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 Medicing
Reynolds 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 disease
Vascular dementia
Lewy Body dementia
Frontotemporal dementia
2. Discriminate neuropsychiatric conditions associated
with dementia syndromes.
Normal Aging
STRUCTURAL BRAIN CHANGES
Thinning of the Cortical Gray Matter
Age-Related changes in Neuronal Morphology
Oxidative Stress
DNA Damage
Less efficient Neural Circuits and Brain Plasticity
CHEMICAL BRAIN CHANGES
Dopamine
Serotonin
Glutamate
GENETIC CHANGES
Decline in Gene expression functions
Normal Age-Related Cognitive Changes
SLIGHT DECLINES
Attention/Concentration
Processing speed slowing
Word finding
“Tip of the Tongue”
Memory “senior moments”
Executive abstract reasoning
Compensatory strategies
INTACT FUNCTIONING
Sensory Motor
Visual Spatial
Receptive & Expressive
Language
Memory for personal
history & recent events
Executive – Intelligence,
fund of information, math
skills, judgment, decisional
capacity
IADLs
RISK FACTORS FOR ABNORMAL
COGNITIVE DECLINE
Increasing Age
Hypertension
Cardiac disease
Diabetes
Poor nutrition
Social isolation
Family history of dementia
Psychological factors: stress & depression
Stages of Assessment
Stage One
1. Medical & psychocial hx
with pt & informant
2. Physical & Neuroexam
3. Mood & behavioral screening –
SIGECAPS & Anxiety
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.
4. Cognitive Screening- MMSE,
MoCA, SLUMS, etc. Make sure
vision, hearing, or accents are
NOT lowering score
Stage Four
Rescreen cognition after tx & if still
abnormal – refer for Neuropsych
eval
Stage Two
Assess effort if secondary monetary
gain is present – such as disability or
civil suits are present (more likely in
younger patients)
Labs – CBC, Chem 7, Liver fx,
Thyroid, Metals, Vit B-12, D-3,
serological test as indicated, etc.
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 Alcohol, drugs, heavy metals, Bromide, CO,
to med side effects,
Benzodiazepines, Psychotropics (ie, antipsychotics,
substance abuse, or toxins
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 Pituitary, Parathyroisis, Thyroid, Adrenal dysfunction
to Endocrine disorders
Neurocognitive Disorder due Pernicious anemia, Pellagra, Folic Acid, Thiamine
to nutritional deficiencies
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 NCD
Onset
Acute to Sub-acute
Insidious
Course
Fluctuating
Stable and Progressive
Duration
Hours to day (rarely weeks)
Months to years
Attention
Fluctuates
Steady
Sensorium
Often impaired – can
fluctuate rapidly
Clear 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
Disrupted, reversed Sun
Sleep/wake
cycle
Manepali, et al. Primarydowning
Psychiatry. Vol 14, No. 8, 2007
Sun downing
DEPRESSION
NCD – Alzheimer’s
Onset
Duration
Mood
Rapid
Short
Insidious
Long
Diurnal variation,
usually depressed
Fluctuating 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
Associated Sx
Poor
Anxiety, insomnia,
anorexia
Normal
Rare, 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
DSM-IV
Mild Cognitive Impairment
Dementia due to …
DSM-5
DSM-5
Mild Neurocognitive Disorder
ICD-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
Mild NCD
Major
NCD
http://www.mind.uci.edu/wp-content/uploads/2013/08/Normal-aging-to-dementia.jpg
AGING VS DISEASE CONTINUUM
Normal Aging
Primarily
intact cognition,
subtle processing
speed slowing &
less efficient
attention &
executive
reasoning
Mild
Neurocognitive
Disorder
Decline from
lifelong abilities
in 1 or more
areas of
thinking +
inefficiency in
daily activities
Major
Neurocognitive
Disorder
Needs help
with daily
activities +
substantial
decline in 1 or
more
cognitive
abilities
Functional/Clinical Decline
COGNITIVE DOMAINS
DAILY FUNCTIONING
General Intelligence
BASIC transfers, ambulation,
bathing, hygiene, & feeding
Sensory Motor
Attention/Concentration
Processing Speed
Visual Spatial Functions
Language Functions
Memory – Auditory & Visual
Executive – higher thinking &
reasoning
MOOD & BEHAVIORS
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 DISORDER
Evidence 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; AND
2. 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 IADLs
2. Moderate: difficulties with basic activities of daily living
3. Severe: fully dependent
NeuroCognitive
Disorder
due to
Alzheimer’s
disease
Vascular
Neurocognitive
Disorder
Fronto-Temporal
Neuro-Cognitive
Disorder
Neurocognitive
disorder
with
Lewy
Bodies
OTHERS:
Parkinson’s
Depression
Seizures
NPH
Trauma
Infection
Metabolic
Drugs/Toxins
Neoplasms
Anoxia
PROPORTIONAL RANGE OF DEMENTIA SUBTYPES
http://cargocollective.com/ritamaldonadobranco/Visualising-dementia
“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:
AD10 (continued):
1. Memory loss
6. Problems with abstract
thought
2. Difficulty performing
familiar tasks
3. Problems with language
4. Disorientation to time and
place
5. Poor or decreased
judgment
www.ALZ.org
7. Misplacing things
8. Changes in mood or
behavior
9. Changes in personality
10. Loss of initiative
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.
AGE IS HIGHEST RISK FACTOR FOR AD
Age 30 – 65
Early Onset
Age 65 – 74
10% of total AD pts – some autosomal dominant mutation in
ALZHEIMER’S
DISEASE
Amyloid precursor protein, presenilin 1 or presenilin 2
7% of total AD pts –
Age 75 – 84
43% of total AD pts
Age 85 & up
40% of AD pts
Total AD pts
Genetics
100% - Female:Male = 2:1 ratio
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
Vascular risk factors AD by cerebrovascular pathology or thru
Risk Factor / direct effects on AD pathology
Typical course 8 to 10 yrs after dx, but some live 20 years
Disease
Late stage AD become mute and bed bound
Course
Early onset more likely to survive full course
Late onset dx more complex multiple comorbidities
Death commonly due to aspiration
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 disease
A. 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 &
wandering
Rummaging, hiding, & hoarding
Delusions: Paranoia & persecutory themes
LATE 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 Game
Invasive, 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 AD
46 of the 74 were incidental cases
28 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 Inhibitors
donepezil (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 therapy
Highest 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 events
Evidence 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 NCD
POSSIBLE 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 Bodies
Criteria 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 Pathology
Braak & 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 severity
Donaghy 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 progression
Either (1) or (2):
BEHAVIORAL VARIANT:
3 or more of the following behavioral symptoms:
Behavioral disinhibition
Apathy or inertia
Loss of sympathy or empathy
Perseverative, stereotyped or compulsive/ritualistic behavior
Hyperorality 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)
Progressive
Nonfluent Aphasia
Language
Variant (lvFTNCD)
Motor Neuron
Disease
Picks Complex
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 motivation
Changes 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-toside, 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 (FTNCDMND)
MND affects motor nerve cells in spinal cord, brain stem, and cerebral
cortex
Motor 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
Mild or Major Neurocognitive Disorder
Mild Neurocognitive Disorder
Subjective cognitive complaint
corroborated by informant
Objective cognitive impairment,
preserved general cognition
INTACT IADLs
Gradual onset,
progressive decline,
ADL deficits,
memory loss,
aphasia, apraxia,
agnosia, executive
dysfunction
mNCD
AD
Acute onset,
stepwise decline,
vascular risks,
frontal deficits,
neurological signs,
neuroimaging
findings
Vascular
NCD
Potentially Reversible Causes
Depression, drug side effects,
metabolic d/os, vitamin deficiency,
infectious disease, neoplams NPH,
subdural hematoma
Hallucinations,
parkinsonism,
attn / arousal
fluctuations,
executive dysfx,
visuospatial
deficits
Early onset, family
history, executive
dysfx, disinhibition,
personality change,
aphasia (fluent /
non-fluent
NCD LB
or PD
http://openi.nlm.nih.gov/imgs/512/143/3104685/3104685_jmdh-4-125f3.png
bvFTNCD
lvFTNCD
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.
2.
3.
4.
Memory  26% improved
Reasoning  74% improved
Processing Speed  87% improved
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!