DEMENTIA NEUROCOGNITIVE DISORDER 2015

37th Annual Family Medicine Intensive Review Course

May 16, 2015

Shelia R. Cassidy, Psy.D.Asst. Professor & Clinical Neuropsychologist

UAMS College of MedicingReynolds Institute on Aging

DISCLOSURES

The following speaker of this CME activity has no relevant financial relationships with commercial interests to disclose:

SHELIA R. CASSIDY, PSYD

OBJECTIVES

1. Differentiate 4 MOST COMMON types of dementia syndromes through functional clinical presentations.

Alzheimer’s diseaseVascular dementia Lewy Body dementia Frontotemporal dementia

2. Discriminate neuropsychiatric conditions associated with dementia syndromes.

Normal AgingSTRUCTURAL BRAIN CHANGES

Thinning of the Cortical Gray MatterAge-Related changes in Neuronal MorphologyOxidative StressDNA DamageLess efficient Neural Circuits and Brain Plasticity

CHEMICAL BRAIN CHANGESDopamineSerotoninGlutamate

GENETIC CHANGESDecline in Gene expression functions

Normal Age-Related Cognitive Changes

SLIGHT DECLINES Attention/ConcentrationProcessing speed slowingWord finding “Tip of the Tongue”Memory “senior moments”Executive abstract reasoning

Compensatory strategies

INTACT FUNCTIONINGSensory MotorVisual SpatialReceptive & Expressive Language Memory for personal history & recent eventsExecutive – Intelligence, fund of information, math skills, judgment, decisional capacityIADLs

RISK FACTORS FOR ABNORMAL COGNITIVE DECLINE

Increasing AgeHypertensionCardiac diseaseDiabetesPoor nutrition Social isolation Family history of dementiaPsychological factors: stress & depression

Stages of AssessmentStage One

1. Medical & psychocial hx with pt & informant

2. Physical & Neuroexam

3. Mood & behavioral screening – SIGECAPS & Anxiety

4. Cognitive Screening- MMSE, MoCA, SLUMS, etc. Make sure vision, hearing, or accents are NOT lowering score

Stage Two

Labs – CBC, Chem 7, Liver fx, Thyroid, Metals, Vit B-12, D-3, serological test as indicated, etc.

Stage Two (cont.)Neuroimaging – dependent on findings of H & P – if over 75 & consistent with AD may not meet medical necessity

Stage Three

Treat potentially reversible conditions, medications, mood, sleep apnea, B-12 deficiency, etc.

Stage FourRescreen cognition after tx & if still abnormal – refer for Neuropsych eval

Assess effort if secondary monetary gain is present – such as disability or civil suits are present (more likely in younger patients)

http://primarypsychiatry.com/wp-content/uploads/import/_C_F1_big.gif

Disease TYPE Neurocognitive Disorder Etiology Parenchymal Brain Disease

Alzheimer’s disease, Parkinson’s disease, Huntington’s Chorea, Progressive Supranuclear Palsy

Vascular Neurocognitive Disorder

Multi-Infarct, Focal Infarct, Subcortical Ischemic Vascular Dementia (Binswanger disease)

Neurocognitive Disorder due to med side effects, substance abuse, or toxins

Alcohol, drugs, heavy metals, Bromide, CO, Benzodiazepines, Psychotropics (ie, antipsychotics, opiates, sedatives, etc.) (toxin exposure/drugs)

Neurocognitive Disorder due to metabolic dysfx

Chronic hepatic/uremic encephalopathy, dialysis, Wilson’s disease (metabolic dysfunction)

Neurocognitive Disorder due to Endocrine disorders

Pituitary, Parathyroisis, Thyroid, Adrenal dysfunction

Neurocognitive Disorder due to nutritional deficiencies

Pernicious anemia, Pellagra, Folic Acid, Thiamine

Neurocognitive Disorder due to Infectious dissease

HIV/AIDS, Neurosyphyllis, Chronic Meningitis, Creudtzfeldt Jacob disease (Infectious disease)

Increased Intracranial Pressure

Brain tumor, Head Trauma, Hematoma, Hydrocephalus

DELIRIUM Mild or Major NCDOnset Acute to Sub-acute InsidiousCourse Fluctuating Stable and ProgressiveDuration Hours to day (rarely weeks) Months to yearsAttention Fluctuates SteadySensorium Often impaired – can

fluctuate rapidlyClear until later stages

Etiology Usually immediate cause identified

Usually no immediate cause

Psychomotor activity

Increased, decreased, or unpredictable

Can be normal

Cognitive function

Globally impaired, poor attn span

Poor short-term memory, attn span less affected

Perception Visual hallucinations, fleeting common delusions

Simple delusions & hallucinations

Sleep/wake cycle

Disrupted, reversed Sun downing

Sun downing

Manepali, et al. Primary Psychiatry. Vol 14, No. 8, 2007http://primarypsychiatry.com/wp-content/uploads/import/0807PP_Manepalli_T1.gif

DEPRESSION NCD – Alzheimer’s Onset Rapid InsidiousDuration Short LongMood Diurnal variation,

usually depressedFluctuating from apathy to normal to irritability

Intellectual fx Impaired; answers “I don’t know”

Impaired; answers questions incorrectly; minimizes or rationalizes errors

Memory Loss Recent and remote answers

Recent most affected

Self Image Poor NormalAssociated Sx Anxiety, insomnia,

anorexiaRare, occasional insomnia or uncooperative

Consultation reason

Self-referral Family referral

Previous History Previous depression, social problems

Family hx of dementia

RECENT TERMINOLOGY CHANGES

DSM-IV

Mild Cognitive Impairment

DSM-5

Mild Neurocognitive Disorder

DSM-IV

Dementia due to …

DSM-5ICD-9/1CD-10

+Major Neurocognitive

Disorder

DSM-5 Pertinent Cognitive Domains

COMPLEX ATTENTION

EXECUTIVE FUNCTION

LEARNING AND MEMORY

LANGUAGE

PERCEPTUAL MOTOR

SOCIAL COGNITION

Normal Aging vs. Progressive dementia

http://www.mind.uci.edu/wp-content/uploads/2013/08/Normal-aging-to-dementia.jpg

Mild NCD

MajorNCD

AGING VS DISEASE CONTINUUM

Normal Aging

Decline from lifelong abilities

in 1 or more areas of

thinking + inefficiency in daily activities

Needs help with daily

activities + substantial

decline in 1 or more cognitive

abilities

Major Neurocognitive

Disorder

Mild Neurocognitive

Disorder

Primarily intact cognition,

subtle processing speed slowing &

less efficient attention & executive reasoning

Functional/Clinical DeclineCOGNITIVE DOMAINS

General Intelligence

Sensory Motor

Attention/Concentration

Processing Speed

Visual Spatial Functions

Language Functions

Memory – Auditory & Visual

Executive – higher thinking & reasoning

MOOD & BEHAVIORS

DAILY FUNCTIONING

BASIC transfers, ambulation, bathing, hygiene, & feeding

INSTRUMENTAL ACTIVITIES• Safe use of appliances• Phone answering & dialing• Laundry• Housekeeping• Meal Preparation• Shopping• Management of finances• Management of meds• Driving

DSM-5 MILD NEUROCOGNITIVE DISORDEREvidence of modest cognitive decline from premorbid fx in 1 or more cognitive domains based on:

CONCERN of pt OR a knowledgeable informant, OR the clinician that there has been a mild decline in cognitive fx

+MODESTLY IMPAIRED cognitive performance on standardized neuropsychological testing or, in its absence, another quantified clinical assessment.

Cognitive deficits do NOT affect independence in IADLs, but may require greater effort or compensatory strategies.

The cognitive deficits do not occur exclusively in the context of a delirium & are NOT better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

DSM-5 MAJOR NEUROCOGNITIVE DISORDER A. Evidence of significant cognitive decline from previous abilities in one or more cognitive domains based on:

1. Concern of pt OR a knowledgeable informant OR clinician that there has been a significant decline in cognitive function; AND2. SUBSTANTIALLY IMPAIRED cognitive performance on standardized neuropsychological testing or, in its absence , another quantified clinical assessment.

B. Cognitive deficits INTERFERE with independence in activities. C. Cognitive deficits not due exclusively to a delirium.

D. Cognitive deficits not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

Major NCD

SPECIFY: 1. Without behavioral disturbances 2. With behavioral disturbances: if cognitive disturbance plus a clinically significant behavioral disturbance psychosis, mood disturbance, agitation, or apathy.

SPECIFY:1. Mild: difficulties limited to IADLs2. Moderate: difficulties with basic activities of daily living3. Severe: fully dependent

Neuro-CognitiveDisorder due to

Alzheimer’sdisease

Vascular Neuro-

cognitiveDisorder

Neuro-cognitive disorder

with Lewy

Bodies

OTHERS:Parkinson’sDepressionSeizuresNPHTraumaInfectionMetabolicDrugs/ToxinsNeoplasmsAnoxia

Fronto-Temporal Neuro-Cognitive

Disorder

http://cargocollective.com/ritamaldonadobranco/Visualising-dementia

PROPORTIONAL RANGE OF DEMENTIA SUBTYPES

“Alzheimer’s disease is bankrupting America”

AD – 6th-leading cause of death in US.

AD - only disease in top 10 causes of death in America without a way to prevent it, cure it or significantly slow its progression.

Currently $172 billion is spent caring for people with AD & other dementias.

By 2050, the costs may reach over $1 trillion without adjusting for inflation.

Almost 1/2 of all AD costs are paid by Medicare & more than one in every six Medicare dollars is spent on a pt with AD

Between 2010 & 2050, Medicare costs Medicare of caring for a pt with AD will increase over 600 % & out of pocket costs to families will grow more than 400 %.

Ten Key Warning Signs for AD

Alzheimer’s Assoc. AD10:1. Memory loss

2. Difficulty performing familiar tasks

3. Problems with language

4. Disorientation to time and place

5. Poor or decreased judgment

AD10 (continued):6. Problems with abstract

thought

7. Misplacing things

8. Changes in mood or behavior

9. Changes in personality

10. Loss of initiative

www.ALZ.org

Alzheimer’s disease facts and figures

5.3 million Americans have AD - 5.1 million are aged 65 and over (1 in 8).

By 2050, 13.5 to 16 million in US will have AD

Nearly 1 in 2 aged 85 and over has the disease.

Every 70 seconds, someone in US develops Alzheimer’s.

In 2050, every 33 secs an American will develop AD

Survival is an average of 4 to 8 years after diagnosis with AD, but many live for as long as 20 years with the disease.

On average, 40 % of person’s years with AD are in the most severe stage of the disease.

ALZHEIMER’S DISEASEAGE IS HIGHEST RISK FACTOR FOR AD

Age 30 – 65 Early Onset

10% of total AD pts – some autosomal dominant mutation in Amyloid precursor protein, presenilin 1 or presenilin 2

Age 65 – 74 7% of total AD pts – Age 75 – 84 43% of total AD pts

Age 85 & up 40% of AD pts

Total AD pts 100% - Female:Male = 2:1 ratio Genetics

Familial 5 to 15% of cases; APOE4 risk factor NOT dx marker – not necessary for AD Susceptibility - polymorphism APOE-4 & earlier onset in homozygous individuals. Down’s syndrome (trisomy 21 gene) AD if survive to midlife

Risk Factor / Disease Course

Vascular risk factors AD by cerebrovascular pathology or thru direct effects on AD pathologyTypical course 8 to 10 yrs after dx, but some live 20 yearsLate stage AD become mute and bed boundEarly onset more likely to survive full courseLate onset dx more complex multiple comorbiditiesDeath commonly due to aspiration

(Weuve et al 2012

MILD NCD DUE TO ALZHEIMER’S DISEASE

A. Criteria met for MILD neurocognitive disorder. B. Insidious onset & gradual progressive impairment in 1 or more cognitive domains. C. Not interfering with IADLs but more difficult & use compensatory strategies.

1. May or may NOT have evidence of a causative AD genetic mutation from family history or genetic testing, BUT

2. All 3 of the following are present: a. Clear evidence of decline in memory & learning + at least 1 other cognitive domain (detailed history or serial neuropsychological testing). b. Steadily progressive, gradual decline in cognition, without extended plateaus. c. No evidence of mixed etiology

DSM 5 MAJOR NCD due to Alzheimer’s diseaseA. Criteria met for MAJOR NCD.

B. Insidious onset & gradual progressive impairment in 2 or more cognitive domains.

POSSIBLE AD if only one of the following are present PROBABLE AD if either of the following is present

Interferes with IADLs fx

The following CRITERIA are also met:

a. Clear evidence of decline in memory & learning + at least 1 other cognitive domain (based on detailed history or serial neuropsychological testing). b. Gradual progressive decline in cognition w/o long plateaus. c. NO evidence of MIXED etiology

NEUROPSYCHIATRIC FEATURES AD~ 80% of pt with MAJOR NCD due to Alzheimer’s disease behavioral & psychological SX – that are also frequent at the MILD stage.

Behavioral symptoms = or more distressing than cognitive SX & are frequently the reason health care is sought.

MILD STAGE NCD due to AD depression & apathy

MODERATE STAGE NCD due to AD psychotic features, irritability, agitation, combativeness, sundowning & wanderingRummaging, hiding, & hoardingDelusions: Paranoia & persecutory themesLATE STAGE NCD due to AD gait disturbance, dysphagia, incontinence, myoclonus, and seizures

Neurofibrillary Tangle Amyloid Plaque

http://www.drugdevelopment-technology.com/projects/caprosinol/images/2-graph.jpg

Biomarkers in the GameInvasive, time consuming, & expensive• Structural & functional magnetic resonance imaging• Cerebrospinal fluid tau and amyloid-β levels• Pittsburg compound amyloid imaging or “inflammaging”

Blood based biomarkers will likely become more pragmatic

Mark Mapstone, Howard Federoff et al @ Georgetown University 525 people aged 70 & over for 5 years.74 developed aMCI or mild AD46 of the 74 were incidental cases28 of 74 (the "converters") converted from nonimpaired memory status at entry to aMCI or AD, over an average time of 2.1 years.Validated set of 10 peripheral blood lipids that predicted phenoconversion to either amnestic MCI or AD within a 2–3 year timeframe with a sensitivity and specificity of 90% accuracy

NCD pharmacological treatment for AD

Acetylcholinesterase Inhibitorsdonepezil (Aricept)rivastigmine (Exelon)galantamine (Razadyne)tacrine (Cognex) – less used due to side effects

memantine (Namenda) – NMDA antagonist

Vascular Neurocognitive Disorder

2nd most common cause of dementia in elders

Potentially preventable condition/slow progression tight BP & BG control (90 – 150 mg/dL) + cholesterol lowering therapyHighest 5-year mortality rate (61%) of all dementias

TYPES:1. CADASIL (Cerebral autosomal dominant arteriopathy with

leukoencephyalopathy) gene mutation Notch 3

2. Multi-Infarct Dementia

3. Subcortical Ischemic Vascular Dementia (SIVD)Beers MH, Porter RS, Jones TV, et al. The Merck Manual of Diagnosis and Therapy. 18th ed. Whitehouse Station, NJ: Merck Research Laboratories; 2006:1635,1727,1808-1822,2541-2545.

What is Dementia? National Institute of Neurological Disorders and Stroke. National Institutes of Health. Available at: http://www.ninds.nih.gov/disorders/dementias/dementia.htm. Accessed March 31, 2015

Vascular NCD

http://cspl.uis.edu/illaps/doa/conferences/NeurocognitiveDisorders.Chicago.2014.pptx.

MAJOR OR MILD VASCULAR NEUROCOGNITIVE DISORDER

Criteria are met for major or mild NCD

Clinical features are consistent with a vascular etiology, as suggested by the following:

Onset of cognitive deficits is temporally related to 1 or more cerebrovascular eventsEvidence for decline is prominent in complex attention (including processing speed) and frontal-executive function.

There is evidence of the presence of cerebrovascular disease from history, physical examination, and/or neuroimaging considered sufficient to account for the neurocognitive deficits.

The symptoms are not better explained by another brain disease or systemic disorder.

Possible vs. Probable Vascular NCDPOSSIBLE vascular NCD symptoms meet clinical criteria but NO neuroimaging +TEMPORAL relationship of the neurocognitive syndrome with 1 or more cerebrovascular events is not established.

PROBABLE vascular NCD is diagnosed if 1 of the following is present

Clinical criteria supported by neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular disease (neuroimaging-supported).

The neurocognitive syndrome is temporally related to one or more documented cerebrovascular events.

Both clinical & genetic (CADASIL) evidence of cerebrovascular disease is present.

Neuropsychiatric features of Vascular Neurocognitive Impairment

• Personality change• Apathy / Dependent behaviors / lack of insight• Impaired social communication with family and friends• Mistrust• Repetitive fixated behaviors• Neglect of hygiene & appearance• Guilt or shame• Generalized Anxiety• Frequently Depressed• Agitation /Anger /Disrespectful • Increased risk of self harm – impulsivity, dangerous risk-taking• When severe, may have delusions, hallucinations, delirium

Neurocognitive Disorder due to Lewy BodiesCriteria are met for major or mild NCD.Insidious onset & gradual progression.Combination of CORE dx features & suggestive dx features for either PROBABLE or POSSIBLE NCD with Lewy bodies.PROBABLE major or mild NCD with Lewy bodies, the individual has 2 core features, or 1 suggestive feature with 1 or more core features. POSSIBLE major or mild NCD with Lewy bodies, the individual has only 1 core feature, or 1 or more suggestive features.

CORE diagnostic features:FLUCTUATING cognition with pronounced variations in attention & alertness.RECURRENT visual hallucinations that are well formed and detailed.SPONTANEOUS features of parkinsonism, with onset subsequent to the development of cognitive decline.SUGGESTIVE diagnostic features:

• Meets criteria for rapid eye movement sleep behavior disorder• Severe neuroleptic sensitivity

Disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder.

Lewy Body PathologyBraak & collegues – staging system in PD applied to LB

Stage 1: pathology in dorsal motor nucleus of CN 9/10 & intermediate reticular zone of medulla

Subsequent LB ascension thru pons, midbrain, & subcortical structures to finally the neocortix in stages 5 & 6

Susceptible – olfactory bulb, dorsal motor nucleus of vagal nerve, other brainstem structures & PNSincluding enteric nervous system

Actual amount of LB pathology does NOT correlate with symptom severityDonaghy and McKeith The Clinical characteristics of dementia with Lewy bodies and a consideration of prodromal diagnosis Alzheimer's Research & Therapy 2014, 6:46 http://alzres.com/content/6/4/46

Lewy Body Pathology (cont.)

DLB & PDD pathological differences - DLB - higher amyloid plaque deposition in the striatum

More αSyn deposition in CA2/3 area of hippocampus & higher frontal cortical 5-HT1A receptor density

DLB less cell loss - substantia nigra & minimal D2 receptor up-regulation in striatum

Coexisting LB & AD pathology (amyloid-beta (Aβ) and tau) postmortem

DLB < structural brain changes compared with AD

MILD OR MAJOR NEUROCOGNITIVE DISORDER WITH LEWY BODIES

Affects 2ce as many men

Fluctuations in alertness, attention, & cognition

Decline in smell (hyposmia)

Postural Dizziness

Constipation

Parkinsonian symptoms - muscles that go abnormally rigid or tremble uncontrollably

Relative preservation of short-term memory unlike AD

Later in course - memory loss, poor judgment, and confusion

Supportive features of NCD due to Lewy Bodies

Repeated Falls & Syncope

Transient unexplained loss of consciousness

Severe autonomic dysfunction (orthostatic hypotension, incontinence)

Relative preservation of medial temporal structures on CT or MRI

Generalized low uptake on PET / SPECT perfusion scan with reduced occipital activity

Abnormal low uptake on MIBG myocardial scintigraphy

Prominent slow wave activity on EEG with transient temporal lobe sharp waves

Neuropsychiatric features of NCD due to Lewy Bodies

Rapid Eye Movement (REM) sleep d/o – parasomnia characterized by enactment of dreams (kicking, punching) that often results in injury

Systematized Delusional thinking

Ego Syntonic well formed visual hallucinations

Hallucinations in other modalities

Depression – ¼ pts

Anxiety – ¼ pts

Frontotemporal Neurocognitive Disorder (FTNCD)

Criteria met for major or mild neurocognitive disorder

Disturbance - insidious onset and gradual progressionEither (1) or (2):

BEHAVIORAL VARIANT:3 or more of the following behavioral symptoms:

Behavioral disinhibitionApathy or inertiaLoss of sympathy or empathyPerseverative, stereotyped or compulsive/ritualistic behaviorHyperorality and dietary changes

Prominent decline in social cognition and/or executive abilities.

LANGUAGE VARIANT:PROMINENT DECLINE in language ability, speech production, word finding, object naming, grammar, or word comprehension

Relative sparing of learning and memory & perceptual-motor function.

Frontotemporal NCD (cont.)

The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder.PROBABLE frontotemporal neurocognitive disorder is diagnosed if either of the following is present:

Evidence of a causative Frontotemporal neurocognitive disorder genetic mutation, from family history or genetic testing.Evidence of disproportionate frontal and/or temporal lobe involvement on neuroimaging.

POSSIBLE frontotemporal neurocognitive disorder is dx’d if: NO evidence of a genetic mutation NO neuroimaging has not been performed.

VARIANTS

Frontotemporal NCD

Behavioral Variant

(bvFTNCD)

Language Variant (lvFTNCD)

Motor Neuron Disease

Picks Complex

Progressive Nonfluent Aphasia

Semantic Dementia

Corticobasal Degeneration (CBD)

Progressive Supranuclear

Palsy (PSP)

BEHAVIORAL VARIANT Frontotemporal Neurocognitive Disorder

60 % of FTNCD pts have (bvFTNCD)

Dysfunction in frontal & temporal lobes

Diminished social skills, emotional regulation, personal conduct, & self awareness

Mood changes – stubbornness, emotinal coldness or distance, apathy, & selfishness

Initially limited confusion about place or time

FTNCD (cont.)

Inability to control impulsive urges /impulsive behavior

Poor decision-making

Loss of the ability to empathize with others

Decrease in personal motivationChanges in grooming or eating habits

Language- or speech difficulties – aphasia or dysarthria

Loss of the ability to use words that make sense for a given conversational context

Less frequently FTNCD – impaired body movement Rigid or trembling & weak muscles Loss of the ability to coordinate the activity of different muscles Swallowing problems.

Frontotemporal Neurocognitive Disorder Language Variant PROGRESSIVE NONFLUENT APHASIA (PNFA)

20% of FT NCD cases – temporal lobe dysfunction

Receptive language deficits – difficulty understanding complex sentences.

Expressive language deficits - difficulty producing language fluently though they still know the meaning of the words they are trying to say; talk slowly, have trouble saying words, difficulty talking in groups of people or on the telephone

Eventually, many pts with PNFA develop severe Parkinsonian symptoms overlapping with Progressive Supranuclear Palsy (PSP) & Corticobasal degeneration (CBD) – inability to move eyes side-to-side, muscle rigidity in arms & legs, falls, & weakness of muscles around the throat.

FT NCD SEMANTIC DEMENTIA (SD)

20 % of FTD cases – Temporal lobe dysfunction

Left Hemispheric onset – loss of meaning for words, decline in reading & spelling, decline in people’s names; Memory not affected until later; intact orientation to place & time, intact muscle control

Right Hemispheric onset – trouble recalling faces of friends & familiar people; deficits understanding emotions of others; loss of empathy

Eventually both hemispheres will become dysfunctional

SD patients eventually develop behavioral problems – disinhibition, apathy, diminished insight

FT NCD with Motor Neuron Disease

15 % of pts with FTNCD also develop motor neuron disease (FTNCD-MND)

MND affects motor nerve cells in spinal cord, brain stem, and cerebral cortexMotor sx = tremors, jerks (chorea or myoclonus), excessive startle response, seizures

More frequently found in pts with bvFTNCD

Rare in SD or PNFA

Most common MND is amyotrophic lateral sclerosis (ALS). Often pts with ALS have behavioral or cognitive problems similar to those seen in FTNCD.

MND Symptoms: slurring of speech, difficulty swallowing, choking, limb weakness, or muscle wasting.

Often a family history of the disease

Neuropsychiatric features of FTNCD

Inattention

Low Motivation, Apathy or inertia

Poor Insight

Behavioral disinhibition

Aggression

Impulsivity

Sexual Impropriety

Loss of sympathy or empathy

Perseverative, stereotyped or compulsive behavior

Hyperorality and dietary changes

http://openi.nlm.nih.gov/imgs/512/143/3104685/3104685_jmdh-4-125f3.png

Mild or Major Neurocognitive Disorder

Mild Neurocognitive DisorderSubjective cognitive complaint corroborated by informant Objective cognitive impairment, preserved general cognition INTACT IADLs

Potentially Reversible Causes

Depression, drug side effects, metabolic d/os, vitamin deficiency, infectious disease, neoplams NPH, subdural hematoma

Gradual onset, progressive decline, ADL deficits, memory loss, aphasia, apraxia, agnosia, executive dysfunction

Acute onset, stepwise decline, vascular risks, frontal deficits, neurological signs, neuroimaging findings

Hallucinations, parkinsonism, attn / arousal fluctuations, executive dysfx, visuospatial deficits

Early onset, family history, executive dysfx, disinhibition, personality change, aphasia (fluent / non-fluent

mNCD AD

Vascular NCD

NCD LB or PD

bvFTNCDlvFTNCD

PREVENTION & NONPHARMACOLOGICAL TREATMENT

Controlling risk factors for chronic disease, such as heart disease and diabetes (e.g., tight control of blood cholesterol and blood pressure at healthy levels & maintaining a healthy weight)

Enjoying Consistent exercise regimen and physical activity

Reduce stress – limit caffeine, meditation routine &/or MINDFULNESS

Eating a healthy lifestyle diet - including plenty of vegetables & fruits, such as the Mediterranean diet

Engage in intellectually stimulating activities and maintaining close social ties with family, friends, and community

Don’t smoke & Limit alcohol intake

Get 7 to 9 hours of sleep each night

Do activities that require quick responses – ping pong, tennis, board games, computer games

Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE)

2,802 healthy adults ages 65 & up living independently – 4 Groups @ 10 computer sessions

1. Memory 26% improved2. Reasoning 74% improved3. Processing Speed 87% improved4. Control group

11 mos later 60% 75-minute “booster” sessions

5 years later Groups 1 - 3 > controls

REASONING & PROCESSING SPEED groups

Any Questions?

Thank you!