Alcohol Related Dementia

Transcription

1 Alcohol Related Dementia A DIAGNOSIS WE SHOULD NOT BE HAVING TO MAKE Bob Batey a seeker after a broader view of the issue

2 Alcohol Related Dementia Mr JD 49 Now in Nursing Home unable to survive independently Loss of short term memory, confabulating Unable to undertake ADL s without direction Disruptive when drunk but sociable when sober Also troubled by cirrhosis, cerebellar damage and incoordination and heart failure

3 Alcohol Related Dementia All these conditions complicate his management and impact on cerebral function With abstinence all will improve BUT IT IS ALL TOOOOOOO LATE!

4 ALCOHOL INDUCED BRAIN IMPAIRMENT A MUCH HEALTHIER VIEW OF ARBD Bob Batey I will get my way on this if it kills me!!

5 Alcohol Related Dementia What are the outcomes I would like? An earlier diagnosis of this process A greater understanding of the complexity of AIBI A willingness to assess for EARLY signs of AIBI

6 PLUS An increased awareness of all staff in your units of the need for a change in our thinking about ARBI Better assessment protocols - Better management plans for less damaged patients - A LOSS OF THE NIHILISM that marks our thinking about ARD because it is now thought of as AIBI!

7 Alcohol Related Dementia What I will cover Defining the Condition Some thoughts on pathogenesis Imaging inadequacies The current diagnostic features Management strategies Prevention Treatment Management

8 AIBI - Definitions What it is and What it is not!

9 AIBI What it is Brain impairment which may be Functional &/or Structural Resulting from the effects of alcohol BUT it usually also includes: nutritional impairment, hypoxia and trauma on normal brain development, function and ageing. One could argue that the additional components should be isolated out along with other factors & In time maybe it will be

10 AIBI What it is NOT Ischaemic injury associated with alcohol use disorders Traumatic brain injury acquired while under the influence of alcohol Hypoxic brain injury resulting from episodes of hypoxia when under the influence Toxic brain injury from other ingested agents Metabolic brain impairment from hepatic, renal cardiac encephalopathy BUT REMEMBER Many of our patients will have some or all of these compounding the problem of pure AIBI

11 Pure AIBI does it exist? The answer is probably - yes but maybe as with ALD There is a cascade Alcohol + brain leads to altered neurophysiology but We need a second trigger To Promote damage and impairment

12 What could those second insults be? Nutritional deficiency!! Hypoxia Inflammation chemical, infectious, immunological A second toxin bacterial toxin/protein, another drug WHO KNOWS??

13 3 pictures Representing 1800 years of thinking To encourage us to do it quicker!!

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16 Beautiful isn t it!

17 SO? At present ARDementia is like the end stage or stage 5 of coeliac AIBI is an attempt to get us thinking about patients when they are In Stages 0-3 and preferably Stages 0-1 when some help can be offered that is likely to work!

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19 Pathogenesis Pour alcohol on a brain and nothing much seems to happen. Pour it on a cockroach and it is dead in milliseconds As I learned in my doctoral study years at RPAH! Survival of the fastest Drink too much of it and you are in trouble sooner or later Problem is too much for me may have no effect on him or even her We are all different and those differences relate to:

20 Genetic & Environmental Differences GENETIC: Metabolic pathways Hepatic CNS Inflammatory responses Immune regulation Reaction to drugs e.g IL28B Reaction to other insults we experience ENVIRONMENTAL Nutrition Drugs Weight itself as an inflammatory mediator Infections With or without hypoxia Trauma Physical Psychological

21 Pathogenesis Whereas until recently we talked of ARBD as being: Alcohol induced damage Aggravated by nutritional deficiencies Complicated by trauma, ischaemia etc We now read of AIBI being as subtle and complex as inflammation and tissue damage anywhere else Oxidative stress Cytokine mediation of injury and inflammation Cytokine regulation of apoptosis and altered neuroplasticity Genetic control of these steps to brain loss

22 3 pictures that changed my thinking

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26 If this is our Brain How dare we wait till it is totally stuffed Before we start to think about ARBD We are working with an incredibly beautiful, complex, wonderful structure And we treat it so poorly!!

27 Science and ARD Where to start? Most studies have been describing brain volumes Of patients with DEMENTIA Some studies are trying to dissect out: Alcohol related from Co-occuring traumatic/hypoxic INJURY More recent studies have started looking at the biology of brain disease much earlier Some work is now talking about brain regeneration

28 Brain studies What do people measure? Cortical thickness Brain surface area Brain volumes Structural changes Connectome studies Protein expression Biochemical changes in response to stimuli Cytokine levels in CNS and peripheral blood in brain disease

29 Brain studies what do they tell us? Many studies for many years have shown changes in various parts of the brain including: Prefrontal white matter Superior frontal association cortex Corpus callosum Hypothalamus Cerebellar white matter Brain reward systems Rostral and caudal anterior cingulate cortex Insula Medial and lateral orbitofrontal cortex Rostral and caudal middle and superior frontal gyri Amygdala Hippocampus

30 AIBI 130 years post Wernicke! Still a field for much more endeavor We still can t agree on whether Wernicke s remains a clinical problem or not: In the past 3 months I have heard of cases of WE in emergency departments in NSW and Heard people saying blandly that thiamin in bread has made WE a thing of the past We cannot chart a pathway from early alcohol related injury to severe damage Patients still end up with severe AIBI and nowhere to get help

31 AIBI things I have learned in reading for today The corpus callosum is significantly affected in AIBI The cerebellum is possibly involved in executive functioning Changes in AIBI involve both changes in myelin metabolism and axonal integrity Myelin rapidly degrades post mortem making studies in humans impossible Animal models show reduced myelin thickness in alcohol models of neuronal injury MRI and MR spectroscopy can show brain gain with abstinence

32 The current diagnostic features

33 We don t have a good list Impaired cognition But how bad do you have to be How do we measure this Impaired function in community But if family covers for failing performance how do we know Impaired memory But by what degree Progressing at what rate Specific neurological impairments

34 We tend to wait till blind Freddy can see there is a problem

35 Now to the Clinical experience How many have wrung their hands over placing patients with ARD? And still had problems placing them!! What is the problem?

36 Clinical ARD issues Patients with ARD are hard to manage They improve to a degree with abstinence They do not fit well into psychotherapy group work They get bored with poorly regulated days They need living skills programs They can be so damaged that they need total nursing care NO UNITS EXIST TO MEET ALL THESE NEEDS

37 So We need earlier intervention AND Better resourced Units for these patients

38 The Scottish Report 2004 A major report with great recommendations INCLUDING: The Scottish Executive and Alcohol & Drug Action Teams (SEADT) should undertake work to increase public and professional awareness of ARBD highlighting risk factors such as: Poor nutrition Sustained heavy drinking Co-existing head injury And the association with deprivation

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40 Recommendations - Australianised Work to challenge stigma and discrimination associated with ARBD Provide information for assessing need, and then providing services for people with ARBD Monitor local protocols between addiction, neuropsychology, psychiatry, children, family and older people s services Agree on care pathways and appropriate referral and assessment arrangements.

41 Recommendations Train relevant staff Relevant National body should consider the development of specific standards of care for people with ARBD The research community should improve the evidence base in relation to: Epidemiology Population needs assessment Early identification Rehabilitation Community living and Care home provision

42 Recommendations If only!!