Degenerative Dementias: MRCPsych Course

Dr Chris Davison, Consultant Old Age Psychiatrist Content

• Dementia • Cases • Exams • Images

2 Aims

• Describe the clinical presentation and course of the common degenerative dementias of late life, particularly AD and DLB • Introduce the concept of mild cognitive impairment as a possible early presentation of dementia • Encourage the use of operationalised diagnostic criteria for these disorders • Raise awareness of less common causes of degenerative dementia that may be encountered in the practice of old age psychiatry

3 Learning Outcomes

• Be able to diagnose the dementia syndrome and aetiological subtypes, using systematic methods and with an awareness of the probable diagnostic accuracy • Understand the issues around diagnosing dementia at an early stage and to know the approach to assessment that will best assist in this. • Understand the specific importance of accurate diagnosis for optimal management of each of the common disorders

4

What is dementia?

5 What is dementia?

 Clinical syndrome with multiple and persisting cognitive impairments  Memory plus other cognitive functions affected  Impairment lasting 6 months

 Functional impairment in daily living e.g. repetitive questions, inability to make a cup of tea, putting clothes on wrong

 Exclusion of other conditions interfering with cognitive function  Depression  Delirium  Hypothyroid etc. 6 What is dementia?

Executive function  Memory plus Impaired decision making, apathy

other cognitive Spatial neglect, visuo

functions affected

Space perception Space impairment, impairment, agnosia

Memory

 -

Functional constructive

impairment or

Language Language & motor Aphasia, Alexia, Apraxia, Apraxia, Alexia, Aphasia, decline from premorbid function Visual function Agnosia, Prosopagnosia

7 What is dementia?

 Can be progressive e.g. Alzheimer's dementia

 Can be static e.g. secondary to head injury

8 What is dementia?

 Degenerative Dementia in old age is huge problem

 Risk doubles every five years over age of 65

 800,000 people in UK affected by dementia

 Numbers set to grow significantly – 1 million by 2021

 Costs 17 billion pounds

9 DSM 5

 DSM 5:

 Dementia

 = Major Neurocognitive Disorder

10 Dementia prevalence

 Dementia prevalence in the UK

11 Causes of Dementias Parkinsons Disease Fronto-temporal dementia dementia Dementia with Lewy Bodies

Alzheimer’s

Huntingtons disease disease Mixed dementia Vascular dementia Rare causes 12 Progressive Dementias

Alzheimer's Disease 50%

Mixed Other Causes Alzheimer's/ 10% Vascular Disease 10%

Vascular Disease Dementia with 10% Lewy Bodies 20%

13 Case study

• 69 year old lady • 3 year history of progressive worsening of short term memory • On a couple of occasions put electric kettle on gas hob • Keeping out of date food in fridge and missing appointments • On clinical assessment: • MMSE 22/30. Mood apathetic and some depression • Experienced musical hallucinations. Doesn’t think memory is that bad. • Physically well otherwise

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Case study

• 81 year gentleman • 1 year history of progressive worsening of short term memory • Nominal aphasia - mild • On clinical assessment: • MMSE 19/30. Reduced verbal fluency. • High BP – but treated • Mild MI when 74 • History of prostate cancer • Physically slightly stooped. No focal neurological signs. • At research clinic has CSF sample – high tau and low beta amyloid 15

16 AD: NINCDS-ADRDA criteria

 Dementia established by clinical examination and cognitive examination e.g. MMSE  Deficits in two or more areas of cognition  Progressive worsening of memory / other cognitive functions  No disturbance of consciousness  Onset between 45 and 90 (most often >65)  No systemic or other brain disorders which could account for progressive cognitive deficits

McKhann et al. Neurology 1984;34:939-944.

AD: NINCDS-ADRDA criteria

 Supported by  Impaired activities of daily living or altered behaviours  Family history of Alzheimer’s  Cerebral atrophy on CT head scan and progressive atrophy noted with serial scans or normal CT

McKhann et al. Neurology 1984;34:939-944. AD: NINCDS-ADRDA criteria

 Other clinical features  Plateaus in course of progression  Associated behavioural and psychological symptoms  Depression  Insomnia  Incontinence  Delusions  Hallucinations  Verbal, emotional or physical outbursts  Weight loss  Neurological signs (especially advanced AD)  Increased muscle tone, myoclonus, gait disorder, seizures

McKhann et al. Neurology 1984;34:939-944.

 Timeline of neuropathology and symptoms in AD

Alzheimer’s Dementia

 Brain changes in Alzheimer’s dementia

Normal Alzheimer’s Widened sulci Alzheimer’s Dementia

 Brain changes in Alzheimer’s dementia

Hippocampus – memory function

Normal Alzheimer’s Biomarkers in AD

Biomarkers in AD

 Brain changes in Alzheimer’s dementia

Normal

Mild Increasing hippocampal atrophy Moderate

Severe Biomarkers in AD

 Neuroimaging  Structural  PET – metabolism (FDG) and amyloid load (PIB)

Biomarkers in AD

 CSF sampling  High total tau  High phosphorylated tau

 Low beta amyloid (A-Beta40 and A-Beta42)

Predictive of Alzheimer’s

Biomarkers in AD Proposed new diagnostic criteria for AD ADD Workgroup, McKhann et al, Alzheimer’s and Dementia, 2011 • Probable AD: • Dementia (amnestic or non-amnestic presentation) • Gradual onset • Evidence decline/ progression • No related stroke/ CVD on imaging/ presence of DLB/FTD etc • Probable AD with evidence of AD pathological process: • Evidence neuronal injury (MRI, FDG PET, CSF tau) • Alterations in A-beta (Amyloid PET or CSF) • AD like profile (history and course) • Possible AD with evidence of AD pathological process: • Meet criteria for another dementia but AD biomarker positive • Pathophysiologically proved AD: • Meet clinical criteria and autopsy positive Case study 2

• 69 year old lady • 1 year history of subjective worsening of short term memory • Forgetting appointments and needs to write things down to remember. • On clinical assessment: • MMSE 27/30 • Intact activities of daily living • Physically well otherwise

Research amyloid scan Research PET FDG scan

Mild Cognitive Impairment

Petersen et al. 1999,2004 Mild Cognitive Impairment • Definition – Memory complaint by patient, family or physician – Normal activities of daily living – Essentially preserved general cognitive abilities – Objective impairment of cognitive function (> 1.5 or 1.0 SD of age mean i.e. 7% or 16% of normal population) – Clinical dementia rating score of 0.5 – Not clinically demented

Petersen et al. 1999,2004 Mild Cognitive Impairment

• Yet another in a long line of attempts to define a subclinical syndrome • However gained much wider acceptance

Petersen et al. 1999,2004 Strengths of MCI concept

– Significant research evidence supporting it as a syndrome – Requires objective element to assessment – Relies on a holistic and in-depth clinical assessment and not just a cognitive cut-off – Other criteria been applied loosely – Provided basis for predicting progression to dementia – Focus of major randomised controlled trials

Areas of controversy

• Normal or abnormal aging – absent minded or in the early stages of dementia • Definition • Validity • Reliability • Prognosis • Pathological basis Limitations with the MCI concept

Farias et al 2009; Petersen et al. 2009 Limitations with the MCI concept Instability of diagnosis over time  E.g. Ritchie et al 50% of MCI return to normal after 1 year.  But likely related to education, psychiatric co-morbidity (depression), medications, hormonal changes and genetics

Reliability varies with setting & retrospective surveys  However prospective studies provided more stable estimates Farias et al 2009; Petersen et al. 2009 Progression

 In Memory Clinic/Hospital samples  Progression to dementia: 10 – 15 % / year  Stable over time, few recover  Higher prior probability of having underlying disorder  In population  Progression to dementia: 6 – 10 % / year  More unstable with people becoming “cognitively normal” again  Broader spectrum of MCI severity and more heterogeneity

Farias et al 2009; Petersen et al. 2009 MCI Subtypes People with MCI are probably at greater risk of progressing to Alzheimer’s disease if:

• they are older • they have a family history of dementia • they have had high blood pressure • they have high cholesterol • they have a risk gene (ApoE4)

Biomarkers in AD Case study

• 63 year old retired physics teacher • Complaining of blurring of vision and seeing lights, with a normal ophthalmic examination • CT head was normal • She re-attended one year later complaining of subjective short term memory difficulties and “bumping into things”. Struggling to dress herself and gets easily confused • On examination, no neurological signs • MMSE 22/30. Deficits in visuo-spatial, writing, calculation and following command. Memory intact • Has finger agnosia, left-right disorientation

Posterior cortical atrophy

• Atypical variant of AD • Also called Benson's syndrome • Characterised by posterior atrophy • Affects occiptial and parietal lobe areas • Tend to have well preserved memory and language • However often progressive, dramatic and relatively selective decline in vision and/or literacy skills such as spelling, writing and arithmetic • Can present with Gerstmann’s syndrome • Dysgraphia/agraphia: deficiency in the ability to write • Dyscalculia/acalculia: difficulty in learning or comprehending mathematics • Finger agnosia: inability to distinguish the fingers on the hand • Left-right disorientation • Can also present with Prosopagnosia • Also Balint’s syndrome • inability to perceive the visual field as a whole (simultanagnosia) • difficulty in fixating the eyes (ocular apraxia) • inability to move the hand to a specific object by using vision (optic ataxia)

• Often younger onset than AD

Case study

• 72 year old gentleman • 1 year history of worsening of short term memory • Frequent falls • Occasionally sees “a pink elephant” out of the corner of his eye and the stripped carpet tends to “ripple like the sea”. • On cognitive assessment: • MMSE 27/30

Dementia with Lewy bodies

 Dementia with Lewy

Alzheimer's bodies (DLB) is a Disease common cause of 50%

dementia Mixed Other Causes Alzheimer's/ 10% Vascular Disease  10% DLB is related to Vascular Disease Dementia with 10% Parkinson’s disease Lewy Bodies 20%

Lewy Body Disease

MSA RBD Parkinson’s Lewy Body Disease Dementias

PD Dementia Dementia with Lewy Bodies (DLB)

50 -60 Increasing age 70 - 80 Dementia with Lewy bodies

 Evidence of dementia of sufficient magnitude to interfere with normal social and occupational function.

 Core features (at least 2)  Fluctuating cognition with pronounced variations in attention and alertness  Recurrent visual hallucinations which are typically well formed and detailed  Spontaneous features of parkinsonism

 Suggestive features  REM sleep behaviour disorder  Severe neuroleptic / antipsychotic sensitivity  Low dopamine transporter uptake in basal ganglia demonstrated by SPECT or PET imaging Dementia with Lewy bodies

Supportive features  Falls and syncope  Unexplained loss of consciousness  Autonomic dysfunction  Hallucinations in other modalities  Systematized delusions  Depression  Preserved medial temporal lobe structures on CT/MRI  Generalised low uptake on HMPOA SPECT/PET perfusion scan with reduced occipital activity  Prominent slow wave activity on EEG with temporal lobe transient sharp waves Dementia with Lewy bodies: Neuropsychological profile • DLB and AD equally impaired on composite batteries e.g. MMSE, CAMCOG • AD worse than DLB on immediate and delayed recall e.g. episodic memory • DLB worse than AD for : • attention e.g. reaction time, digit vigilance • visuospatial performance e.g. clock drawing • visual perception e.g. fragmented letters

AD DLB

MMSE 18/30 MMSE 20/30 Orientation 5/10 Orientation 8/10 Short term memory 0/3 Short term memory 2/3 Dementia with Lewy bodies

Cognitive deficits in DLB vs AD

DLB AD Attention Moderate Mild Executive functions Moderate / Severe Moderate Psychomotor speed Moderate / Severe Mild Free recall Mild Severe Recognition Mild Severe Retention Mild Severe Constructional praxis Severe Mild Visuo-perceptual Severe Mild Fluctuating cognition in DLB

minute to minute / hour by Lucidity and hour capable task variation performance

Cognitive baseline time

Transient Communication Glazed / interruption in difficulties switched off awareness Medial Temporal Lobe Atrophy in DLB and AD Subjects Matched for Global Impairment

AD

DLB

Absence of medial temporal lobe atrophy is more common in DLB (40-60%) than AD (10%) Barber et al. Neurology. 2000;54:1304-1309. Neuroleptic sensitivity in DLB

 Increased mortality 2-3x in 50% - no predictors

 Atypicals seem similar to conventional anti-psychotics but no RCT evidence!

 Tolerance of anti-psychotics does not exclude DLB

 Anti-psychotic challenge is not advocated

 Anti-psychotics do not affect DA transporter uptake imaging

REM Sleep Behaviour Disorder

 High specificity for a diagnosis of Lewy body disease / -synucleinopathy when associated with neurodegenerative disease

 A potential risk indicator for LB disease

 A useful diagnostic marker

 An important treatment target

Dementia with Lewy bodies

 Low dopamine transporter uptake in basal ganglia demonstrated by SPECT or PET imaging

Alzheimer's DLB Dementia (AD)

DaTSCAN

59 Dopamine transporter imaging as a diagnostic biomarker for DLB.

Sensitivity for probable DLB v probable AD was 78% and specificity 90%. Independent of age, MMSE or UPDRS.

Note: A negative DaTSCAN does not exclude a diagnosis of DLB! (20% will be negative!)

Dementia in PD (Aarsland et al, Arch Neurol 2003; 60: 387-392)

% 90 80 70 60 Dementia 50 "Probable DLB" 40 Cumulative dementia 30 20 10 0 1993 (n=238) 1997 (n=139) 2001(n=76)*

Mean time from onset of PD to dementia is 10.5 yr (range 4-27) (Apaydin et al, 2002) Diagnostic Criteria for PD dementia (Emre M et al, Movement Disorders 2007 2007 Sep 15;22(12):1689-707)

• Parkinson’s disease • Dementia – > 1 cognitive domain – ADL > motor and autonomic deficits • Associated clinical features – Cognitive – attention, executive, visuospatial, memory, language – Behavioural – apathy, personality and mood, hallucinations (v), delusions, daytime sleepiness • Exclusions include other conditions causing confusion or unknown time course of motor/cognitive symptoms

Can diagnose probable or possible PDD DLB and PDD are similar with respect to:

• Cognitive profile • LB distribution and density • Fluctuating cognition • Cholinergic and dopaminergic • Extrapyramidal deficits features • Neuroleptic • Neuropsychiatric sensitivity symptoms • Response to cholinesterase inhibitors

Couple of case studies - 1

A 51-year-old male lawyer began to embezzle money at work using the money to buy pornographic materials via the internet. Also noted to be inappropriate at work to female staff

His work had dramatically deteriorated, and rather than working with his clients, he spent most of the day at work shuffling papers, reading magazines or downloading pornography onto his computer

Subsequently fired and not working. Over past year has last interest and tends not to speak

He developed a strong desire for potato chips and gained 6 kgs

His manners deteriorated, and he stuffed his mouth, often choking at the dinner table Upon examination, the patient was profoundly apathetic and indifferent

MMSE 27/30 missing one point each for the name of the hospital, the season and for spelling "world" backwards

Verbal fluency, abstract thinking and performance on Luria motor task were impaired

Basic neurologic examination revealed pathologically brisk jaw jerks. Palmo-mental reflex evident.

Fasciculations, as well as subtle atrophy and weakness, were evident in the arms and legs.

Plantar responses were flexor. Couple of case studies - 2

A successful architect began to have trouble finding names for people and objects.

He continued to design buildings but had trouble filling out paper orders, making frequent spelling mistakes.

Surprisingly, he was caught stealing a shiny necklace from a client's home.

While at home he began to play solitaire compulsively for 6 hours per day.

He developed a new interest in squash, and his game steadily improved. He stopped working as an architect but obtained a courier job and learned and remembered a complex route for delivering packages.

There was no family history of dementia. MMSE score was 24/30.

Speech was fluent but somewhat lacking specific nouns.

Comprehension was mildly impaired due to deficits in understanding some words.

The items missed were two of three words on memory, naming of the watch and pen, and two items on the three-step command.

Neurologic examination was normal Case 1 Case 1

Progression Pathology

Within six months, the patient was Extensive gliosis and spongiform even more apathetic and unable changes of the frontal cortex. to speak. Ubiquitin and TDP-43-positive, Swallowing liquids became tau-negative inclusions were seen difficult, and aspiration became in the dentate gyrus of the frequent. hippocampus.

Died 9 months after diagnosis as Diagnosis of FTD-MND was a result of pneumonia diagnosed

Case 2 Case 2

Progression Pathology

Subsequently, deficits in Extensive atrophy of the anterior recognizing faces of others temporal lobes, orbitofrontal and became apparent, and he was medial frontal cortex was evident unaware when his wife became upset. Extensive spongiosus, gliosis and neuronal loss were evident in Four years after diagnosis, these frontotemporal regions. comprehension for spoken and written language had Ubiquitin-positive inclusions were disappeared, and he called all evident in the frontal and anterior people and items in his temporal lobes environment "thing."

Subtle problems with swallowing Diagnosis: Semantic dementia emerged 5 1/2 years after diagnosis, and the patient died 6 months later.

FTD: Manchester-Lund criteria

CORE SYMPTOMS (all must be present)

• insidious onset and gradual progression • early decline in social interpersonal conduct • early impairment in regulation of personal conduct • early emotional blunting • early loss of insight

FTD: Manchester-Lund criteria

SUPPORTIVE SYMPTOMS

• Behavioural disorder: • decline in personal hygiene and grooming • mental rigidity and inflexibility • distractibility and impersistence • hyperorality and dietary change • utilization behaviour

• Speech and language: altered speech output (aspontaneity and economy of speech, press of speech), stereotypy of speech, echolalia, perseveration, mutism

FTD: Manchester-Lund criteria

SUPPORTIVE SYMPTOMS

• Physical signs: primitive reflexes, incontinence, akinesia, rigidity, tremor, low/labile blood pressure

• Investigations: • neuropsychology: impaired frontal lobe tests; no amnesia or perceptual deficits • EEG: normal on conventional EEG despite clinically- evident dementia • brain imaging: predominant frontal and/or anterior temporal abnormality

Frontotemporal dementia (FTD)

• Dementia of frontal lobe type • Semantic dementia • Progressive non-fluent aphasia • FTD with motor neurone disease • FTD with parkinsonism • Chr 17 • Chr 3 • No linkage established Case study

• 69 year old previously highly functional lady presents with a 3 month history of rapid decline in short term memory and displays confusion. She is quite paranoid and needs to be admitted under MHA section

• MMSE is 20/30

• She has problems with her balance and co-ordination and has occasional “jerks”

Case study

Sporadic CJD

• Dementia100% • Myoclonus 80% • Pyramidal signs 50% • Cerebellar signs 50% • Extrapyramidal signs 50% • Less common:cortical visual defects,LMNL,abnormal extraocular movt.,sensory defects,seizures,vestibular disturbance,autonomic dysfunction • Mean survival five months

Sporadic CJD Investigations

• EEG:characteristic periodic sharp- wave complexes superimposed on slow background rhythm present in>90% • MRI: T2 hyperintense signal in basal ganglia in 80% • CSF:Elevated levels of protein 14- 3-3 without pleocytosis in 96%

Other prion diseases

• Kuru • Familial Creutzfeldt-Jacob disease • Gerstmann-Straussler-Scheinker disease • Familial fatal insomnia • New variant Creutzfeldt-Jacob disease sCJD vs. vCJD

Case study 4

• An 80 year old nursing home resident has fluctuating confusion, recurrent urinary incontinence and apathy.

• Nursing staff are finding it more difficult to get the gentleman up and mobile as his walking and gait has deteriorated.

• He scores 14/30 on his MMSE and seems slowed in his thinking

• The gentleman’s gait is shuffling and he is stooped but there is no rigidity or tremor

Case study 4

Normal pressure hydrocephalus

• Symptoms • Gait dysfunction • Unsteadiness and impaired balance • “magnetic gait” • May mimic Parkinsonian gait but no tremor • Urinary incontinence – urgency and detrusor hyper-reflexia • Cognitive impairment – subcortical / dyexecutive Normal pressure hydrocephalus

• Investigations • Structural scan • Lumbar puncture (Miller-Fisher test) • In most cases, CSF pressure is usually above 155 mmH2O • Clinical improvement after removal of CSF (30 mL or more) has a high predictive value for subsequent success with shunting • A "negative" test - very low predictive accuracy. Many patients may improve after a shunt in spite of lack of improvement after CSF removal Neuropsy- Disease First Symptom Mental Status Neurology Imaging chiatry Entorhinal cortex Episodic AD Memory loss Initially normal Initially normal and hippocampal memory loss atrophy Apathy; poor Apathy, May have vertical Frontal, insular, Frontal/ judgment/ disinhibition, gaze palsy, axial and/or temporal executive, FTD insight, speech/ hyperorality, rigidity, dystonia, atrophy; spares language; language; euphoria, alien hand, or posterior parietal spares drawing hyperorality depression MND lobe Visual hallucinations, Drawing and Visual Posterior parietal REM sleep frontal/ hallucinations, atrophy; DLB disorder, executive; depression, Parkinsonism hippocampi larger delirium, Capgras' spares memory; sleep disorder, than in AD syndrome, delirium prone delusions parkinsonism Cortical ribboning Variable, Dementia, and basal ganglia frontal/ Myoclonus, mood, anxiety, or thalamus CJD executive, Depression, anxiety rigidity, movement hyperintensity on focal cortical, parkinsonism disorders diffusion/ memory FLAIR MRI Often but not Frontal/ Cortical and/or always sudden; executive, Apathy, Usually motor subcortical Vascular variable; apathy, cognitive delusions, slowing, spasticity; infarctions, falls, focal slowing; can spare anxiety can be normal confluent white weakness memory matter disease HIV & the Brain Definition of HAND

Acquired No Pre- Interferes Delirium Impairment in existing with Daily Absent ≥ 2 Cognitive Cause Functioning Abilities Asymptomatic Neurocognitive ✔ ✔ ✔ No Impairment (ANI) Mild Neurocognitive ✔ ✔ ✔ Mild Disorder (MND)

HIV-Associated Marked Marked Dementia (HAD) ✔ ✔

Antinori et al, Neurology 2007, 69: 1789-99 86 Investigation

 Exclude opportunist infection

 CNS imaging . atrophy in basal ganglia & frontal white matter

 Look for other causes (B12 / folate deficiency, HCV, syphilis, TFT)

 Check CSF HIV Viral Load

 Cognitive screening tools • Cheaper & more available alternative than formal neuropsychological testing, but inferior 87 HAND Prognosis

 Unclear if mild HAND leads to HIV associated dementia

 Increased risk of death (HR 3.1, 95% CI 1.8 – 5.3)

Source: UpToDate http://www.uptodate.com/contents/hiv-associated-neurocognitive- disorders?source=search_result&search=hiv+dementia&selectedTitle=1%7E150 – Accessed 13/06/13 88 HIV Dementia

 Marked reduction in HAART era - <2%

 CASCADE study showed incidence of HAD from 6.49 per 1000 person-years in the pre-ART era to 0.66 per 1000 person-years by 2003 to 2006

Source: UpToDate http://www.uptodate.com/contents/hiv-associated-neurocognitive- disorders?source=search_result&search=hiv+dementia&selectedTitle=1%7E150 – Accessed 13/06/13 89 HIV & the Brain

 Clear direct effect on the brain

 We can optimise treatment to help reduce impact (we think)

 Patients may present with cognitive impairment alone

 Further research ongoing

90 What you need to know for the MRCPsych exam and

dementia  Know about associated behavioural and neuropsychiatric symptoms associated with each dementia e.g. Visual hallucinations with LBD.  Be aware of:  risk factors & genetics associated with each dementia e.g. APP with AD  neuropathological changes associated with each dementia e.g. balloon cells with Pick’s  molecular biology theories of dementia e.g. amyloid cascade hypothesis  epidemiology of dementias including prevalence and incidence  Know functional neuroanatomy e.g. If patient with dementia has prosopagnosia - where is the lesion? 91 Less common dementias and the MRCPsych exam

 In addition to “bread and butter” degenerative dementias need be aware of:  Huntingtons and genetics  CJD and other transmissible spongiform encephalopathies e.g. Kuru  Normal pressure hydrocephalus  HIV dementia & Alcohol dementia  Corticobasal degeneration  Progressive supranuclear palsy  Neuroinflammatory conditions e.g. HSV encephalitis, SLE etc.

92 MRCPsych exam

 Flashbulb Memory

93 MRCPsych exam

 Flashbulb Memory

 A detailed and vivid memory that is stored on one occasion and retained for a lifetime. Usually, such memories are associated with important historical or autobiographical events

Autobiographical / Declarative

94 MRCPsych exam

95 MRCPsych exam

 ApoE

96 MRCPsych exam

 ApoE

 apolipoprotein e gene

ApoE on chromosome 19 has been implicated in late-onset Alzheimer’s disease

97 MRCPsych exam

 Go / No Go

98 MRCPsych exam

 Go / No Go

Ask the patient to place a hand on the table. Tap under the table. Tell the patient to raise one finger when you tap once and not to raise the finger when you tap twice. Show the patient how it’s done and then do the test.

Frontal / Impulse control

99 MRCPsych exam

Perseveration ? Which lobe

100 MRCPsych exam

Perseveration ? Which lobe

Frontal (Lateral orbitofrontal cortex or inferior prefrontal convexity (Brodmanns area)

101 MRCPsych exam

 Gerstmann Syndrome

102 MRCPsych exam

 Gerstmann Syndrome

 Dominant Parietal Lode lesion

•Agraphia or dysgraphia •Acalculia or dyscalculia •Finger agnosia •Left-right disorientation

103 MRCPsych exam

 Stroop Test – Tests what?

104 MRCPsych exam

 Stroop Test – Tests what?

 Processing Speed / Attention  Prefrontal Non Dominant

105 MRCPsych exam

 Subcortical Dementias

 Cortical

106 MRCPsych exam

 Subcortical Dementias

 Parkinson's disease dementia,  Huntington's disease  AIDS dementia complex

 Cortical

 AD  CJD  FTD 107 MRCPsych exam

 HIV Ring Lesion 

108 MRCPsych exam

 HIV Ring Lesion  Toxoplasmosis

109 MRCPsych exam

 FTD Genes

110 MRCPsych exam

 FTD Genes

 Tau (MAPT),  progranulin (GRN),  chromosome 9 open reading frame 72 (C9ORF72),

111

 A 78-year-old, previously independent. His wife said that 1 month ago he was in a supermarket, buying gift for their daughter. He started crying uncontrollably for no reason. What is the most likely diagnosis?

 Anxiety disorder

 Dementia

 Depression

 Diogenes syndrome

 Post-stroke delirium

112  Donepezil - most common side effect

 A. Bradycardia

 b. Nausea

 C. Headaches.

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