Register Now! Sat, Oct 28, PSP/CBD Research Update and Family Conference

UPDATED (11-27-17):  This was a great conference!  See our complete conference webpage here:


Registration is now open!

Brain Support Network will host the:

PSP/CBD Research Update and Family Conference
Saturday, October 28, 2017
Crowne Plaza Foster City (San Francisco Bay Area)
8am Continental breakfast/check-in
9am Speakers begin
5pm Conclusion

Cost: $55 per person until October 7; $65 until October 27
No registration at the door

Register now:

This conference is for families coping with progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD).   Professionals and anyone in the community are also welcome to attend.

The conference will be run from 8am to 5pm. The morning will feature international researchers in town for a major conference on PSPCBD, and tau. The afternoon will feature Bay Area clinicians (from UCSF and Stanford), healthcare professionals, and those on the PSP/CBD journey.

See the great speaker line-up on the agenda.

In recent days, several people have asked how this conference is different from the CurePSP conference on October 26-27.  That CurePSP conference is for international researchers. All of the talks at the CurePSP conference will be at a very high-level.  (I don’t know of any laypeople who can understand even 20% of those talks.)

It seemed like a great opportunity to ask those international researchers to stay in town through Saturday noon to give shorter and easier-to-understand talks to laypeople. That’s what we’ve done!  We’ve worked with CurePSP to know who was speaking at their conference.

Our main planning partner is Dr. Adam Boxer and the team at the UCSF Memory & Aging Center. UCSF is the lead institution for PSP and CBD clinical trials. We are lucky to have them in our backyard!

Space is limited so register now:

If the $55 ticket is a hardship for you, we do have a small number of scholarships available. Please contact us.

We are looking for sponsorship for videorecording ($2K) the conference.  Can you help us sponsor this so more people can benefit from the great conference?  Contact us.

We are also looking for an all-day volunteer:  (contact us)

  • digital photographer. (Requires someone with a digital camera, photography skills, interest in roaming around the ballroom and foyer the whole day, and good with people.)

We’ve opened up exhibitor registration here:

Soon, we’ll be opening up registration for:  (contact us)

  • RNs, LVNs, LMFTs, and LCSWs who want CEUs.  Six CEUs are being offered through the Alzheimer’s Association.

Stay tuned.

Click here for a flyer to print and share.


Recording + Notes from “Diagnosing PSP” Webinar, August 2017

Brain Support Network and Stanford University co-hosted a webinar on Wednesday, August 30th about diagnosing Progressive Supranuclear Palsy.



We’ve posted the webinar recording here —

It’s the speaker’s presentation (about 30 minutes).



For additional information on the topics addressed during the webinar, see:

PSP Education, by Brain Support Network



Our terrific volunteer, Denise Dagan, took notes from the webinar.

Diagnosing Progressive Supranuclear Palsy

Speaker: Kathleen Poston, MD, movement disorders specialist, Stanford University
Host: Robin Riddle, CEO, Brain Support Network
August 30, 2017


We are focusing on the diagnosis of progressive supranuclear palsy today, and particularly paying attention to why the new diagnostic criteria was developed, how it can be applied in a clinical setting both from the perspective of clinicians and the patient and patient’s family.


Why have there been revisions in the clinical diagnostic criteria?

PSP can be a very difficult disorder to properly diagnose. The more classic of the PSP syndromes, called Richardson Syndrome, is one of the easier versions of PSP to diagnose.

In several studies, only about 63% of people diagnosed with PSP, who donated their brains for scientific research, actually had PSP confirmed by autopsy.

That’s a pretty low number especially for clinical trials because when you are studying a treatment for PSP you only want to recruit people who have PSP. If it turns out only 63% of the people enrolled in your study actually have PSP, your results are askew. The results are showing you your treatment only works on about half the people in your study which doesn’t look very effective. When, in fact, it may be working very well on every person who has PSP but you can’t see it because there are so many people enrolled who don’t have PSP.


What is misdiagnosed at PSP?

Dr. Poston showed a slide showing a Venn diagram of the types of disorders commonly misdiagnosed as PSP from a study of 181 patients who’s brain underwent autopsy, including one circle labeled as the 63% who actually had PSP.

The biggest group of misdiagnosed disorders is “Parkinsonism,” which is a collection of disorders which includes Parkinson’s disease (PD), Dementia with Lewy Bodies (DLB) and a broader parkinsonism, which in these autopsy cases means the clinician thought it was some form of parkinsonism but couldn’t definitively say it was either Parkinson’s disease or Dementia with Lewy Bodies versus some other parkinsonism disorder.
This group is 13% of cases misdiagnosed as PSP during life, but found to have Parkinsonism on autopsy.

The other commonly misdiagnosed disorders were less frequent:
corticobasal degenerative disease, which is also frequently confused with PSP = 2%
frontotemporal degeneration = 3%
Alzheimer’s disease = 4%


What are the clinical features of PSP:

* Parkinsonism, a syndrome defined by axial rigidity (rigidity in the neck and trunk), postural instability (poor balance), bradykinesia (slowness of movement and facial expression muscles), reduced blink

* Supranuclear gaze palsy (SGP) – This is the feature that most accurately helps diagnose PSP. When we quickly look up, down, right, or left it is called a saccadic eye movement. When we move our eyes slowly, it is called called a smooth pursuit. These movements are controlled by the cortex of the brain, above the nucleus that controls the eye muscles (supranuclear). That is the part of the eye movement that is most impacted by PSP. Patients, at first, have trouble with the saccadic movements, and eventually have trouble looking up or down at all, even with smooth pursuit. This is in contrast to a gaze movement below the level of the nucleus (infra nuclear) in which you move the head in one plane can the eyes move around and the eyes are not affected.

* Dysphagia/dysarthria – speech and swallowing difficulties

Cognitive Profile:
* Executive dysfunction – cognitive profile / thinking challenges

* Apathy, obsessive/compulsive behaviors, lack of inhibition

When these cognitive and behavior dysfunctions are present, it can make it difficult to distinguish PSP from other types of memory problems, like Alzheimer’s disease (AD) and Frontemporal Dementia (FTD). When there’s more of a motor component to presenting symptoms, it becomes difficult to distinguish PSP from Parkinson’s disease and parkinsonisms.


The original diagnostic criteria was developed in 1996. They were based on a series of autopsy cases for people who had been followed throughout their life and were found at autopsy to have PSP in their brains. When they looked back at the clinical symptoms to see what clinical symptoms distinguished PSP from other disorders they came up with:
– Gradually progressive (to distinguish from stroke, which causes sudden changes)
– Presenting symptoms over the age of 40
– Vertical supranuclear gaze palsy
– Postural instability with a propensity to fall within the first year of symptoms

There are a lot of other supporting features but those tended to differentiate PSP from other disorders, but were unspecific, like rigidity in the neck and trunk, tendency to fall backward, poor response to levodopa, and some cognitive symptoms. These supporting features didn’t do a good job of distinguishing people who had PSP from other disorders, and what was used in the study of 181 people thought to have PSP in which only 63% actually had PSP on autopsy.

What has been identified since is that most patients would have the classic parts of PSP (supranuclear gaze palsy, and tendency to fall) early on and can be properly diagnosed within 1-3 years. But a lot of patients didn’t have those particular features early on in the disorder. Over time those symptoms tend to emerge into the classic Richardson syndrome, but it can be so many years (6 or 7 years) before those symptoms present and getting the right diagnosis. In fact, people have actually died before presenting the classic Richardson syndrome symptoms of PSP.

This is frustrating for patients, their families, and clinicians trying to only enroll people who actually have PSP in their clinical trial studies.


Dr. Poston showed a slide at time stamp 14:52 showing the accuracy of a PSP diagnosis, depending on early symptom presentation.
1. PSP Richardson syndrome – supranuclear gaze palsy & early falls = very likely properly diagnosed with PSP
2. PSP-P Parkinsonism symptoms – slowness, stiffness, subtle eye movement abnormalities, no early falls = less than 1/2 the time accurately diagnosed with PSP
3. PSP Primary Freezing of Gait – difficulty initiating walking early on. Not part of the classic Richardson Syndrome. Very difficult to diagnose, but more accurately diagnosed with PSP than those below.

These four disorders are a very small percentage of people with PSP, but they do exist and it is important to understand that. That is part of the logic behind the somewhat complex nature of the new diagnostic criteria. Because they are a small percentage, we will focus on the first three.
4. Cortobasal syndrome
5. Nonfluid Primary Progressive Aphasia
6. Behavior variant FTD
7. Cerebellar ataxia


PSP- RS / PSP Richardson Syndrome is the most common clinical variant. People presenting these symptoms are most likely to actually have PSP pathology on autopsy.
* Unexplained falls, Unsteady gait, Bradykinesia (slowness of movement)
* Personality changes (apathy, disinhibition)
* Cognitive slowing, Executive dysfunction (difficulty problem solving and organizing your day)
* Slow, spastic, and hypophonic speech, Dysphagia (difficulty swallowing)
* Impaired eye movement (slow vertical saccades, apraxia eyelid opening)
* Vertical supranuclear gaze palsy, but onset is variable, for example:
— Might not present for 3-4 years after disease onset
— May present early on as decreased velocity, amplitude of vertical > horizontal saccadic (can’t look all the way up or all the way down)
— May present as decreased or absent optokinetic nystagmus. There are some easy to use apps to test OKN in your doctor’s office.


PSP-P / PSP-Parkinsonism is the one that has the most difficulty distinguishing between PSP and Parkinson’s disease or PSP and Dementia with Lewy Bodies. This subtype of PSP was identified in the last 10 years by an autopsy study done in the UK where they looked at a bunch of patients who had donated their brain and had PSP on autopsy but did not have a diagnosis of PSP during their life. A lot of those patients had features very similar to classic Parkinson’s disease, particularly early on.

We always thought PSP should be very symmetric without a lot of tremor, but these folks had a lot of asymmetry and a lot of tremor and a good many of them had an early, good response to Levodopa. As years progressed this response went away and the asymmetry became symmetric, but early on it really resembled classic Parkinson’s disease and this made us realize that early on some patients are early to distinguish.

It was uncommon for these people with PSP Parkinsonism to develop the classic Levodopa-induced dyskinesias, they didn’t have the autonomic dysfunction (blood pressure drops common in Parkinson’s), or hallucinations common in Dementia with Lewy Bodies (DLB) and that’s really important in distinguishing PSP from DLB. DLB is a variant of Parkinson’s disease where the visual hallucinations are a distinguishing feature. Asking whether visual hallucinations are present is key in distinguishing PSP from DLB.

(Slide summary)
PSP-P Parkinsonism. People presenting these symptoms are less than 1/2 the time accurately diagnosed with PSP.
* Early features of PD
* Asymmetric onset tremor, Bradykinesia, Rigidity, Moderate initial response to Levodopa
* Resembles idiopathic Parkinson’s disease
* Levodopa-induced dyskinesias, autonomic dysfunction, and visual hallucination are less common in patients with PSP-P (compared to the patients with PD)


PSP-PGF / PSP Primary Gait Freezing – very tough to diagnose but important to recognize it is a variant of PSP as almost all patients have PSP pathology at autopsy.
* Pure Akinesia with Gait Freezing – primarily have difficult initiating walking, feet really stick to the floor
* Isolated gait disorder (5-6) years before development of other PSP-RS
* Progressive gait disturbance with start hesitation
* Subsequent freezing of gait
* Sometimes difficulties with initiating or completing speech or writing
* Without tremor, rigidity, dementia, or eye problems during first 5 years


The new 2017 diagnostic criteria:
* Sporadic occurrence (to distinguish from stroke)
* Age 40 or older at onset
* Gradual progression of PSP-related symptom
* Core Features:
— Oculomotor dysfunction
— Postural instability
— Akinesia
— Cognitive dysfunction

What does Probably PSP mean?
We cannot say someone definitely has PSP without autopsy finding. It is not possible at this point, based on clinical exam, brain imaging, or blood test to say someone definitely has PSP. Research is underway.

Highly specific: If someone meets probable PSP criteria, there is a very high chance that the underlying pathological diagnosis will be PSP. These are the people we are most certain about.

Good for use in clinical trials where you only want to enroll people who have the real underlying pathology.

But not very sensitive for PSP. Most people who have PSP pathology will not fully meet the Probable Criteria. Means that if you don’t have Probable PSP based on criteria, there’s still a really good chance you have PSP.


Slide at time stamp 26:10 showing the diagnostic levels of certainty when certain symptoms are present early on. In all cases, the oculomotor dysfunction must be present or it would be too hard to distinguish from PD or DLB.
To be diagnosed with Probable PSP-RS (Richardson Syndrome) you must have:
1. Either a vertical supranuclear gaze palsy or slow velocity of vertical saccades AND
2. Either repeated unprovoked falls within 3 years or a tendency to fall on the pull-test within 3 years.

To be diagnosed with Probable PSP-P (Parkinsonism) you must have:
1. Either a vertical supranuclear gaze palsy or slow velocity of vertical saccades AND
2. Parkinsonism, akinetic-rigid, predominantly axial, and levodopa resistant or Parkinsonism, with tremor and/or asymmetric and/or levodopa responsive.

To be diagnosed with Probable PSP-PGF (Gait Freezing) you must have:
1. Either a vertical supranuclear gaze palsy or slow velocity of vertical saccades AND
2. Progressive gait freezing within 3 years


Dr. Poston showed a slide at time stamp 29:30 showing imaging scans that are helpful in diagnosis when they appear. Similar to the eye movement abnormalities, when doctors see these they are very helpful in making a diagnosis. Unfortunately, most patients do not present so clearly on imaging. The lack of these distinguishing scan features does not mean you do not have PSP, it just means this tool didn’t present any compelling evidence for a PSP diagnosis. Clinical observation will have to suffice.
* The hummingbird sign shows thinning of the midbrain, which is classic to PSP
* The morning glory sign or mickey mouse ears, also shows thinning of the midbrain.


Dr. Poston showed slides of PSP pathology under the microscope at autopsy at time stamp 30:33, and discussed:
* Neurofibrillary tangles or neuropil threads or both, in the basal ganglia and the brainstem.
* Microscopic features:
— Neuronal loss
— Gliosis
— Neurofibrillary tangles
— Neuropil threads
— Tufted astrocytes
— Oligodendroglial coiled bodies


Carbonated liquids may help swallowing dysfunction (small Swedish study)

This is interesting research from Sweden on the effect of carbonated liquid on swallowing dysfunction. Though the study was done on 48 patients with Lewy body dementia, the findings likely apply to all in the Brain Support Network community.

Two interesting points were made:

1- While 40 patients had swallowing dysfunction confirmed through videofluoroscopy, 14 of these did not perceive they had swallowing symptoms.

2- Out of the patients with swallowing dysfunction, 87% had “an overall improved swallowing function with carbonated liquid.” This was true even that the pharyngeal transit time of carbonated liquid was quicker than think liquid or thickened liquid.

Of course you can test whether carbonated liquids work (for you or for your family member) by requesting they be tried during videofluoroscopy.

The abstract is below.



Clinical Interventions in Aging. 2017 Aug 8;12:1215-1222.

Effects of carbonated liquid on swallowing dysfunction in dementia with Lewy bodies and Parkinson’s disease dementia.

Larsson V, Torisson G, Bülow M, Londos E.


Swallowing dysfunction is an increasingly recognized problem in patients with dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), which can result in aspiration pneumonia and death. Few studies have examined potential ways of improving swallowing function in this fragile patient group. The aim of this study was to evaluate swallowing dysfunction and carbonated liquid using videofluoroscopy in DLB and PDD patients.

A total of 48 patients with DLB and PDD were referred for a clinical examination with videofluoroscopy. Descriptive overall assessments were provided at the time of the examination regarding swallowing function and the effects of different modifications, including carbonated thin liquid (CTL). Additionally, a repeated measures quantitative retrospective analysis has been performed comparing 1) thin liquids; 2) thickened liquids and 3) CTLs, with regard to the quantitative variables 1) pharyngeal transit time (PTT); 2) pharyngeal retention and 3) tracheal penetration.

In all, 40/48 (83%) of the patients had a swallowing dysfunction, which was confirmed on videofluoroscopy, with 34/40 (85%) patients having a pharyngeal-type dysfunction. A total of 14/40 (35%) patients with an objective swallowing impairment did not have any subjective swallowing symptoms. Out of the patients with swallowing dysfunction, 87% had an overall improved swallowing function with carbonated liquid. PTT for carbonated liquid (median 633 ms, interquartile range [IQR] 516-786 ms) was quicker than for thin liquid (760 ms, IQR 613-940 ms, P=0.014) and thickened liquid (880.0 ms, IQR 600-1,500 ms, P<0.001). No significant effect was seen in residue or penetration.

The majority of patients with DLB or PDD had a swallowing dysfunction, sometimes without subjective swallowing symptoms, which improved with carbonated liquid. This highlights the importance of investigating patients with videofluoroscopy and to carry out a prospective interventional study to further evaluate carbonated liquid, also addressing the effects on quality of life, aspiration and mortality.

Results from AbbVie phase 1 study of tau antibodies in PSP

At the recent Alzheimer’s Association International Conference, reports were given on phase 1 trials of tau antibodies. Tau is the protein involved in Alzheimer’s, progressive supranuclear palsy, and corticobasal degeneration. Phase 1 studies are focused on safety, not efficacy.

Alzforum posted a summary over the weekend on this tau research that involved PSP volunteers. Basically, the experimental drug seemed safe, and AbbVie is proceeding to a phase 2 trial in PSP. UCSF is one of the trial sites.

You will hear plenty more about this research is you attend our October 28th PSP/CBD Research Update and Family Conference in the SF Bay Area. Registration will open soon. We are hoping that AbbVie will sponsor part of our conference. Keep your fingers crossed!

Here’s a link to the Alzforum summary about this PSP research:

High-Dose Aβ and Tau Immunotherapies Complete Initial Safety Tests
Series – Alzheimer’s Association International Conference 2017
27 Aug 2017



Benefits of palliative care, and list of palliative care programs in Northern California

Recently I came across a research article on the emerging role of palliative care in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). The article makes the point that palliative care emphasizes “quality of life in progressive disorders” and is beneficial for all neurodegenerative disorders.

If you’d like to read the full article, check out this link:

Palliative Care and its Emerging Role in Multiple System Atrophy and Progressive Supranuclear Palsy
Parkinsonism & Related Disorders
January 2017, volume 34, pages 714

I had a feeling that if I shared this link, many of you would ask “where can I find a palliative care program?” Brain Support Network volunteer Denise Dagan created a list of as many palliative care programs as she could find on the Peninsula and in the South Bay. Since many of these medical clinics exist throughout Northern California — Sutter Health, Kaiser, PAMF, etc — this list should be useful to most of you on this list.



By Denise Dagan (Brain Support Network volunteer)
August 2017

California Pacific Medical Center (CPMC), in San Francisco, is part of Sutter Health. Information about their program can be found here:, or for more information contact Linda Blum, RN, NP, at 415-600-4576.

The Chinese Hospital, San Francisco Call 415-677-2349 for information.

Community Hospital of the Monterey Peninsula Ask your doctor for more information.

El Camino Hospital, Mountain View Call 650-988-7624 for information or visit

Hospice By the Bay offers palliative care in collaboration with these hospitals:
Marin General, Sonoma Valley, Sonoma Acres and Broadway Villa Sonoma. Call 415-927-2273 for information.

Jewish Family and Children’s Services of San Francisco, the Peninsula, Marin and Sonoma Counties offers palliative care through Seniors At Home. Call 844-222-3212 or visit the JFCS’ Seniors At Home website.

Kaiser Permanente offers palliative care at several locations around the bay:
Oakland – Inpatient 510-801-7246, Outpatient 510-752-1834
Richmond – Outpatient 510-752-1834
San Francisco – Outpatient 415-833-0204
San Jose – Inpatient 408-972-6888, Outpatient 408-972-7311

Palliative Care

Santa Clara – Inpatient 408-851-7578, Outpatient 408-851-0537,

Palliative Care

Laguna Honda Hospital, San Francisco Call 415-682-1230 for information or to arrange a tour.

Mission Hospice & Home Care, San Mateo, offers in-home palliative care. Call the Clinical Outreach Team 650-554-1000 for information or visit

Palo Alto Medical Foundation (PAMF) offers palliative care in several locations:
Dublin, Fremont, Mountain View, Palo Alto, Santa Cruz, and Sunnyvale

Pathways offers palliative care for any individual or private physician referral on the peninsula, south and east bay areas. Call 844-755-7855 for information.

Regional Medical Center, San Jose Call 877-868-4827 for information

St. Francis Memorial Hospital, San Francisco Call 415-353-6856 or 415-353-6180 for information.

St. Mary’s Medical Center, San Francisco Call 415-750-5907 for information.

San Francisco General Hospital offers inpatient palliative care in Comfort Care Suites. Ask your doctor for more information or visit

San Mateo Medical Center, San Mateo County Health System Call 650-573-2381 for Information.

Santa Clara Valley Medical Center, San Jose Call 408-793-5974 for information.

Season’s Hospice and Palliative Care offers palliative care in both San Mateo and Santa Clara Counties. Call 855-812-1136 or email [email protected] for information.

Sequoia Hospital, in Redwood City, offers palliative care through Pathways. Sequoia Hospital is a co-owner of Pathways. Call 888-755-7855 for information.

Stanford offers palliative care in these locations:
Palo Alto – Lucile Packard Children’s Hospital. Call 650-497-8963 for information.
Palo Alto – Palliative Care at Stanford Hospital. Call 650-724-0385 for information.
San Jose – Cancer Center South Bay. Call 408-426-4900 for information.

Sutter Health This page has a list of 33 palliative care doctors affiliated with Sutter Health (including, CPMC, Mills-Peninsula Medical Center, PAMF and Sutter Pacific Medical Foundation) in several locations:
Alameda, Auburn, Berkeley, Burlingame, Castro Valley, Fremont, Hayward, Modesto, Oakland, Palo Alto, Roseville, Sacramento, San Francisco, San Jose, San Mateo, Santa Cruz, Santa Rosa, Sunnyvale, and Yuba City

UCSF Medical Center offers inpatient and outpatient palliative care at both Parnassus and Mission Bay, and inpatient palliative care at SF General Hospital. Call 415-502-6861 for more information.

Veterans Affairs (VA) offers palliative care at several locations:
Palo Alto VA Health Care System – contact them through [email protected]
San Francisco VA Medical Center offers hospice and palliative care through Geriatric Services. Call 415-221-4810, ext. 2-3224 for information.

Visiting Angels offers palliative care in several locations:
Burlingame – Call 650-344-2178 for information.
Fremont – Call 510-284-0000 for information.
San Jose – Call 408-241-5100 for information.
Sunnyvale – Call 408-735-0977 for information.

Vitas Healthcare offers palliative care in several locations:
Milpitas – Call 408-964-6800 for information.
San Francisco – Call 415-874-4400 for information.
San Mateo – Call 650-350-1835 for information.

With Grace Hospice and Palliative Care, San Jose Call 408-444-5500 for information.


Stanford/BSN Webinar – Diagnosing PSP, Wed, Aug 30, 2-3pm PT – Register Now!

Brain Support Network is kicking off a webinar series with Stanford Movement Disorders Center, one of our Northern California partners.

Join us for a free, one-hour webinar on diagnosing progressive supranuclear palsy (PSP). The speaker is Stanford movement disorders specialist Kathleen Poston, MD. Please spread the word!


Diagnosing Progressive Supranuclear Palsy

When: Wednesday, Aug 30, 2017
2-3pm Pacific Time (US and Canada)

Speaker: Kathleen Poston, MD, MS, movement disorders specialist, Stanford Movement Disorders Center

Register in advance for this webinar:

After registering, you will receive a confirmation email containing information about joining the webinar.

Note: If you can’t make it on August 30th, we encourage you to register for the webinar so that you will be alerted when the recording is available online.


Further details on the webinar topic:

Dr. Kathleen Poston, a movement disorder specialist with extensive experience with PSP, will address these topics:

* how is PSP diagnosed?
* how many years does the average person wait for a diagnosis?
* what are the two main types of PSP?
* what’s the new diagnostic criteria for probable PSP?
* what’s the accuracy of a PSP diagnosis?

There will be time for audience questions on PSP.


Further details on the speaker:

The speaker is Dr. Kathleen Poston, a movement disorders specialist at Stanford University. Dr. Poston research focuses on the development of novel neuroimaging biomarkers to improve diagnostic accuracy and monitor the efficacy of investigational treatments for Parkinson’s Disease and other movement disorders, such as PSP. She is the co-investigator for the NINDS-funded Udall Center of Excellence for Parkinson’s Disease Research.


Further details on the webinar host:

The webinar will be hosted by Robin Riddle, who coordinates a Parkinson’s Information & Referral Center at Stanford. She is also the CEO of Brain Support Network, a nonprofit focusing on the four atypical parkinsonism disorders, including PSP.

Brain Support Network is organizing a research update and family conference on Progressive Supranuclear Palsy and Corticobasal Degeneration on Saturday, October 28th, in the San Francisco Bay Area. To be notified when registration opens for this conference, please join the PSP email list.


Register in advance for this webinar:


Questions? Please contact Robin Riddle.

BSN’s Allan Marcus Fund Gave Six Grants in 2017

The Allan Marcus Fund for Families in Need with PSP has successfully completed its giving for 2017.  The Marcus family and Brain Support Network (BSN) approved six grants to families with loved ones with progressive supranuclear palsy (PSP).

The grants to PSP families provided in-home caregiving, travel to family reunions, needed physical therapy, and more.  Congratulations to all the families in the US who received grants.  It was an honor to hear your stories and help make what we hope will be precious memories.

The Marcus family aims to provide this fund annually.  Please join BSN’s PSP email list to be kept informed as more information is available in the new year.

PSP and CBS excerpts from curriculum on dementia for healthcare professionals

Someone in our local support group recently sent me this link to US Dept. of Health and Human Services’s curriculum for physicians (especially primary care physicians) and healthcare professionals (social workers, psychologists, pharmacists, emergency department staffs, dentists, etc.) on dementia. Though the web address includes the term “Alzheimer’s,” frontotemporal dementia is also mentioned in this curriculum:

Training Curriculum: Alzheimer’s Disease and Related Dementias
Health Resources and Services Administration (part of Dept of HHS)

One of the types of frontotemporal dementia is the “motor type,” which include corticobasal syndrome and progressive supranuclear palsy.

Here are some excerpts on frontotemporal dementia.



Overview of Mild Cognitive Impairment and Dementia for an Interprofessional Team (Module 1)

Frontotemporal Dementia Types
* There are at least 3 distinctive clinical syndromes, each with heterogeneous neuropathology.
– Progressive behavior/personality decline: behavioral variant FTD (bvFTD)
– Progressive language decline: Primary progressive aphasia (PPA)
– Progressive motor decline: corticobasal syndrome, amyotrophic lateral sclerosis, or [progressive] supranuclear palsy. FTD with progressive motor decline is rare. FTD with progressive motor decline can involve movement problems/slowed movement, muscle rigidity (Parkinsonian symptoms), body stiffness, and changes in behavior or language.
* Behavioral variant FTD (bvFTD) is the most common variant. It is characterized by marked personality changes and changes in social conduct.

Understanding Early-Stage Dementia for an Interprofessional Team (Module 5)

Early-Stage Frontotemporal Degeneration (FTD): Overview
* FTD is a heterogeneous group of diseases with overlapping clinical symptoms but different causative genes and differing underlying pathologies.
* FTD is caused by damage to frontal and/or temporal lobes. Impairments generally progress quickly but memory often remains intact.
* Persons with FTD demonstrate changes in behavior and personality, language problems, and motor problems.
( Memory impairment is minimal in early stages.

Palliative and End-of-Life Care for Persons Living with Dementia (Module 12)

When to Consider Hospice Care in Persons with End-Stage FTD
* Persons with end-stage FTD are generally younger and healthier than persons with other types of end-stage dementia.
* As with other dementias, FTD is often not recognized as a terminal diagnosis.
* End-stage FTD may “look different” than other advanced dementias.


Apathy – description and treatment

Brain Support Network volunteer Denise Dagan came across this article in a recent Parkinson’s Disease (PD) organization’s newsletter about apathy in PD.  Certainly apathy occurs in many of the disorders in the Brain Support Network community as well — especially progressive supranuclear palsy (PSP).  That’s why I’m sharing the article within our network.

These statements in the article caught Denise’s eye:

“Persons with apathy generally do not recognize the symptoms, so caregivers will need to bring it to medical attention. … It is important to assess for apathy because those with apathy are 2.5 times more likely to report poor quality of life in comparison to those without apathy. Apathy is also associated with more severe motor impairment. PD patients with apathy are less physically active and may not adhere to medical recommendations. Relationships may suffer as well since caregivers often experience more frustration and stress.”

The author of the article is Rosa Chuang, MD.  She may be familiar to some in our multiple system atrophy (MSA) group.  She used to practice at Stanford but is now in Seattle.

The article is copied below.



Apathy in Parkinson’s Disease
Parkinson’s Pathfinder (Newsletter by APDA Northwest)
Summer 2017
By Dr. Rosalind Chuang

Apathy is a common non-motor symptom of Parkinson’s disease but often times not recognized or commonly mistaken for depression. Some studies show that 30-40% of PD patients have apathy, but the frequency can range from 20-70%, depending on how patients are asked. It can occur at any stage of PD and can even occur before motor symptoms develop. It is important to assess for apathy because those with apathy are 2.5 times more likely to report poor quality of life in comparison to those without apathy. Apathy is also associated with more severe motor impairment. PD patients with apathy are less physically active and may not adhere to medical recommendations. Relationships may suffer as well since caregivers often experience more frustration and stress.


Apathy is defined as:
• Loss of motivation or lack of initiative
• Loss of pleasure
• Decreased goal directed behaviors
• Decreased goal directed cognitive activity
• Decreased interests and emotions (reduced display of emotions)


A common complaint from family and friends is that the PD patient just “sits around” or “doesn’t seem to care about anything.” Nothing gets done and a person often declines social activities if given a choice. This can be misinterpreted as fatigue, laziness, or lack of empathy/ uncaring.

Persons with apathy generally do not recognize the symptoms, so caregivers will need to bring it to medical attention. Medical providers may ask specific questions from the Starkstein apathy scale to determine apathy. Some questions on the scale include:

• Any interest in learning new things?
• Does anything interest you?
• Do you look for things to do?
• Are you concerned about your condition? Or unconcerned about many things?
• Does someone have to tell you what to do each day? Do you need a push to get started on things?
• Are you neither happy nor sad, just in between?

As you can see, these questions are similar to those to assess for depression, so sometimes it can be difficult to separate apathy from depression. Often times, patients can have both depression and apathy, but in ~10- 28% of time, patients can have apathy alone.


In both depression and apathy, a person may no longer enjoy things. However, someone with depression may endorse feeling “blue” or sad. Other “negative” symptoms of depression include inappropriate guilt, loss of appetite, loss of sleep, or thoughts of death. An apathetic person does not cry frequently or have suicidal thoughts.


It is important to evaluate if the symptoms are from apathy alone because it can affect treatment. If apathy is associated with depression or anxiety, treatment of co-morbid conditions can help reduce apathy. Sometimes isolated apathy can also respond to the SSRIs used to treat depression, but generally studies don’t show good response. Dopamine medications (levodopa or dopamine agonists) may also improve apathy. (In some patient who have undergone deep brain stimulation for PD, rapid withdrawal of their PD medications resulted in apathy.) In one trial, PD apathy responded to rivastigmine, a medication used for dementia, even though the patients did not actually have dementia.

For isolated apathy, I generally recommend non-pharmacologic treatment. These include:

• Write down at least 3 daily goals and 3 weekly goals. These goals can be physical, social, or thinking activities.
• Daily goals should be specific and can be reasonably achieved.
• Create a schedule: be specific when each task will should be accomplished.
• Review the written list at breakfast, lunch and dinner to remind yourself of the next goal.
• Cross off each task as you complete them.
• Say “yes” to at least one thing every day even if you don’t feel like it.
• Maintain routine: continue to do things you used to do, even if you don’t feel like it.
• Recall an activity that you used to enjoy and try to restart that activity.
• Exercise even if you don’t feel like it.
• Must leave the house at least once a day

Even though apathy is not as easily treated as the motor symptoms of PD or other non-motor symptoms such as depression, simply recognizing and understanding apathy is an important part of overall management of Parkinson’s disease.

Save the Date! Saturday, October 28, PSP/CBD Research Update and Family Conference

Save the date!

Brain Support Network will host the:

PSP/CBD Research Update and Family Conference
Saturday, October 28, 2017
Crowne Plaza Foster City (San Francisco Bay Area)

This conference is for families coping with progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD).   Professionals and anyone in the community are also welcome to attend.

BSN’s planning partner is Dr. Adam Boxer and the team at the UCSF Memory & Aging Center. UCSF is the lead institution for PSP and CBD clinical trials. We are lucky to have them in our backyard!

The conference will be run from 9am to 5pm. The morning will feature international researchers in town for a major conference on PSP, CBD, and tau. The afternoon will feature Bay Area clinicians (from UCSF and Stanford), healthcare professionals, and families.

We anticipate registration will open in early September. Join our PSP or CBD email lists and we’ll send you an update when registration opens. Alternatively, check back at our website in September to register. Our meeting facilities are planned to accommodate 150 participants.

Stay tuned for more details!