Category Archives: CBD

Treating blood pressure, bladder, constipation, etc. – article by Dr. Golbe

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Dr. Lawrence Golbe is a movement disorder specialist at Robert Wood Johnson Medical School in NJ.  He is an expert on progressive supranuclear palsy (PSP), and is the head of the CurePSP Science Advisory Board.  In the latest CurePSP (psp.org) newsletter, there’s a short article he authored on palliative measures in multiple system atrophy (MSA).  He defines “palliative measures” as those that will “lessen the severity of…symptoms and…improve both the quality and quantity of life.”

Dr. Golbe addresses these symptoms or treatments:
* anti-parkinson treatment
* low blood pressure
* bladder problems
* constipation
* swallowing problems

As many of these symptoms are found in all the disorders within our group (MSA, LBD, PSP, and CBD) – not just MSA – the article may be of interest to everyone.

The full article is copied below.

Robin

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https://web.archive.org/web/20120514113101/http://www.psp.org/file_download/b9b6fe18-8ac0-4354-8e23-b35734be1767 –> article on page 3

MSA: Palliative Measures
Lawrence I. Golbe, MD, UMDNJ-Robert Wood Johnson Medical School
CurePSP Newsletter
March/April 2012

There is still no cure for MSA nor any way known to slow its progression, but there are many ways to lessen the severity of the symptoms and to improve both the quality and quantity of life. These are called “palliative” measures.

Antiparkinson treatment: Many people with MSA who have stiffness of limbs and slowness of movement find that carbidopa/levodopa, the main drug used for Parkinson’s disease, can help those symptoms. The duration and intensity of the drug’s effect is usually less than in Parkinson’s.

Low blood pressure: There are many ways to treat low blood pressure. If one is taking drugs or limiting salt intake to treat what once was high blood pressure, these measures could be reduced, but only under the supervision of a physician. Drugs that can increase the blood pressure include fludrocortisone (Florinef), midodrine (Pro-Amatine) and pyridostigmine (Mestinon). There are a handful of other drugs that are often worth a try. Non-drug measures include increasing the salt and fluid intake (if there are no heart or kidney problems that would make that risky), elevating the head of the bed by putting six-inch blocks under the legs at that end and using pressure stockings.

Bladder problems: The need to urinate frequently can be reduced by drugs that inhibit the muscle that empties the bladder. These are called “peripherally acting anticholinergics” and are widely advertised in the popular media.

Constipation: This symptom in MSA is treated as in any other setting. It is best to start with a stool softener (docusate; Colace) or a bulk-forming agent (Metamucil).

Swallowing problems: This is best treated by changing one’s habits regarding choice of foods and food textures, chewing technique and swallowing technique. This is best assessed by a trained speech/swallowing pathologist and often guided by an x-ray video of the person swallowing various food textures, called a “modified barium swallow.”

For severe swallowing difficulties that present a high risk of “aspiration” (food going down the wrong pipe into the lungs), a soft rubber tube can be placed through the skin of the abdomen directly into the stomach (“percutaneous endoscopic gastrostomy” or “PEG”). But this step should not be undertaken lightly. If such a technique becomes necessary to prevent aspiration, a careful decision should be reached by the patient, family, physician and other available advisors. They may decide that while the PEG may prolong life, the quality of life at that point in the disease becomes too low.

Sharon’s Treatment Regimen for CBD (revised in 2012)

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I know Sharon Comden from the CBD-related online support group.  She was diagnosed with corticobasal degeneration (CBD) in 2009.  She has a doctorate in public health from UCLA and, as you’ll see, she’s one smart cookie.

Sharon gave me her permission to circulate three recent posts in early 2012 about her treatment regimen (using supplements).  As CBD and PSP are similar disorders, her approach may be of interest to those with PSP (progressive supranuclear palsy).

One insignificant change I made to her posts is that I substituted “CBD” for “CBG.”  The old acronym for CBD was CBGD.

Sharon asks that you contact her via the CBD-related online support group (if you are a member there).  Let me know if you want to join; I’m a moderator of the group.

Robin

Editor’s Note: Sharon Comden died in late 2015. We at Brain Support Network were honored to help her make advance arrangements for her brain donation. She was a remarkable woman.

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(In this post, Sharon is responding to Elaine, whose mother is 91 and has a CBD diagnosis.)

Re: Treatment Options for PSP and CBD (Review)
Posted by: “Sharon Comden”
Date: Wed Feb 15, 2012 5:14 am ((PST))

Elaine, I have had CBD since 2009, when the first symptoms of hand apraxia (difficulty w/zippers, putting earrings on, and later deterioration of keyboard skills) showed up. In late 2010, I began having speech issues–slowing and intermittent difficulty pronouncing some words. It got progressively worse and my search of the “emerging therapies” literature paid off for me; I’ve seen significant improvements over the last eight months that I’ve been on my supplement regimen. My symptoms included: loss of sensation and fine motor coordination of my fingers (apraxia), slowed gait and upper limb movements, curling fingers of both hands when at rest (dystonia), speech slower and more hesitant than normal and difficulty pronouncing polysyllable words like “degenerative.”

Since there are no medical treatments currently available, I decided to look for promising therapies that had good preliminary results in animal studies, seeking low toxicity “emerging therapies” based on lab research results, if not clinical trials. I also contacted leading researchers with many years of experience working with drugs/supplements that act on neurodegenerative diseases. I have a doctorate in public health from UCLA and have research training (though not in neuroscience). I don’t pretend to understand everything–this is very technical research–but I am fairly confident in what I’m personally taking to delay progression of my CBD. It takes a multifactorial approach to combat CBD/PSP because there is no magic bullet that impacts all the elements of this disease, so a cocktail of different drugs/supplements is necessary, depending on what symptoms or part of the disease process we want to target.

Last May, I started taking 1000 mgs of bioavailable curcumin (Longvida, available in capsule and powder forms from phytosensia.com) w/ at least 500 mgs. vit. C and one 1200 mgs enteric coated DHA/omega 3 fish oil from Costco (Kirkland brand) on an empty stomach in the morning and at bedtime. Like your Mother, I also take 600 mgs. of CoQ10.

After four weeks on the curcumin/DHA/etc., I began to see improvements in my speech, at 4.5 weeks the curling fingers were gone, and my gait/limb movements returned to normal speed. Those benefits continue and most of the time, my speech is near normal. I subsequently lowered my dose of Longvida to 500 mgs. to twice a day after a few weeks, following what I call the initial induction phase when the curcumin levels are rising to therapeutic levels in the brain.

At the suggestion of my neurologist, I’ve added 25 grams of trehalose (NeuroCoatT, 1 tablespoon twice a day dissolved in a beverage or with food), a commercial sweetener shown to be safe and beneficial with Huntington’s Disease. It seems to be improving my articulation as well and compliments the action of the Longvida formulation curcumin. I understand there will be a clinical trial of the Longvida formulation, perhaps later this year. I also take a baby aspirin every other day.

Your Mother’s advanced age may or may not color her response to this regimen, all reputable over-the-counter supplements. Some caveats:

1. There is data available on the safety/efficacy of these supplements in animals and often humans too, but limited or no data on what happens when you take several concurrently. Many are common foodstuffs, e.g. curcumin (tumeric), trehalose (widely used commercial sweetener), but there is a risk that some combinations don’t work together or produce adverse reactions. Since I know what will happen if I do nothing, my personal decision is to accept that risk and keep good records of what I’m taking and how I respond. After eight plus months, I can report only benefits.

2. It takes three to six weeks to see changes after you start taking some supplements because it takes that long for them to build to therapeutic levels. Sometimes you feel a bit out of focus mentally before you feel better too. The “fuzziness” cleared up in a couple of weeks. I’ve been taking this combination for 8.5 months with no ill effects.

I hope your Mom does well with these supplements, if she decides to try them. This combination is based on hundreds of hours of reviewing scientific papers to find something that offers some hope for tauopathy sufferers (see First and Second Line of Defense maps on Yahoo CBD website). It’s the best we can do for ourselves right now, while researchers are looking for a cure.

Best regards,
Sharon Comden, Dr.PH

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(In this second post, Sharon is responding to Dawn, whose husband has a CBD (corticobasal degeneration) diagnosis and has not had the use of his left hand for over a year.  Dawn’s husband takes Aricept, Cipralex, and Crestor.)

Re: Treatment Options for PSP and CBD (Review)
Posted by: “Sharon Comden”
Date: Wed Feb 15, 2012 4:26 pm ((PST))

Dawn, this is a learning journey. My Mayo neurologist is cautiously watching what I’m doing–but he has also told colleagues about it and the results so far–so he is respectful of what appear to be symptom reversal for some things. I would normally refer you to your neurologist to help you assess potential contraindications, however, the likelihood of help there is about nil because outside of the research community, most neurologists are unfamiliar with supplements. I can share several scientific papers supporting the regimen, if you or your physician wants some reading.

As you note, I still enjoy a high level of function. Your husband may get some or no symptomatic relief at his stage; we just don’t know until the clinical trials are done with people at different disease stages. Here is reason to hope because at least one study of late curcumin intervention with mice, suggests that cognitive function can be improved by curcumin even in later stages of disease. We don’t have the luxury of waiting three to five years for human clinical trial results, unfortunately. Here is how I would proceed if it were my husband.

*    Crestor is a hybrid drug that can adversely affect muscles through its “statin” component. The evidence of the value of CoQ10 to treat myopathies caused by statin drugs is mixed, but some physicians advise their statin patients to take CoQ10 to reduce risks of side effects, so it would seem reasonable that the 600 mgs. in the anti-CBD regimen (300 mgs. morning and at bedtime) would not be contraindicated. To the contrary, there is evidence of benefit in neurodegenerative disease. Lahey Clinic has a clinical trial with PSP patients on very high doses of CoQ10.

*    The most powerful component of the anti-CBD regimen is the Longvida curcumin, originally developed in the lab of respected UCLA  researchers Drs. Sally Frautschy and Greg Cole and subsequently licensed by the University to an outside manufacturer. If your husband is  debilitated or sensitive to drugs in general, you might start with less Longvida and build up to the 1000 mgs. morning and at bedtime. One of curcumin’s actions is it stimulates autophagy, the cellular clean-up mechanism for the fragments of tau proteins created during abnormal hyperphosphorylation and destruction of normal neuron function. Not surprisingly, I did notice some cognitive effects after a week or so at a 1000 mgs. and my solitaire scores went down 500-1000 points. The fuzziness abated and the scores returned to normal after about three or four weeks. That is also when I began to see functional improvements.

*    I would start the regimen as described in the last post, but leave out the trehalose, so you can first establish his response to the curcumin.

Keep good notes of what he is taking and changes in his condition. You have to use your judgment if he reacts poorly to the supplements. Even with FDA approved drugs, sometime people will have adverse reactions.

TIPS: digestion of a meal will interfere with the absorption of the curcumin in the gut, so take it at least 45 minutes before or after meals. Liquids are ok and if swallowing capsules is a problem, it’s ok to mix the curcumin into yogurt, a smoothie; even hot liquids like a latte or cocoa are ok. The manufacturer, Phytosensia, sells it in powder form as well as capsules.

www.phytosensia.com/Longvida-Curcumin-Supplements.item

I have problems opening the capsules, so the powder is great. Rough measure if you elect to use the powder is one-quarter tsp = 500 mg and one-half tsp = 1000 mgs. It doesn’t taste bad either–cinnamon works well in hot cocoa to blend the flavors nicely and I like it in peach yogurt.

Let me know if you decide to proceed or if you want more information.

Sharon

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(In this post, Sharon is responding to me, when I’ve told her that her analysis is incredibly impressive.)

Re: Treatment Options for PSP and CBD (Review)
Posted by: “Sharon Comden”
Date: Wed Feb 15, 2012 4:49 pm ((PST))

Robin, thanks for the compliment. There is a strong possibility of a Longvida trial. The animal studies are very promising, as well as the results from my n=1 experiment. As you know, buying time until the cure is found is essential for tauopathy patients. I believe that I have bought time with this regimen. Coupled with regular exercise and cognitively challenging work–I feel good most all the time.

UCLA uses PET scans to study tau tangles

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This news out of UCLA on Monday February 13th has relevance for the PSP (progressive supranuclear palsy) and CBD (corticobasal degeneration) communities.  Both PSP and CBD are disorders of tau.  In Alzheimer’s Disease (AD), tau is a problem along with a second protein called beta amyloid.  A couple of years ago, researchers out of the University of Pittsburgh developed a compound that attaches itself to amyloid in the brain such that PET scans can help identify those with a high chance of having Alzheimer’s Disease.  A year or so ago, it was announced that researchers at UCLA had developed a compound that attaches itself to tau in the brain such that PET scans can help identify those with tauopathies, such as AD, PSP, and CBD.

This study published out of UCLA this week is about using this new PET scan compound to identify which subjects had tau tangles in the brain and predicted which subjects would experience cognitive decline.  Though this particular study focused on mild cognitive impairment (which can “convert” to Alzheimer’s Disease), it has implications for the PSP and CBD communities.

The full press release is copied below.  (Note that there are quite a few typos in this press release.)

Robin

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newsroom.ucla.edu/portal/ucla/ucla-imaging-technique-predicts-220856.aspx

UCLA brain-imaging technique predicts who will suffer cognitive decline over time
By Rachel Champeau
UCLA Newsroom
February 13, 2012

Cognitive loss and brain degeneration currently affect millions of adults, and the number will increase, given the population of aging baby boomers. Today, nearly 20 percent of people age 65 or older suffer from mild cognitive impairment and 10 percent have dementia.

UCLA scientists previously developed a brain-imaging tool to help assess the neurological changes associated with these conditions. The UCLA team now reports in the February issue of the journal Archives of Neurology that the brain-scan technique effectively tracked and predicted cognitive decline over a two-year period.

The team has created a chemical marker called FDDNP that binds to both plaque and tangle deposits — the hallmarks of Alzheimer’s disease — which can then be viewed using a positron emission tomography (PET) brain scan, providing a “window into the brain.” Using this method, researchers are able to pinpoint where in the brain these abnormal protein deposits are accumulating.

“We are finding that this may be a useful neuro-imaging marker that can detect changes early, before symptoms appear, and it may be helpful in tracking changes in the brain over time,” said study author Dr. Gary Small, UCLA’s Parlow–Solomon Professor on Aging and a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Small noted that FDDNP–PET scanning is the only available brain-imaging technique that can assess tau tangles. Autopsy findings have found that tangles correlate with Alzheimer’s disease progression much better than do plaques.

For the study, researchers performed brain scans and cognitive assessments on the subjects at baseline and then again two years later. The study involved 43 volunteer paricipants, with an average age of 64, who did not have dementia. At the start of the study, approximately half (22) of the participants had normal aging and the other half (21) had mild cognitive impairment, or MCI, a condition that increases a person’s risk of developing Alzheimer’s disease.

Researchers found that for both groups, increases in FDDNP binding in the frontal, posterior cingulate and global areas of the brain at the two-year follow-up correlated with progression of cognitive decline. These areas of the brain are involved in decision-making, complex reasoning, memory and emotions. Higher initial baseline FDDNP binding in both subject groups was associated with a decline in cognitive functioning in areas such as language and attention at the two-year follow-up.

“We found that increases in FDDNP binding in key brain areas correlated with increases in clinical symptoms over time,” said study author Dr. Jorge R. Barrio, who holds UCLA’s Plott Chair in Gerentology and is a professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA. “Initial binding levels were also predictive of future cognitive decline.”

Among the subjects with mild cognitive impairment, the level of initial binding in the frontal and parietal areas of the brain provided the greatest accuracy in identifying those who developed Alzheimer’s disease after two years. Of the 21 subjects with MCI, six were diagnosed with Alzheimer’s at follow-up, and these six subjects had higher initial frontal and parietal binding values than the other subjects in the MCI group.

In the normal aging subjects, three developed mild cognitive impairment after two years. Two of these three participants had had the highest baseline binding values in the temporal, parietal and frontal brain regions among this group.

Researchers said the next step in research will involve a longer duration of follow-up with larger samples of subjects. In addition, the team is using this brain-imaging technique in clinical trials to help track novel therapeutics for brain aging, such as curcumin, a chemical found in turmeric spice.

“Tracking the effectiveness of such treatments may help accelerate drug discovery efforts,” Small, the author of the new book “The Alzheimer’s Prevention Program,” said. “Because FDDNP appears to predict who will develop dementia, it may be particularly useful in tracking the effectiveness of interventions designed to delay the onset of dementia symptoms and eventually prevent the disease.”

Small recently received research approval from the U.S. Food and Drug Administration to use FDDNP–PET to study people with mild cognitive impairment to determine whether a high-potency form of curcumin — a spice with anti-amyloid, anti-tau and anti-inflammatory properties — can prevent Alzheimer’s disease and the accumulation of plaques and tangles in the brain.

UCLA owns three U.S. patents on the FDDNP chemical marker. The Office of Intellectual Property at UCLA is actively seeking a commercial partner to bring this promising technology to market.

Small and study authors Jorge R. Barrio and S. C. Huang are among the inventors. Disclosures are listed in the full study.

Additional authors included Prabha Siddarth, Linda M. Ercoli, Alison C. Burggren, Karen J. Miller, Dr. Helen Lavretsky and Dr. Susan Y. Bookheimer, all of the UCLA Department of Psychiatry and Biobehavioral Sciences, and Vladimir Kepe and S.C. Huang, who are part of the UCLA Department of Molecular and Medical Pharmacology.

The study was funded by the National Institutes of Health and the U.S. Department of Energy.

Treatment Options for PSP, CBD, and FTD (Review)

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Treatment Options for PSP, CBD, and FTD (Review)

This medical journal article is a review of what we know about treatment of PSP (progressive supranuclear palsy), CBD (corticobasal degeneration), and FTD (frontotemporal dementia). Some general statements are made about “diet and lifestyle,” then several medications are discussed including anti-depressants (SSRIs in particular), dementia medications, antipsychotics, and levodopa. Finally, “emerging therapies” are briefly described.

I’ve copied the abstract below.

For me, the one new piece of information is that Abilify and Seroquel are the two most commonly prescribed antipsychotics “in parkinsonian disorders.” It would be interesting to know how frequently they are prescribed in PSP and CBD. Certainly most of the prescriptions are for Parkinson’s Disease and Parkinson’s Disease Dementia (Lewy Body Dementia). Though we have a few local support group members with PSP and CBD taking these medications, the majority do not.

Robin

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Current Treatment Options in Neurology. 2012 Feb 4. [Epub ahead of print]

Treatment Options for Tauopathies.

Karakaya T, Fußer F, Prvulovic D, Hampel H.
Department of Psychiatry, J.W. Goethe-University, Frankfurt, Germany.

Abstract
OPINION STATEMENT: To date, there are no approved and established pharmacologic treatment options for tauopathies, a very heterogenous group of neuropsychiatric diseases often leading to dementia and clinically diagnosed as atypical Parkinson syndromes.

Among these so-called Parkinson plus syndromes are progressive supranuclear palsy (PSP), also referred to as Steele-Richardson-Olszewski syndrome; frontotemporal dementia (FTD); and corticobasal degeneration (CBD).

Available treatment strategies are based mainly on small clinical trials, miscellaneous case reports, or small case-controlled studies. The results of these studies and conclusions about the efficacy of the medication used are often contradictory.

Approved therapeutic agents for Alzheimer´s dementia, such as acetylcholinesterase inhibitors and memantine, have been used off-label to treat cognitive and behavioral symptoms in tauopathies, but the outcome has not been consistent.

Therapeutic agents for the symptomatic treatment of Parkinson’s disease (levodopa or dopamine agonists) are used for motor symptoms in tauopathies.

For behavioral or psychopathological symptoms, treatment with antidepressants-especially selective serotonin reuptake inhibitors-could be helpful.

Antipsychotics are often not well tolerated because of their adverse effects, which are pronounced in tauopathies; these drugs should be given very carefully because of an increased risk of cerebrovascular events.

In addition to pharmacologic options, physical, occupational, or speech therapy can be applied to improve functional abilities.

Each pharmacologic or nonpharmacologic intervention should be fitted to the specific symptoms of the individual patient, and decisions about the type and duration of treatment should be based on its efficacy for the individual and the patient’s tolerance.

Currently, no effective treatment is available that targets the cause of these diseases. Current research focuses on targeting tau protein pathology, including pathologic aggregation or phosphorylation; these approaches seem to be very promising.

PubMed ID: #22307450 (see pubmed.gov for this abstract only)

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

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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:
http://www.smw.ch/content/smw-2011-13293/

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.

Robin

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

Abstract
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