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Saturday, March 26, 2011

Aricept - Aricept 23 and My bvFTD - Update 2

More about Aricept (Donepezil) 23, the benefits, and my side effects.

“The reason people find it so hard to be happy is that they always see the past better than it was, the present worse than it is, and the future less resolved than it will be”     ~Marcel Pagnol

"How poor are they that have not patience! What wound did ever heal but by degrees?"    ~William Shakespeare

First a short review from my previous post about taking Aricept . I started taking Aricept (Donepezil) 5 mg on September 13, 2010. I increased the dosage to 10 mg after about 6 weeks, and on December 13, 2010, I increased the dosage to 23 mg. My Neurologist is very supportive of this treatment, and reports having very good results in other patients with FTD.

Though not approved for use with bvFTD, Aricept is frequently prescribed off-label. It has a large enough effect on cognition that it is a highly sought-after drug by students taking exams such as the BAR, or Medical Boards. Well, if the wannabe doctors are taking it to help pass their exams there is probably something to it. That is worth more than a pill manufacturer's advertising any day.

For the first few days at the lowest dosage of 5mg I did not notice any side effects, or any improvement. Then I developed a sore throat, and a head cold. This actually may have been a side effect, but there is really no way to tell. By Thursday I had insomnia, and nausea. These are definitely side effects of the Aricept. Though I did not seem to have any adverse behavioral issues, I did have some gastrointestinal problems when I increased the dosage to 10mg. The most bothersome of which eventually was heartburn. The insomnia was not too bad to cope with, but the itching was horrible, and almost caused me to discontinue taking the drug. It started suddenly on the bottoms of my feet one night, and then got worse. Much worse! I cannot express in words how severe the itching was - think poison ivy on top of mosquito bites... and add a few chiggers! Then multiply by two! Everywhere! It moved around. Then, after a particularly uncomfortable drive back from chasing Elk around Pennsylvania, the itching abruptly stopped. So far it has not recurred, but it was a miserable couple of weeks.

Overall most of the side effects lasted about 6 - 10 weeks after each dosage increase, but were considerably more manageable near the end of that period. There may still be a little nausea and insomnia now and then, but that may have nothing to do with the Aricept because of some other medications I occasionally take which also can cause both nausea and insomnia. In any case it does not happen often, doesn't last more than a few minutes, and is not severe.

So, back on December 10, 2010, with the support of my neurologist, I increased the dosage to see if I could tolerate the higher 23 mg dosage of Aricept without having a return of the adverse side effects. It is now the end of March 2011. I have been taking the higher dosage Aricept for more than 12 weeks, and "Yes!" - there are side-effects!

Just like when I first started taking Aricept, I got sick again. I had Strep Throat, and then a couple of head colds. I have a runny nose most of the time - kinda like a slight case of hay-fever, but no sneezing or itchy eyes. The runny nose is listed as a pretty common side effect, so is to be expected. I mostly felt pretty lousy for about 5 weeks catching one thing after another, and still have a slight cough. I even got a skin infection on my nose that lasted a full 2 weeks. Looked pretty awful, but was nothing serious. It is finally healing, and should be gone in another few days. It seems that Aricept really gives your immune system a challenge fighting off infections of any kind. I have had more sickness in the past few months than I have in the past 10 years.

I also have the same gastrointestinal problems with the Aricept 23 as when I first started taking Aricept 5mg, but the nausea is not as severe, and the rest is worse. I don't want to dwell on it, but constipation and diarrhea can occur all in the same day, or for a few days at a time. Sometimes unpleasant, but something I can tolerate. It is getting better, but is still unpredictable.

For a couple of weeks I had some pretty bad incidents of vertigo. The worst was one morning when I actually fell down in the shower. How trite is that? At least I didn't break a hip or anything. I just got dizzy, grabbed onto the sliding door of the tub for balance, and gradually blacked out and slid-half-fell into the tub as the shower door rolled open. OK, so maybe it wasn't the best thing to grab on to, but it was all I had within reach at the time. I was a little sore the next day, but not bruised. It shook me up though, and made me very careful. At least a couple other times I had to sit down, or fall down. I spoke to my Neurologist about it on the insistence of my then girlfriend (actually, she told him all about it), and his advice was, and I quote, to "Be more careful!", and "don't worry! It will go away." Gotta like that guy ; )

Another side-effect is blurred vision
. This is rather subtle. I noticed it when I increased my dosage to 10mg because one day I walked outside onto my deck, and the morning was clear. Everything looked sharp. It was then that I realized that I had been having blurred vision, and just didn't notice it. Well, I have it again with the 23mg dose of Aricept. It isn't very bad, but when I am driving, the street signs are a little blurry and harder to read. This is already getting better, and may be completely gone already.

I forgot to mention, I have also gained about 10 pounds since I started taking Aricept. It seems that no matter what I eat, and even if I severely cut down on my calories, I cannot seem to lose this extra weight. Both "Weight Gain", and "Weight Loss", are listed as known side-effects of taking Aricept, so my guess is that my weight gain is related. I have also been taking Ibuprofen, and that can cause a weight gain also, but my best guess is that it is the Aricept. Though I am still at an acceptable weight for my height, I don't like the extra pounds around my middle. But hey! Even though my brain is turning to Lime Jello - I am still "lookin' good"!

According to the research I found, the biggest problem with taking Aricept with bvFTD is the possibility of it making the behavioral symptoms worse. This is difficult for me to evaluate in myself, but I may notice a slight increase in some of my behavioral symptoms. I think I may be having even more difficulty than before initiating actions which translates into just "doing stuff", or getting things done. I am even better than before at procrastinating. Thinking about doing something is just as good as actually doing it. Part of the symptom is that I am happy not doing stuff, so though frustrating after-the fact sometimes, it hasn't been horrible. I still manage to go shopping, and pay the bills on time ...mostly. My attention issues may also be slightly worse. Of course, that may all be due to the normal progression of my disease. There is no way for me to tell for sure.

So, except for some insomnia, and gastrointestinal distress occasionally, I think I am doing well taking the Aricept 23. Some may ask, "Why put up with all the discomfort?" The answer is that for me the benefits far outweigh the minor inconvenience of the side-effects.

As I mentioned in my earlier post, some beneficial changes in me that I and others have noted in the first 12 weeks when I started taking Aricept included: being able to do mental math again, not using a daily to-do list, quicker thinking and speech. I am generally more like my "old self".  All of those benefits have continued, or even improved with the increased dosage.

I still don't really have too many ways to objectively evaluate any benefits. I can still say that without a doubt I feel like my thinking is sharper, and my cognition has improved. Subjectively I think I have seen a huge improvement regarding my Dysexecutive Syndrome, and maybe a slight improvement in attention. As I recounted in my earlier post, the only objective test is that I can now add a couple numbers in my head, and do other mental math. The example I gave then was: "I was at a store a couple days ago, and as I was being checked out I was adding the stuff up in my head as it was being tallied into the cash register. When the total was given, I was confident enough in my math capability to question it because it was about $22 higher than what I had added it up to be. I was right! I had been double charged for a bag of a hundred wine corks!"

Additionally, I was out counting frogs again last week. It is finally Spring, or it was there for a few days at least, and the frogs were happily singing. At the end of the count, I tallied up the sheet. My friend, whom I have been counting frogs with for the past 10 years was astounded. According to her, last year I was unable to tally up the count sheets at all, and had great difficulty with even the simplest arithmetic. I zipped through the sheet easily last week totaling the counts. It seemed effortless to me, and I loved it! It made me feel really good to see such a positive change.

I could not add up the tally sheet a year ago, and another person also noticed the change! So, in my opinion, Aricept is helping. Aricept is helping a lot! I am also still taking a couple of herbal supplements as well, specifically Ginkgo and Melatonin. I strongly believe that the combination of the Ginkgo and the Aricept is having a huge impact. The two have been shown to interact in numerous studies, and as soon as I started taking the Ginkgo Biloba I noticed an increase in the effects of the Aricept. Of course, it may also increase the adverse side-effects. Maybe it is a coincidence... if you believe in that sort of thing. I take 120mg Ginkgo Biloba in the morning and again at night. There is more about  Ginkgo Biloba here.

But remember, all of that is just a bonus. I am not taking Aricept to improve my FTD symptoms. My purpose in taking it is to slow or stop the progression of my bvFTD. If I can gain even a couple years any nasty side-effects (except the itching!) would be well worth it. Unfortunately there is no way I can think of to objectively measure if it is working to slow the progression or not. Only time will tell.

 So, I am going to continue taking the Aricept 23 as long as I can afford it - it is expensive even with my current insurance - and there are no other adverse effects. I am also going to continue to explore other options such as Alternative Medicine, and Namenda (Memantine) in the coming weeks.

Everything here is my account of what happened to me, or my interpretation of stuff. Every case of FTD is different. Keep in mind as you read this that the person who wrote this has Frontotemporal Degeneration. That would be ME.  Medical Disclaimer.

Questions and Comments are welcome.

Wednesday, March 16, 2011

Melatonin may may act as an antioxidant in the brain - So I take it

A flock of sheep that leisurely pass by
One after one; the sound of rain, and bees
Murmuring; the fall of rivers, winds and seas,
Smooth fields, white sheets of water, and pure sky -
I've thought of all by turns, and still I lie
                ~William Wordsworth, "To Sleep"

One of the dietary supplements I have been taking for several months is Melatonin. Melatonin is available from just about any source that carries supplements. It is a very inexpensive supplement, and has a long track record for safety. I do not seem to have any nasty side-effects though an occasional very vivid dream may occur after taking it. Nothing out of the ordinary, but more vivid is the best way I can describe those dreams I associate with taking melatonin.

I do not take Melatonin to help me sleep. Taking Melatonin does not seem to have any affect on my quantity, or quality, of sleep. I typically sleep for a few hours, and then wake up. I frequently get up in the middle of the night, and watch TV or read for a couple hours before going back to sleep. I get about 8 hours of sleep a night - just not all at once. I generally do not feel tired during the day though sometimes I take a short afternoon nap or rest.

So? If I do not take Melatonin to help me sleep, why am I taking it? I take Melatonin because it is a strong antioxidant, and is particularly active in the brain. Melatonin has been shown to provide some protection from cell death due to collections of Tau proteins, and specifically Amyloid Plaques. Sounds pretty good to me! Did I mention the part about it being very inexpensive, and safe? Once again there is little downside to this one, and a huge possible benefit if it can help to slow the progression on my bvFTD. That is the purpose in just about everything I take - to try and slow the progression of the disease. If something helps with my symptoms, that is great, but it is a bonus rather than the true purpose. One of those extra bonus features is that Melatonin may also provide a huge boost to the immune system.

The following information is collected from many places, but I think it gives a pretty clear reason for me to give it a try - and every once in a while I do get a really great night's sleep out of it ...but maybe that is just a coincidence. I have been taking it nightly for several months without any bad effects. I take between 600-900 mcg per night right before going to sleep in the form of 2-3, 300 mcg pills. If you decide to take it please follow the directions on the package. Too much is probably worse than too little.

What is Melatonin anyway? Melatonin is a natural hormone in the body that helps regulate our circadian rhythm. Melatonin helps the brain to sleep at night, and be awake during the day.

People take melatonin supplements to fight insomnia and circadian rhythm sleep disorders. Prolonged release melatonin has shown good results in treating insomnia in adults over 55. So ot said, but the few people that I talked to have had mixed results, or said it was no help at all in treating their insomnia. Of course I have no idea if they took it correctly, or in the right dosages.

Dr. Crawford, the author of a study on Melatonin and Dementia, explained, “Melatonin does not currently exist as a treatment for dementia but is registered in Europe and the UK for use in older patients. It has proven remarkably safe and virtually free from side effects."

Sundowning & Melatonin - supposedly about 45% of people with dementias such as Alzheimer's or FTD suffer from "sundowning," which often causes heightened afternoon or evening agitation. Not getting enough melatonin is a suspected cause.

There is a clear connection behind this suspicion. In Alzheimer's, the two hallmarks of the disease are amyloid plaques and neurofibrillary tangles (Tangles, for short). In a person with Alzheimer's, these tangles can be found in the part of the brain called the hypothalamus. Tangles in the hypothalamus adversely affect the body's production of melatonin. The implication is that Alzheimer's dries up melatonin production. This throws a wrench into the body's daily rhythm.

To make things worse, a vicious cycle ensues. Melatonin has been shown to prevent hyperphosphorylation of the tau protein in rats. In other words, melatonin prevents tangles.

Therefore, less melatonin means less "tangle-prevention." The result is even more Alzheimer's tangles which means even less melatonin. This cycle could well be why many studies have shown that sundowning can be effectively treated with melatonin supplements in the evening.

Amyloid Plaque & Melatonin

The first published evidence that melatonin may be useful in fighting dementias such as Alzheimer's was the demonstration that this neurohormone prevents neuronal death caused by exposure to the amyloid beta protein. Amyloid beta is a neurotoxic substance that is poisonous to brain cells.

Melatonin also inhibits the aggregation of the amyloid beta protein into neurotoxic microaggregates. These "toxic bunches" form the "plaque" characteristic of full-blown Alzheimer's. By blocking this bunching up of amyloid beta, melatonin helps fight plaque.

Melatonin is produced in the dark, while we sleep, and wanes upon daybreak: bright light signals the production cycle to shut down. It is secreted by the pineal gland, a small organ set behind and between the eyes. The pineal is called the "third eye," a reference to our evolutionary heritage-a time when the pineal may have extended the sensory capacities. The pineal gland serves as the timekeeper of the brain, helping to govern the sleep-wake cycle and, in animals, seasonal rhythms of migration, mating, and hibernation. In the human population, melatonin levels are highest in children, and decline with age.

Melatonin is made from an amino acid called tryptophan. Tryptophan is an essential amino acid-we can get it only from the foods that we ingest. The tryptophan we consume during the day is converted into serotonin, a brain chemical involved with mood. Serotonin, in turn, is converted into melatonin.

(some of this will undoubtedly be dis-proven in the near future)

Although research on melatonin has been ongoing since its discovery in 1958, it is only recently it has attracted high interest. Why? Research breakthroughs over the past decade have revealed some startling properties of this amazing substance:

    * Studies by immunologist Dr. Walter Pierpaoli of the Biancalana-Masera Foundation for the Aged in Ancona, Italy, and various colleagues have shown that melatonin treatments extended the life span of mice by as much as 25 percent. Moreover, mice that had been treated with melatonin not only lived longer, they also appeared younger, healthier, more vigorous, and sexually rejuvenated.
    * Researchers at Tulane University School of Medicine in New Orleans have done studies suggesting that melatonin can stop or retard the growth of human breast cancer cells. Cancer specialists in Milan have added melatonin treatments to chemotherapy and immunotherapy in their treatment of cancer patients. They have found that such patients experienced tumor regression, in addition to living longer and suffering from fewer side effects than patients who received chemotherapy and immunotherapy alone.
    * Studies suggest that melatonin may be a kind of "natural" sleeping pill, inducing sleep without suppressing REM (dream) sleep and without producing side effects, such as those caused by sedatives and other artificial sleep aids.
    * Travelers have found that by using melatonin they can "reset their biological clocks" after flying across one or more time zones. Numerous studies have confirmed melatonin's efficacy in combating jet lag and restoring restful sleep patterns.
    * Melatonin may help to prevent heart disease by lowering blood cholesterol in people with high cholesterol. (Interestingly, melatonin seems to have no such effect on those with normal cholesterol.)
    * In a study conducted by the Medical University of Lodz (Poland) in April 2002, women between ages sixty-four and eighty years took melatonin at bedtime for six months, and were found to have a slight but significant increase in IGF-1 and an increased level of DHEA.
    * New research suggests that melatonin may be effective in combating, treating, or preventing AIDS, Alzheimer's disease, Parkinson's disease, asthma, cataracts, diabetes, and Down's syndrome. Some scientists also believe that it may be the basis of a new estrogen-free birth control pill that combats breast cancer at the same time that it prevents conception.

Studies conducted by pioneering University of Texas melatonin researcher Dr. Russel Reiter show melatonin to be the most potent scavenger of free radicals-unstable molecules that promote cancer and heart disease by damaging DNA, cells, and tissue.

So, that is why I decided to add Melatonin to my cocktail of supplements to try and slow the progression of my disease. Does it work? I don't know, but it seems to have a lot going for it. So, at the end of the day, I take Melatonin.

Even thus last night, and two nights more I lay,
And could not win thee, Sleep, by any stealth:
So do not let me wear to-night away.
Without thee what is all the morning's wealth?
Come, blessed barrier between day and day,
Dear mother of fresh thoughts and joyous health!

                                        ~William Wordsworth, "To Sleep"

Everything here is my account of what happened to me, or my interpretation of stuff, except what I copied from somewhere else. Wikepedia is a constant source of information. Every case of FTD is different. Keep in mind as you read this that the person who wrote this has dementia. That would be ME.
Medical Disclaimer.

Comments and questions are welcome.

Monday, March 7, 2011

Increasing brain enzyme may slow Alzheimer's disease progression; Study finds damaging accumulation of tau proteins removed

"Our research demonstrated that increasing the brain enzyme known as PSA/NPEPPS can effectively block the accumulation of tau protein that is toxic to nerve cells and slow down the progression of neural degeneration without unwanted side effects," said Stanislav L. Karsten, PhD, the corresponding author for the study and a principal investigator at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed). "These findings suggest that increasing this naturally occurring brain peptidase, PSA/NPEPPS, may be a feasible therapeutic approach to eliminate the accumulation of unwanted toxic proteins, such as tau, that cause the neural degeneration associated with the devastating effects of Alzheimer's disease and other forms of dementia."

 See the full article by following the link below.

Increasing brain enzyme may slow Alzheimer's disease progression; Study finds damaging accumulation of tau proteins removed

Comments are welcome.

Sunday, March 6, 2011

Review of FTD Symptoms

The best way to behave is to misbehave.
~ Mae West

A. Behavioral Variant FTD (bvFTD)/Frontal Variant FTD (FvFTD)/Pick's/Frontotemporal Lobar Degeneration (FTLD)

bvFTD is characterized by the insidious onset of personality changes, behavioral abnormalities and poor insight. The division of frontal lobe function into three separate areas (orbitobasal, medial, and dorsolateral) offers a way to understand the clinical presentation of bvFTD. Orbitobasal involvment leads to some of the most common symptoms encountered in this disorder. These include disinhibition, poor impulse control, antisocial behavior, and stereotypical behaviors. Examples of stereotypical, or ritualized behaviors, include insisting on eating the same food at exactly the same time daily, cleaning the house in precisely the same order, or simple repetitive behaviors such as foot-tapping. Ritualized acts may also include the use of a "catch-phrase" and a change in food preference. A patient's decline in social conduct can include breaches of interpersonal etiquette and tactlessness. Verbally inappropriate sexual comments and gestures are common.

Apathy is correlated with the severity of medial frontal-anterior cingulate involvement. Dietary changes are frequent and typically take the form of overeating, i.e. hyperorality, with a preference for sweet foods. Patients also exhibit emotional blunting. Speech output is attenuated and mutism eventually develops. Echolalia and perseveration may be present.

The most common cognitive deficit in bvFTD is an impairment of executive function or working memory, which is indicative of frontal and prefrontal cortex involvement. Other frequently encountered cognitive abnormalities include attentional deficits, poor abstraction, difficulty shifting mental set, and perseverative tendencies. Deficits in planning, organization, and other aspects of executive function become universal as the disease progresses, and this reflects the involvement of the dorsolateral prefrontal cortex.

Within the clinical subtypes of bvFTD, there is marked heterogeneity of clinical presentations, often as a result of differential involvement of brain regions. Some patients are disinhibited, fatuous, purposelessly overactive, easily distracted, socially inappropriate, and lacking in concern. At the other extreme, others are bland, apathetic, inert, lacking volition, mentally rigid, and perseverative. Social behavior has been shown to be more disrupted in patients with predominantly right-hemisphere pathology. Moreover, Mc Murtray., demonstrated that patients with frontal FTD showed hypoactivity and apathy, whereas patients with temporal FTD showed hypomania-like behavior. Decreased insight was associated with right frontal hypoperfusion, while decreased hygiene and grooming with left frontal hypoperfusion. Patients with left hemisphere FTD had early speech and language difficulty but greater normal behavior, whereas patients with right hemisphere FTD had normal speech and language but more frequent inappropriate behavior.

Review the parts of the brain by clicking here.

B. Semantic Dementia (SD)

Temporal FTD, also known as semantic dementia (SD), is associated with bilateral atrophy of the middle and inferior temporal neocortex. The most common initial presentation in these patients is an abnormality of language, which includes loss of memory for words or a loss of word meaning. Patients with SD are often unaware of their difficulties with comprehension. Speech is fluent, but patients tend to use substitute phrases such as "thing" or "that". Patients lose the ability to name and understand words and to recognize the significance of faces, objects and other sensory stimuli. They also show deficits on non-verbal tasks using visual, auditory, and other modalities, suggesting that the key impairment in SD is a breakdown in conceptual knowledge rather than a specific problem with language. Working memory and autobiographical memory, at least for the recent past, tend to be preserved. However, patients with SD perform poorly on standard anterograde verbal memory tests, such as word-list learning.

Behavioral symptoms may occur early or late in the clinical course. Patients with SD may present as less apathetic and more compulsive than those with FvFTD. They may show interpersonal coldness and impairments in emotional processing. Patients with more marked right temporal lobe involvement tend to present with significant changes in personality, such as emotional disturbances, bizarre alterations in dress, and limited, fixed ideas.

Snowden et al., compared behavioral patterns and functional imaging in patients with FTD to those with SD. Whereas lack of emotional responsiveness was pervasive in FTD, it was often more selective in semantic dementia and particularly affected the capacity to show fear. Apathetic FTD patients also had a higher pain threshold, whereas patients with SD had an exaggerated response to pain. Overall, emotional, repetitive, and compulsive behaviors discriminated FTD from SD with an accuracy of 97%.

C. Progressive aphasia (PNFA)

Progressive non-fluent aphasia (PNFA) is a disorder predominantly of expressive language, in which severe problems in word retrieval occur in the context of preserved word comprehension. This disorder is associated with asymmetric atrophy of the left hemisphere. Patients present with changes in fluency, pronunciation, or word finding difficulty. They do not present with behavioral problems until later in the disease. In a study that assessed discourse in patients with both semantic dementia and PNFA, patients with PNFA had the sparsest output producing narratives and had the fewest words per minute.

This was just a short article I found which addressed the differences in the various forms of FTD. I found it to be a good review in a short amount of space. It is important to always keep in mind that every case of FTD is different. Everybody does not have to have all of the symptoms listed, and some of them may never develop. Though current research is correlating parts of the brain affected with behavior, nobody knows much about it yet.

Everything here is my account of what happened to me, or my interpretation of stuff, except what I copied from somewhere else. Wikepedia is a constant source of information. Every case of FTD is different. Keep in mind as you read this that the person who wrote this has dementia. That would be ME.
Medical Disclaimer.

Questions and comments are welcome.