Organic Mental Disorders Flashcards

1
Q

Delirium

A

Acute, Generalised Impairment of Brain Function; Crucially, impaired
consciousness; Primary cause often outside of the brain

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2
Q

Dementia

A

Chronic, Generalised Impairment; Main feature is Global Intellectual Impairment;
Might also involve changes in Mood and Behaviour
o Primary cause within brain e.g. Alzheimer’s Disease

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3
Q

Specific Syndromes

A

Includes disorders with predominant impairment of Memory, Thinking,
Mood or Personality Change
o Includes Neurological disorders which frequently lead to Organic Psychiatric
complications e.g. Epilepsy

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4
Q

Delirium Features

A

• Acute Impairment of Consciousness producing Generalised Cognitive Impairment; =Acute
Confusional State; 15% of patients on wards, with primary cause often systemic illness
• Impaired Consciousness most important (Deficit in Attention, Concentration, Awareness);
Often not able to follow/engage in logical conversation
o Fluctuates in intensity, often worse in the evening
• Disorientation, Overactive/Underactive Behaviour, Disturbed Sleep, Impaired thinking, Ideas
of Reference and Delusions, Labile, Disordered Mood
• Misinterpretations, Illusions and Visual Hallucinations; Tactile and Auditory Hallucinations
occur but are less frequent; Disturbances of Memory and Insight

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5
Q

Delirium Epidemiology

A

Extremely common; May occur in all age groups; Those at Extremes of Age, Pre-existing
Dementia or Serious Physical Illness make up majority; More common with Primary Mood or
Anxiety Disorders; Half of Delirium occurs in people with underlying Dementia syndrome
o Highest incidence on Intensive Care (40 – 60%)

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6
Q

Aetiology of Delirium

A

• Usually multifactorial; Each relevant at different points of illness
• Consistent clinical presentation suggests common pathological pathway for all aetiologies
• Diffuse slowing of EEG, global changes in Cerebral Circulation; Neuroimaging suggests
involvement of PFC, Thalamus, Post Parietal, Subcortical
o Unclear why Speech, Motor and Sensory intact in delirium while rest deranged
• Relative deficit in Cholinergic action compared to Excessive Dopaminergic Action

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7
Q

Assessment of Delirium

A

• Aim to identify underlying physiological cause; Place in context with patient’s premorbid level
of Cognition and Functioning; Clinical Diagnosis, usually obvious on speaking to patient
• Collateral history valuable to identify course of illness; Medication History, Systems Review
and Full Neurological Examinations
• Bloods – FBC, U/Es, LFTs, TFTs, Ca, Phos, Mg, Glu, Lactate, Trop, Alb, Haematinics
• BC, U Dip and MC+S, ABG, ECG, CXR
• Consider further investigations – CT Head, LP, EEG if appropriate
• Quantify Delirium ≤6/10 on AMTS; MMSE < 25 (Although primarily for Dementia)

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8
Q

Management of Delirium: Medical

A

Treat Underlying Cause – Oxygen requirement, Fluids, Antibiotics, Analgesia; Invasive
procedures and Intravenous access should only be done if valid indication
o Avoid unnecessary medications/ Polypharmacy

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9
Q

Management of Delirium: Nursing

A

• Reassurance and Reorientation – Clock visible at all times; Constantly reminded of Time,
Place, Day and Date regularly
• Predictable, Consistent Routine – Nursed either Quiet side room, or near to Nursing Station;
Reasonably dark at night, light during day; Meals at standard times, Relatives and Friends
encouraged to stay or visit frequently

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10
Q

Management of Delirium: Family

A

Explanation to Relatives and Friends – Allows them to help reassure and reorientate patient

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11
Q

Management of Delirium: Sleep

A

Small dose of Hypnotics (Zopiclone 3.75mg nocte) or Benzodiazepines (Temazepam
10mg nocte); Avoid during daytime as sedative effects increase disorientation

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12
Q

Management of Delirium: Disturbed/Violence/Distressed Behaviour

A

2/3rds of patient have clinical improvement on
Antipsychotics; Haloperidol, or Atypical Antipsychotics (E.g. Olanzapine)
o Lorazepam also effective but moderate risk of worsening the mental state
o IM dose might be required in acute setting, with follow-on oral therapy
o Should be regularly reviewed and never used unless other methods of management
have been exhausted

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13
Q

Dementia

A

• Generalised decline of Intellect, Memory and Personality without Impairment of
Consciousness; Clinical syndrome caused by variety of pathologies
o Acquired disorder although onset might be any age; Onset before 65yrs = Presenile
o Increasing incidence, likely due to ageing population
• 25 million people worldwide; Increases dramatically as Life Expectancy increases further; Four
times more common in women

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14
Q

Clinical Features of Dementia: Onset

A

• Insidious onset; might occur after acute deterioration; Might be trigged by social
circumstances or intercurrent illness; Might include uncharacteristic aggressive behaviour or
sexual disinhibition; Social lapses that are out of character

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15
Q

Clinical Features of Dementia:Cognition

A

Decline in cognitive function, Increased Forgetfulness; Difficulty in new learning; Memory loss
more obvious for recent vs remote events; Might have Aphasia, Agnosia and Apraxia

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16
Q

Clinical Features of Dementia: Behaviour

A

– Disorganised, Restless or Inappropriate; Loss of Initiative and Reduction of
Interests; When taxed beyond their restricted capabilities, might develop Catastrophic
Reaction (Sudden Tearfulness or Anger)

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17
Q

Clinical Features of Dementia:Mood

A

– Anxiety, Irritability, Depression; Important to differentiate from Pseudodementia

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18
Q

Clinical Features of Dementia Thinking

A

Slows; Impoverished thinking; Difficulty in abstract thinking, Impaired judgment
Grossly Fragmented and Incoherent Thought
o Persecutory and Paranoid Delusions
o Disturbed thinking becomes reflected in speech – Syntactical Errors and Nominal
Dysphasia; Eventually might utter only meaningless noises or become mute

• Perceptual Disturbances, Visual Hallucinations

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19
Q

Clinical Features of Dementia : Insight

A

Lacking into the degree, and nature of disorder

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20
Q

Depressive Pseudo-dementia

A

Poor Memory, Appears Intellectually Impaired because Poor
Concentration leads to Inadequate Registration
o Depressed Mood may lead to Slowness and Self-Neglect
o Depressed Mood precedes Memory issues; Memory impairment improves when
interest is aroused; Patient is retarded and unwilling to cooperate (C/f Dementia)

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21
Q

Differential Diagnosis of Dementia

A

Differential also includes Psychotic disorders and Delirium
• In Older Patients, Dementia is caused by 55%
Alzheimer’s Dementia, 20% Vascular Dementia,
15% Lewy Body Dementia

22
Q

Alzheimer’s Dementia

A

• Significantly reduced brain area and size; Widened
Sulci, Enlarged Ventricles; Cell loss, Shrinkage of
Dendritic Tree, Proliferation of Astrocytes and
Gliosis
o Amyloid Plaques – Dense, Insoluble Beta-
Amyloid Peptide surrounded by Abnormal Neuritis, Filled with Highly Phosphorylated
Tau Protein
o Neurofibrillary Tangles – Helical Filaments
of Microtubule-associated Proteins (Tau) in
a Highly Phosphorylated state; Found
throughout Cortical and Subcortical Grey
• Plaques and Tangles initially occur in Hippocampi,
and spread more widely after; Occipital Lobe and
Cerebellum sparing; Neurones lost tend to be
primarily Cholinergic

23
Q

Alzheimer’s Dementia: Classical Presentation

A

Forgetfulness is often first symptom; Disorientation, Mood Variation,
Poor Sleep, Social Behavioural Declines and Self-Neglect (Although some can compensate)
• Personality Changes (Exaggeration of less-favourable Traits)
• Progression might involve Parietal Lobe Dysfunction – Dysphagia, Dyspraxia, Agnosia

24
Q

Alzheimer’s Dementia:Risk Factors

A

FH, Age, Genetic Mutation, Previous Head Injury, Down Syndrome,
Hypothyroidism, Parkinson’s Disease, Cardiovascular Disease, Lower Education and IQ

25
Q

Alzheimer’s Dementia: Prognosis

A

Death occurs usually within 5 – 8years after first signs of disease; Most Pneumonia

26
Q

Vascular Dementia

A

=Multi-infarct; Clinical syndrome can be caused by variety of Cerebrovascular Pathologies;
Associated with Ischaemia and Non-Ischaemic changes
o Both large and small blood vessels might be affected; Infarcts tend to be Bilateral and
Involve Full Thickness of White Matter
o Multiple Infarction and Ischaemic Lesions in the White Matter
o Atrophy of Old Infarcted Areas; Blood Flow changes in Unaffected Regions
o Entire brain is smaller and Ventricles expanded

27
Q

Vascular Dementia: Presentation

A

Presents in Late 60s – Early 70s; More sudden onset than Alzheimer’s; May present after
Stroke; Emotional and Personality Changes tend to happen earlier C/f Alzheimer’s

28
Q

Vascular Dementia: Symptoms

A

Symptoms characteristically Fluctuating; Episodes of confusion common, especially at night;
Depression is common; Fits, TIA or other signs of Cerebral Ischaemic might occur

29
Q

Vascular Dementia: Diagnosis

A

Diagnosis from Alzheimer’s difficult unless clear CVA history; Risk factors include CVS disease,
Smoking, FH, AF, DM, Coagulopathies, Carotid Disease

30
Q

Lewy Body Dementia

A

• Spherical, Neuronal Inclusion Bodies; Clinically can manifest as Parkinson’s Disease, Dementia
with Lewy Bodies, and Autonomic Failure, associated with Degeneration of Sympathetic
Neurones of the Spinal Cord
o Dense, Intracytoplasmic Inclusions made of Phosphorylated Neurofilament Proteins
associated Ubiquitin and Alpha-Synuclein
o Primarily in Basal Ganglia and later spread into Cortex; Neuronal Loss is Prominent
with slight reduction in Total Brain Volume
o Mixture of Lewy Bodies and Alzheimer’s-type Amyloid Plaques and Tangles

31
Q

Lewy Body Dementia Clinical Features

A
  • Relative Sparing of Memory with Fluctuating Cognitive Ability and LOC is typical
  • Parkinsonianism – Postural Instability, Shuffling Gait; Only 20% of Tremor
  • Visual Hallucinations, Falls, Depression and Sleep Disorders
32
Q

Lewy Body Dementia Prognosis

A

Life Expectancy 4 – 10 years; Rate of Cognitive Decline like Alzheimer’s; Pronounced
Parkinsonism affects movement; Perceptual and Behavioural Disturbance can be severe in later stages with Antipsychotics, requiring Residential Care

33
Q

Lewy Body Dementia Treatment

A

Levodopa and Antiparkinsons medications for Parkinsonianism; Anticholinergics
avoided as they might increase Confusion and Visual Hallucination
o Atypical Antipsychotics should be used before Typical agents as higher risk of Neuroleptic Malignant Syndrome in LBD

34
Q

Assessment of Dementia

A

• Memory Assessment Clinics – Includes Detailed History Taking, which covers Collateral
History and Mood; Full Physical Examination
• Cognitive Testing – MMSE widely used, with high sensitivity and specificity
• FBC, U/Es, LFTs, TFTs, B12, Folate, Thiamine, Ca, Glucose
o Special Investigations E.g. HIV, Syphilis only if high clinical suspicion
• Imaging – CT/MR Head if suspicion of Organic Brain Disease up to late middle age, or if
suggestion of Focal Lesions >65yrs

35
Q

MANAGEMENT OF DEMENTIA

A

Aim to reduce disability and provide support; Where possible, care outside hospital, either
with relatives or Residential care; Admission if at risk of harm to themselves or others, or
Complex Physical or Psychiatric Co-morbidities
o Maintain remaining ability, Relieve Distressing Symptoms, Arrangement of Practical
Requirements and Support for Relatives/Carers

36
Q

MANAGEMENT OF DEMENTIA: Written Care Planning

A

Includes views on Residential Care, EOLC, Resus status; Input from
OT, PT and Dietician should be offered

37
Q

MANAGEMENT OF DEMENTIA: Psychoeducation

A

Symptoms, Course, Prognosis, Treatments, Support Groups, Financial and Legal Considerations, and further information

38
Q

MANAGEMENT OF DEMENTIA: Psychoeducation

A

Symptoms, Course, Prognosis, Treatments, Support Groups, Financial and
Legal Considerations, and further information

39
Q

MANAGEMENT OF DEMENTIA: Structured Group Cognitive Stimulation Programmes

A

Improve MMSE scores and QOL for

patients with mild-moderate Dementia in medium term

40
Q

MANAGEMENT OF DEMENTIA: Management of Agitation and Challenging Behaviour

A

Aromatherapy, Music/Dance, Animal-Assisted Therapy, Massage Therapy

41
Q

Pharmacotherapy for Dementia

A

Acetylcholinesterase Inhibitors (E.g. Donepezil, Galantamine, Rivastigmine) – Increase
Concentration and Duration of Acetylcholine in CNS; Evidence for moderate-severe
Dementia; For use if MMSE 10 – 20, or agitation not managed conservatively or with
Antipsychotics; Not recommended if non-Alzheimer’s Dementia
Benzodiazepines avoided, especially in the day; Same indications as Antipsychotics

42
Q

Memantine

A

Glutamine NMDAR Antagonist; Improves Cognition, Mood, Behaviour in moderate-severe Dementia

43
Q

Antipsychotics

A

Avoided whenever possible; Used for Severely Distressed or Agitation
causing Risk to Self and Others
o Avoid in mild-moderate Dementia due to risk of Cerebrovascular Events

44
Q

Cortical and Subcortical Dementia

A
  • Controversial Distinction – Cortical (Alzheimer’s Pattern) or Subcortical (Parkinson’s)
  • Cortical – Memory > Motor; Aphasia, Apraxia, Acalculia more common
  • Subcortical – Motor prominent with less marked Memory issues; Dysarthria > Aphasia; Impaired Coordination with Abnormal Posture
45
Q

Psychiatric Manifestations of Head Injury

A

• Majority Head Injuries associated with RTA and ETOH; Peak age 15 – 24yrs, M>F
• Difficulty to predict likelihood of brain injury; Neuropsychiatric consequences variable in
terms of severity and symptoms

46
Q

Acute Phase of Head Injury (Hours to Days)

A

o Post-Traumatic Amnesia – Loss of Memory for the period of injury until normal
memory resumes; Amnesia >24hrs associated with higher risk of impairment
o Retrograde Amnesia – Loss of Memory for Distinct Period of time leading up
o Acute Post-Traumatic Delirium – Confusion, Anxiety, Mood Lability, Paranoia,
Hallucinations occurring soon after regaining consciousness

47
Q

Longer Term Psychiatric Syndromes

A

o Cognitive Impairment – Global Dementia, or Focal Deficits in Memory, Attention,
Concentration or Speech; Repetitive Trauma can lead to Progressive Deterioration in
Intellectual Function
o Personality Change – Often most serious complication; Particularly after Frontal Lobe
damage; Irritability, Loss of Spontaneity and Drive, Coarsening of Behaviour, Reduced Control of Aggressive Impulses
o Emotional – Post Concussional Syndrome of Interaction of Minor Brain Damage with Anxiety and Depression

48
Q

Psychiatric Manifestations of Head Injury: Specialist Rehabilitation

A

PT and graded increased in physical activity, Occupational Therapy,
Working around and minimising Disabilities in ADL and specific Cognitive Deficits
• Depression, Psychosis and Agitation treated as with standard guidelines

49
Q

Psychiatric Manifestations of Epilepsy

A

4× risk of Psychiatric Disorders; Wide variation depending in type of Epilepsy
o Due to Effects of Stigma and Social Restrictions, Behavioural Disturbance associated
with Seizures, Disorders between Seizures or Disorders due to cause of Epilepsy

50
Q

Psychiatric Manifestations of Epilepsy: Prodromal

A

Period of Tension, Irritability, Depression lasting hours to days
• Ictal – if Focal Onset type, may have Automatic Behaviours; If prolonged, may appear as
Abnormal Mental State, Abnormal Behaviours or Social Withdrawal

51
Q

Psychiatric Manifestations of Epilepsy: Postictal

A

Prolonged period of Confusion, Disorientation, Inattention, Agitation that usually lasts few hours; Psychosis might occur if severe Epilepsy

52
Q

Psychiatric Manifestations of Epilepsy: Between Seizures

A

Cognitive Dysfunction (Either due to Residual Abnormal Electrical Activity,
or Anti-Epileptic Medications), Personality Disorders (Which may occur due to Social, or
Organic causes), Depression, Anxiety, Suicide (5×) and DSH (7×) Sexual Dysfunction
o Chronic Interictal Psychosis (Uncontrolled Epilepsy >10yrs; Similar presentation to
Schizophrenia, treated with Antipsychotics
o Forensic – Although might be confounded by Lower IQ, Lower SES