“Different Forms of Dementia” including Lewy Body Dementia – webinar notes

The American Society on Aging (asaging.org) hosted a webinar on Monday, November 21st on the topic of “Understanding the Different Forms of Dementia.”  The speaker was Teepa Snow (teepasnow.com), a dementia education specialist.

Though I think Teepa Snow is typically an incredible presenter, the one-hour webinar format didn’t suit her.  She raced through the material, and didn’t cover many slides.  I thought her discussion of Alzheimer’s and mixed dementia were very good.  For Lewy Body Dementia, I think she would’ve done better by looking at the diagnostic criteria.  I thought she was very unclear on FTD (frontotemporal dementia).  And I think she under-rates the challenge of diagnosing dementia.

She said two things about Lewy Body Dementia that were new to me:
* “This is not AD plus PD.”
* “About 50% of those with LBD can’t get into REM sleep.”

You can find an online recording of the webinar here:

Put your mouse over the “11-21-11” area.  Click on the file folder that appears below the word “Understanding.”

And, I’ve copied my notes from the webinar below.  (In some cases, I’ve combined my notes with Teepa Snow’s slides, particularly for the many slides that she didn’t cover in full.)



Robin’s Notes from

Understanding the Different Forms of Dementia
Speaker – Teepa Snow, a dementia education specialist
11/21/11 Webinar

Three sponsors =
Alzheimer’s Foundation of America (alzfdn.org)
Senior Helpers (seniorhelpers.com)
American Society on Aging (asaging.org)

Recording will be posted on asaging.org (American Society on Aging) within a week.

Learning objectives of this webinar:
* Distinguish the difference between normal and abnormal changes in brain functions associated with the aging process.
* Describe similarities and differences among dementia, delirium, and depression.
* Compare various dementias regarding initial symptoms, progression patterns, and management and treatment strategies.
* Discuss the importance of the role of the care partner in helping to effectively manage the care plan and treatment of individuals living with various dementias.

Dementia is caused by changes in the brain:
* Structural changes:  permanent; cells are shrinking and dying
* Chemical changes:  variable; cells are producing and sending less chemicals; people can “shine” when least expected (“chemical rush”)

“Dementia” – umbrella term that covers 70-80 different disorders, such as Alzheimer’s Disease (50-60%), vascular dementias, Lewy body dementia, fronto-temporal lobe dementias, other dementias.  The “other dementias” category includes genetic syndromes, drugs/toxin exposure, white matter diseases, and Parkinson’s.  Most of AD co-occurs with other dementias.  These are terminal disorders.  These are life-altering disorders.


Alzheimer’s has two forms — young onset (used to be called “early onset”; younger than 65), and late onset (or “normal onset”; more common; after age 65; average onset is 75).  People in their 20s have AD!

Over 65, 5-10% of population has AD.  At 85, closer to 50% of population has AD.  Dramatic increase between 65 and 85!

With AD, brain shrinks by one-third.

PET scans of glucose activity by Gary Small, MD, at UCLA.  Most with “Early Alzheimer’s” don’t have an AD diagnosis.  Person and family might be aware of subtle changes.  Similarities in PET scans between 90 YO with late AD and a child!

Young onset AD:  genetics can be involved or lifestyle (high stress; sedentary; not socializing) can be involved.  Many have young families (children in the house).  Misdiagnosis (including psychiatric illnesses; mid-life crises; menopause; substance abuse) and non-diagnosis are common.  Work may be the first place to notice changes (may be fired).  Relationships are strained early.  Services can be a problem.  Finances are often problematic.

Down Syndrome:  beta-amyloid plaques are in the brain at birth; young onset.

Late onset AD:  New info is lost.  Recent memory worse.  Problems finding words.  Misspeaks.  More impulsive or indecisive.  Gets lost in time and place.  Notice changes over 6 months to 1 year.  Can last 8-12 years, on average.


Problems not due to disease.  Damage is related to blood supply, not primary brain disease.  White spots on CT scan indicate dead cell areas — mini-strokes.  Symptoms depend on where the dead areas are.

Sudden changes, known as stepwise progression.

Treatment can plateau.  Treatment involves managing vascular health.

Other conditions:  diabetes, hypertension, heart disease.

Picture varies by person (blood/swelling/recovery).

Can have bounce back and bad days.

Least-predictable of all the dementias.

Judgment and behavior is “not the same”

Spotty loss (memory, mobility).

Emotional and energy shifts.  Person is very labile:  go from one extreme to another pretty quickly.  Example:  ask someone “how are you doing?” and they start crying and say “I don’t know.”  Advice:  leave the room, come back with Kleenex.  This distraction solves problem.  Another situation is that the person is very apathetic.

Can last 3-30 years.


Important to know about.  This is not AD plus PD.  This is a different phenomenon.

Most mis-diagnosed and missed as a diagnosis.

Can be misidentified as PD.  It does involve movement problems (especially frequent falls) early in the disease.  Often falls are in bathrooms and bedrooms.

Can have visual hallucinations.  Almost always involve animals, children, or people.  Usually in the late afternoon and evening.  Some people have insight into their hallucinations.

Can have fine motor problems — hands and swallowing.

Don’t often have rest tremor.  The person is often awkward due to an intention tremor.  (This is a distinguishing characteristic.)

Episodes of rigidity.  The person might get stuck.  They are NOT getting stuck on purpose!

Episodes of syncope.

Can have nightmares.  Think dreams are real.  Can have a dark edge of the dreams.

Can have insomnia.  About 50% of those with LBD can’t get into REM sleep.

Fixed delusional thinking.

Fluctuations in abilities.

Drug responses can be extreme and strange.  This is probably the most important thing.  Often, MDs, if they are thinking PD, will prescribe Sinemet.  Sinemet can make the hallucinations worse.  Often the drugs used to treat hallucinations are antipsychotics.  50% of those with LBD have a seriously strong reaction (extrapyramidal side effects) to antipsychotics.  This is one of the reasons for a black-box warning on antipsychotics.

Often drugs used to treat agitation can make the problem worse.

Average:  live 7-9 years with symptoms.


Many types:
* Frontal – loses impulse and behavior control (no memory issues).  Says unexpected, rude, mean, odd things to others.  Disinhibited with food, drink (so serious the person can get hyponatremia), sex, emotions, actions.  OCD-type behaviors.  Hyperorality.
* Temporal – language loss.  Cannot speak or get words out.  Cannot understand what is said.  Sounds fluent but using nonsense words.

Those with frontal lobe dementias:  can end up arrested.  Highest risk:  genetic and head injury.

“PPA (Primary Progressive Aphasia) Nonfluent” – older term for temporal dementia

* FvFTD – frontal variant of FTD
* FTD – frontal-temporal lobe dementia
* TLD – non-fluent aphasia
* TLD – fluent aphasia
[Robin’s note:  yes, those last two both say “TLD”]

Temporal Lobe Non-Fluent Aphasia:  very frustrating; locked-in dementia; cannot name items; hesitant speech; not speaking; worsening of speech production over time; echolalia; misspeaking; word salad; receptive inability; other skills intact — early; 25% never develop global dementia

Fluent Aphasia

FTD (Pick’s Disease)
* Frontal Issues:  poor decision making; problems sequencing; reduced social skills; lack of self-awareness; hyperorality; egocentric; disinhibited (food, drink, words, actions); OCD behaviors early; excessive emotions
* Temporal Issues:  reduced attempts to talk; reduced content in speech; poor volume control; public use of “forbidden words”; sing-song speech; cannot understand others’ words


Could be atypical dementia, other dementia, or mixed dementia

40% of those with PD will develop dementia

Up to 50% of those with depression will develop dementia late in life.

Those with toxic exposure (drugs, heavy metals) or pesticide exposure can develop dementia

Other dementias:
* genetic syndromes:  Huntington’s Chorea
* ETOH related
* white matter diseases:  MS
* mass effects:  tumors and NPH
* infections that cross the blood brain barrier:  Creutzfeld-Jakob, HIV/Aids

Some progress very rapidly.  Some are unique while some follow more traditional patterns.

In a mixed picture, it is possible to:
* have multiple forms
* start with one and add another
* have some symptoms, but not all
* have other life-long issues and then develop dementia (Down syndrome, mental illness, personality disturbances, substance abuse)


If you begin to notice changes, what should you do?
* Get it assessed
* Go see the doctor!

Why see a doctor?
* Future plans:  progression and prognosis; finances; health
* Being in control
* Medications can make a difference in quality of life
* Get educated about the disease
* Take advantage of the right support services

Old screening option is the MMSE.  It’s short but helpful.

New screening options:
* AD8 interview
* SLUMS:  7 minute screen; short but helpful
* Animal fluency:  # of animals that can be named in one minute
* Clock drawing:  2 step
* Full neuropsychological testing panel
* Mini-Cog

AD8 dementia screening interview:
* Does your family member have problems with judgment?
* Does your family member show less interest in hobbies/activities?
* Does your family member repeat the same things over and over?
* Does your family member have trouble learning how to use a tool, appliance, or gadget?
* Does your family member forget the correct month or year?
* Does your family member have trouble handling complicated financial affairs?
* Does your family member have trouble remembering appointments?
* Does your family member have daily problems with thinking or memory?
AD8 score:  Changed, Not Changed, Don’t Know

If the screening identifies concern:
* Review current medications
* Complete work-up and follow up OR Send for a full neuropsychological evaluation
* Then, follow up with you OR Refer to a specialist


Depression:  cannot think; cannot remember; not worth it; loss of function; mood swings; personality change; change in sleep

Delirium:  swift change; hallucinations; delusions; on and off response; infection; toxicity; dangerous


* If person is aware and cooperative, partner and support
* If person is not aware and not interested or willing, look for authority figure to help.  Be willing to change how you talk about your concern.  Weigh the cost-benefit.  Ask for the person’s help FOR you….not about them.  Do you have a healthcare POA?


What should happen?
* A complete physical, medical, and psychological history
* A good history from the person and the family of the situation
* A thorough PE neurological and cardiac exam with blood work
* A complete medication review
* Imaging study (CT, MRI, PET)
* Neuropsychological testing – what works and what does not
* Follow-up and counseling or at least a referral

When should you get a second opinion?
* When what we talked about did not happen
* When you feel un-listened to about concerns
* When you are not offered options that seem reasonable
* When you think or feel that the doctor is not skilled enough to do a good job of managing this
* When it is an atypical dementia

How you can help?
* Be supportive
* Be an advocate
* Work out healthcare support (HC-PoA)
* Check with your doctor – raise your concern
* Consider a neuropsychological assessment
* Consider seeing a specialist — geriatrician, neurologist, gero-psychiatrist

* Alzheimer’s Foundation of America:  www.alzfdn.org
* Senior Helpers:  www.seniorhelpers.com
* American Society on Aging:  www.asaging.org
* Teepa Snow:  www.teepasnow.com


Question:  How do we interact with someone with FTD?

Answer:  For frontal lobe dementia, the most important thing to know is that the person can be impulsive, and although the person may know they are not supposed to do something, they are still going to do it.  We need to quit creating opportunities where the impulse will create a bad outcome.

You can’t stand in front of the door and say “you can’t go out and drive,” as you will get hurt.  You want to remove the car keys from the immediate vicinity, and let someone else be the bad guy.

This person needs a controlled environment early on.

When someone is doing something, use positive social engagement.  Rely on automatic responses.

If it’s a temporal lobe problem, stop using so many words.  Slow down your speech.  Don’t get too close.  Don’t put your hands on them.  Repeat a few of the words they said.

If it’s a fluent aphasia, go along with their speech.

If it’s a nonfluent aphasia, say:  “You are a very smart person.  I’m so sorry but I can’t understand what you are saying.”  Don’t say “It’s OK, it’s OK.”

Q:  Meds for AD?

A:  AChEIs (Aricept, Exelon, Razadyne) – help with symptom management.  Don’t help with the disease.  Helps brain produce more acetylcholine in some people.  Can only help living cells.  Most effective early in the disease.  Late in the disease, acetylcholine may be helping your brain to remember to put food in your mouth and chew.  We don’t know when this medication becomes ineffective.  It’s not for everyone.  Always consider giving it a dry.  These drugs are for AD, but not necessarily for FTD.

There’s also Namenda.  Controls glutamate in brain.  Can keep brain on an even keel.

We don’t know if people are short on acetylcholine and need to have their glutamate level moderated.  Must weigh downsides (GI, may bother heart, may bother gut).

Q:  Tool to tell difference between these conditions?

A:  What were the very first symptoms anyone noticed?  The first symptoms tell us where the disease started.  Where the disease started is important.  This helps identify the primary dementia.

Upon brain autopsy, for those cases where we got a really good history, 90% of the time we are accurate.

Key indicators:
AD – memory; immediate recall
LBD – movement; hallucinations; delusional thinking
FTD – behaviors or language
Benson’s – visual processing (we haven’t talked about this one)

Q:  We are seeing more LBD and vascular dementia diagnoses these days.  Is the frequency increasing?

A:  We are diagnosing people better.

For the first time, Alzheimer’s is no longer a diagnosis of exclusion.

“The Immense Value of the Family Caregiver Support Group”

Family Caregiver Alliance (caregiver.org) is a wonderful organization focused on caregivers.  They have a blog series on the “30 Days of Caregiving.”  Day 10 focuses on the value of caregiver-only support groups.  Brain Support Network coordinates a caregiver-only support group in the San Francisco Bay Area for Lewy Body Dementia, Progressive Supranuclear Palsy, Multiple System Atrophy, and Corticobasal Degeneration.  Here’s the FCA post as to why you should join!




Day 10: The Immense Value of the Family Caregiver Support Group
By Lois Esobar, MSW, Family Consultant at Family Caregiver Alliance
November 10, 2011

The role of a family caregiver is difficult. Aside from taking care of their loved one, they must also continue to lead their lives, which includes working, caring for family, grocery shopping and a seemingly endless list of potentially stress-inducing responsibilities! Many family caregivers need time to vent in a safe place. Caregiver support groups allow caregivers to have that special time to be with other people who have similar issues.

Support groups are a place to receive and give support—so essential to the family caregiver. About eight years ago, I taught a caregiver class in Spanish here in San Francisco. Participants in the class appreciated having the class in their language, but they also wanted more, and so began our Spanish caregiver support group which I have facilitated for the past eight years. Many family caregivers have attended the group since its inception and have told me how much they look forward to the meetings. At the beginning of the meetings, caregivers check in with each other to see how they’re doing. Blanca, one of the members stated: “this support group is the place that I can go to and be understood. I learn so much from my group of friends.”

Time and again, caregivers have told me that the support they receive is so beneficial. Many of the participants have formed friendships and stay in contact with eachother in between the monthly meetings. Participants also look forward to the different types of food that members bring to the meetings- whether it’s Columbian, Cuban, El Salvadoran, or Mexican. Members are even planning a Thanksgiving gathering! Over the years many family caregivers have told me that they feel isolated. They often do not talk to anyone for days. Rosa says: “Sometimes I feel very isolated and alone, but when I come to the group, I know that there are others who care.”

Being in a caregiver support group allows the caregiver to focus on their needs, not only the needs of the care receiver. The meeting once a month is a gentle reminder that family caregivers need to put themselves first . . . even if only for a couple of hours each month! The caregivers in the group are caring for loved ones affected by stroke, Alzheimer’s disease, Parkinson’s disease, and Lewey Body Dementia and we’ve had guest presenters come to the group and talk about these diseases. Besides the guest speakers, I have learned from the caregivers about their stressors, challenges, and frustrations, and this has made me a better social worker.

People hear about the support group most often from word-of-mouth from a friend, but other social workers will also make referrals. Family caregivers need to be mindful of when it is time to look for more support. Some of the signs can be as follows: You feel exhausted and have less energy. You become overwhelmed easily and feel helpless. You also become easily frustrated, angry and irritable. Most importantly, you begin to neglect your own needs.

Some Resources to Help

1. “Support groups a lifesaver for caregivers” By Paula Falk. Herald Tribune. July 12, 2011. Available at www.heraldtribune.com/article/20110712/WIRE/110719938/2059/LIVING?p=1&tc=pg

2.  FCA: “Caregivers Online: Using Support Groups on the Internet”

3.  FCA: “How To Form A Support Group”

4.  FCA: “Family Caregiver Alliance’s 4 Online Support Groups”

Creative Commons License
The Immense Value of the Family Caregiver Support Group by Lois Escobar, MSW, Family Consultant at Family Caregiver Alliance is licensed under a Creative Commons Attribution-NoDerivs 3.0 Unported License.

Michigan man with MSA

This newspaper article is about a Michigan man with multiple system atrophy (MSA).  Vera James posted this today on the ShyDrager Yahoo!Group.  (Vera is referred to in the article as a “California woman.”)


A Birthday to Remember: MMR paramedic takes Frankenmuth man with degenerative Shy-Drager syndrome to see family as birthday treat

By Lindsay Knake
The Saginaw News
Published: Sunday, October 23, 2011, 2:00 PM


Differential diagnosis – PSP, CBD, MSA, DLB, and PD

The recent issue of the journal Swiss Medical Weekly offers a great overview of the terms “parkinsonism” and “atypical parkinsonism.”

The article also offers very detailed explanations of how to differentially diagnose the atypical parkinsonism disorders (PSP, CBD, MSA, and DLB) and Parkinson’s Disease. The authors give three reasons why they believe it’s important to identify the subtype of parkinsonism at the time of diagnosis:

* “the prognosis can be estimated.”

* “some of the atypical features such as autonomous or cognitive problems may be targeted by pharmacological treatment”

* because “identification of atypical parkinsonism may prevent unnecessary iatrogenic harm from ineffective drugs, to which these patients typically react very sensitively.”

The full article is available in English at no charge on the Swiss Medical Weekly’s website:

Note that in a section on the role of imaging in the differential diagnosis of parkinsonism, an MRI is shown with the “hummingbird sign” of PSP.

I’ve copied some excerpts below as well as the abstract.


Swiss Medical Wkly. 2011 Nov 1;141.

Parkinsonism: heterogeneity of a common neurological syndrome.

Bohlhalter S, Kaegi G.
Division of Restorative and Behavioral Neurology, Department of Internal Medicine, Luerner Kantonsspital, Luzern, Switzerland

Parkinsonism refers to a neurological syndrome embracing bradykinesia, muscle rigidity, tremor at rest and impaired postural reflexes, and involving a broad differential diagnosis.

Having ruled out secondary causes (most importantly drugs), distinguishing levodopa-responsive idiopathic parkinson’s disease (PD) from chiefly treatment-resistant and hence atypical parkinsonism is essential.

Recent clinico-pathological studies using data-driven approaches have refined the traditional classifications of parkinsonism by identifying a spectrum of subtypes with different prognoses. For example, progressive supranuclear palsy (PSP), characterised by early vertical gaze limitation and falls, probably has a milder variant with predominant parkinsonism (PSP-P) which may respond quite well to levodopa before converting to the classical disease, relabelled Richardson syndrome (PSP-RS).

Analysis of PD subcategories has shown that tremor-dominant forms are probably less benign than was hitherto thought and that in mild cases dystonia should rather be considered. In addition, life expectancy in early onset PD may be shortened.

Despite the clinical and pathological overlap of the various subtypes, appreciating the heterogeneity of parkinsonism also includes identifying non-motor features such as early autonomous or cognitive problems which are potentially amenable to pharmacological treatment. Not least, non-motor symptoms, along with postural instability, render the patient particularly vulnerable to side effects, and hence avoiding unnecessary treatment is equally important in the management of parkinsonian disorders.

PubMed ID#: 22052571

“Dementia Care Without Drugs” – did you know…?

The “Dementia Care Without Drugs: A Better Approach for Long Term Care Facilities” conference on October 27, 2011 turned out to be well-attended. There were so many people that I don’t know if any other support group member was there??

I will go through the three presentations at some later point, and share any recommendations. In the meantime, let me share the “Did you know….” facts that were flashed on the screen during the breaks. #1 and #2 are incredible.


“Dementia Care Without Drugs: A Better Approach for Long Term Care Facilities”
Thursday 10-27-11
Organized by Ombudsman Services of San Mateo County (ossmc.org)

Did you know….

#1 – 40 skilled nursing facilities (SNFs) in California have no residents who receive antipsychotics.

#2 – 33 SNFs in California give antipsychotics to every resident.

#3 – A chemical restraint is any drug used to control behavior rather than treat a person’s medical condition.

#4 – Psychotrophics may not be given without informed consent of the patient or the patient’s legally responsible party.

#5 – Federal and state laws prohibit the use of antipsychotics in nursing homes unless it is necessary and required to treat symptoms. Non-pharmacological options must be used as a first resort.

#6 – People taking atypical antipsychotics are approximately 70% more likely to develop blood clots than those who aren’t.

#7 – Using antipsychotics to treat dementia is “off-label” and has a black box warning indicating that risk of death is doubled.

#8 – In a 2005 study, nearly one-fourth of all antipsychotic prescriptions in nursing homes did not include a clinical indication for use.

#9 – Regularized pain medication has been shown to be as effective in controlling dementia symptoms as psychotropics.

#10 – The five senses are not severely impacted by dementia and can be used to provide comfort.