7 Subjective memory complaints Disorientationforget time, place, trace of timeDisorganizationforget appointments, instructionsOmissionleave things behind, losing things, forgetting lightsRepetitionasking same question, telling same storyAll can occur in healthy people!Testing memory – list of words and cues – verbal recall
8 Assessment Memory problems Cortical regions involved Assessment Memory problems Cortical regions involved Frontal (judgment, reasoning, finances, attention, planning, motivation, impulsivity) Temporal (memory, word finding, remembering names, irritability, misinterpretations) Parietal (disorientation, spatial misjudgment, left- right confusion, dressing apraxias)
9 Structure of MemoryMemory – 3 Rs: registration (encode - needs attention and arousal),retain (store), and recall (retrieve)Implicit/procedural Declarative/explicit(unconscious) (conscious)(learning of skills and (learning of information)automatic behaviours)Motor/conditioning/priming Working/short term memory (over seconds) (over seconds to minutes)Phonological loopVisuo-spatial sketch padLong term memory (over days)Semantic memory(knowledge and memory about things)Episodic memory(narrative memories)
10 Neuroanatomy of Memory Episodic memory – limbic system and hippocampus Semantic memory – widely distributed in cortex Implicit memory – basal ganglia, cerebellum, spinal cordDisorders of MemoryDisorders of working memory - problems with attention and ‘central executive function’ - the ‘scratchpad’ or RAMDisorders of episodic memory - inability to retain new information/material (amnesia) - hippocampus basedDisorders of semantic memory (knowledge) - more difficult to erode, less affected by diseaseDisorders of ‘metamemory’ - inability to judge own memory function - insight
11 Subjective cognitive complaints (SCC) Benign course, forgets names, misplaces things, needs more reminders, reduced concentration and increased distraction, anxiety and depression, excess demandCognitive impairment not dementia (CIND) also known as mild cognitive impairment (MCI)1/3 better, 1/3 same, 1/3 worse over two yearsMCI single domain – amnesicMCI multiple domain – memory, concentration, complex activities (cooking, finances), new learningEarly dementiaMulti domain impairment plus functional effects and impairments on instrumental ADLs
12 Mild Cognitive Impairment – Sub-types • Mild Cognitive Impairment (MCI) is considered a transitional state between ‘normal’ cognitive changes of ageing and the earliest clinical presentation of dementia. The original definition of amnestic MCI has empirical support as a prodrome to Alzheimer’s disease with conversion rates of 10-15% per year.• MCI is now recognised as a heterogeneous syndrome and diagnosticcriteria have been broadened to include 4 clinical subtypes* Amnestic MCI single domain (aMCI) – memory impairment only* Amnestic MCI multiple domain (maMCI) – impairment in memory + other cognitive domain(s)* Non-amnestic MCI single domain (nMCI) – impairment in a single nonmemory domain* Non-amnestic MCI multiple domain (mnMCI) – impairment in multiplenon-memory domains.• Individuals with MCI affecting multiple domains may be more severelycognitively impaired and represent a more advanced prodromal stage.
13 Dementia ‘epidemic’ explodes. Main types of dementia Dementia ‘epidemic’ explodes Main types of dementia Alzheimer’s disease (35%) Vascular dementia (20%) Mixed Alzheimer’s/vascular (20%) Dementia with Lewy bodies (10%) Focal lobar atrophies (frontal variant FTD, semantic dementia, progressive non-fluent aphasia, and motor neuron dementia) (5%) Sub cortical dementias (Parkinson’s disease, progressive supranuclear palsy, multiple system atrophy, Huntington’s disease) (5%) Alcohol related (3%) Head injury (2%)Memory loss a cardinal feature of dementia along with either aphasia, apraxia, agnosia or a disturbance of executive functioning (planning, organizing, sequencing, abstracting)
14 Dementia Conditions Most Common Dementias Less than 1% of the under age 65 population compared with 20% of over 80s individualsMost Common DementiasAlzheimer’s diseaseVascular dementiaDementia with Lewy bodiesFrontotemporal dementiaMost common. Inflammatory plaques of amyloid outside neurones, and deposition of tau tangles inside neurones. Initially concentrated in hippocampus and acetylcholine producing neurones. First causes learning and recent memory problems, and attention difficulties. Early onset Alzheimer’s disease more often inherited (chromosomes 14, 1, and 21 including Down’s syndrome)
15 Vascular dementiaMulti-infarct dementia and Binswanger’s disease (deep white matter ischemia or subcortical vascular dementia)Vascular risk factors prominent (smoking, high blood pressure, diabetes, high lipids/cholesterol)Early onset may indicate an inherited Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL). Causes migranes, recurrent strokes and dementia. Chromosome 19 NOTCH3 gene mutation.Some early onset vascular dementias are autoimmune conditions affecting blood vessels in brain and may be treatableMemory less affected compared with Alzheimer’s disease. Frontal lobe executive functions, language, emotion and apathy, walking problems and incontinence more prominent.Stepwise deterioration
16 Differentiating Alzheimer’s disease and vascular dementia The most important differential diagnosis is between AD and VD, although in some cases AD and VD will overlap. Some key differences between the two diseases are listed on the slide.
17 Frontotemporal dementia Previously known as Pick’s diseaseSecond most common degenerative disease causing dementia in younger adults (after Alzheimer’s disease)More localised damage in frontal or temporal lobes causing changes in personality, language skills, and later memoryPathology includes severe loss of neurones (causing focal atrophy), as well as deposition of tau protein as ‘Pick bodies’ in neurones and accumulation of ubiquitin protein. A small number (20%) of cases are due to chromosome 17 mutations (tau and progranulin genes).Three clinical presentations of frontotemporal dementiaBehavioural variantPersonality change most distinctive – loss of empathy and warmth, apathy, and disinhibition. Poor judgment, reasoning, planning and organisation. Reduction in conversation, eating changes, decline in self-care and loss of independent ADLs.Progressive aphasia – semantic dementia (fluent)Loss of memory for words, impaired comprehension of word meaning, reading and spelling affected, numerical abilities preserved.Progressive nonfluent aphasiaSlow and tortuous production of words causing distortion of speech, wrong words and grammatical errors. Problems with using telephone or talking in groups. Apraxia of hand movementsBoth types of aphasia can progress to behavioural disturbance
18 Parkinsonian disorders associated with dementia Parkinson’s diseasePathology of Lewy bodies (clumps of alpha-synuclein protien) in substantia nigra region of brain stem20% to 40% later develop dementia characterised by difficulties with abstract thought, memory, behavioural regulation and visual hallucinations.Dementia with Lewy bodiesSimilar pathology to Parkinson’s disease, but in addition plaques and tanglesA ‘cross’ between Parkinson’s disease and Alzheimer’s disease – cognitive features of Alzheimer’s disease with movement disorder of Parkinson’s disease (‘Parkinson’s plus’).Vivid visual hallucinations (faces, animals), rapid fluctuations of alertness, and falls are commonAttention is impaired more than memoryCopying shapes and understanding visual material is affectedSensitive to antipsychotic medication, may respond to ACEIsProgressive supranuclear palsyRigid Parkinson’s disease, gaze palsy, swallowing problems and frontal dementiaCorticobasal degeneration (CBD)Rigidity, bradykinesia, apraxia (‘alien limb’ syndrome), and behavioural variant of frontotemporal dementia
19 Less Common Early Onset Dementias Motor Neurone Disease with dementiaHuntington’s diseaseAlcohol related dementia and Korsakoff’s syndromeMultiple sclerosisHIV-related dementia
20 Rare Causes of Younger Onset Dementia Creutzfeldt-Jacob disease (CJD)Dementia after head injuryDementia in Down syndromeHomocystinuriaVasculitisWilson’s diseasePorphyriaAdrenoleukodystrophyLipid storage diseasesMitochondrial disordersDentatorubralpallidoluysian atrophy (DRPLA)Neuroacanthocytosis
21 History taking questions Recent narrative memory, past narrative memory, people's names, names items, learning problems, forgetting things and appointments, word finding problems, comprehension and expression problems, semantic difficulties, topographical disorientation, R/L disorientation, dressing and other apraxias, gait problems, posture, EPS, involuntary movements, incontinence, confusion episodes, mood and affect, psychotic symptoms, motivation and passivity, personality changes, agitation, aggression, planning and sequencing problems, sleep, appetite, weight, ADLs, cooking, shopping, driving
22 The Clinical ProblemAge Related Changes or Subjective Cognitive Complaints (SCC)VsMild Cognitive Impairment (MCI) or Cognitive Impairment Not Dementia (CIND)Early Dementia?
23 Beyond the Mini Mental State Exam Beyond the Mini Mental State Exam? The Addenbrooke’s Cognitive Examination
24 Int J Geriatr Psychiatry 2006; 21: 1078–1085. The Addenbrooke’s Cognitive Examination Revised (ACE-R): a brief cognitive test battery for dementia screeningEneida Mioshi1,2, Kate Dawson2, Joanna Mitchell2, Robert Arnold1 and John R. Hodges1,2*1MRC Cognition and Brain Sciences Unit, Cambridge, UK2University of Cambridge Department of Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge, UKSUMMARYThere is a clear need for brief, but sensitive and specific, cognitive screening instruments as evidenced by the popularity of the Addenbrooke’s Cognitive Examination (ACE).ObjectivesWe aimed to validate an improved revision (the ACE-R) which incorporates five sub-domain scores(orientation/attention, memory, verbal fluency, language and visuo-spatial).MethodsStandard tests for evaluating dementia screening tests were applied. A total of 241 subjects participated in this study (Alzheimer’s disease=67, frontotemporal dementia=55, dementia of Lewy Bodies=20; mild cognitive impairment–MCI=36; controls=63).ResultsReliability of the ACE-R was very good (alpha coefficient=0.8). Correlation with the Clinical Dementia Scalewas significant (r=0.321, p <0.001). Two cut-offs were defined (88: sensitivity=0.94, specificity=0.89; 82:Sensitivity=0.84, specificity=1.0). Likelihood ratios of dementia were generated for scores between 88 and 82: at a cut-off of 82 the likelihood of dementia is 100:1. A comparison of individual age and education matched groups of MCI, AD and controls placed the MCI group performance between controls and AD and revealed MCI patients to be impaired in areas other than memory (attention/orientation, verbal fluency and language).ConclusionsThe ACE-R accomplishes standards of a valid dementia screening test, sensitive to early cognitivedysfunction.
25 ADDENBROOKE'S COGNITIVE EXAMINATION - ACE-R Prof John Hodges (Prince of Wales Hospital Randwick, NSW)Revised Version A (May 2004) - Australian VersionOrientation (time and place)*Registration (three words)*Attention and concentration (“world” backwards, serial 7s)*Memory - recall (three words)*Memory - anterograde memory (learning name and address)Memory - retrograde memory (recent and past historical figures)Verbal fluency - letter P [phonemic fluency] and animals [semantic fluency]Language - comprehension (follow written instruction and three stage command)*Language – writing (sentence)*Language – repetition (words and phrases)*Language - naming (pictures)Language - comprehension (pictures)Language - reading (words)Visuo-spatial abilities (copying figures* and clock drawing)Visuo-spatial perceptual abilities (count dots and identify letters)Memory - recall (name and address)Memory - recognition (name and address)Overall score (max 100; below mid 80s suggests dementia)*Includes MMSE score (max 30; below mid 20s suggests dementia)
32 Neuropsychological Testing Refer to NeuropsychologistPen and paper testing, up to 4 hours, but can be reduced to 2 hoursCan be expensiveOrTouch-screen, computer-based neuropsychological testingBrain Resource Company (BRC) Integneuro programNo keyboard skills requiredTakes about 1.5 hoursBest for patients with MMSE score 25 and aboveSome patients need assistance
34 Memory Clinic ProgramInitial ConsultationThe initial consultation involves a medical review, a mental health assessment, and a memory and cognitive screening evaluation.InvestigationsFurther comprehensive assessment procedures include a touch screen, computer-based diagnostic and baseline neuropsychological assessment of memory and cognitive function, laboratory blood tests, EEG/QEEG, ECG, structural & functional brain imaging tests (CT/MRI, SPECT, Doppler carotid ultrasound), and interviews with family or carer.Second ConsultationAt a second consultation the results of all tests are reviewed with the patient (and family/carer) and a diagnosis determined. A personalized management plan is then developed.Memory Rehabilitation ProgramA unique 12-session (24 hours total) Memory Rehabilitation Program is offered to reduce risk factors for memory loss and to enhance protective factors for preserving memory function.Follow-upAssessment of clinical and cognitive status. At further consultations the plan is monitored and reviewed in collaboration with the GP/local doctor.
41 Providing a rationale for treatment: Dementia The diagram on the slide, or a similar diagram, could be used as a tool when providing a treatment rationale for dementia.
42 Effects of treatment on target symptoms Antidepressant agents are helpful in managing depressive symptoms in patients with dementia. Antipsychotic agents are useful in managing psychotic symptoms and associated behavioural disturbance. Atypical antipsychotic agents are preferred due to reduced risk of adverse side effects. Care should be taken to exclude patients with DLB.
44 Acetylcholinsterase Inhibitors (AChEIs) Evidence from studies indicate:AChEIs are effective in the treatment of mild to moderate AD40-50% of patients show improvement in cognitive symptoms and delay in progression of illnessImprovement in non-cognitive symptoms (apathy, hallucinations, behaviour disturbance) are reportedBenefits last between 6 months to 2 yearseg. Donepezil 5mg nocte to start, 10mg after one monthN-methyl-D-aspartate (NMDA)-receptor antagonist - MemantineBlock glutamate toxicityEffective in moderate - severe ADCombination therapy – AChEIs plus Memantine
45 Acetylcholinsterase Inhibitors (AChEIs) Evidence from studies indicate:AChEIs are effective in the treatment of mild to moderate AD40-50% of patients show improvement in cognitive symptoms and delay in progression of illnessImprovement in non-cognitive symptoms (apathy, hallucinations, behaviour disturbance) are reportedBenefits last between 6 months to 2 years
46 Management of Dementia with Lewy Bodies Patients demonstrate neuroleptic sensitivityAChEIs have been shown to improve cognition, psychotic symptoms and neuropsychiatric symptoms in some patients with DLBEvidence is accumulating for the use of AChEIs as first-line pharmacological treatment of cognitive dysfunction, apathy, psychosis and agitation in some patients (McKeith, 2002, p. 146)If DLB is suspected, patients should be referred for specialist assessment.Patients demonstrate neuroleptic sensitivity, so specialist advice should be sought before prescribing antipsychotic agents to patients who present with features of dementia, depression and fluctuating cognition.AChEIs have been shown to improve cognition, psychotic symptoms and neuropsychiatric symptoms in some patients with DLB.Evidence is also accumulating for the use of AChEIs as first-line pharmacological treatment of cognitive dysfunction, apathy, psychosis and agitation in some patients. (McKeith, 2002, p. 146)
47 Frontotemporal dementia – associated features Patients with FTD may present with slowness and apathy or restlessness, overactivity, distractibility and disinhibitionNeurological signs of Parkinsonism, rigidity, dyspraxia, dysarthria, tremor or ocular problems occur with disease progressionPharmacological treatments are limited; there have been reports of some symptomatic response to SSRIs, possibly AChEIsPatients with FTD may present with slowness and apathy or restlessness, overactivity, distractibility and disinhibition. Neurological signs of Parkinsonism, rigidity, dyspraxia, dysarthria, tremor or ocular problems occur with disease progression. Pharmacological treatments are limited; although there have been reports of some symptomatic response to SSRIs.
49 Memory Rehabilitation Program Lifestyle Interventions**[ ] Exercise - 30 min walking (or equivalent) per day five days a week[ ] Resistance strength exercises three times a week for 20 min[ ] Reduce weight, BMI and abdominal girth[ ] Diet – low saturated fat Mediterranean style diet (colored vegetables, monounsaturated oils, lots of fish, garlic)[ ] Reduce alcohol (max. 2 standard drinks per day), no tobacco, no drugs[ ] Social interaction[ ] Intellectual stimulation[ ] Active leisure pursuits[ ] Protect the headNutrient Supplements[ ] Mega-folate (5 mg per day)[ ] Multivitamins (antioxidants [vitamins A, D, C, E], B-group vitamins [B1, B2, B3, B6, B12], and trace elements [copper, iodine, manganese, phosphate, selenium])[ ] Omega 3 fish oil capsules (DHA long chain type)Memory and Cognition Training**[ ] Memory aids and techniques (books, guides)[ ] Computer-based and counselor-guided memory training programsStress Management**[ ] Stress reduction, increase resilience, and manage depression and anxietyCommunity Organizations[ ] Alzheimer’s Australia (Living with Memory Loss courses) PhMedical Interventions[ ] Low dose aspirin (or other blood thinner)[ ] Blood pressure control[ ] Anti-cholesterol and anti-triglyceride medications (satins)Memory enhancing medications (nootropics)[ ] Acetyl-cholinesterase inhibitor drugs[ ] Memantine[ ] OthersAccommodation and home care support[ ] ACAT assessment** Included in the Memory Rehabilitation Program
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