Tuesday, October 31, 2006
And so it occurred to me that as a patient with a chronic disease who needs treatment regularly and who has a fairly long life expectancy, I am a cash cow in the cancer business. Most other patients at this office either beat their cancer, or don’t, and their files probably cover fewer treatments over a shorter period of time. Having chronic lymphocytic leukemia makes me a frequent flyer, so to speak, a prize customer.
So where are my rewards? I mean, airlines have private lounges for their best customers. Even Camping World has something called the President’s Club. Why not a President’s Club for CLL patients?
For example, I might enjoy a private infusion room -- nay, suite -- with a genuine leather recliner, none of that vinyl stuff. And why can’t my IV pole be at least gold-plated? Where, oh where, is my plasma TV? My private nurse? The dessert tray, fer chrissakes?
“Champagne with your Rituxan, sir?”
“Don’t mind if I do.”
But no, I’m stuck in there with the hoi polloi, some of them using cheap, off-patent drugs. I am a Rituxan user. My insurance pays $5,000 a pop for this stuff; in the last three years I have brought this office around $150,000 in gross income. Yet the management is forcing me to root, raccoon-like, for bags of peanuts from an oversized communal snack basket. What is this, the Motel 6 of oncology?
In all seriousness, or at least partial seriousness, there are times when having CLL can be used to one’s advantage. After one recent Rituxan treatment, Marilyn and I went to our favorite hotel in Phoenix. I plopped my bandaged hand on the counter and announced to the twenty-something clerk that I had been doing chemotherapy and that I needed a quiet room in which to rest. This led to a free upgrade.
When Marilyn and I flew to Florida recently during the height of the gels-on-planes scare, we were able to bring a bottle of Purell hand sanitizer on board with us. This required showing the TSA guards a report stating I have CLL and am immune-compromised, which was backed up by me pointing to my neck and saying, “It looks puffy because I have swollen lymph nodes from my leukemia.”
Indeed, at the Miami airport one of the Northwest Airlines clerks fell all over himself being helpful and gladly agreed to give our bags priority handling even though we weren’t flying first class.
The best story I’ve heard came from a fellow patient in the infusion room, not a CLLer, who lost her hair to chemotherapy. While speeding down the freeway, she was pulled over by a cop.
“Officer,” she said, whipping off her baseball cap to reveal her bald head, “I am late for my chemotherapy.”
It worked, of course. No ticket.
Let that be an inspiration to you the next time Cytoxan does nasty things to your hair follicles.
And while I still wish I could get a complimentary foot massage while being hand-fed Godiva chocolates, I'll take what I can get.
Saturday, October 14, 2006
The same could be said of Rituxan and the other CLL treatments. Rituxan is imperfect -- effective in the peripheral blood, only mildly effective in the marrow, chancy in the larger lymph nodes. Other things work better, but at a far greater cost to the immune system. To put it another way, Mussolini made the trains run on time, but was it worth it?
Looking at my situation, the question is: “What really needs to be done?” Not “What could be done if I wanted to do the most possible?” This is an important distinction for a tortoise, or any CLL patient, to make.
So, what needs to be done? The lymph nodes need to be reduced, the spleen needs to be reduced, and the marrow needs to keep treading water.
I have written about my bothersome pelvic nodes. It has been a year since I last started Rituxan maintenance and I am getting rather chunky all over. (Only part of the blame can be placed on excessive consumption of Tire Tread licorice.) The discomfort in my lower left side will only get worse the longer I let things go.
So, how far do I let things go?
Letting things go was Dr. John Byrd’s suggestion to me, and at first I was rather taken with it. Letting the nodes go to 10 cm, double the size of the largest ones I have now. Letting my platelets and/or hemoglobin drop below normal. Letting my spleen get big enough to press on my stomach, making me feel full. Then using his protocol of Rituxan three times a week for four weeks, which he said would have a 40% chance of giving me a partial remission for 10 months. And, afterward, hope that something else would come along, maybe start thinking about a transplant, for which I would need RFC as preparation.
For awhile there I was tempted to put my head firmly in the sand and say “the doctor told me not to worry,” but then I started thinking. (Damned brain!)
The thing is, I am not so anxious to get a transplant. And I see HuMax-CD20 on the horizon. It should provide better disease control than single-agent Rituxan, which has itself probably kept me in Stage 2 and feeling pretty healthy for almost three years now. I can see myself going several more years controlling the disease with better monoclonals before even thinking about starting chemotherapy, let alone a transplant. This is called playing for time.
In Part 1, I talked about how science presents data, but is at a loss when it comes to value judgments. As much as it pains me to disagree with some of Dr. Byrd’s analysis, it has come to pass. Above all other considerations, I must make what I feel is the best value judgment, and I must remain true to myself.
I read Dr. Byrd’s single-agent Rituxan study. In it. 56% of patients at Stage I/II responded to the treatment; that number dropped to 42% of Stage III/IV. Similarly, there was a 56% overall response in patients whose nodes were 2 to 5 cm. That dropped to 40% among those with nodes from 5 cm to 10 cm.
In other words, if I wait until I am sick as a dog and do his Rituxan protocol, there is about a 40% chance it will work, which is exactly what he told me -- “work” being defined in the study as a reduction of 50% in disease bulk lasting for 10 months. If I don’t wait that long, the odds of it working are better.
Another point: Assuming I get that 50% reduction in bulk when my nodes are at 10 cm, that would put me right where I am right now. Given the discomfort from my pelvic nodes, I am not sure that this is the ideal baseline for a remission.
I also read Dr. Susan O’Brien’s single-agent Rituxan dose escalation study from MD Anderson. It told me two things: First, the more Rituxan you give someone, the better the response. Second, at dosages commonly given (375mg/m2 once a week for four weeks) one can expect perhaps a 9% reduction in CLL in the marrow.
Finally, and very, very important in all this, I know how I have responded to Rituxan the first three times I had it. It does very well in my peripheral blood and in nodes up to 2 cm. It is almost useless in nodes bigger than 3 cm. At times, prior to treatment, I have had very small declines in red blood cell count and hemoglobin and it has reversed those declines, indicating perhaps that it has some effect in my marrow. Rituxan sends my spleen, which has been as large as 10 cm below the costal margin, back under my rib cage. When it does this there is usually a bump up in platelets, which had probably been sequestered there.
The Rituxan maintenance idea
If Rituxan were not available and starting chemotherapy were the only option, I would avoid treatment until I was half dead. This is the traditional view held by treatment conservatives, and in a world of few choices, it made sense. But Rituxan is available, and it changes the game for some of us.
There is a hardy band of CLL patients doing single-agent Rituxan. I know of maybe ten through the internet and there are no doubt more. The patient who has been managing the longest on this maintenance (that I know of) has been doing it for about five years. Our choice is unorthodox and experimental, though not off the wall. (Among those who have said they think it makes sense for some patients are Chaya Venkat of CLL Topics, who has written about it extensively, and Dr. Terry Hamblin, who comments on it here. MD Anderson often puts older patients, past age 70, on Rituxan + GM-CSF, aka Leukine, because older people have a harder time with hard chemo.)
The Rituxan maintenance rationale is to keep the disease at bay with the least collateral damage. For most people (but not all) Rituxan is essentially toxicity-free. Most CLL docs don’t think it is worth using by itself given the middling remission it gives. As an academic exercise, they are correct that the depth of remission provided by Rituxan pales in comparison to that given by combination therapy or even individual drugs such as fludarabine. But my body is not an academic exercise.
As Dr. Hamblin famously asks, “What is the aim of treatment?” For me, the answer is to keep me going, nothing more, with the least collateral damage. I don’t care how unpretty my remission is -- that is not the point. Beauty is in the eye of the beholder, and I like looking into the distance and seeing all those beautiful unburnt bridges ready to be used if I need them.
I have used Rituxan maintenance three times thus far. (My first hem/onc wanted me to use fludarabine alone. My second suggested RFC but went along with the Rituxan when I objected. She later quit her practice and I am now on my third hem/onc, who is open-minded and whom I like.) My first treatment was starting January ’04, 8 weeks at 375mg/m2. Second was starting April ’05, 4 weeks at 500mg/m2 (along with some G-CSF (Neulasta) shots to try to boost the effectiveness, which appeared to have little effect). Third was starting October ’05, 8 weeks at 375mg/m2. So it has been a year since I last started treatment.
There is no control to my experiment -– no cloned version of myself who chose another path –- so I can only make educated guesses at what the Rituxan has done for me. I would like to think that I have been keeping the marrow from becoming impacted; Rituxan’s modest effects on it may be just enough. I have kept the node growth reasonable among the smaller nodes, at least. Rituxan has been effective on my spleen. My Rituxan maintenance system has probably allowed me to drag Stage 2 out longer than I might have otherwise.
Now is the time
The deal with Rituxan maintenance is that you are using Rituxan, and Rituxan works better on earlier-stage patients and those with less bulky disease. I could wait longer to treat and take pain meds for my pelvic node(s) -- and more and more of them as the problem grows bigger and bigger, literally -- but what about the marrow? If I were to wait long enough for it to crash, Rituxan’s 9% reduction in CLL will probably be too little too late. I will have boxed myself in, likely leaving myself no choice but to add stronger agents that I would rather avoid.
I meet three of the NCI guidelines for treatment: Spleen swollen greater than 6 cm below the costal margin, lymphocyte doubling time of less than 6 months, and progressive lymphadenopathy.
To recap my prognostics: I am IgVH unmutated; ZAP-70 positive as per the reliable lab at UC San Diego; I tested positive for the 11q deletion on 24% of cells in March; and I am CD 38 negative, a blessed 1%.
Prognostics only tell some of the story. Based on my experience since diagnosis in 2003, I know my disease is steady in advance and can be steadily pushed back. I do not have the wild over-the-top escalation that some patients with my prognostic markers have, and I have so far been spared the sudden onset of major surprises. Maybe that negative CD 38 is helpful in some way, or maybe the planets have aligned right, or maybe I just haven't reached the point in time when the disease starts to go berserk.
For all these reasons, I think it makes sense to treat now if that treatment is to be Rituxan maintenance.
Why not the rest?
As readers of this blog know, I have explored Rituxan + HDMP and Rituxan + chlorambucil as possible options. But since my marrow is holding steady, I do not feel the need to jump to a stronger agent that might clear it better than plain old Rituxan.
I think both options do make sense for people who need better marrow clearance but who wish to avoid heavy-duty chemo combinations.
R + HDMP has been the subject of somewhat spirited debate in patient forums and among leading doctors as well. (I have recounted opposing views by Dr. Januario Castro and Dr. Byrd in this blog.) It is being pioneered in chemo-naive patients at UC San Diego, which has had generally good results with it, and I feel it is best done there, under their watchful and experienced eyes. I would not rule it out as a future treatment for myself under the right circumstances.
R + chlorambucil, advocated by Dr. Hamblin, appears to have good anecdotal results. My concern here is the possibility that alkalyting agents can be mutagenic. There is a study that lumps chlorambucil and cyclophosphamide together and reports a somewhat higher incidence of p53 mutations in patients who have received those alkalytors. While the chance may be small, especially at small doses, acquisition of a p53 (aka 17p) deletion is the last thing I want to bring upon myself. Still, under the right circumstances, I could see using R + low-dose chlorambucil.
My plan: festooning the shark
What I am opting for is the minimal amount of treatment I think I can get away with, but something a little stronger than I have had in the past.
Having a blog means sharing an evolving learning process. I was a little premature in March when I posted “Single agent Rituxan jumps the shark.” Since March, HuMax-CD20 has begun to loom on the horizon, and the likely advent of this promising new tool has changed the outlook for me, as discussed in Part 1.
The treatment plan ahead is single-agent Rituxan with some Beta-Glucan added, probably with a second step involving a steroid tweak.
I looked back at my prior experience with two courses of once-a-week-for-eight-weeks Rituxan. After week 5, I reached a plateau in blood counts and node reduction. Is there a way to improve on that dosing schedule? The O’Brien study showed that the more Rituxan you get, the better. (Yes, yes, Rituxan shaving may be a drawback, but there appears to be something causing it to work better at higher doses.) Byrd’s protocol uses more frequent dosing, three times weekly. By extension, even at 375mg/m2, that gets more Rituxan into you in a shorter space of time.
So, on the theory that more frequent dosing is likely to be no less effective than the once-a-week schedule -- and hopefully more -- I will be following the first half of Byrd’s protocol: six infusions of Rituxan at 375mg/m2 over two weeks. The decision to use half of Byrd’s protocol is made given my past plateau after infusion 5 and the fact that the extra Rituxan may 1) go to waste, or 2) be more than I really need right now, and 3) always carries the risk of developing disease resistance, which I want to keep to a minimum, since I will probably have to use Rituxan maintenance of some kind again before I can use HuMax. Hopefully the shorter, more intense schedule will lead to a more intense result. We shall see.
Added to the mix will be Beta-Glucan, which may have the benefit of boosting macrophage activity and thus the cell kill. Researchers at the University of Louisville in Kentucky are now accruing CLL patients for a Rituxan + Beta-Glucan clinical trial. The Beta-Glucan they are using is available commercially.
Failure to clear the larger nodes adequately –- I am not expecting miracles here, just a decrease in discomfort -- would lead to Step 2. After an interval designed to allow the body’s complement to recover from the Rituxan, I would receive a course or two of dexamethasone (Decadron), perhaps 20 mg daily for four days. The idea is to push the CLL out of the nodes and into the bloodstream, where Rituxan can get at it better. I have done some research on dex and it is lympholytic on its own –- that is, it kills CLL cells (though it is not a major player in this department).
The question of whether it would have synergy with Rituxan is another matter and there are no definite answers, it seems. It may, or it may tamp down macrophages and the CDCC (complement dependent cytotoxicity) and ADCC (antibody dependent cytotoxicity) that helps with the Rituxan cell kill. So after administration, there would be a wait of a week or two before doing two final rounds of Rituxan -– enough to clear the dex from my system without allowing the CLL to return in large numbers to the nodes. (The immunosuppressive effects of the dex may well continue for some time, despite the wait; sometimes there are no elegant options. Also, as I have skin cancer issues, I will also be monitored by a dermatologist.) Since Rituxan works best in the peripheral blood, it will hopefully kill off some of the formerly node-based CLL. Again, we shall see, but there is little downside in trying.
(As an aside, one reason not to frontload the dex is to avoid the possibility of tumor lysis syndrome, since I already anticipate significant cell-kill during the first week. Another reason is not to gum up the works -- I know I get my best response from Rituxan after the first two or three infusions, and I would just as soon let it do its thing before doing anything that might inadvertently dampen its effects.)
In the end, I am hoping for 8 or 10 or 12 months of CLL control, with the nodes knocked back further than when I started, a petite spleen, and any decline in the marrow arrested. And “control” is the operative word. Call my hoped-for remission incomplete, crappy, or whatever name you wish. As my father once said when asked many years ago why he wasn’t going to get rid of his clunky old 1967 station wagon, “It gets me from Point A to Point B.”
That’s my goal.
Monday, October 09, 2006
The search for what to do next led to my Doctor Quest, which I have described at length in these pages. I explored options such as Rituxan + high dose methylprednisolone (HDMP), Rituxan + chlorambucil, and even Rituxan + fludarabine, and I picked the brains of a few leading experts. This being chronic lymphocytic leukemia, of course, I got different and even contradictory answers. But in the process I have become more familiar with my case, what the criteria might be for treating it, and the options for that treatment. I also had a chance to mull over the conventional wisdom as well as some opposing viewpoints about depth of remission, long-term survival, and various other things that go bump in the night.
And now, here I am, ready to embark on a course of treatment. I will tell you what I have decided, and why.
I have decided who is in charge
Meeting with some top doctors, as well as some lesser lights, I quickly realized what so many CLL patients learn: four rabbis, five opinions. Or, as one world-renowned expert told me about my treatment timing and prospects, “There isn't a right or wrong answer. I could construct an argument for almost any approach.”
So the one thing I have learned in my Doctor Quest is that nobody knows my disease quite like I do. Or, as I wrote to a friend of mine, “After seeing all the experts and learning all I can, I have learned one thing: my guess is as good as anyone's and it is all a crapshoot.”
This is not hubris. I may be a fairly well-educated patient, but my knowledge of the disease pales in comparison to that of the experts. We patients need our doctors, and I have learned a great deal in my conversations with them. I would not want to be left to my own devices even if I could buy Rituxan at Costco and set up an IV pole next to the living room sofa. Doctors are needed not only for their expertise but also for their skill and experience at monitoring symptoms and managing complications that can blindside us. And not every patient has the time or inclination to make the effort I have made to get to know the lay of the land. Nor does everyone have the same personality type; some people would rather just pick a doctor they are comfortable with and follow that person’s advice. I respect that choice, which seems on the surface to be quite sensible.
For me, personally, it is not enough given the uncertainty that surrounds CLL. I am the recipient of a disease without consensus, a disease termed “heterogeneous” because it is about as individual as a fingerprint, and mine in particular is rather quirky. Understanding of CLL is in flux, old assumptions are being questioned, new treatment ideas go every which way. The experts are left to debate and disagree among themselves. And you and I are cursed with living in interesting times. I wish it were easier to be a patient, but it’s not.
In terms of how to put it all in perspective, someone named Andy once left a comment on this blog that offers sage advice:
“Nothing can substitute for common sense, especially when one's life hangs in the balance. Science is indispensable to the understanding of the pros and cons but when it comes to making a value judgment, science has nothing to say -- that's something many patients (and many doctors as well) fail to grasp.”
So, while I know that I will never have the scientific knowledge of a John Byrd or a Januario Castro, my ability to make the right value judgment is probably equal to anyone’s. And since my life is on the line, I had better become adept at it.
I have decided what makes common sense to me
The more I have learned, the more I am convinced that, as a rule, less is more when it comes to treatment. The least toxic route to disease control is to be preferred to nuking the sumumbitch and risking very real complications that I have written about many times, that CLL Topics has warned about many times, that Dr. Terry Hamblin’s blog has discussed many times, and that basically fall under one category: I done blowed up my CLL and my immune system’s all shot, too.
If there is one thing I fear more than death by CLL, it is becoming sickly and having a lousy quality of life, being in and out of the hospital, being at the mercy of every bacteria or virus that comes waltzing along. CLL means my immune system is in decline -- this is why our immunoglobulins drop -- but why speed up that process?
I said this was my view “as a rule.” There are exceptions. There are people whose marrow becomes impacted, whose platelets and hemoglobin drop to dangerous levels, whose nodes grow to enormous size, and who have no choice but to do something pretty drastic to clear the marrow and deal with the problem. I may be one of those people one day, and if that time comes, I will welcome fludarabine, cyclophosphamide, and god knows what else with open arms and open veins.
But now is not that time.
I have decided I am a tortoise
I know, you’re thinking “What has Dave been smoking? Does he also think he’s the Eggman, coo-coo-ca-choo?”
Let me explain about the tortoise and the hare and how it applies to CLL.
There is a school of thought, the conventional wisdom, that depth of remission leads to longer overall survival. This may make sense in many cancers, but does it hold true in CLL? One problem is that long-term studies are very difficult to do, and CLL is a long-term disease. A must-read is Dr. Hamblin’s “What is the aim of treatment?” series. In it, he posits that the acute leukemia model, in which a cure is the desired goal, may not be realistic in CLL.
“Most doctors who design clinical trials for CLL have trained as acute leukemia doctors, “ Hamblin writes. “Faced with a disease that may span decades they revert to type. Pharmaceutical companies are not much interested in a clinical trial that may last 20 years -- their patents will have run out. Current clinical trials, by common consent, have abandoned overall survival as an end-point; instead they have adopted “complete response rate” and “progression free survival” as surrogates. There are problems with both of these . . .”
Hamblin goes on to discuss this in detail, and I will leave it to you to read his thoughts (see “Resources” below) if you have not already done so. His views may be somewhat heretical on this topic, but that does not make them wrong.
The point is that there is not sufficient evidence, to my mind, that depth of remission will lead to longer overall survival for all CLL patients. The problem is that patients relapse from those deep remissions and are left with fewer treatment choices. Another big-name doctor told me that the weakest spot in CLL therapy is finding things that work on the fludarabine-refractory. And there is plenty of anecdotal evidence, at least, that some patients who get big remissions set themselves up for other big problems in the process, notably immune suppression that can lead to life-threatening complications.
So, will you live longer by running hard out of the gate, or by plodding along only as fast as you need to?
My intuition says to bet on the tortoise.
The tortoise rewarded
Good things come to he who waits, or at least he who moves slowly. HuMax-CD20, the monoclonal antibody, has received fast-track status from the FDA and is now in Phase III trials. Everything I read and hear, officially or through the grapevine, is that this stuff puts Rituxan to shame. It adheres better to the CLL cell, it leads to better cell kill, and being fully-humanized it guards against some of the nasty allergic reactions that can accompany mouse-based Rituxan.
For those of us who have been saying “Do the minimum you need to do, avoid burning bridges if you can, keep your immune system as functional as possible to maximize the effectiveness of new drugs that may come along,” HuMax-CD20 is evidence of our logic, the proof in our pudding. I would be shocked if it were not approved for commercial distribution sometime in 2008, at the latest.
So, how does this tortoise get from here to there?
I’ll conclude my thoughts in Part 2.
Dr. Terry Hamblin's three-part "What is the aim of treatment?" series:
Part I: http://tinyurl.com/qgd2f
Part II: http://tinyurl.com/rxnpt
Part III: http://tinyurl.com/rmjv5
Thursday, October 05, 2006
Having chronic lymphocytic leukemia, I have another strike against me: the prospect of getting "chemo brain" from heavy-duty chemotherapy, should it ever become necessary. This is one of the hidden dangers of CLL and most cancer therapy, and yet another reason to avoid the alphabet soup treatments such as RFC. RFC+M, CFAR, et al until you have no choice and really need to use them.
Researchers tend to talk about "multiple non-overlapping toxicities" and doctors tend to use phrases like "well-tolerated" when describing some of these regimens. (I suppose whatever doesn't kill you is something that, grading on a curve, you can tolerate well.) But in plain old common sense English, pump your body full of stuff that destroys cells and don't be surprised if it does something in the brain.
Of course, chemo brain is one of those areas that is not really the subject of too many studies. After all, drug companies have little incentive to reveal yet another potential problem with their products. And researchers looking for a cure or effective control may feel their time is better spent on that rather than on tracking down amorphous side effects that can vary from person to person. Type "chemo brain" in quotes into PubMed and you get exactly three results (though there are other areas which better catalog the information available -- see "Resources" below).
It is on internet CLL patient forums that one hears stories about chemo brain: people becoming disoriented and not knowing where they're going when they're driving down the street, people who go to work and can no longer answer the phone and type into the computer at the same time. Some people seem to be spared these sort of effects, some have mild or transient cases, some have long-term problems.
Depression complicates matters
Chemo brain is a very real risk, though matters of depression and stress can lead to an impression of brain fog in some people that may not be entirely chemo-related.
A PubMed abstract of a 2003 study at the University of Indianapolis provides this analysis:
"Oncology patients often complain that their "mind does not seem to be clear." This subjective perception, sometimes referred to as "chemo brain," may be due to situational stressors, psychological disorders, organic factors, or effects of neurotoxic medications. Cognitive decline cannot only diminish quality of life, but can also interfere with a patient's ability to make decisions regarding complex treatment issues."
The authors of the study tried to quantify and clarify the results in 61 patients. They found this to be difficult, and concluded: "While the perception of cognitive impairment is common in cancer patients, there may be problems in interpreting the nature of these complaints, particularly in separating them from depressive preoccupation."
Certainly depression can lead to reduced clarity of thought and action. Many older people have CLL and may already be experiencing a bit of brain slowdown as part of the natural aging process. But chemo brain cannot be dismissed as a figment of the imagination. A study reported today by UCLA researchers finally pins down in hard science what many cancer patients have felt to be true all along.
New study: chemo alters brain metabolism
Entitled "Chemo has long-term impact on brain function: study," Reuters reported the following:
Chemotherapy causes changes in the brain's metabolism and blood flow that can last as long as 10 years, a discovery that may explain the mental fog and confusion that affect many cancer survivors, researchers said on Thursday.
The researchers, from the University of California, Los Angeles, found that women who had undergone chemotherapy five to 10 years earlier had lower metabolism in a key region of the frontal cortex. Women treated with chemotherapy also showed a spike in blood flow to the frontal cortex and cerebellum while performing memory tests, indicating a rapid jump in activity level, the researchers said in a statement about their study.
"The same area of the frontal lobe that showed lower resting metabolism displayed a substantial leap in activity when the patients were performing the memory exercise," said Daniel Silverman, the UCLA associate professor who led the study. "In effect, these women's brains were working harder than the control subjects' to recall the same information," he said in a statement.
Experts estimate at least 25 percent of chemotherapy patients are affected by symptoms of confusion, so-called chemo brain, and a recent study by the University of Minnesota reported an 82 percent rate, the statement said.
"People with 'chemo brain' often can't focus, remember things or multitask the way they did before chemotherapy," Silverman said. "Our study demonstrates for the first time that patients suffering from these cognitive symptoms have specific alterations in brain metabolism."The article goes on, and this link will take you to the full text.
But the message is simple: chemo brain is real, and it is a risk. Yes, there have been no studies of it in CLL, but there is more than ample anecdotal evidence that some people are affected by it. For those of you who feel your body is crumbling but "at least I have my mind," take heed.
The website http://www.chemobraininfo.org/ offers a fairly encyclopedic roundup of studies and other information.