Transcript Dementia and Mild Cognitive

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
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Based upon the DSM-IV, TR criteria (which are soon
to be revised)
• Impairment of memory
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Impairment in at least one other cognitive domain:
1. Aphasia
2. Agnosia
3. Apraxia
4. Disturbance in executive function
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The above interference with social, work or daily
activities and represent a significant decline from
previous functioning.
DIAGNOSIS
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Diagnosis is based on:
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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.
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‘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
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The risk factors for dementia include:
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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
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RISK FACTORS
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Factors resulting in a lower risk for AD include:
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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).
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ALZHEIMER’S DISEASE (AD)
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AD is generally defined with reference to its specific
neuropathology
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toxic amyloid plaques,
neurofibrillary tangles and
cerebrocortical atrophy predominantly involving
the medial aspect of the temporal lobe
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Diagnosis rests on the clinical findings
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History: generally an insidious onset and progressive
cognitive decline with predominant memory loss in a
patient with normal (i.e. not clouded) consciousness.
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Typically occurs between the ages of 40 and 90.
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In a small number of patients the cognitive decline
may plateau for a time or it may decline rapidly
ALZHEIMER’S DISEASE (AD)
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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).
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The major functions affected are learning and
memory as well as thinking and planning.
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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.
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Histological confirmation can only be done after death;
therefore the diagnosis can only be ‘probable AD’.
ALZHEIMER’S DISEASE
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In advanced AD there is global loss of cerebral
function and marked shrinkage of the brain
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Findings on autopsy after death do not always
correlate.
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Diagnosis is primarily based on the clinical
examination (+ cognitive testing)
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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
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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:
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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
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Degeneration of the brain tissue (which represents a decline in
the substance of the brain) is due to decline or depletion of the
KIDNEY.
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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).
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Collapse of the ORIGINAL OR SOURCE QI (yuan qi ) together
with obstruction of the channels and Heart orifices by
pathogens.
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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.
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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
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MEMOR-AID FORMULA CM144
PLUS
 Bu Yang Huan Wu Wan (Astragalus & Lumbricus
Formula) BP069
Also pay attention to:
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Stress
Mood (depression, anxiety)
General level of vitality
Nutrition
TCM TREATMENTS
FORULA DETAILS
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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
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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.