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PROFESSIONAL SEMINAR SERIES DEMENTIA AND MILD COGNITIVE IMPAIRMENT How to approach patients with early signs of dementia using TCM SCOPE OF THE PROBLEM The incidence of dementia is steadily increasing. The prevalence rates rise with increasing age. In Australia, the prevalence is 2% for people in their 60’s increasing to over 32% for those in their 80’s and beyond. The figures are expected to double by the year 2020, partly because of increasing numbers of people living into old age impending HEALTHCARE CRISIS. Huge burden on patients, their care-givers and the community; ‘disability weight’ for dementia is higher than for almost any other health condition, apart from spinal-cord injury and terminal cancer. THE DEMENTIAS Alzheimer’s disease (AD) Vascular dementia (VaD) Mixed (Vascular + Alzheimer’s) dementia Dementia with Lewy Bodies (DLB) Fronto-temporal dementia (FTD) Mild cognitive impairment (MCI) a.k.a. ‘cognitive decline’, ‘cognitive impairment no dementia’. MAIN TYPES OF DEMENTIA Alzheimer’s disease (AD) Vascular dementia (VaD) Mild cognitive impairment (MCI) = precursor to Dementia Within 4 years of detection of MCI ~ half of these patients progress to clinical dementia (mostly AD). MCI patients: 10 – 12% per year dementia General population (same age group): 1 – 2% per year dementia DIAGNOSIS The criteria for diagnosis are still evolving. Reversible (due to curable medical conditions) and irreversible types (= true dementia) Reversible: chronic drug intoxication, vitamin deficiencies (B12 and folate), subdural hematoma/s, major depression, normal pressure hydrocephalus, hypothyroidism, head trauma and infections (bacterial, viral, fungal). DIAGNOSIS - dementia Based upon the DSM-IV, TR criteria (which are soon to be revised) • Impairment of memory • Impairment in at least one other cognitive domain: 1. Aphasia 2. Agnosia 3. Apraxia 4. Disturbance in executive function • The above interference with social, work or daily activities and represent a significant decline from previous functioning. DIAGNOSIS Diagnosis is based on: • • • • • Case history from the patient A collateral history from an informant Physical examination (rule out medical conditions apparent dementia; also determine cardiovascular and other risk factors, e.g. diabetes) Brief cognitive assessment, using one of the brief cognitive tests such as the Mini-Mental State Examination (MMSE) Referral to neurologist for detailed cognitive assessment Laboratory tests and imaging studies only used to rule out other causes of dementia. DIAGNOSIS – *ISSUES* The key symptom of memory loss is now being questioned, and many clinicians prefer to define dementia as impairment in at least two domains of cognitive function. ‘The comforting notion of the gold standard no longer seems valid. Although neuropathology has an important contribution to make …. people with apparently identical lesions can differ widely in their cognitive function and that differing sets of neuropathologic criteria yield differing estimates of dementias in the same brains ….. Similarly, the sharp line between normal aging and pathology is not as clear as it once was.” - Rockwood, K., Bouchard, R., Camicioli, R., Léger, G. (2007). Toward a revision of criteria for the dementias. Alzheimers Dement. 3(4):428-40. Defining the various dementias by neuropathological features may neither be valid nor clinically useful On autopsy many patients have mixed pathology, although they had been diagnosed with either AD or VaD RISK FACTORS The risk factors for dementia include: Elevated as well as low blood pressure Type 2 diabetes Clinical strokes or silent infarctions (detected on neuroimaging) Elevated total serum cholesterol High serum homocysteine levels Higher levels of total estradiol in women Depression Smoking High dietary fat intake and low omega 3 fat intake History of moderate to severe head injury with loss of consciousness Low education level (less than 12 years of education) Occupational exposure to pesticides, fertilizers, fumigants and defoliants RISK FACTORS Factors resulting in a lower risk for AD include: Adherence to a Mediterranean-style diet Consumption of fish Regular physical activity (particularly high level exercise, i.e. greater intensity than walking, 3 or more times per week) Intellectually challenging activity Moderate consumption of wine (250-500 ml/day). ALZHEIMER’S DISEASE (AD) AD is generally defined with reference to its specific neuropathology toxic amyloid plaques, neurofibrillary tangles and cerebrocortical atrophy predominantly involving the medial aspect of the temporal lobe Diagnosis rests on the clinical findings History: generally an insidious onset and progressive cognitive decline with predominant memory loss in a patient with normal (i.e. not clouded) consciousness. Typically occurs between the ages of 40 and 90. In a small number of patients the cognitive decline may plateau for a time or it may decline rapidly ALZHEIMER’S DISEASE (AD) The underlying pathology: accumulation of betaamyloid causing toxic amyloid plaques (‘senile plaques’) development of neurofibrillary tangles (NFT) widespread neuronal cell death cerebrocortical atrophy, predominantly in the association regions (particularly the medial aspect of the temporal lobe). The major functions affected are learning and memory as well as thinking and planning. As the disease progresses, there is progressive impairment of the ability to speak and understand speech as well as the sense of where the body is in relation to surrounding objects. Histological confirmation can only be done after death; therefore the diagnosis can only be ‘probable AD’. ALZHEIMER’S DISEASE In advanced AD there is global loss of cerebral function and marked shrinkage of the brain Findings on autopsy after death do not always correlate. Diagnosis is primarily based on the clinical examination (+ cognitive testing) Laboratory tests and imaging studies are only used in order to rule out other causes of dementia. NFT’s & SP’s ALZHEIMER’S DISEASE ALZHEIMER’S DISEASE MANAGEMENT Baseline and ongoing assessment of behavioral and psychological symptoms as well as assessment of activities of daily living degree of deterioration of function Administration of appropriate forms of therapy Decisions re the patient’s expected degree of autonomy (i.e. driving, cooking, taking meds, handling money) to live at home or in an institution. Evaluation of the complex needs of the patient and caregiver during the course of the disorder. ALZHEIMER’S DISEASE MANAGEMENT – Pharmaceutical Centrally acting cholinesterase inhibitors (ChEI’s) increase levels of acetylcholine in brain Memantine, a noncompetitive N-methylD-aspartate (NMDA) receptor antagonist. For moderate to severe AD. Prevents excitotoxicity ) ± ChEI Unfortunately the results of drug treatment are very poor. ALZHEIMER’S DISEASE PROGNOSIS Most patients do not respond to treatment and in those that do (1 out of 10 – 12 patients) the effects are modest and temporary, with small improvements in the rate of decline of cognitive function and activities of daily living. Most pharmaceutical studies show a STATISTICALLY significant improvement but not a CLINICALLY significant improvement. AD is the third leading cause of death in the USA (after cardiovascular disease and cancer). The primary cause of death is intercurrent illness, (usually pneumonia). Patients become severely demented and lose the ability to walk and swallow. Difficulty swallowing may lead to aspiration pneumonia. ALZHEIMER’S DISEASE TCM TREATMENTS The best available evidence for the CHM treatment of AD is not of a very high level However, it does point to the possibility that this form of treatment is potentially as good as, if not better than current pharmaceutical interventions (which are poor). Yi Gan San (‘yokukansan’ in Japanese) has been shown to ameliorate the behavioral and psychological symptoms in AD and that patents who take this formula require less antipsychotic medication. VASCULAR DEMENTIA A group of preventable dementias that are due to stroke and cerebral ischemia lesions in the cerebral cortex and/or subcortex. Various subtypes (defined by type of lesion): e.g. multiinfarct dementia; VaD due to a strategic single infarct; VaD due to lacunar lesions (‘lacunar state’); VaD due to hemorrhagic lesions; Binswanger disease; subcortical vascular dementia. Diagnosis: clinical findings together with neuroimaging or neuropathological evidence of cerebral ischemia (e.g. hemiplegia or focal neurological signs and symptoms) VaD occurs more commonly together with AD, as mixed dementia. VASCULAR DEMENTIA VASCULAR DEMENTIA VASCULAR DEMENTIA Mostly due to poorly controlled hypertension and/or diabetes mellitus. Also common in patients with coronary heart disease. ‘Typically’ (text book definition) the signs of cognitive impairment are patchy (i.e. not global as in AD); began acutely or subacutely soon after an acute neurological event (e.g. stroke), with a stepwise progression. Most recent evidence is in favor of slowly progressive cognitive deterioration – NOT stepwise. Mood and behavioral disturbances are very common (emotional lability, depression, apathy) VaD – RISK FACTORS Risk factors are same as for cerebrovascular disease: increasing age, male sex, diabetes mellitus, hypertension, cardiomyopathy, smoking and possibly also: elevated homocysteine levels, elevated total serum cholesterol and a high fat diet. Factors for lower risk for VaD include: consumption of fish and seafood; regular physical activity (particularly high level exercise, i.e. greater intensity than walking, 3 or more times per week); intellectually challenging activity; moderate consumption of wine (250-500 ml/day); non steroidal anti-inflammatory drugs; vitamin supplements; oestrogens (in women). VaD – MANAGEMENT Patient and caregiver education is the same as for AD Life expectancy in VaD is poorer than for AD critical issues relating to long term care planning, the patient’s autonomy and estate management be addressed promptly There are no approved drugs for the treatment of VaD; treatment is directed at prevention of new strokes, managing cerebrovascular disease and alleviation of psychiatric disturbances such as depression, agitation or psychosis. VaD – PROGNOSIS Higher mortality rate than with AD 50% die within 4 years of the diagnosis. As dementia progresses: increasingly poor judgment, agitation, aggression, wandering, sleep disorders, inappropriate sexual behavior and psychosis. They are prone to falls; this limits the use of anticoagulant medication. Prone to aspiration pneumonia, decubitus ulcers. Causes of death are generally due to complications of dementia, cardiovascular disease, or miscellaneous factors such as malignancy STRESS FOR CAREGIVER/S Caregivers are placed under increasing stress increased risk of psychiatric and medical disorders. The decision for placement of the patient into an institution should be made when the problem behaviors have become unmanageable or caring duties exceed the capacity of the caregiver/s VaD - TCM TREATMENTS There is some evidence for both acupuncture and Chinese herbal medicine in the treatment of VaD. However, the improvements are modest or minimal, and appear to be about the same as those obtained with pharmaceutical interventions. MILD COGNITIVE IMPAIRMENT Mild cognitive impairment (MCI) is a precursor to dementia. It represents a worse decline in cognitive function than would be expected for the patient’s age. Does not meet the criteria for dementia. Within 4 years of detection of MCI ~ half of these patients progress to clinical dementia (mostly AD). MCI patients: 10 – 12% per year dementia General population (same age group): 1 – 2% per year dementia (note: this figure also includes MCI patients) Huge potential to reduce the incidence of dementia with early intervention. MCI - ISSUES Approx. 5% per year of those diagnosed with MCI improve to normal (possibly misdiagnosed or patient just having a ‘bad day’) Much research into predicting which MCI patients will progress to dementia. However no precise indicators that are clinically useful have as yet been found. Patients are categorized as amnestic (exhibiting memory impairment) and nonamnestic (impairment of non-memory cognitive functions such as language, attention span, executive function or visouspatial skills) Amnestic types tend to progress to AD, the more severe ones progress (i.e. deteriorate) more rapidly, especially if there are multiple domains of impairment. MCI – DIAGNOSIS & ASSESSMENT Be aware that some MCI patients may have lack of insight and denial The patient or relative reports a decline in one or more of the following: • Memory, • Executive function (e.g. driving, handling finances, meal planning) • Behavior and mood (e.g. agitation, anxiety, apathy, disinhibition) • Language • Orientation • Performance of familiar tasks. Or you may suspect cognitive decline when taking the case history assess the patient’s: A B C’s – Activities of daily living; Behaviour; Cognitive state. MCI – DIAGNOSIS & ASSESSMENT COGNITIVE ASSESSMENT • Problems with memory, especially recent memory • Problems with word finding • Forgetting things about family and friends e.g. occupations, birthdays, addresses • Difficulty with learning new material or procedures e.g. using a new gadget • Frequently losing or misplacing things • Confusion with time and place • Difficulty with making decisions on daily matters MCI – DIAGNOSIS & ASSESSMENT FUNCTIONAL ASSESSMENT • Frequently forgetting to turn off taps or electrical or gas appliances • Difficulty with financial matters • Getting lost or unable to find the way • Self-care – dressing, washing, continence (activities of daily living – ‘ADLs’) • Driving or using public transport • Work • Managing medications MCI – DIAGNOSIS & ASSESSMENT BEHAVIOURAL ASSESSMENT • Changes in personality or behaviour • Psychiatric disturbance e.g. hallucinations, delusions (persecution) • Behavioural disturbances o o o o o demanding behaviours aggression, agitation wandering interrupted sleep disturbed eating pattern MCI – DIAGNOSIS & ASSESSMENT If you suspect that you are dealing with a patient with MCI, administer the Folstein Mini Mental State Examination. (A copy has been included in your notes) The Folstein Mini Mental State Examination: • • • • • Orientation (time and place) Registration (i.e. Immediate memory) Attention and calculation (simple numerical exercises) Recall (short term memory) Language (e.g. naming objects, reading, writing, copying) Takes about 20 minutes Score between 18 – 23 = MCI or early dementia MCI & DEMENTIA IN TCM Degeneration of the brain tissue (which represents a decline in the substance of the brain) is due to decline or depletion of the KIDNEY. Memory, cognition and other cognitive functions are regulated by the HEART and may become impaired in any pathology of the Heart, particularly when PHLEGM obstructs the Heart ‘orifices’ (= theoretical opening between the Heart and Brain). Collapse of the ORIGINAL OR SOURCE QI (yuan qi ) together with obstruction of the channels and Heart orifices by pathogens. LIVER QI CONSTRAINT leading to depletion of the Stomach Qi, which in turn impairs the Stomach’s digestive function resulting in the retention of Phlegm, which eventually obstructs the orifices of the Heart. BLOOD STASIS, which is a major feature of ageing and may also arise due to Liver constraint. MCI & DEMENTIA IN TCM CORE PATHOLOGY Deficiency of the Kidney essence Phlegm retention, which obstructs the ‘orifices’ of the Heart (= mind and senses) Blood stasis (in the brain) OTHER PATHODYNAMICS • Liver Qi constraint, Qi stagnation (= stress) • Heart deficiency (= mood disturbances) • Spleen Qi deficiency (vitality / energy, digestive function) • Liver Yin deficiency (= precursor to hypertension) • Heat (red face, red eyes, red tongue, sensations of heat) • Interior Wind due to Liver Yang hyperactivity (= hypertension) TCM TREATMENTS KIDNEY DEFICIENCY Liu Wei Di Huang Wan (Rehmannia Six Formula) BP015 Fu Gui Ba Wei Wan (Rehmannia Eight Formula) BP011 Qi Bao Mei Ran Dan (Polygonum & Cuscuta Formula) BP057 MEMOR-AID FORMULA CM144 BLOOD STASIS Bu Yang Huan Wu Wan (Astragalus & Lumbricus Formula) BP069 Salvia tablets (Dan Shen Pian) RP451 TCM TREATMENTS PHLEGM OBSTRUCTION An Shen Ding Zhi Wan (Zizyphus & Polygala Formula) BP001 Wen Dan Tang (Bamboo & Hoelen Formula) BP050 Xiang Sha Liu Jun Zi Tang (Saussurea & Cardamon Formula) BP028 TCM TREATMENTS BASIC PROTOCOL MEMOR-AID FORMULA CM144 PLUS Bu Yang Huan Wu Wan (Astragalus & Lumbricus Formula) BP069 Also pay attention to: • • • • Stress Mood (depression, anxiety) General level of vitality Nutrition TCM TREATMENTS FORULA DETAILS • Liu Wei Di Huang Wan (Rehmannia Six Formula) BP015 – nourishes the Kidney Yin-essence. For patients with signs of Kidney Yin deficiency: low back pain; seminal emissions; overactive libido; dizziness; tinnitus; poor memory; dry mouth; night sweating; red tongue with little or no coat. • Fu Gui Ba Wei Wan (Rehmannia Eight Formula) BP011– warms and invigorates the Kidney Yang-essence. For patients with signs of Kidney Yang deficiency: low back pain with a cold sensation; intolerance of cold; cold extremities and lower abdomen; sexual hypofunction; urination is copious and clear • Qi Bao Mei Ran Dan (Polygonum & Cuscuta Formula) BP057 – nourishes the Kidney and Liver. Traditionally developed to prevent hair loss, this formula has a marked action on patients exhibiting the early signs of ageing. Essential clinical features include: pain in the hypochondrium; pain and weakness of the low back and knees; tinnitus; seminal emissions (male); vivid sexual dreams (female); signs of deficiency Heat or Fire (dry mouth and throat, red cheeks, night sweats, red tongue with little or no coat, rapid pulse, etc.) • Memor-Aid Formula CM144 - an empirical formula that mainly nourishes the Kidney essence; also nourishes the Heart and calms the Spirit, resolves Phlegm and opens the Heart orifices, activates the Blood and dispels stasis. Clinical features include: sleep disturbance; fatigue; postural dizziness; tinnitus; pain and weakness of the low back and knees; cold hands and feet; tongue is pale; pulse is weak and thready or deep and weak TCM TREATMENTS FORMULA DETAILS • Bu Yang Huan Wu Wan (Astragalus & Lumbricus Formula) BP069 – resolves Blood stasis, tonifies the Qi and nourishes the Blood. Traditionally used for hemiplegia, this formula has broad applications in muscle wasting disorders and various neuropathies. This would be the formula of choice to address Blood stasis in patients with early dementia/MCI. Possible reasons not to use it (and use Salvia tablets instead) would include: very mild condition; inability of the patient to tolerate a treatment composed of many different herbal ingredients. • Salvia tablets (Dan Shen Pian) RP451– a gentle on the stomach treatment for Blood stasis. It has a calming action, is cooling and detoxifying and mildly Blood nourishing. TCM TREATMENTS FORMULA DETAILS • An Shen Ding Zhi Wan (Zizyphus & Polygala For.) BP001– Clears the Heart orifices, nourishes the Heart and calms the Spirit. Clinical features include: insomnia or disturbed sleep, forgetfulness, anxiety, agitation, timidity, apprehensiveness, palpitations, depressed mood, poor concentration, nervous laughter, pale tongue, thready and weak pulse • Wen Dan Tang (Bamboo & Hoelen Formula) BP050 – resolves Phlegm, mildly clears Heat and redirects counterflowing Qi. Key clinical features include: thick and greasy tongue coat; slippery pulse; nausea, vomiting or acid reflux; sense of fullness and discomfort in the chest. • Xiang Sha Liu Jun Zi Tang (Saussurea & Cardamon Formula) BP028 – resolves Phlegm and tonifies the Spleen Qi. This formula is more appropriate for patients with clear signs of Spleen deficiency. Key clinical features include: Fatigue, muscular weakness; sensation of bodily heaviness; poor appetite with a sensation of fullness after eating small amounts; epigastric or abdominal distension with mild pain; nausea, vomiting or belching; loose stools; pale tongue with a white greasy or thick white coat; weak pulse that is also slippery.