declines.
o All the following increase with age and have been related to memory loss:
Neurofibrillary tangles.
Senile amyloid plaques.
Lewy bodies.
Hirano bodies.
Lipofuscin accumulation.
Intellectual functioning
o IQ peaks at 25 years, plateaus until 60-70 years and then declines.
o Performance IQ declines after the age of 30 years and drops markedly after age 65 years.
224

o Verbal IQ is less affected.
o Short-term memory does not alter with age, but working memory declines.
o Long-term memory declines, except for remote events of personal significance which may be
recalled with great clarity.
o Verbal comprehension shows little or no decline.
o Scientific creativity peaks in the 30s.
o Artistic creativity peaks in the 50s.
Note: dementia is not part of normal aging.
Body changes
o Decreased
Total body mass.
Body water.
Body muscle.
Rate of gastric emptying.
Blood flow in splanchnic circulation.
Gastrointestinal absorptive surface.
Metabolically active tissue.
Liver volume and blood flow.
epatic biotransformation.
Renal blood flow and renal function.
Renal tubular function.
o ncreased
Body fat.
Gastric pH (i.e. less acidic).
Dementia
Introduction
Dementia is a syndrome due to disease of the brain, usually of chronic or progressive nature in
which there is a disturbance of higher cortical functions, including memory, thinking, orientation,
comprehension, calculation, learning capacity, language and judgement.
The impairment of memory typically affects the registration, storage and retrieval of new
information. Previously learned and familiar material may also be lost, particularly in the later
stages.
Consciousness is not clouded (versus delirium where it is clouded).
Many people with dementia experience periods of confusion and wandering at which are worse
night. This is referred to as sundowning.
The four As of dementia:
o Amnesia: loss of recent rather than remote memory.
o Agnosia: inability to recognise objects, a family member or even ones own reflection in the
mirror.
o Apraxia: inability to carry out simple tasks, e.g. dressing, eating.
o Aphasia: inability to speak, which can be receptive or expressive.
Epidemiology
Prevalence 5% of people > 65 years
20% of people > 80 years
Gender Alzheimers disease: females > males
Vascular dementia: males > females
Race Caucasian race is a risk factor for dementia
Aetiology
Irreversible causes
o Alzheimers disease (the most common type of dementia).
o Vascular dementia (the second most common type of dementia).
o Dementia in Picks disease (frontotemporal dementia).
o Dementia in Creutzfeldt Jakob disease.
o Dementia in Huntingtons disease.
o Dementia in Parkinsons disease.
o Dementia in human immunodeficiency virus (HIV) disease
o Lewy body dementia.
225

Treatable causes
o Head injury.
o Chronic alcohol use.
o Infections, e.g. meningitis or encephalitis.
o Normal pressure hydrocephalus.
o Brain tumours.
o Heavy metal exposure, e.g. lead, arsenic, mercury or manganese.
o Hypoxia.
o Endocrine disorders
Addisons disease.
Cushings disease.
Diabetes.
Hyperparathyroidism or hypoparathyroidism.
Hypothyroidism or hyperthyroidism.
Phaeochromocytoma.
o Metabolic disorders
Hypercalcaemia.
Hyponatraemia.
Renal failure with uraemia.
Hepatic failure.
Porphyria.
o Nutritional deficiencies
B
1
(thiamine) deficiency.
B
12
(cobalamin) deficiency.
Pellagra (deficiency of niacin or tryptophan).
Protein calorie malnutrition.
o Drug reactions or misuse
Hypnotics.
Anticholinergic medications.
Illicit substances (especially heroin and cocaine).
Clinical picture
Stage 1 early dementia
o Word-finding difficulties.
o Short-term memory loss.
o Difficulties performing activities of daily living (ADLs), e.g. cooking, feeding, shopping,
washing, using the telephone.
o Confusion, disorientation in unfamiliar surroundings - may wander, trying to return to familiar
surroundings.
o Personality changes
A sociable person becomes withdrawn or a shy person becomes more extraverted.
o Mood swings, often with periods of irritability or anger.
o Paranoia.
Stage 2 intermediate dementia
o Deterioration of early dementia symptoms.
o Unable to learn new material.
o Needs help with ADLs.
o Increasing disorientation and confusion even in familiar surroundings.
o Confabulation.
o Inappropriate sexual behaviour.
o Anxiety, depression and agitation.
o Paranoid delusions and hallucinations.
Stage 3 severe dementia
o Worsening of symptoms seen in early and intermediate dementia.
o Loss of short-term and long-term memory.
o Complete dependence on others for ADLs.
o Impaired swallowing.
o Incontinence.
o Contractures.
Note: short-term memory loss occurs early in dementia. Long-term memory loss occurs late in the
illness.
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Diagnosis of dementia
History.
Mental state examination.
Collateral history.
Physical examination (including neurological examination).
Investigations.
Review of medications in order to identify and minimise the use of drugs, including over-the-
counter products that may adversely affect cognitive functioning.

1. History
History of presenting complaint
o Onset, duration, progression and impact of symptoms.
o Features suggestive of dementia
Chronic or progressive disorder in which there is a disturbance of higher cortical
functions, including memory, thinking, orientation, comprehension, calculation,
learning capacity, language and judgement.
Clear consciousness.
o Attempt to distinguish Alzheimers dementia from vascular dementia
Insidious onset in Alzheimers dementia (versus abrupt onset in vascular dementia)
and slow steady progression over years in Alzheimers dementia (versus stepwise as
in vascular dementia).
o Features suggestive of Picks disease (a type of frontotemporal dementia)
Predominance of frontal lobe features (euphoria, emotional blunting, coarseness of
social behaviour, disinhibition and either apathy or restlessness).
o Features suggestive of Lewy body dementia
Parkinsonian motor features.
Visual hallucinations.
Fluctuations in cognitive function with varying levels of alertness and attention.
Sensitivity to antipsychotic (neuroleptic) medication.
Past psychiatric history
o Previous contact with the psychiatric services.
Family history
o Family history of dementia or other neurological disease
Past medical and surgical history
o History of stroke, transient ischaemic attacks with brief impairment of consciousness,
fleeting pareses or visual loss (all of these are risk factors for vascular dementia).
o Identify other disorders that can cause loss of memory, confusion, attention deficit or
symptoms similar to dementia that include:
Anaemia, malnutrition or vitamin deficiencies.
Diabetes.
Kidney or liver disease.
Thyroid abnormalities.
Problems with the heart, lung or blood vessels.
Alcohol and substance misuse history
Current medications
Personal history
Forensic history
Premorbid personality
2. Physical examination (including neurological examination)
Evidence of hypertension or stroke (e.g. paresis) vascular dementia.
Focal neurological signs and symptoms vascular dementia.
3. Collateral history
Onset, duration and progression of symptoms.
Ability to carry out activities of daily living (e.g. bathing, grooming, toileting, eating or more
complex activities).
Prior level of functioning.
Any recent changes in medications, environment and health status.
Assessment of social support system for both the patient and caregiver.
4. Mental state examination
Appearance and behaviour (e.g. impairment of consciousness, evidence of self-neglect).
227

Speech.
Mood (e.g. anxious, depressed).
Abnormalities of thought (e.g. obsessional thoughts, thought disorder, delusions, suicidal and
homicidal thoughts).
Perception (e.g. hallucinations).
Cognition (e.g. impairment in: memory, orientation, comprehension, calculation, judgement).
Insight (e.g. does she believe she is unwell and in need of treatment?).
5. Investigations
Biological
o Bloods: FBC, RFT, LFT, TFT, fasting glucose, B
12
, folate.
o ECG, CXR, CT / MRI brain.
o Mini Mental State Examination (MMSE) see Appendix 1.
o Montreal Cognitive Assessment see Appendix 2.
o Clock Drawing Test see Appendix 3.
o Cognitive assessment see Appendix 4.
Psychological
o Risk assessment.
o Neuropsychological testing to identify retained abilities and specific problem areas such
as comprehension, insight and judgement.
Social
o Collateral history (from family, GP, psychiatric services including details of previous risk
assessments).
o Documentation (GP records, psychiatric case notes).
o Occupational therapy: assessment of the patients activities of daily living (ADLs) and
needs.
Memory clinic
o Memory clinics provide multi-disciplinary assessments for people experiencing memory
difficulties and allows for comprehensive investigation and initiation of treatment, where
appropriate.
o Information, education and support are provided for family caregivers.
o Memory clinics have inputs from neuropsychology, psychiatry, nursing and other mental
health disciplines when necessary.

Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA)
Both the MMSE and the MoCA are routine cognitive screening tests rated on a 30-point scale.
The MMSE is a widely used screening tool for dementia, with a diagnostic threshold usually
set at less than 27 points.
o Any score greater than or equal to 27 points (out of 30) on the MMSE is effectively
normal (intact). Below this, scores can indicate severe (10 points), moderate (11-20
points) or mild (21-26 points) cognitive impairment.
The suggested cut-off point on the MoCA is 26 points.
The MoCA has been shown to be more sensitive at detecting mild cognitive impairment and
mild Alzheimers dementia than the MMSE. Mild cognitive impairment is considered a
preclinical stage of Alzheimers disease and may extend over decades. During this preclinical
stage, most patients with mild cognitive impairment score at least 26 out of 30 on the MMSE,
which is within the normal range for elderly patients.
o Mild Alzheimers disease: MoCA sensitivity 100% vs MMSE 78%.
o Mild cognitive impairment: MoCA sensitivity 90% vs MMSE 18%.
Overall, the MMSE is likely a better test than the MoCA for more severe cases of Alzheimers
disease.
The MoCA has more emphasis on tasks of frontal executive functioning and attention than the
MMSE, which may make it more sensitive in detecting non-Alzheimers dementia (e.g.
frontotemporal dementia, vascular dementia, dementia with Lewy bodies and dementia in
Parkinsons disease).

ICD-10 classification
1. Dementia in Alzheimers disease
A. Dementia in Alzheimers disease with early onset.
B. Dementia in Alzheimers disease with late onset.
C. Dementia in Alzheimers disease, atypical or mixed type.
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2. Vascular dementia
A. Vascular dementia of acute onset.
B. Multi-infarct dementia.
C. Subcortical vascular dementia.
D. Mixed cortical and subcortical vascular dementia.
3. Dementia in other diseases classified elsewhere
A. Dementia in Picks disease.
B. Dementia in Creutzfeldt Jakob disease.
C. Dementia in Huntingtons disease.
D. Dementia in Parkinsons disease.
E. Dementia in human immunodeficiency virus (HIV) disease.
F. Dementia in other specified diseases classified elsewhere.
1. Alzheimers disease
A 65 year old man is brought to the Emergency Department by his daughter. She is concerned about
her father due to his gradual deterioration in short-term memory over the past five years, associated
with a decline in his ability to perform daily activities. He has difficulty undertaking household tasks
such as preparing meals, which he had previously enjoyed doing. He no longer feels able to use his
computer as he cannot remember how to use it. She described that he had started to wander away from
home, more frequently in the late afternoon and evening.
ICD-10 criteria
Presence of a dementia.
Insidious onset with slow deterioration.
Absence of clinical evidence, or findings from special investigations, to suggest that the mental
state may be due to other systemic or brain disease which can induce a dementia (e.g.
hypothyroidism, hypercalcaemia, vitamin B
12
deficiency, niacin deficiency, neurosyphilis, normal
pressure hydrocephalus or subdural haematoma).
Absence of neurological signs of focal damage such as hemiparesis, sensory loss, visual field
defects and incoordination occurring early in the illness (although these phenomena may be
superimposed later).
Note: the delusions in Alzheimers disease tend to be simple in comparison to those in someone with
schizophrenia. In Alzheimers disease for example, the person may believe that someone is stealing
their belongings.

Subtypes
A. Dementia in Alzheimers disease with early onset
Dementia in Alzheimer's disease beginning before the age of 65 years.
There is relatively rapid deterioration, with marked multiple disorders of the higher cortical
functions. Aphasia, agraphia, alexia, and apraxia occur relatively early in the course of the
dementia.
Family history of Alzheimer's disease is a contributory but not necessary factor for the
diagnosis, as is a family history of Downs syndrome or of lymphoma.
B. Dementia in Alzheimers disease with late onset
Dementia in Alzheimers disease where the clinically observable onset is after the age of 65
years and usually in the late 70s or thereafter.
Slow progression, usually with memory impairment as the principal feature.
C. Dementia in Alzheimers disease, atypical or mixed type
Dementias that do not fit the descriptions and guidelines for either A or B above.

Aetiology risk factors
Age
o The main risk factor for Alzheimers disease is increased age. As the population ages, the
frequency of Alzheimers disease increases.
o Advanced maternal age at birth.
Gender
o Females > males.

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Downs syndrome (trisomy 21)
o Develop the brain changes of Alzheimers disease by 40 years of age.
Education
o People who have completed less than eight years of education are at increased risk of
developing Alzheimers disease.
Mild cognitive impairment (MCI)
o More than 50% of people with MCI later develop dementia.
Systemic vascular disease or risk
Small head size
History of head trauma
Genetics
o A family history of Alzheimers disease increases the risk.
Molecular genetics
Chromosome Implicated gene Pattern of onset of Alzheimers disease
1 Presenilin 2 (PS-2) Early onset autosomal dominant
14 Presenilin 1 (PS-1) Early onset autosomal dominant
19 Apolipoprotein e4 (ApoE4) Late onset sporadic
21 Amyloid precursor protein (APP) Early onset autosomal dominant

Possible protective factors
Apolipoprotein E2 genotype.
History of oestrogen replacement therapy in postmenopausal women.
Higher educational level.
History of use of non-steroidal anti-inflammatory agents (NSAIDs).
Smoking.
Moderate alcohol consumption.
Fish consumption.
Apolipoprotein E (ApoE)
ApoE exists in 3 forms:
o ApoE2 protective against Alzheimers disease.
o ApoE3 increases the risk of developing late onset Alzheimers disease.
o ApoE4 increases the risk of developing late onset Alzheimers disease 4 times if one copy of
ApoE4 gene is inherited and 10 times if two copies of ApoE4 gene are inherited (one from
each parent).
Neuropathology
Alzheimers disease begins in the entorhinal cortex and proceeds to the hippocampus, which is
essential to the formation of short- and long-term memories. Affected brain regions atrophy.
Cortical atrophy.
Enlargement of the lateral ventricles.
Neurofibrillary tangles
o Intracellular protein accumulations.
Amyloid plaques (extracellular)
o Plaques are made of beta-amyloid, a protein fragment snipped from a larger protein called
amyloid precursor protein (APP).
Granulovacuolar degeneration of neurons.
Glial proliferation (gliosis).
Loss of cortical neurons.
Hirano bodies.
Astrocyte proliferation.

Neurochemistry
Decreased acetylcholine
o The cholinergic system is involved in memory functioning.
o Cholinergic deficiency has been implicated in the cognitive decline and behavioural changes
of Alzheimers disease.
o Both acetylcholinesterase and butyrylcholinesterase play an important role in the degradation
of acetylcholine.
230

Decreased norepinephrine.
Decreased epinephrine.
Decreased serotonin.
Decreased somatostatin.
Decreased gamma aminobutyric acid (GABA).
Decreased creatine kinase.
Management
Reversible causes of cognitive impairment must be identified and corrected as far as possible (e.g.
physical conditions such as delirium and hypothyroidism).
Biological
o Anticholinesterase (AChE) inhibitors (e.g. donepezil, rivastigmine or galantamine) prevent
the breakdown of acetylcholine
Donepezil and galantamine are selective inhibitors of AChE.
Rivastigmine affects both AChE and butyrylcholinesterase (BuChE).
The three AChE inhibitors are licensed in Ireland for the treatment of mild to moderate
Alzheimers disease.
Side effects of the AChE inhibitors: nausea, vomiting, loss of appetite, diarrhoea.
Medication cannot cure Alzheimers disease. It may however help to stabilise symptoms
for a limited amount of time before the illness progresses.
o Memantine
NMDA antagonist.
Used for treatment of moderate to severe Alzheimers disease.
Main effect is to delay progression of some of the symptoms of moderate to severe
Alzheimers disease. It may allow patients to maintain certain daily functions a little
longer than they would without the medication.
o Ginkgo biloba
Cognitive enhancer that may have neuroprotective effects.
May be effective in mild to moderate Alzheimers disease.
o Depression: SSRIs (e.g. fluoxetine, paroxetine, sertraline).
o Psychosis: low dose atypical antipsychotics (e.g. quetiapine) as the elderly are very sensitive
to side effects.
Note: clinical trials in dementia have shown an association between risperidone and olanzapine with
cerebrovascular accidents.
Psychological
o Risk management.
o Psychoeducation.
o Art therapy
Provides meaningful stimulation, improves social interaction and improves levels of self-
esteem.
o Music therapy
Involvement in a musical activity (e.g. singing or playing an instrument) or listening to
songs and music.
Can increase levels of well-being, improve social interaction and improve
autobiographical memory.
o Behavioural therapy
Has been shown to decrease wandering and incontinence.
o Reality orientation
Aims to help people with memory loss and disorientation by reminding them of facts
about themselves and their environment.
People with memory loss are orientated to their environment using a range of materials
and activities, e.g. signposts and notices identifying the bathroom, fridge etc.
o Validation therapy
Attempts to communicate with people with dementia by empathising with their feelings
and meanings hidden behind their confused speech and behaviour.
o Reminiscence therapy
Helps people with dementia relive past experiences, e.g. showing photographs of family
holidays and weddings.

231

Social
o Meals on wheels
Meals can be delivered to peoples homes in the case of those who are unable due to age,
illness or disability, to cook their own meals.
For many elderly people the volunteer delivering their meal may be their only social
contact for the day and as far as possible volunteers try to take the opportunity to spend a
little time with them.
o Home help
Assist with normal household tasks such as shopping and cleaning and are assigned to
people who are unable to carry out such tasks themselves.
o Activity therapy
Involves recreations such as dance, sport and drama.
Physical exercise in dementia can reduce the number of falls and improve mental health
and sleep.
o Complementary therapy
Massage, reflexology, reiki, herbal medicine and aromatherapy.
o Animal assisted therapy (pet therapy)
Pairing of animals and people with specific needs.
The ideal pet is gentle and placid, never aggressive.
While a variety of animals are used, dogs are particularly well suited for therapy sessions
with elderly people.
Reduces isolation and provides a social context to share time with others in a comfortable,
non-confrontational atmosphere.
Particularly useful in people who were life-long pet lovers. It is a window into the past
allowing the recall of long forgotten animal companions.
o Social work input to assist with supported accommodation if needed.
o Occupational therapy input to improve skills.
o Carer support
Consider the psychological and practical needs of carers.
Care plans for carers of people with dementia should involve a range of tailored
interventions
Individual or group psychoeducation.
Peer-support groups with other carers, tailored to the needs of individuals depending
on the stage of dementia of the person being cared for and other characteristics.
Support and information by telephone and through the internet.
Training courses about dementia, services and benefits, and communication and
problem solving in the care of people with dementia.
Involvement of other family members as well as the primary carer in family meetings.
Transport or short break services should ideally be provided for carers to enable them
to participate in interventions.
Carers of people with dementia who experience psychological distress and negative
psychological impact should be offered psychological therapy, including cognitive
behavioural therapy.
o Support groups
Alzheimer Society of Ireland offers:
Day care centres.
Home care.
Respite care.
Social clubs (weekly drop in centre for people with dementia and their carers, family
and friends).
The Dementia Rights Advocacy Service
Helps people with dementia voice their needs and wishes, access their entitlements and
assert their rights.
Other possible treatment strategies
o Bright light therapy (may improve fluctuations in diurnal rhythms that might account for
night-time disturbances) and multisensory approaches (which involve using a room designed
to provide several types of sensory stimulation such as light often in the form of fibre optics
which can move and are flexible, texture in the form of cushions, smell and sound).
o Antioxidants (vitamins C and E, alcohol and green tea).
o Anti-inflammatory agents (NSAIDs may offer a neuroprotective effect by inhibition of both
cyclo-oxydenases COX-1 and COX-2).
232

o Secretase inhibitors.
o Metal chelators.
o Amyloid--peptide vaccination.
o Cholesterol lowering medications.
o Physical activity (decreases cardiovascular risk and increases insulin-like growth factor [IGF-
1] which has been shown to decrease -phosphorylation, a process implicated in Alzheimers
disease).

Prognosis
There is no known cure for Alzheimer's disease. The disease naturally progresses and worsens over
time.
On average, people with Alzheimers disease live eight years after their diagnosis, with a range
from 1-20 years.
The most common cause of death is an infection such as pneumonia.
Factors associated with poor prognosis:
o Males.
o Onset before the age of 65 years.
o Severe cognitive deficits.
o Severe behavioural problems.
o Parietal lobe involvement.
o Absence of misidentification syndrome (see Chapter 20).

2. Vascular dementia

A 70 year old man with a history of memory deterioration has a mild hemiparesis, nocturnal confusion
and persecutory delusions.
ICD-10 criteria
Dementia.
Abrupt onset with stepwise deterioration.
History of transient ischaemic attacks (or less commonly a major stroke) with brief impairment of
consciousness, fleeting pareses or visual loss.
Associated factors: hypertension, carotid bruit.
Presence of focal neurological signs and symptoms.
Note: the Hatchinski Ischaemic Score is a tool used to differentiate vascular dementia from other forms
of dementia.

Subtypes
A. Vascular dementia of acute onset
Usually develops rapidly after a succession of strokes from cerebrovascular thrombosis,
embolism or haemorrhage.
In rare cases, a single large infarction may be the cause.
B. Multi-infarct dementia
A more gradual onset than the acute form, following a number of minor ischaemic episodes
which produce an accumulation of infarcts in the cerebral parenchyma.
C. Subcortical vascular dementia
There may be a history of hypertension and foci of ischaemic destruction in the deep white
matter of the cerebral hemispheres which can be suspected on clinical grounds and
demonstrated on computerised axial tomography scans.
The cerebral cortex is usually preserved.
D. Mixed cortical and subcortical vascular dementia
Mixed cortical and subcortical components of the vascular dementia may be suspected from
the clinical features, the results of investigations (including autopsy), or both.
Epidemiology
In most countries, vascular dementia is a less common form of dementia than Alzheimers disease.
This is true in North America and Europe but is not so in Japan, where it is more common than
Alzheimers disease.
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Overall, vascular dementia is the second most common form of dementia, after Alzheimers
disease.
Aetiology risk factors
Age
o As the population ages, the frequency of vascular dementia increases.
o Vascular dementia usually occurs at a younger age than Alzheimers disease.
Gender
o Males > females.
Genetics
o Apolipoprotein E4 (ApoE4) gene is a risk factor for both Alzheimers disease and vascular
dementia.
o Mutations in the Notch 3 gene on chromosome 19 is a risk factor for a form of vascular
dementia known as cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy (CADASIL). The Notch 3 gene is on the same locus as the gene for
familial hemiplegic migraine.
Vascular risk factors
o Hypertension.
o Smoking.
o Excessive alcohol consumption.
o Obesity.
o Hypercholesterolemia.
o Diabetes mellitus.
o Cardiovascular and cerebrovascular disease.
Management
Biological
o Reduction of vascular risk factors
Antihypertensive.
Aspirin.
Smoking cessation.
Avoidance of excessive alcohol consumption
Diet.
Exercise.
Statin.
o Anticholinsterase inhibitors have been used for vascular dementia (unlicensed).
Psychological
o As for Alzheimers disease above.
Social
Comparison between Alzheimers disease and vascular dementia
Alzheimers disease Vascular dementia
Ranking Most common form of dementia Second most common form of dementia
Gender Females > males Males > females
Age Later age of onset Earlier age of onset
Onset Insidious (gradual) Abrupt
Progression Slow and steady Stepwise
Vascular risk factors Less common More common
Focal neurological signs and
symptoms
Risk of co-existent depression,
persecutory delusions, anxiety
and emotional disturbance
Personality changes More common Less common
Deterioration in insight and
judgement
More common Less common
Anticholinsterase inhibitors and
memantine
Licensed for use Not licensed for use
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CT scan Mainly temporal lobe atrophy Infarcts. White matter change
EEG Usually abnormal even early in
the disease. It shows a slowing of
alpha waves initially, later
increased delta and theta waves
EEG is of limited help, although it is
possible that there may be focal activities
at the site of a thrombosis
3. Dementia in other diseases classified elsewhere
ICD-10 criteria
Cases of dementia due, or presumed to be due, to causes other than Alzheimers disease or
cerebrovascular disease.
Onset may be at any time in life, though rarely in old age.

Subtypes
A. Dementia in Picks disease (a type of frontotemporal dementia)
Dementia in Picks disease scenario
o The wife of a 55 year old man expresses concern that her husbands memory has deteriorated
and his personality appears to have changed. When he is assessed, he is noted to be giggling
inappropriately and is restless.
Features of the condition
o A progressive dementia.
o Occurs at an earlier age than Alzheimers disease.
o Frontal and temporal lobes are predominantly affected.
o A predominance of frontal lobe features with euphoria, emotional blunting, and coursing of
social behaviour, disinhibition and either apathy or restlessness.
o Behavioural manifestations which commonly precede frank memory impairment.
o Argyrophilic inclusions (Pick bodies) and swollen cells (Pick cells) in the atrophic frontal and
temporal brain regions.
o Knife blade atrophy occurs due to neuronal loss.
Note: the Wisconsin Card Sorting Test is a measure of executive functioning due to the sensitivity in
detecting frontal lobe dysfunction.
B. Dementia in Creutzfeldt Jakob disease (CJD)
Dementia in Crutzfeldt Jakob disease scenario
o A 65 year old woman presented with a functional decline and memory loss of one month
duration. She had previously been a capable, active member of the community but is now
having difficulty dressing herself and undertaking other activities of daily living.
Investigations are unremarkable apart from a triphasic EEG pattern.
o Rapidly progressing dementia.
o Pyramidal and extrapyramidal disease with myoclonic jerks.
o Characteristic triphasic EEG.

C. Dementia in Huntingtons disease
Dementia in Huntingtons disease scenario
o A 45 year old man has a history of memory decline, progressive writhing bodily movements
and a family history of dementia.
o Dementia.
o Choreiform movement disorder.
o Family history of Huntingtons disease.
D. Dementia in Parkinsons disease
Dementia in Parkinsons disease scenario
o A 50 year old man has a history of a memory decline, tremor at rest, rigidity, slowness of
movement, and postural instability.
o Dementia developing in an individual with advanced, usually severe, Parkinsons disease.

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E. Dementia in human immunodeficiency virus (HIV) disease
Dementia in human immunodeficiency virus disease scenario
o A 50 year old man with HIV has a history of memory decline.
o A disorder characterised by cognitive deficits meeting the clinical diagnostic criteria for
dementia, in the absence of a concurrent illness or condition other than HIV infection that
could explain the findings.
F. Dementia in other specified diseases classified elsewhere
o Dementia can occur as a manifestation or consequence of a variety of cerebral and somatic
conditions.
Lewy body dementia

A 60 year old woman presents with a fluctuating cognitive impairment, visual hallucinations, tremor
and rigidity. The GP prescribed risperidone which resulted in severe extrapyramidal side effects
Dementia.
Features of Parkinsons disease, e.g. tremor, rigidity, bradykinesia, postural change, gait
disturbance.
Fluctuations in cognitive function with varying levels of alertness and attention.
Visual hallucinations (most commonly of people or animals).
Note: visual hallucinations in Lewy body dementia are linked to attentional dysfunction and
cholinergic hypofunction.
Sensitivity to antipsychotic medication and to antiemetic medications that affect dopaminergic and
cholinergic systems
o Can cause dramatic EPSEs and neuroleptic malignant syndrome.
Pathology
Lewy bodies, clumps of alpha synuclein and ubiquitin protein in neurons, present in the substantia
nigra.
Note: lewy bodies are also found in 10-20% of cases of Alzheimers disease and in Parkinsons
disease. Lewy bodies are therefore not specific to Lewy body dementia.
Loss of dopamine-producing neurons in the substantia nigra similar to that seen in Parkinson's
disease.
Loss of acetylcholine producing neurons similar to that seen in Alzheimers disease.
Alzheimer-type changes with plaques present in a similar density and distribution, but fewer
neurofibrillary tangles and less tau pathology.
Cerebral atrophy.

Management
Biological
o Anticholinesterase inhibitors
People with lewy body dementia who have non-cognitive symptoms causing significant
distress to the individual or leading to behaviour that challenges, should be offered an
anticholinesterase inhibitor.
Anticholinsterase inhibitors can be helpful for hallucinations and agitation in Lewy body
dementia.
o Antipsychotics
Care should be taken with prescribing antipsychotics due to sensitivity to these agents.
If an antipsychotic is needed, a low dose atypical such as quetiapine is preferable.
o Levodopa/carbidopa
May improve motor function.
Many patients this combination has no effect and may exacerbate psychiatric symptoms
or confusion.
Psychological
Social
236

Normal pressure hydrocephalus

A 62 year old man is referred with a history of worsening memory and urinary incontinence. He has
broad based gait. A CT scan showed ventricular enlargement.

Introduction
An abnormal increase of cerebrospinal fluid in the ventricles of the brain.
It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way.
This causes the ventricles to enlarge, putting pressure on the brain.
Usually affects people over the age of 50 years, with most people being age 60 years or older.
Clinical picture
Insidious onset of dementia.
Unsteady gait.
Urinary incontinence.

Management
Surgical placement of a shunt in the brain to drain excess CSF into the abdomen where it can be
absorbed. This allows the brain ventricles to return to their normal size.

Dementia versus pseudodementia

Pseudodementia scenario: a 72 year old woman presented with memory deficits following the death of
her husband one month previously. She also described lethargy, disturbed sleep, weight loss and a loss
of interest in activities that she would normally enjoy.
Depression is the illness that is most commonly mistaken for dementia.
Dementia Pseudodementia
Features Disturbance of higher cortical
functions, including memory,
thinking, orientation,
comprehension, calculation,
learning capacity, language
and judgement
Depression in the elderly that may
resemble dementia
Typical symptoms of depression are
present
Patients may complain of memory
impairment and other cognitive
problems. However, upon careful
testing, memory and language
functioning are intact. The history of
cognitive problems is usually short,
with depressive symptoms appearing
before cognitive symptoms
Onset Slow Acute
Focus of patients Patient focuses on past
success
Patient focuses on failures
Confusion at night Present Absent
Answers Guesses at answers
(confabulation)
Often avoids answering questions and
makes little effort to find the correct
answer (dont know answers)
Past history of
depression
Less likely More likely
Awareness of
difficulties
Less likely More likely - the person is more likely
to complain of memory problems
Neurological signs More likely Less likely
Geriatric Depression Scale see Appendix 16
Self-rated questionnaire which is used to assist with the diagnosis of depression in the elderly.
It focuses on the cognitive rather than the physical aspects of depression.

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Dementia versus delirium
ICD-10 criteria for delirium
Impairment of consciousness and attention.
Global disturbance of cognition (perceptual distortions, illusions and hallucinations - most often
visual, impairment of abstract thinking and comprehension with or without transient delusions but
typically with some degree of incoherence, impairment of immediate recall and of recent memory
but with relatively intact remote memory, disorientation for time as well as in the more severe
cases, for place and person).
Psychomotor disturbances (hypo- or hyperactivity and unpredictable shifts from one to the other,
increased reaction time, increased or decreased flow of speech, enhanced startle reaction).
Disturbances of the sleep-wake cycle (insomnia, or in severe cases, total sleep loss or reversal of
the sleep-wake cycle, daytime drowsiness, nocturnal worsening of symptoms, disturbing dreams or
nightmares, which may continue as hallucinations after wakening).
Emotional disturbances (depression, anxiety or fear, irritability, euphoria, apathy, or worsening
perplexity).
Feature Delirium Dementia
Onset Acute (abrupt) Insidious (gradual)
Course Fluctuating Progressive
Duration Days to weeks Months to years
Consciousness Altered Clear
Cognitive testing Rapid fluctuations Slow decline
Visual hallucinations Common Uncommon
Psychomotor changes Increased or decreased Often normal
Sleep wake cycle Disrupted Preserved
Reversibility More common Less common
Note: consider delirium in a patient with post-operative agitation and confusion.
Note: the symptoms of delirium are usually worse at night compared to other times during the day.
Management
Fluid and nutrition
o These should be carefully given because the patient may be unwilling or physically unable to
maintain a balanced intake.
o For the patient suspected of having alcohol toxicity or alcohol withdrawal, therapy should
include multivitamins, especially thiamine.
Environmental modifications
o Re-orientation techniques or memory cues such as a calendar, clock and family photos may be
helpful.
o The environment should be stable, quiet and well-lit. Support from a familiar nurse and family
should be encouraged.
o Family members and staff should explain proceedings at every opportunity reinforce
orientation and reassure the patient.
o Physical restraints should be avoided.
Biological management
o Antipsychotics (e.g. haloperidol, olanzapine).

Testamentary capacity
(i.e. the ability to make a will)

You have been asked to see Alice Jones, who is a 74 year old woman with a recent diagnosis of
Alzheimers disease. She lives with her husband. She wishes to make her will. Assess her testamentary
capacity.
In order to have testamentary capacity, an individual
1. Should be aware of what a will constitutes (i.e. should understand what a will is, what it means and
the consequences of leaving a will).
2. Should know the general extent of their assets. This does not have to be detailed knowledge but a
general one, e.g. ownership of a house, car, furniture etc.
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3. Must be aware of the people who might reasonably expect to benefit from the assets (i.e. does the
person know the names of, and relevant claims of relatives).
4. Must be free from delusional beliefs that might affect the distribution of assets and affect his
judgement.
5. Must not be under the influence of any drugs that tend to distort mental capacity as far as making a
will is concerned.

It is important to realise
Not all delusions or mental illnesses will impact on a persons decisions sufficiently to cause a loss
of testamentary capacity. In many cases of mental illness, the individual will have lucid intervals
and it is important to note that a will made during one of these intervals will be valid.
Examples of delusions which will influence decisions include:
o Where a person holds persecutory delusions about a family member, causing the individual to
exclude that person from their will.
o Delusions of poverty whereby the person does not realise the worth of his estate.
Someone with an illness such as paranoid schizophrenia or dementia may fulfill the above criteria
for testamentary capacity.
Note: the criteria for testamentary capacity are legal and not medical.

Power of Attorney

Introduction
Power of Attorney is a legal device that can be set up by a person (the Donor) during his/her life
when he/she is in good mental health.
It allows another specially appointed person (the Attorney) to take actions on the Donors behalf if
he/she is absent, abroad or incapacitated through illness.
If someone is mentally incapacitated (e.g. because of illness, disability or a progressive
degenerative illness), all of their assets and property are normally frozen and cannot be used by
anyone else unless they are jointly owned or, someone has Power of Attorney to deal with their
property or money.
A Donor can appoint anyone to be their Attorney, including a spouse, family member, friend,
colleague, etc.
Power of Attorney ceases on the death of the Donor.
There are two types of Power of Attorney allowed under Irish law
Power of Attorney which gives either a specific power (limited to a particular purpose, e.g. sale of
the Donors house in their absence) or a general power (entitling the Attorney to do almost
everything that the Donor could do themselves) and ceases as soon as the Donor becomes
incapacitated. General Power of Attorney allows the Attorney to may make payments from the
specified accounts, make appropriate provision for any specified persons needs, and make
appropriate gifts to the Donors relations or friends.
Enduring Power of Attorney which takes effect on the incapacity of the donor. An Enduring Power
of Attorney allows the Attorney to make personal care decisions on the Donors behalf once he/she
is no longer fully mentally capable of taking decisions him/herself. Personal care decisions may
include deciding where and with whom the Donor will live, who he/she should see or not see and
what training or rehabilitation he/she should get. However, if the Donor wants, he/she can
specifically exclude any of these powers when setting up the Power of Attorney or can make the
Attorneys powers subject to any reasonable conditions and restrictions.

Ward of Court

When a person becomes unable to manage his or her assets because of mental incapacity, an
application can be made to the courts for this person to become a Ward of Court.
The court must make a decision as to whether the person is capable of managing his/her own
property for his/her own benefit and the benefit of his/her dependants.
If it is decided that the person cannot manage his or her own property because of mental
incapacity, a Committee is appointed to control the assets on the Wards behalf.
A person under 18 years old may also be taken into Wardship as a minor.
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Elder abuse

An 80 year old man who has been lonely after the death of his wife five years ago, was befriended at
his local pub by a young couple who bought him a glass of whiskey. He started inviting them to his
house for drinks, and after a while, they moved in. He ended up moving into the back bedroom of the
house. He later found out that he no longer owned the house and that his bank account had been
emptied of his life savings.
Introduction
Abuse of older people is a hidden and often ignored problem in society.
The prevalence of elder abuse is difficult to quantify for a number of reasons. Abuse is frequently
hidden, may not be obvious even to the victim and is likely to be underreported.
In the Abuse and Neglect of Older People in Ireland Report on the National Study of Elder Abuse
and Neglect (Naughton et al., 2010), 2,021 people aged 65 years and older were interviewed in
their own home in Ireland between April and May 2010, using face to face interviews. All the
interviewers were older women and all interviews were conducted in private with the older person.
The results of the study showed that 2.2% of the study population experienced abuse or neglect
during the previous 12 months. These results were similar to the prevalence estimate obtained in
the UK (2.6%).

Types of elder abuse
Physical abuse.
Emotional abuse.
Sexual abuse.
Discriminatory abuse (includes abuse that is racist, sexist or based on a persons disability).
Neglect and acts of omission (includes ignoring medical or physical care needs, failure to provide
access to appropriate health, social care or educational services, the withholding of the necessities
of life, such as medication, adequate nutrition and heating).
Financial exploitation.

Risk factors for elder abuse
Carer risk factors
o Depression.
o Alcohol and substance misuse.
o Lack of support from other potential caregivers.
o Opinion that care giving is burdensome and without psychological reward.

Elder risk factors
o Severe illness or dementia.
o Behavioural disturbance associated with irritability and verbal/physical aggression.
o Previous role as an abusive parent or spouse.
o History of domestic violence.
o Social isolation.

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MCQs Chapter 23
Question 1: Which ONE of the following statements regarding brain changes associated with
normal aging is FALSE?
A. Brain volume decreases.
B. Lipofuscin decreases.
C. Ventricle volume increases.
D. White matter volume decreases after age 40 years.
E. Sulci increase.

Question 2: Which ONE of the following statements regarding intellectual functioning associated
with normal aging is TRUE?
A. Performance IQ declines after the age of 40 years.
B. Scientific creativity peaks in the 20s.
C. Artistic creativity peaks in the 40s.
D. IQ peaks at age 30 years.
E. Short-term memory is unaffected by age.

Question 3: Which ONE of the following statements regarding body changes associated with
normal aging is FALSE?
A. Gastric pH decreases.
B. Hepatic biotransformation decreases.
C. Liver volume decreases.
D. Body water decreases.
E. Body muscle decreases.
A. Stage 3 dementia - incontinence.
B. Stage 2 dementia confabulation.
C. Stage 2 dementia impaired swallowing.
D. Stage 1 dementia - personality changes.
E. Stage 2 dementia unable to learn new material.
Question 5: Which ONE of the following statements is TRUE?
A. A score of 19 on the Mini Mental State Examination suggests mild dementia.
B. The Mini Mental State Examination is probably a better test for the detection of vascular
dementia than the Montreal Cognitive Assessment.
C. The Montreal Cognitive Assessment places greater emphasis on the examination of executive
functioning than the Mini Mental State Examination.
D. The Montreal Cognitive Assessment is based on a 26-point scale.
E. The Mini Mental State Examination is probably a better test than the Montreal Cognitive
Assessment at detecting mild cognitive impairment.
Question 6: Which ONE of the following is LEAST LIKELY to be a risk factor for Alzheimers
disease?
A. Mild cognitive impairment.
B. Advancing age.
C. Less than 8 years of education completed.
D. Systemic vascular disease.
E. Large head size.
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Question 7: Which ONE of the following associations is TRUE?
A. Chromosome 21 late onset Alzheimers disease.
B. Chromosome 14 Presenilin 1.
C. Chromosome 17 Apolipoprotein E4.
D. Chromosome 19 Presenilin 2.
E. Chromosome 1 early onset autosomal recessive Alzheimers disease.
A. Galantamine is recommended for the management of severe dementia.
B. Memantine is a NMDA agonist.
C. Constipation is a side effect of anticholinesterase inhibitors.
D. Rivastigmine affects butyrylcholinesterase.
E. Medication is curative for Alzheimers disease.

Question 9: Which ONE of the following statements regarding Alzheimers disease is TRUE?
A. The most common cause of death in people with Alzheimers disease is a stroke.
B. Parietal lobe involvement is associated with poor prognosis of Alzheimers disease.
C. The presence of misidentification syndrome is associated with a poor prognosis of
Alzheimers disease.
D. On average, people live for 12 years after the diagnosis of Alzheimers disease.
E. Females have worse prognosis than males for Alzheimers disease.
A. Personality changes are more common in Alzheimers disease than vascular dementia.
B. Vascular dementia is associated with an abrupt onset.
C. Vascular is the commonest form of dementia in Japan.
D. The progression of Alzheimers disease is slow and steady.
E. The risk of co-existent depression is more common in Alzheimers disease than vascular
dementia.
A. Ubiquitin protein is present in the substantia nigra in Lewy body dementia.
B. Picks dementia occurs at an earlier age than Alzheimers disease.
C. Dementia in Creutzfeldt Jakob disease is associated with a characteristic biphasic EEG.
D. Acetylcholine producing neurons are decreased in Alzheimers disease.
E. Picks dementia is associated with a predominance of frontal lobe features.
Question 12: Which ONE of the following statements is MORE LIKELY to be associated with
delirium than dementia?
A. Disturbance of the sleep wake cycle.
B. Insidious onset.
C. Clear consciousness.
D. Visual hallucinations are uncommon.
E. Slow decline on cognitive testing.
Question 13: Which ONE of the following statements regarding testamentary capacity is
FALSE?
A. A diagnosis of dementia does not signify the absence of testamentary capacity.
B. A person does not need to know the general extent of their assets in order to have testamentary
capacity.
C. The criteria for testamentary capacity are legal.
D. A person with testamentary capacity should be aware of the people who might expect to
benefit from the assets.
E. In order to have testamentary capacity, an individual should understand what a will
constitutes.
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Questions 14-18: Dementia and related conditions
A. Vascular dementia
B. Dementia in Huntingtons disease
C. Normal pressure hydrocephalus
D. Picks disease
E. Delirium
F. Alzheimers disease
G. Lewy body dementia
H. Pseudodementia
I. Dementia in Creutzfeldt Jakob disease
J. Dementia in Parkinsons disease
For each of the presentations below, choose the single most likely diagnosis from the above list of
options. Each option may be used once, more than once or not at all.
14. A 75 year old woman with a three month history of a reduction in her sleep, appetite, energy
and interest in activities, describes distress at her deteriorating memory. On testing, her
memory is found to be normal. It is difficult to obtain a full history from her as she frequently
replies I do not know, when a question is asked.
15. A 60 year old man with a resting tremor and rigidity presents with a deterioration in his
memory, varying levels of alertness and attention, and the description of seeing animals at
home that his wife denies are present.
16. A 68 year old woman with a history of memory deterioration is noted to have difficulty in
using the cooker and the washing machine which she had been able to use in the past. She is
also having difficulty in naming the characters in her favourite soap opera, which she has been
watching three times a week for the past 20 years. She has become withdrawn and has
decreased interest in interacting with friends.
17. A 66 year old man is accompanied to the clinic by his daughter who describes a deterioration
in her fathers memory over the past 5 years. The daughter says that she is surprised that she
has heard her father swearing on a regular basis for no apparent reason over the past 3 years,
which she says is totally out of character for him. During the interview, he picks up a paper
weight and throws it into the air while laughing loudly.
18. A 55 year old man presents with deterioration in his memory, unsteady gait and urinary
incontinence.

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1. B
2. E
3. A
4. C
5. C
6. E
7. B
8. D
9. B
10. E
11. C
12. A
13. B
14 H
15 G
16. F
17. D
18. C
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Chapter 24
Intellectual disability

245

Chapter 24: Intellectual disability
Introduction
Mental handicap is a condition of arrested or incomplete development of the mind which is
characterised by an impairment of skills, manifested during the developmental period, which
contribute to the overall level of intelligence, i.e. cognitive, language, motor and social abilities.
Intellectual disability is a significantly reduced ability to understand new or complex information,
to learn new skills (impaired intelligence), with a reduced ability to cope independently (impaired
social functioning), which started before adulthood, with a lasting effect on development.
World Health Organisation (WHO) definitions:
o Impairment: abnormality of structure or function.
o Disability: reduction of ability to perform secondary to impairment.
o Handicap: disadvantage limiting role fulfilment secondary to impairment or disability.
Intellectual disability can occur with or without any other mental or physical disorder.
People with an intellectual disability are at an increased risk of developing mental health disorders,
e.g. mood disorders, anxiety, schizophrenia, personality disorder, ADHD etc.
o The age of onset of schizophrenia tends to be earlier in people with an intellectual disability.
o Delusions and hallucinations tend to be less complex in someone with an intellectual disability
who has schizophrenia than in someone with schizophrenia who does not suffer from an
intellectual disability.
The more severe the intellectual disability, the higher the prevalence of psychiatric disorder.
Compared to members of the general population, individuals with an intellectual disability are at a
greater risk of exploitation and physical/sexual abuse.
Intellectual disability psychiatrists are specialists who deal with patients who have mental health
problems associated with an intellectual disability, such as emotional and behavioural disorders.
Services include:
o Day services
Educational programmes for children and adults with intellectual disabilities.
Day activation programmes include aromatherapy, massage therapy, music therapy, sport
and recreation, swimming, cookery and socialisation.
Sheltered work activities, e.g. horticulture, animal care, knitting and restaurant work
(meeting customers, taking orders, preparation of food, serving the food).
o Community houses
Aim to integrate individuals into a home-like environment in family sized groups and to
provide them with the opportunities to improve their quality of life.
Residents participate in day activities, sheltered work or supported employment, each
week from Monday to Friday.
Staff in the community houses provide support by assisting residents in achieving life
skills.
Residents are encouraged to participate in the running of the house by means of such
activities as shopping for food, preparing the meals, doing laundry and maintaining the
garden.
Families are encouraged to facilitate residents spending time at home at weekends and
during holiday breaks.
o Inpatient care
Caters for people who require intensive support and care.
Adult respite services provide additional support for patients and their families living in
the community.
IQ
Normal IQ = 85-115.
Borderline intellectual disability = 70-84.

Classification of intellectual disability
Intellectual
disability
category
ICD-10 IQ DSM-IV
IQ
ICD-10 guidelines
Mild 50-69 50-55 to 70 Understanding and use of language is delayed to
a varying degree but most can use speech for
246

everyday purposes.
Most achieve full independence in self-care
(eating, washing, dressing, bladder/bowel
control).
Main difficulties are usually in academic school
work, reading and writing.
Organic aetiology is identified in only a
minority of subjects.
Associated conditions such as autism, other
developmental disorders, epilepsy, conduct
disorders or physical disability are found in
varying proportions.
Moderate 35-49 35-40 to 50-55 Level of language development is variable.
Some can take part in simple conversations
while others have only enough language to
communicate their basic needs.
Achievement of self-care and motor skills are
impaired and some need supervision throughout
life.
Progress in school work is limited, but some
learn basic skills for reading, writing and
counting.
Complete independent living in adult life is
rarely achieved.
Most can establish contact, communicate and
engage in simple social activities.
Organic aetiology can be identified in the
majority.
Childhood autism or other pervasive
developmental disorders are present in the
minority.
Epilepsy and neurological and physical
disabilities are common, but mot people can
walk without assistance.
Severe 20-34 20-25 to 35-40 Similar to moderate IQ, but lower level of
achievement of visuospatial, language, or social
skills.
Most have marked motor impairment.
Profound <20 <20-25 Comprehension and use of language is limited
to, at best, understanding basic commands and
making simple requests.
Most are immobile or severely restricted
mobility, incontinent, and capable at most of
only very rudimentary forms of non-verbal
communication.
Little or no ability to care for their own basic
needs and require constant help and supervision
Organic aetiology identified in most cases.
Severe neurological or other physical disabilities
affecting mobility are common, as are epilepsy
and visual and hearing impairments.
Pervasive developmental disorders, especially
atypical autism are particularly frequent,
especially in those who are mobile.
Epidemiology
Males > females.

247

Aetiology
Genetics (see the table below)
o Chromosomal abnormalities.
o Autosomal dominant and recessive conditions.
o X linked dominant and recessive conditions.
o Polygenetic conditions.
o Mitochondrial disorders.
Prenatal
o Infections
TORCH
T Toxoplasmosis/Toxoplasma gondii.
O Other infections (see below).
R Rubella.
C Cytomegalovirus.
H Herpes simplex virus.
Syphilis.
HIV.
Other causes of meningitis and encephalitis.
o Toxins
Alcohol
Foetal alcohol syndrome
Caused by maternal alcohol use.
Illicit substances.
Medications.
Heavy metal poisoning.
o Maternal illnesses
Hypertension.
Hypothyroidism.
Diabetes.
Malnutrition.
Perinatal
o Birth injury.
o Birth asphyxia.
o Neonatal meningo-encephalitis.
Postnatal
o Hypoxic ischaemia.
o CNS infection.
o Brain trauma.
o Epileptic encephalopathies.
o Toxins.
o Deprived psychosocial environment.
Genetic causes of intellectual disability
Cause Example
Chromosomal
abnormality
Trisomy 21 (Downs syndrome)
o Risk factors for giving birth to a child with Downs syndrome:
Maternal age > 40 years
Paternal age > 40 years when having a child with a women aged > 35
years
Females > 35 years who smoke
Fifth or subsequent number child
Previous child with Downs syndrome
Mother has Downs syndrome
About 15-30% of women with trisomy 21 are fertile and they have
a 50% risk of having an affected child
Males with Downs syndrome are less fertile than females with the
condition
o Causes of Trisomy 21
Full trisomy 21 (non-disjunction) in ~95% of cases
Robertson translocation in ~5% of cases
Mosaicism (a mixture of normal and trisomic cell lines) in ~2-5% of
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cases
22q11 deletion syndrome (velo-cardio-facial syndrome/Di George syndrome)
o Characterised by abnormal pharyngeal arch development that results in
defective development of the parathyroid glands, thymus, and conotruncal
region of the heart.
o Occurs in one in 4,000 newborns.
o Caused by the deletion (microdeletion) of a small segment of the long arm
(q) of one of the chromosomes in the number 22 chromosome pair
(22q11).
o In ~ 90% of the cases, 22q11 deletion syndrome is caused by a new
mutation, meaning that the mutated gene has not been inherited and is not
present in the affected individuals family.
o In ~ 10% of cases, the syndrome is passed down by autosomal dominant
inheritance.
o Most common symptoms include congenital cardiac and palatal defects,
calcium deficiency, increased susceptibility to infections, delayed
development, and mild to moderate intellectual disability.
o Increased rates of ADHD, anxiety, oppositional defiant disorder, and
autistic spectrum disorders.
o ~ 25-30% of people with 22q11 deletion develop schizophrenia or other
psychotic disorders.
Trisomy 18 (Edwards syndrome)
Trisomy 13 (Patau syndrome)
Trisomy 8 (Warkany syndrome)
Turners syndrome (karyotype 45, XO)
Trisomy X (karyotype 47, XXX)
Klinefelters syndrome (karyotype 47, XXY)
XYY male (karyotype 47, XYY)
Angelman syndrome (karyotype 15q11.2-12)
o Mostly caused by a microdeletion of maternally derived chromosome 15
Prader Willi syndrome (karyotype 15q11-13)
o Mostly caused by a microdeletion of paternally derived chromosome 15
o Self-injury through skin picking
Williams syndrome (karyotype 7q11.23)
o Microdeletion
Cri du chat syndrome (karyotype 5p-)
o Deletion of the short arm of chromosome 5
Autosomal
dominant
Neurofibromatosis
Tuberous sclerosis
Von Hippel Lindau syndrome
Sturge Weber syndrome
Autosomal
recessive
Phenylketonuria
o Deficiency in the hepatic enzyme phenylalanine hydroxylase which is
necessary to metabolise phenylalanine to tyrosine
o When phenylalanine hydroxylase is deficient, phenylalanine accumulates
in the body
o Diagnosed after birth by the Guthrie Test (Heal Prick Test), designed to
detect elevated blood levels of phenylalanine
Hurler syndrome (Mucopolysaccharidosis Type I)
o Build-up of mucopolysaccharides due to a Deficiency of alpha-L
iduronidase, an enzyme responsible for the degradation of
mucopolysaccharides in lysosomes
o Without alpha-L iduronidase, a buildup of heparan sulphate and dermatan
sulphate occurs in the body
Laurence Moon syndrome
X linked
dominant
Fragile X syndrome
o Males > females
o Expansion of a single trinucleotide gene sequence (CGG) on the X
chromosome, results in a failure to express the protein coded by the FMR1
gene, which is required for normal neural development
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X linked
recessive
Lesch Nyhan syndrome
o Caused by a deficiency of the enzyme hypoxanthine-guanine
phosphoribosyltransferase (HGPRT), produced by mutations in the HPRT
gene located on the X chromosome
o The HGPRT deficiency causes a build-up of uric acid in all body fluids.
This results in both hyperuricemia and hyperuricosuria, associated with
severe gout and kidney problems
o Beginning in the second year of life, a particularly striking feature is self-
mutilating behaviours, characterised by lip and finger biting
Hunter syndrome (Mucopolysaccharidosis Type II)
o Lysosomal storage disease caused by a deficient (or absent) enzyme,
iduronate-2-sulphatase
Polygenetic
conditions
Neural tube defects
Pervasive developmental disorders
Mitochondrial
disorder
Myoclonic epilepsy with ragged red fibres
Note: the most common genetic cause of intellectual disability is Trisomy 21 (Downs syndrome).
Note: the second most common genetic cause of intellectual disability is Fragile X syndrome.
Rating scales
Wechsler Abbreviated Scale of Intelligence (WASI)
o Observer rated scale which measures adolescent and adult IQ.
National Adult Reading Test (NART)
o Measures premorbid IQ and educational level.

Dementia in Downs syndrome
Epidemiology
Prevalence at birth of Downs syndrome (DS) increases with maternal age, ranging from
~0.7/1,000 births for a woman aged 20-24 years to 16/1,000 births for a woman 40-44 years.
The prevalence of Alzheimers disease (AD) in people with DS rises with increasing age.
In the general population, approximately 10% of 65 year olds and 40% of 80 year olds develop
symptoms of AD. In contrast, the incidence of AD in people with DS is estimated to be 3-5 times
greater than that of the general population.
At autopsy, the presence of AD-type neuritic plaques and neurofibrillary tangles

have been
reported in the brains of 7.5% of people with DS as

early as the second decade of life, with a rise in
prevalence

to 80% of cases by the fourth decade and 100% over 60 years

of age.

Aetiology
The markedly high frequency of AD neuropathology and early onset in DS may be related to
having trisomy chromosome 21, because this chromosome carries the amyloid precursor protein
(APP) gene which is implicated in the development of amyloid plaques in the general population.
Hence, it has been hypothesised that the presence of an extra copy of the APP gene in DS leads to
abnormalities in APP processing in neuronal membranes and subsequently to the formation of
amyloid plaques, neuronal death and clinical AD.
The presence of APOE 4 allele is associated with early onset of AD, whereas the presence of the
APOE 2 allele is associated with a delay in disease onset and is possibly protective.
Menopause occurs earlier in women with DS. It is thought that the loss of oestrogen may be
important in the development of AD in women.
Women treated with hormone replacement therapy (HRT) seem to have reduced risk of developing
the disease. However, HRT given to women with cognitive impairment does not appear to prevent
further cognitive decline.

Presentation of dementia in Downs syndrome
Cognitive
o Forgetfulness of recent events (and at a later stage, long-term events).
o Geographical disorientation.
o Loss of previously learned skills.
o Confusion.
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Affective
o Low mood.
o Loss of interest.
o Insomnia/hypersomnia.
o Decreased concentration.
o Irritability.
o Anxiety.
Behavioural
o Increased dependence on others.
o Social isolation.
o Excessive over-activity or restlessness.
o Excessive uncooperativeness.
o Personality change.
Perceptual
o Hallucinations in any modality.
Neurological
o Dysphasia leading to aphasia.
o Agnosia.
o Apraxia.
o Gait disturbance.
o Seizures.
o Myoclonus.
o Dystonias.
o Loss of mobility.

Investigations
Biological
o Bloods: FBC, RFT, LFT, TFT, fasting glucose, B
12
and folate.
o ECG, EEG, CXR, CT/MRI brain.
o Clock Drawing Test see Appendix 2.
o Cognitive status can be measured using the Cambridge Cognitive Examination (CAMCOG), a
composite index of episodic memory, orientation, language, attention, praxis and executive
function.
Psychological
o Risk assessment.
o Dementia Scale for Downs syndrome.
o Dementia Questionnaire for Persons with Mental Retardation.
o Neuropsychological testing to identify retained abilities and specific problem areas, such as
comprehension, insight and judgement.
Social
o Collateral history (from family, GP, psychiatric services if the person had previous contact).
Onset, duration and progression of symptoms.
Ability to carry out activities of daily living (e.g. bathing, grooming, toileting, eating or
more complex activities).
Prior level of functioning.
Any recent changes in medications, environment and health status.
Assessment of social support system for both the patient and caregiver.
o Documentation (GP records, psychiatric case notes).
o Occupational therapy: assessment of the patients needs and activities of daily living (ADLs).
Management
Reversible causes of cognitive impairment must be identified and corrected as far as possible, e.g.
physical conditions such as delirium and hypothyroidism.
Biological (monitor for the side effects of medications)
o Anticholinsterase (AChE) inhibitors (e.g. donepezil, rivastigmine or galantamine).
o Depression: SSRIs (e.g. fluoxetine, paroxetine, sertraline).
o Psychosis: low dose atypical antipsychotics (e.g. quetiapine).
Psychological
o Risk management.
o Psychoeducation.
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o Art therapy: provides meaningful stimulation, improves social interaction and improves
levels of self-esteem.
o Music therapy: engagement in a musical activity (e.g. singing or playing an instrument) or
listening to songs and music. Can increase levels of well-being, improve social interaction and
improve autobiographical memory.
o Behavioural therapy: has been shown to decrease wandering and incontinence.
o Reality orientation: aims to help people with memory loss and disorientation by reminding
them of facts about themselves and their environment. People with memory loss are orientated
to their environment using a range of materials and activities (e.g. signposts and notices
identifying the bathroom, fridge etc).
o Validation therapy: attempts to communicate with people with dementia by empathising
with their feelings and meanings hidden behind their confused speech and behaviour.
o Reminiscence therapy: helps people with dementia relive past experiences e.g. family
holidays and weddings.
Social
o Meals on wheels
Meals can be delivered to peoples homes in the case of those who are unable due to age,
illness or disability, to cook their own meals.
o Home help
Assist with normal household tasks such as shopping and cleaning and are assigned to
people who are unable to carry out such tasks themselves.
o Activity therapy
Involves recreations such as dance, sport and drama. Physical exercise in dementia can
reduce the number of falls and improve mental health and sleep.
o Complementary therapy
e.g. massage, reflexology, reiki, herbal medicine and aromatherapy.
o Animal assisted therapy (pet therapy)
Pairing of animals and people with specific needs.
The ideal pet is gentle and placid, never aggressive.
Reduces isolation and provides a social context to share time with others in a comfortable,
non-confrontational atmosphere.
o Social work input to assist with supported accommodation if needed.
o Occupational therapy input to improve skills
o Carer support
Consider the psychological and practical needs of carers.
o Support groups
Alzheimer Society of Ireland offers:
Day care centres, home care, respite care.
Social clubs (weekly drop in centre for people with dementia and their carers, family
and friends).
The Dementia Rights Advocacy Service (helps people with dementia voice their needs
and wishes, access their entitlements and assert their rights).
Other therapies
o Bright light therapy.
o Snoezelen room or controlled multisensory stimulation.
Snoezelen rooms are specially designed to deliver stimuli to various senses, using lighting
effects, color, sounds, music, scents, etc. The combination of different materials on a wall
may be explored using tactile senses and the floor may be adjusted to stimulate the sense
of balance.

Foetal alcohol syndrome

Introduction
Foetal Alcohol Syndrome (FAS) is a pattern of mental and physical defects which develops in
some unborn babies when the mother drinks too much alcohol during pregnancy.
One of the major causes of intellectual disability.
May be due to the effects of alcohol on N-Methyl-D-aspartic acid (NMDA) receptors which alter
cell proliferation
People with FAS are at a higher than average risk for physical and sexual abuse and neglect.

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Epidemiology
Incidence 0.2-3 per 1,000 live births.
10-20% of cases of mild intellectual disability may be caused by maternal alcohol use.

Aetiology
Alcohol in a pregnant womans bloodstream circulates to the foetus by crossing the placenta.
There, the alcohol interferes with the ability of the foetus to receive sufficient oxygen and
nourishment for normal cell development in the brain and other body organs.
Clinical picture
Signs of alcohol withdrawal
o Irritability.
o Hypotonia.
o Tremor.
o Seizures.
Growth deficiencies
o Small body size and weight.
o Developmental delay.
o Failure to thrive.
Skeletal deformities
o Microcephaly.
o Hip dislocations.
o Bent, fused, webbed or missing fingers or toes.
o Limited movement of joints.
Facial abnormalities
o Small eye openings.
o Nearsightedness.
o Indistinct philtrum.
o Flattened cheekbones.
o Small jaw.
o Low-set or poorly formed ears.
Organ deformities
o Heart defects (ASD, VSD).
o Genital malformations.
o Renal hypoplasia.
o Bladder diverticuli.
o Hearing loss.
CNS
o Small brain.
o Intellectual disability.
o Epilepsy.
o Poor coordination/fine motor skills.
o Receptive and expressive language deficits.
Social skills
o Poor socialisation skills, i.e. difficulty building and maintaining friendships and relating to
groups.
Management
There is no cure for FAS because the CNS damage creates a permanent disability.
Due to their poor social judgement, underdeveloped independent living skills and impaired
intellectual functioning, most people with FAS will require a structured, sheltered living situation
throughout their lives.
Biological
o Stimulants (e.g. methylphenidate) may be recommended to treat inattention and hyperactivity.
Psychological
o Psychoeducation for parents.
o Behaviour therapy.
o Family therapy.
Social
o Appropriate placement in special education classes.
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Prevention
The only certain way to prevent FAS is to simply avoid drinking alcohol during pregnancy.
A number of studies have shown that light to moderate drinking during pregnancy might not pose
a risk to the foetus, although no amount of alcohol during pregnancy can be guaranteed to be
absolutely safe.

254

MCQs Chapter 24
Question 1: Which ONE of the following statements regarding the classification of intellectual
disability is FALSE?
A. Profound intellectual disability has an IQ of <20-25 in DSM-IV.
B. Mild intellectual disability has an IQ of 50-55 to 70 in ICD-10.
C. Severe intellectual disability has an IQ of 20-34 in ICD-10.
D. Moderate intellectual disability has an IQ of 35-49 in ICD-10.
E. Profound intellectual disability has an IQ of <20 in ICD-10.

Question 2: Which ONE of the following associations regarding the classification of intellectual
disability is FALSE?
A. Moderate intellectual disability some patients only have enough language to communicate
their basic needs.
B. Profound intellectual disability pervasive developmental disorders are frequent.
C. Mild intellectual disability difficulties in academic school work, reading and writing.
D. Severe intellectual disability most people are immobile or have severely restricted mobility,
incontinent and capable of only rudimentary forms of non-verbal communication.
E. Mild intellectual disability most people can use speech for everyday purposes.

Question 3: Which ONE of the following factors regarding the aetiology of Downs syndrome is
MOST ACCURATE?
A. Maternal age > 35 years.
B. Mother has cystic fibrosis.
C. Fifth or subsequent child.
D. Paternal age > 35 years when having a child with a woman aged > 40 years.
E. Females > 30 years who smoke.

Question 4: Which ONE of the following IS an autosomal dominant condition?
A. Phenylketonuria.
B. Lesch Nyhan syndrome.
C. Prader Willi syndrome.
D. Williams syndrome.
E. Neurofibromatosis.

Question 5: Which ONE of the following is NOT a chromosomal abnormality?
A. Laurence Moon syndrome.
B. Warkany syndrome.
C. Williams syndrome.
D. Velo-cardio-facial syndrome.
E. Patau syndrome.

A. Angelman syndrome chromosomal abnormality.
B. Hunter syndrome autosomal recessive.
C. Myoclonic epilepsy with ragged red fibres mitochondrial disorder.
D. Mucopolysaccharidosis Type II X linked recessive.
E. Von Hippel Lindau syndrome autosomal dominant.

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Question 7: Which ONE of the following statements regarding dementia in Downs syndrome is
TRUE?
A. The incidence of Alzheimers disease in people with Downs syndrome is 10 times that of the
general population.
B. The presence of Alzheimers disease plaques and tangles have been reported at autopsy in the
brains of 100% Downs syndrome individuals over the age of 40 years.
C. The prevalence at birth of Downs syndrome is 16/10,000 births for a woman aged 40-44
years.
D. Menopause often occurs earlier in women with Downs syndrome.
E. In the general population, approximately 20% of 65 year olds develop symptoms of
Alzheimers disease.

Question 8: Which ONE of the following features is LEAST LIKELY to be associated with the
foetal alcohol syndrome?
A. Farsightedness.
B. Poor socialisation skills.
C. Microcephaly.
D. Hypotonia.
E. Hearing loss.

256

1. B
2. D
3. C
4. E
5. A
6. B
7. D
8. A

257

Chapter 25
Capacity to consent

258

Chapter 25: Capacity to consent to treatment

A 50 year old man was admitted two days ago under the care of the surgical team. His left leg has
become increasingly more cold and discoloured. A dark grey/black colour began in the region of his
toes and gradually extended up his leg. Examination and investigations suggest that his leg is
gangrenous. He refuses to sign the consent form for amputation. The surgical team has asked for a
psychiatry assessment of his capacity to consent or to withhold consent to the operation.

Introduction
Capacity
o Capacity means the ability to enter into a valid contract, i.e. to decide whether to undergo an
operation or other procedure.
o Capacity is gained in adulthood and is presumed to be present throughout the lifespan of the
individual unless permanently or temporarily lost. We must assume capacity to be present
unless demonstrably absent.
o Restore/improve capacity before acting against the persons wishes (except in an emergency).
o To treat a person with capacity without consent would be an assault.
o Competent adults are entitled to refuse treatment even when it would clearly benefit their
health. Respect the right to be foolish if capacity is present. An exception to this rule would be
where the person is detained under the Mental Health Act 2001 and is obliged to comply with
the treatment of a mental disorder.
o People can be considered to have the capacity to decide some aspects of their treatment but
not others, e.g. a person with severe learning difficulties may have the capacity to decide on
their day-to-day treatment but lack the capacity to understand the complexities of their long-
term treatment. Capacity is therefore not an all or nothing concept.
Best interests
o Acting in the best interests of a patient involves offering those treatments in which the
possible benefits outweigh any burdens or risks associated with the treatment and avoiding
those treatments where there is no net benefit to the patient.
o If a person lacks capacity, treatment can only be given taking into account the best interests of
the patient.
o Take the least restrictive course of action consistent with the patients best interests.
o Act in the best interests of the patient (not the familys or hospitals interests).
Note: the Mental Health Act 2001 cannot be used to force a patient to have a medical or surgical
procedure.
Consent
o It is necessary to provide sufficient information to patients before they can decide whether or
not to give their consent, e.g. information about the benefits and risks of the proposed
treatment and alternative treatments.
o It is important that the patient is given continuing opportunities to ask further questions and to
review their decision.
o Consent can be:
Verbal.
Implied, e.g. raising your hand to indicate that you are happy for a nurse to take a blood
sample.
Written, e.g. by signing a consent form.
o A signed consent form by itself does not constitute consent. It simply serves as evidence of
consent. The consent form will not be valid if the consent is:
Not voluntary.
Not informed.
The person does not have enough mental capacity to give consent.
Assessment of capacity: to have capacity the patient must be able to:
1. Understand the issue at hand. This involves an assessment of:
The patients understanding of the problem he has.
o What do you understand about the problems that you are having?
o What have the doctors told you about the difficulties you are having?
The patients understanding of the nature of the proposed procedure.
o Do you know what the doctors believe should happen?
o What have you been told about the anaesthetic that would be used?
259

The patients understanding of the purpose of the procedure.
o Why do think that you might need the procedure?
o Why do the doctors think that you might need the procedure?
The patients understanding of the risks of the procedure.
o What have the doctors told you about the possible risks of the procedure?
o Do you think that the procedure might be painful?
o Do you think that the procedure might leave a scar?
o What do think might be the most serious risk of having the procedure?
The patients understanding of the risks of not having the procedure.
o What have the doctors told you about the possible risks of not having the procedure?
o What you think will happen if you do not have the procedure?
o Do you think that you will get better if you do not have the procedure?
o Are you aware of any alternative treatments or procedures?
2. Believe the medical opinion is correct and genuine and accept it applies to them.
o Do you believe that there is a problem with your leg?
o Why do you not believe that there is a problem with your leg?
o What do you think is the difficulty?
3. Retain information long enough to form judgement.
Reassess the patient to ensure that they can retain the information needed to make their
decision.
o Can you summarise for me the discussion that we have had so far today?
4. Use the information to make a decision.
o What is your decision about having the procedure?
5. Communicate their comprehension and viewpoint.
o Why have you (or why have you not) decided to have the procedure?
o Why have you made this decision?
If any of the above criteria (1)-(5) is not present capacity is absent
Conditions in which capacity may be impaired (but not necessarily)
Brain injury.
Delirium/intoxication.
Dementia.
Significant intellectual disability.
Severe mental illness.

Emergency treatment without consent: person with capacity
Treatment may be given without consent to a person with capacity in an emergency, if in the
opinion of the doctor:
o It is not possible to communicate the relevant information to the patient because of a language
barrier or because the person has a disability that prevents the communication from taking
place.
o Steps have been taken to find a means of communicating but no such means has been found.
o The delay required to finding a means to communicate will prolong the patients suffering or
will put the patient at risk of sustaining serious bodily harm.
o There is no reason to believe that the person does not want the treatment.
Note: it is critical that the doctor documents their actions in the patients chart.
Emergency treatment without consent: person without capacity
Treatment may be given without consent to a person without capacity, if in the opinion of a doctor
there is an emergency and the delay required to obtain a consent or refusal on the persons behalf
would prolong the persons suffering or would put the person at risk of sustaining serious bodily
harm.

In the scenario of a patient who has been brought to the Emergency Department after having
engaged in self-harm (e.g. after having taken an overdose) or a general medical/surgical patient
on a ward who wants to take his own discharge
Never allow a patient to take their own discharge without obtaining senior advice.
An assessment of capacity should be done as described above.
Patients who wish to take their own discharge usually fall into one of the following four
categories:
260

1. Patients with capacity, without evidence of mental illness, who have a low risk of suicide and
who are not at risk from their overdose (or by taking their discharge): are entitled to refuse
treatment and can be allowed to take their own discharge.
2. Patients with capacity, without evidence of mental illness, who have a low risk of suicide but
who are at risk from their overdose (and by taking their discharge): are entitled to refuse
treatment. However, all steps should be taken to dissuade them from taking their own discharge.
3. Patients who have capacity but in whom mental illness is suspected, including patients at
high risk of suicide: it may be appropriate to detain these patients under the Mental Health Act
2001.
4. Patients at clinical risk or at risk of suicide who do not have capacity: these individuals should
be kept in hospital for treatment. They can be kept in hospital against their will under common law
if necessary. Mental capacity is often impaired temporarily following an overdose, e.g. with
sedative agents.

261

MCQs Chapter 25
Question 1: Which ONE of the following statements regarding capacity is FALSE?
A. We must assume capacity to be present unless demonstrably absent.
B. If a patient refuses a medical or surgical treatment that is considered necessary, it is not
possible to use to Mental Health Act 2001 to ensure that the patient has the procedure.
C. Capacity is not an all or nothing concept.
D. Capacity is gained in childhood and is presumed to be present throughout the lifespan of the
individual unless permanently or temporarily lost.
E. To treat a person with capacity without consent would be an assault.
Question 2: Which ONE of the following is LESAT LIKELY to be a direct component of a
capacity assessment?
A. Understand the issue at hand.
B. Obtaining a collateral history.
C. Communicate their comprehension and viewpoint.
D. Retain information long enough to form judgement.
E. Believe the medical opinion is correct and genuine and accept it applies to them.

Question 3: Which ONE of the following statements regarding capacity is TRUE?
A. Patients with capacity, without evidence of mental illness should be treated under common
law if they refuse treatment.
B. Patients with capacity, without evidence of mental illness, who have a low risk of suicide but
who are at risk from their episode of self-harm should be encouraged to take their discharge
from the Emergency Department.
C. People can have the capacity to decide some aspects of their treatment but not others.
D. Treatment cannot be given without consent to a person with capacity in an emergency.
E. Capacity is absent in people with severe mental illness.
262

1. D
2. B
3. C
263

Chapter 26
Mental Health Act 2001

264

Chapter 26: Mental Health Act 2001
Introduction
Mental Health Act (MHA) 2001 is an Act to provide for the involuntary admission to Approved
Centres of people suffering from mental disorders, and to provide for the independent review of
the involuntary admission of such individuals.
In this Act mental disorder means mental illness, severe dementia or significant intellectual
disability where:
A. Because of the illness, disability or dementia there is a serious likelihood of the person
concerned causing immediate and serious harm to himself/herself or to other persons, or
B. Because of the severity of the illness, disability or dementia, the judgement of the person
concerned is so impaired that failure to admit the person to an Approved Centre would be
likely to lead to a serious deterioration in his/her condition or would prevent the
administration of appropriate treatment that could only be given by such admission, and
C. The reception, detention and treatment of the person concerned in an Approved Centre would
be likely to benefit or alleviate the condition of that person to a material extent.
Exclusion criteria for involuntary admission exist. It is not lawful to detain a person involuntarily
in an Approved Centre solely because that person is:
A. Suffering from a personality disorder.
B. Is socially deviant, or
C. Is addicted to drugs or intoxicants.

Involuntary admission procedure
1. Step 1: Application
A person may be involuntarily admitted to an Approved Centre and detained there on the
grounds that he/she is suffering from a mental disorder.
People who may apply for involuntary admission:
o The spouse or a relative of the person.
o An authorised officer, i.e. an officer of the Health Service Executive (HSE) Area who is
designated by the Chief Officer of the HSE Area for the purposes of making such
applications.
o A member of the Gardai, or
o Any other person.
People who are disqualified for applying for involuntary admission:
o A person under the age of 18 years.
o An authorised officer or a member of the Gardai who is a relative of the person or of the
spouse of the person.
o A member of the governing body, or the staff, or the person in charge of the Approved
Centre concerned.
o Any person with an interest in payments to be made in respect of the taking care of the
person concerned in the Approved Centre concerned.
o Any registered medical practitioner who provides a regular medical service at the
Approved Centre concerned.
o The spouse, parent, grandparent, brother, sister, uncle or aunt of any of the people
mentioned above, whether of whole blood or half blood.
The applicant must have observed the person who is the subject of the application not more
than 48 hours before the date of making the application.
The applicant completes the relevant form:
o Form 1: Spouse or relative.
o Form 2: Authorised officer.
o Form 3: Garda.
o Form 4: Any other person.

2. Step 2: Recommendation
A registered medical practitioner (i.e. a person whose name is entered in the Medical Council
Register of medical practitioners), who is usually a GP, receives an application on one of the
statutory forms numbered 1-4.
Within 24 hours of the receipt of the application, the registered medical practitioner:
o Examines the person.
o Informs the person of the purpose of the examination.
265

If the registered medical practitioner is satisfied following the examination of the person that
he/she is suffering from a mental disorder, he/she makes a recommendation on Form 5 that
the person can be involuntarily admitted to an Approved Centre (other than the Central Mental
Hospital).
The registered medical practitioner sends the recommendation to the clinical director of the
The registered medical practitioner gives a copy of the recommendation to the applicant.
A recommendation is valid for 7 days after it is made.
If the registered medical practitioner is not satisfied following the examination of the person
that he/she is suffering from a mental disorder, he/she does not make a recommendation.
A registered medical practitioner is disqualified from making a recommendation if he/she:
o Has an interest in payments to be made in respect of the care of the person in the
o Is a member of the staff of the Approved Centre to which the person is to be admitted.
o Is a spouse or relative of the person, or
o Is the applicant.

How is the person brought to the Approved Centre?
The applicant is responsible for arranging for the removal of the person who is the subject of
the recommendation to the Approved Centre.
Where the applicant is unable to make such arrangements, the clinical director of the
Approved Centre (or a consultant psychiatrist acting on his/her behalf) at the request of the
registered medical practitioner, arranges for removal of the person to the Approved Centre by
members of staff of the Approved Centre.
Where the clinical director (or a consultant psychiatrist acting on his/her behalf) and the
registered medical practitioner who made the recommendation are of the opinion that there is
a serious likelihood of the person concerned causing immediate and serious harm to
himself/herself, or to other persons, the clinical director may request the Gardai to assist the
members of staff in the removal by staff of the person to the Approved Centre and the Gardai
shall comply with any such request.

3. Stage 3 Admission Order
The clinical director of the Approved Centre receives the recommendation.
A consultant psychiatrist (on the staff of the Approved Centre) examines the person within 24
hours.
If the consultant psychiatrist is satisfied that the person has a mental disorder, he/she makes an
admission order by completing Form 6.
Within 24 hours of making the admission order, the consultant psychiatrist must send a copy
of the order to the Mental Health Commission and give the patient notice in writing that the
admission order has been made.
An admission order authorises the reception, detention and treatment of the patient.
An admission order is valid for up to 21 days after it is made.

4. Step 4 Renewal Order
Made by a consultant psychiatrist responsible for the care and treatment of the patient if the
mental disorder persists.
The consultant psychiatrist must examine the patient not more than one week before the
making of such an order and certify that the patient continues to be a person with a mental
disorder.
Renewal orders may extend the patients involuntary admission for the following durations
and are made on Form 7.
o First renewal order: a period not exceeding three months from the expiration of the 21
day period provided for in the admission order.
o Second renewal order: a period not exceeding six months from the expiration of the
three month period provided for in the first renewal order.
o Subsequent renewal orders: for any periods not exceeding 12 months in any one
subsequent renewal.

266

Mental Health Tribunals
Aim:
o To independently review all decisions to detain patients in accordance with the Act and either
affirm the order or if not, revoke the order therefore directing that the patient be discharged
from the inpatient facility.
o Tribunal hearings are arranged within 21 days of the admission order commencing, before the
expiry of the three month first renewal order, before the expiry of the six month second
renewal order and before the expiry of the 12 month subsequent renewal orders.
Components of a Mental Health Tribunal:
o A practicing barrister or solicitor who acts of a chairperson.
o A consultant psychiatrist.
o A person other than a barrister, solicitor, consultant psychiatrist, registered medical
practitioner or registered nurse. This person is usually a layperson.
Treatment of involuntary patients
Consent
o Consent from a patient is required for treatment.
o Involuntary admission status does not necessarily mean that consent to treatment is no longer
required.
o Three components of consent:
Provision of adequate information to the patient.
Presence of decision-making capacity.
Voluntarism (i.e. the patients decision should be made freely, without coercion).
o Treatment in the absent of consent may only occur when in the opinion of the consultant
psychiatrist (responsible for the care and treatment of the patient):
The treatment is necessary to safeguard the life of the patient.
To restore his/her health.
To alleviate his/her condition.
To relieve his/her suffering AND the patient concerned is incapable of giving consent by
reason of his/her mental disorder.
Psychosurgery
o Definition: any surgical operation that destroys brain tissue or the functioning of brain tissue
and which is performed for the purposes of ameliorating a mental disorder.
o Requirements
Consultant psychiatrist must be of the opinion that psychosurgery would be in the best
interests of the patient concerned, and
Patient gives his/her written consent, and
The proposal is referred to a Mental Health Tribunal who may authorise the treatment if
they consider that it is in the best interests of the patient, or refuse authorisation if they do
not consider that psychosurgery is in the best interests of the patient.
Note: consent of the patient is required for psychosurgery.
Electroconvulsive therapy (adults)
o Process
Patient gives his/her written consent, or
Patient unable or unwilling to consent.
o When the patient is unwell or unable to give such consent:
The ECT is approved by the consultant psychiatrist responsible for the care and treatment
of the patient, and
The ECT is also authorised by another consultant psychiatrist following referral of the
matter to him or her by the treating consultant psychiatrist.
Note: ECT can be given without the consent of a patient.
Administration of medicine (adults)
o Medicine has been administered to a patient for the purposes of ameliorating his/her mental
disorder for a continuous period of three months.
o Administration of that medicine should not be continued unless:
The patient gives his/her consent in writing.
If the patient is unable or unwilling to consent:
Consultant psychiatrist (responsible for the care and treatment of the patient)
approves the continued administration, and
Refers the matter to another consultant psychiatrist who authorises it.
Administration is valid for three months.
267

Note: medication can be given without the consent of the patient.
Discharge from an Approved Centre
In the case of patients no longer suffering from a mental disorder, the consultant psychiatrist must:
o Be of the opinion that circumstances warranting the admission and detention no longer exists.
o Ensure that discharge is appropriate.
o Have regard that no patient may be detained under an admission order for longer than
necessary.
o A patient may remain in an Approved Centre as a voluntary patient.
Revocation of an involuntary admission
o An admission order or a renewal order may be revoked by the consultant psychiatrist
responsible for the care and treatment of the patient.
o Form 14 must be completed in this regard.

268

269

270

271

272

MCQs Chapter 26
Question 1: Which ONE of the following statements regarding the Mental Health Act 2001 is
TRUE?
A. In the Act, mental illness means mental disorder, severe dementia or significant intellectual
disability.
B. A patient cannot be admitted to an Approved Centre if they are only suffering from borderline
personality disorder.
C. A member of the Gardai may not apply for a patient to be involuntary admitted to an
Approved Centre.
D. Mental Health Act 2001 is an Act to provide for the voluntary admission to Approved Centres
of people suffering from mental disorders, and to provide for the independent review of the
admission of such individuals.
E. A registered medical practitioner who provides a regular medical service at the Approved
Centre concerned may apply for a patient to be involuntary admitted to the Approved Centre.

Question 2: Which ONE of the following statements associations is FALSE?
A. Form 7 - Admission order.
B. Form 3 - Application completed by a Garda.
C. Form 1 - Application completed by a spouse or relative.
D. Form 2 - Application order completed by an Authorised officer.
E. Form 5 - Recommendation.
Question 3: Which ONE of the following statements regarding the Mental Health Act 2001 is
TRUE?
A. Within 48 hours of the receipt of the application, the registered medical practitioner examines
the person.
B. A consultant psychiatrist (on the staff of the Approved Centre) examines the person within 48
hours.
C. The applicant must have observed the person who is the subject of the application not more
than 24 hours before the date of making the application.
D. An admission order is valid for up to 21 days after it is made.
E. A recommendation is valid for 14 days after it is made.

Question 4: Which ONE of the following statements regarding renewal orders is FALSE?
A. A second renewal order should be made during a period not exceeding one month from the
expiration of the three month period provided for in the first renewal order.
B. A renewal order should be made by a consultant psychiatrist responsible for the care and
treatment of the patient if the mental disorder persists.
C. First renewal order should be made during a period not exceeding three months from the
expiration of the 21 day period provided for in the admission order.
D. Third and subsequent renewal orders should be made for any period not exceeding 12 months
in any one renewal.
E. The consultant psychiatrist must examine the patient not more than one week before the
making a renewal order.
A. Tribunal hearings are arranged within 14 days of the admission order commencing.
B. Consent of the patient is not required for psychosurgery.
C. Form 14 - revocation of an involuntary admission.
D. The clinical director of the Approved Centre is responsible for arranging for the removal of
the person who is the subject of the recommendation to the Approved Centre.
E. ECT cannot be given without the consent of a patient.
273

1. B
2. A
3. D
4. A
5. C

274

Chapter 27
Acute behavioural disturbance

275

Chapter 27: Acute behavioural disturbance
A 30 year old man, who is an inpatient in a psychiatric unit, returns to the hospital from a weekend
pass. He is initially noted by nursing staff to be irritable and hostile. His behaviour escalates such that
he is shouting at staff and patients. He puts his fist through a window causing the glass to break and
threatens to cause harm to anyone who comes near him. An empty bottle of vodka and a large quantity
of cannabis are found in his bag.

Introduction
Disturbed or violent behaviour by an individual in an adult inpatient psychiatric setting, general
hospital ward or the Emergency Department, poses a serious risk to that individual, other patients
and staff.
Certain features can serve as warning signs to indicate that a patient may be escalating towards
physically violent behaviour:
o Tense and angry facial expressions.
o Increased or prolonged restlessness, pacing.
o General over-arousal of body systems (increased breathing and heart rate, muscle twitching,
dilated pupils).
o Increased volume of speech.
o Delusions or hallucinations with violent content.
o Verbal threats or gestures.
o Reporting anger or violent thoughts.
The optimal goal in the management of patients with acute behavioural disturbance is to ensure
safety for the patient, staff and other individuals.
Rapid tranquillization involves giving carefully monitored amounts of tranquillizing medication
over brief intervals of time to control agitated, threatening and potentially destructive behaviour in
patients.
The clinical practice of rapid tranquilization is only used when appropriate de-escalation and time-
out approaches have failed to control acutely disturbed behaviour. Rapid tranquilization is
therefore a treatment of last resort.

Management steps
1. Review case notes and the medication kardex, and obtain a collateral history.

2. Endeavour to establish the underlying cause behind the acute behavioural disturbance before
making any treatment decisions. Potential causes which should be considered include:
Delirium (acute confusional state) which can result from:
o Drug/alcohol withdrawal or intoxication.
o Iatrogenic - be suspicious of all prescribed medications, new prescriptions or abrupt
stoppages.
o Infection.
o Fever.
o Metabolic causes, e.g. hypoglycaemia.
o Head injury.
o Brain tumour.
o Brain haemorrhage or infarction.
o Post-surgical complication.
o Constipation.
Psychiatric causes
o Acute psychosis.
o Agitated depression.
o Mania.
o Borderline or antisocial personality disorder.
Other causes
o Intoxication with, or withdrawal from, alcohol or illicit substances which do not result in
delirium.
o Antisocial behaviour.
o Pain.

3. Seek expert advice from a senior colleague.
276

4. Allow a period of de-escalation and time out.
One staff member should take control of a potentially disturbed situation.
Create a safe area by asking other patients and staff who are not directly involved in the
situation to leave the vicinity.
Consider involving security staff and/or the Gardai in the background of the scene.
Move towards a safe place and avoid being trapped in a corner.
Adopt a non-confrontational stance, continuing to engage the patient in conversation,
explaining in simple terms what happening. Do not interview a potentially violent patient
alone.
Listen carefully and show empathy, acknowledging any concerns.
Ask the patient open questions and inquire about the reason for the aggressive or threatening
behaviour.
Ask for any weapons to be placed in a neutral location, i.e. on the floor, rather than handed
over.
Consider if the patient might be too hot or cold, hungry or in pain.
Consider encouraging the patient to make use of a well-lit side room in order to reduce arousal
and/or agitation and to help them to calm down.
Consider 1:1 supervision.
Consider asking a familiar person (e.g. family or staff member) with whom the patient has a
good rapport, to stay with the patient until they calm down.

5. Only when de-escalation has failed to reduce the disturbed behaviour, should medication be
considered. This step is known as rapid tranquilization.

Step 1: Get senior advice and/or inform senior staff at all stages
Step 2: Baseline vital signs: if possible, before giving medication check BP, pulse, respiratory rate and
temperature.
Step 3: Offer oral treatment first: haloperidol 5-10mg + lorazepam 1-2mg.
Repeat every 45-60 minutes if needed, monitoring vital signs every 5-10 minutes if possible.
Go to Step 4 if two doses fail, or sooner if the patient refuses oral medications and/or is putting
themselves or others at risk.
Note: Maximum doses in 24 hours: haloperidol 18mg and lorazepam 8mg.

Step 4: Consider IM treatment: haloperidol 5-10mg + lorazepam 1-2mg.
Monitor vital signs every 5-10 minutes if possible for one hour post-injection; then half-hourly
until ambulatory.
Repeat up to a maximum of three times at 30 minute intervals.
Note: Maximum doses in 24 hours: haloperidol 18mg and lorazepam 8mg.
Note: high dose or cumulative effects of benzodiazepines may cause respiratory depression/arrest.
Flumazenil IV should be available to reverse this effect. If the respiratory rate falls below 10 breaths per
minute, give flumazenil 200g over 15 seconds, then 100g at 60 second intervals if required to a maximum
of 1mg by IV injection.
Note: procyclidine IM (or another anticholinergic agent) should be available for a possible acute dystonic
reaction resulting from the use of an antipsychotic. Procyclidine 5-10mg can be given and may be repeated
after 20 minutes if needed. (Max: 20 mg/day).

Step 5: If no response from the above, consider long-acting IM therapy and/or IV therapy
Zuclopenthixol acetate (clopixol acuphase) 50-150mg IM should never be administered to
those without any previous exposure to antipsychotic medication. It may be considered an
option when:
o It is clearly expected that the patient will be disturbed/violent over an extended period of
time.
o A patient has a past history of good and timely response to zluclopenthixol acetate.
o A patient has a past history of repeated parenteral administration.
Diazemuls (an injectable emulsion of diazepam) 5-10mg IV +/- haloperidol 5mg IV.

Step 6: Prophylactic mediation: in order to maintain control, consider charting regular prophylactic
medication until the precipitants are treated, e.g. haloperidol 5-10mg PO/IM every 8 hours and/or
1-2mg lorazepam PO/IM every 8 hours. These medications must be reviewed daily.
277

6. After rapid tranquillisation is administered, vital signs should be monitored and pulse oximeters
should be available. Blood pressure, pulse, temperature, respiratory rate and hydration should be
recorded regularly, at intervals agreed by a multidisciplinary team, until the patient becomes active
again.

7. Any incident requiring rapid tranquillization, physical intervention or seclusion, should be
recorded in the patients chart.

8. A post-incident review should take place as soon after the incident as possible, but in any event
within 72 hours of the incident ending. The aim of the review is to support staff and patients, seek
to learn lessons and encourage the therapeutic relationship between patients, their carers and staff.
9. Debriefing: both before and after rapid tranquilization, the patient should have the reasons for this
treatment explained to them. In a patient who is lacking capacity, good practice requires that
careful documentation is kept and the patients family should be informed of the clinical situation.
Alternatives to haloperidol for rapid tranquilization
Olanzapine 10mg or risperidone 2mg may be used as an alternative to haloperidol.
Do not give benzodiazepines within 60 minutes of IM olanzapine due to the risk of somnolence
and hypotension.

278

MCQ Chapter 27
Question 1: Which ONE of the following statements regarding acute behavioural disturbance is
TRUE?
A. Two staff members should take control of a potentially disturbed situation.
B. It is important to ask patients to hand over any weapons that they might have in order to
reduce the risk of intensifying the volatile situation.
C. Advice should be sought from a senior colleague.
D. If de-escalation is unsuccessful, proceed to IM mediation.
E. Adopt a confrontational stance.

Question 2: Which ONE of the following doses ARE appropriate for rapid tranquilization?
A. Haloperidol 50-100mg.
B. Zuclopenthixol acetate 5-15mg.
C. Diazemuls 0.5-1mg.
D. Lorazepam 0.1-0.2mg.
E. Procyclidine 5-10mg.

Question 3: Which ONE of the following statements regarding acute behavioural disturbance is
TRUE?
A. Consider encouraging the patient to make use of a well-lit side room in order to reduce
arousal.
B. Risperidone 5-10mg is a useful alternative to haloperidol 5-10mg.
C. If a patient appears particularly tense and angry, it is appropriate to omit the de-escalation
stage and to start with rapid tranquilization in order to achieve a speedy resolution.
D. It is not important to find the cause of the acute behavioural disturbance.
E. IM olanzapine is usually given together with IM lorazepam.

279


1. C
2. E
3. A

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