Dementia. Trainees Weekend 2014

Transcription

1 Dementia Devon Partnership NHS Trust Diagnosis and Tips Colm Owens Consultant Psychiatrist and Clinical Director for Older People s Services, Devon Partnership Trust

2 Overview Background epidemiology Memory systems Memory function and aging Mild Cognitive Impairment (MCI) Dementias Tips on diagnosis

3 Nothing to declare (?)

4 Research funding

5 Diagnosis rate in England <50% There is nothing that can be done

6 Prevalence years: 1 in years: 1 in years: 1 in years: 1 in years: 1 in 3

7 Sub types Alzheimer's disease (AD): 62% Vascular dementia (VaD): 17% Mixed dementia (AD and VaD): 10% Dementia with Lewy bodies: 4% Fronto-temporal dementia: 2% Parkinson's dementia: 2% Other dementias: 3%

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9 Short-term memory Highly abused term by public and doctors. There is no short-term system lasting hours or days STM lasts a few seconds only i.e. remembering a phone number Limited store Prefer to call it Working Memory Reliant on frontal lobe functioning

10 Central executive Working Memory Information integration Monitoring of slave systems Slave systems Phonological loop Visual sketchpad Hold around 7 bits of information at one time Digits forward and backwards tests

11 Episodic memory Recall for specific event Tagged with time and place Often evoke affects and vivid re-imaginings Much knowledge gained from patient HM Bilateral hippocampal and parahippocampal excision for childhood epilepsy Epilepsy cured but episodic memory selectively destroyed Preferentially affected early in Alzheimer s

12 Semantic memory Knowledge of facts Date and time of learning not remembered Temporal lobe neocortex Dissociable from episodic memory HM knew George Bush Snr Selectively affected in semantic dementia Fine grained categories progressively destroyed Alsatian, dog, animal

13 Procedural Implicit memory Riding a bike, playing the flute Preserved in HM Contingent Cleparède s pin Priming

14 Encoding Storage Retrieval Stages of memory

15 Memory and aging Memory relatively stable till 60yo then variable trajectory Episodic memory No decline in well learned episodic memories Decline in recall for incidental recent events (hours to weeks) Recognition less affected than free recall

16 Memory and aging Procedural memory Slower at procedural learning unless able to dictate own pace which negates decline Semantic memory Intact ability to learn and recall semantic knowledge Decline in word-finding Naming pictures & recalling word from definition Increased tip of the tongue phenomenon

17 Memory and aging Working memory Central executive component declines Slave systems hold same amount of information Prospective memory Decline in laboratory settings but better than younger adults in real life situations Metamemory Beliefs about memory Older adults report worse memory and more severe deterioration than found on testing

18 Mild Cognitive Impairment Emerging concept with no internationally agreed criteria Roughly: Memory complaint confirmed by informant Essentially normal general cognitive function No decline in ADLs Objective memory decline for age on neuropsychological testing

19 Types MCI Amnestic MCI (amci) Non-amnestic MCI (namci) Single domain MCI Multi domain MCI Language MCI, Executive MCI etc

20 Prevalence MCI 3-19% depending on age, context and criteria used Incidence (per 1000)

21 Associated features MCI Decline in instrumental ADLs (ie DIY, hobbies etc) Neuropsychiatric features Dysphoria (40%) Apathy (40%) Irritability (29%) Anxiety (25%) Depression (23%) Range 6-9% in controls

22 Prognosis MCI Wide variability of conversion rates to dementia Highest rates of conversion in self-seekers in memory clinic 50% better when re-tested 1 year later amci 12% per year; 80% converted to dementia in 6 years namci 8% per year; 46% converted by 5 years

23 MCI Predictors of conversion APOE ε4 carrier Functional impairment Hippocampal volume reduction Generalised atrophy CSF biomarkers β-amyloid tot and phosphorylated tau (27% per year if present vs 1% per year if not)

24 MCI conversion pattern amci Alzheimer s Executive MCI Vasc dementia Language MCI FrontoTemporal Exec MCI dementia Attentional MCI Lewy Body Visuospatial MCI dementia

25 Memory in early stage Alzheimer s Working memory disease Slave systems unimpaired Central executive unable to co-ordinate and integrate information Demonstrate by tests of divided vs simple attention In real life situations will be unable to juggle tasks (eg. chopping & cooking)

26 Memory in early stage Alzheimer s disease Episodic memory Affected early in Alzheimer s disease Begins with inability to remember recent events Recall for early life events relatively spared initially - temporal gradient Test by story and list learning (verbal) and recall of complex design. Little or no recognition shortly afterwards. In real life become repetitive, forget appointments, misplace objects

27 Remember HM?

28 Memory in early stage Alzheimer s disease Semantic memory Impaired from relatively early Pathology needs to extend out from parahippocampal and hippocampal regions to temporal lobe cortex Poor at naming objects, generating categories, naming to description, Problem with knowledge representation and retrieval

29 ACE-III performance in different types of dementia NB, none of the following is definitive, only suggestive! Severity of dementia, pre-morbid IQ and copathology will also affect pattern of loss Cut off of 82/100 commonly accepted for likely dementia (but would be low if delirious, depressed, psychotic, low IQ, English not first language or tired, physically unwell or uncooperative) Alzheimer s: usually poor performance on memory- both spontaneous recollection of address and prompted recognition (underlying issue is storage)- language (naming objects and naming to description) and sometimes visuo-spatial function Vascular: A real mixed bag depending on where lesions are. In typical sub-cortical vascular dementias, language may be more affected than memory. The deficit with memory may be more to do with retrieval rather than storage so prompted recognition of address may be reasonable despite poor spontaneous recollection. Visuospatial functioning can be relatively preserved. DLB/PDD: problems with attention (which may have a downstream affect on working memory/encoding and prominent visuo-spatial difficulties may be apparent. FTD: VLOM ratio <2.2 (verbal fluency+ language scores/ orientation + memory scores) may be indicative of an FTD- once again, needs to be interpreted with caution. Generally people with early FTDs have fairly intact memory with difficulties with letter fluency and clock drawing. There are other specific frontal battery tests not included on the ACE-R.

30 Consultation- Tips & Pointers Dementia is underdiagnosed Normal for age is overdiagnosed

31 Consultation- Tips & Pointers Difficulties with anterograde ( short term ) memory Repetitious in conversation Forgetting appointments/birthdays New strategies to deal with above Cf difficulties with attention span/working memory

32 Consultation- Tips & Pointers Collateral Useful, especially if from a distance Informant letters Deterioration in function May be subtle or compensated for in highly functioning

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34 Consultation- Tips & Pointers Parietal/occipital Visuo-perceptual deficits eg face processing Visual hallucinations in extremis topographical disorientation dressing apraxia Difficulties with judging depth and distance

35 Consultation- Tips & Pointers Word finding difficulties tip of tongue phenomena

36 Consultation- Tips & Pointers Frontal lobe function Planning Disinhibition Apathy

37 Consultation- Tips & Pointers Associated signs & symptoms Tremor Changes in gait Changes in taste Depression Anxiety Psychosis

38 Consultation- Red Flags Abrupt onset Altered consciousness Significant neurological burden Myoclonus Seizures Clinical evidence of raised ICP

39 Consultation- Risks Aggression Suicidality Self neglect Vulnerability/safeguarding Cooking Smoking Driving Wandering out Falls

40 Consultation Don t Forget the Carer/Spouse/Daughter/Son Huge impact Diagnosis important for them Need to plan Diagnosis is a passport

41 Management Cornerstones are non-pharmacological Cf there s nothing that can be done

42 LPA Planning Driving Management Attendance Allowance Council Tax Exemption Delirium Planning This is me

43 Management- cholinesterase inhibitors Cochrane review of 13 RCTs in AD (NB RCT in PDD) Over 6/12: improvements in cognitive function, on average -2.7 points (95%CI to -2.3), in the midrange of the 70 point ADAS-Cog Scale. Adverse effects 29 % (cf placebo 18%)

44 Memantine Less evidence of efficacy NIHR cost effectiveness review of technology 111: ACIs 99% likely to be more cost effective than TAU, Memantine 38% (in severe only)

45 Cognitive Stimulation Therapy Spector et al BJPsych rt A single-blind, multi-centre, randomised controlled trial recruited 201 older people with dementia.

46 Cognitive Stimulation Therapy Treatment Analysis 1 1 NNT (95% CI) CST, cognitive stimulation therapy; NNT, number needed to treat. Analysis 2 1 NNT (95% CI) 1.Analysis 1 Alzheimer s Disease Assessment Scale Cognition score with no deterioration as improvement; analysis 2 same score with increase of 4 or more as improvement. CST programme 8 (4-144) 6 (4-17) Rivastigmine, 6-12 mg ( Corey-Bloom et al, 1998; Rösler et al, 1999) 4 (3-6) 13 (7-11) Donepezil, 5 mg 5 (4-9) 10 (5-180) Donepezil, 10 mg ( Rogers et al, 1998) Galantamine, 32 mg ( Wilcock et al, 2000) 5 (3-8) 4 (3-7) 5 (4-8) 6 (4-9)

47 BPSD 1/ The most convincing evidence (such as it exists and none is of the highest quality) for reduction of agitation in BPSD is with Risperidone and olanzapine. The only one of these to have a licence for this purpose is Risperidone 2/ The additional risk (absolute risk) of death for patients with dementia treated with any antipsychotic is considerable. Other psychotropics are not without risks either.

48 Summary of risks and benefits for treating1000 people with dementia for BPSD over a 12 week period with an second generation antipsychotic would result in: people with behavioural disturbance showing clinically significant improvement in symptoms 10 deaths (Evidence suggests that risk of mortality increases over time, therefore longer term treatment may result in up to 167 additional deaths over a 2 year period 18 CVAEs of which ~50% would be severe. No additional falls or fractures people with gait disturbance

49 Therefore, advice in BPSD a) treat any underlying cause (this could include a co-morbid psychiatric condition such as depression. Additional common ones not on the list would be dental caries and pressure sores) In patients with difficulty communicating, where pain is suspected, an empirical trial of Paracetamol may be reasonable. b) use non-pharmacological measures wherever possible- and we need to do much more here around training care home staff c) If absolutely necessary, ie if there are significant risks to the patients or others, then the balance of risks may be in favour of a short trial of risperidone. Document when it will be reviewed, by whom, target symptoms and discussion of risks with NOK. Aseessment of cardiac staus shoul dbe documented and if treatment commenced there shoul dbe regular monitoring of fluid balance, sedation and signs of LRTI. Treatment beyond 6-12 weeks should be exceptional and only on specialist advice.