Saturday, December 31, 2011
"When I was a student at Cambridge I remember an anthropology professor holding up a picture of a bone with 28 incisions carved in it. "This is often considered to be man's first attempt at a calendar" she explained. She paused as we dutifully wrote this down. 'My question to you is this – what man needs to mark 28 days? I would suggest to you that this is woman's first attempt at a calendar.' It was a moment that changed my life. In that second I stopped to question almost everything I had been taught about the past. How often had I overlooked women's contributions?"—Sandi Toksvig
In the history of CFS, it will be WOMEN'S contributions that tell the story -- while the men are obfuscating and politicking, it was Elaine DeFreitas and Judy Mikovits working quietly behind the scenes to find the truth. THANK YOU, LADIES!
Friday, December 30, 2011
It's not a frequent topic of discussion, but doctors die, too. And they don't die like the rest of us. What's unusual about them is not how much treatment they get compared to most Americans, but how little. For all the time they spend fending off the deaths of others, they tend to be fairly serene when faced with death themselves. They know exactly what is going to happen, they know the choices, and they generally have access to any sort of medical care they could want. But they go gently. Of course, doctors don't want to die; they want to live. But they know enough about modern medicine to know its limits. How has it come to this—that doctors administer so much care that they wouldn't want for themselves? The simple, or not-so-simple, answer is this: patients, doctors, and the system.
Ken Murray MD, Clinical Assistant Professor of Family Medicine at USC, Zocalo Public Square, Nexus
And to those points, I say "Hooray! Thank you!", and, "I hope the lessons you impart can spread to every other medical student and doctor who can possibly benefit from what you will teach them!" Further, I hope those lessons will be taught (and perhaps pounded into) those doctors practicing today who have already gone off the arrogance charts - those who are, unfortunately, teaching today's medical students how to behave tomorrow.
But yes, there is a downside, and that is, that such a topic needs an expensive, $42 million institute at all. If doctors would simply approach their work using a combination of the Golden Rule, and the manners their mothers taught them, and regard their patients with the dignity and respect their patients deserve, then those $42 million could be put to a much loftier use - toward finding a cure toward a debilitating disease, or improving infant mortality, or helping indigent patients get some of the care they need.
Thursday, December 29, 2011
Defending the indefensible?
Margaret Williams 27th December 2011
Professor Simon Wessely once again attempts to defend what has already been shown to be indefensible, namely his own beliefs about the nature of ME/CFS, including his belief that graded exercise therapy (GET) has "an impeccable safety record" (Simon Wessely; Health in mind and body; The Journal of the Foundation for Science and Technology: 2011:20:7: 9 –11).
The article contains so many insupportable assertions that it cannot go unchallenged.
In his article, although he does not mention ME as such, Wessely refers to Chronic Fatigue Syndrome (CFS), but in countless articles published in medical journals, reports from official bodies such as the Joint Royal Colleges, in medical textbooks and in the media, as well as in the PACE Trial literature itself, the Wessely School insist that ME and CFS are synonymous.
In this latest article (the publishing of which is perhaps surprising, given his frequent assertions that he has relinquished his work on ME/CFS and that he no longer feels safe publishing about the disorder because of the death threats he has received, and that he now feels safer in Afghanistan), Wessely conforms to his track record of appearing to form his conclusions before he has generated the data to support his conclusions (he often states his assumptions and beliefs as though they are established fact, for example, he has asserted that people with ME benefit from "adopting the sick role" and from "secondary gain", and that what "precipitates" ME is not what "perpetuates" it, all of which are supposition not supported by data; a further illustration is to be seen in his study of Vitamin B status in just 12 CFS patients in which he found evidence of reduced functional vitamin B status but concluded: "clearly, many patients with CFS are currently taking vitamin B…with little evidence of benefit", yet nowhere does he provide any evidence that "many" patients are taking supplements with little evidence of benefit and his final conclusion again fails to follow from his data: JRSM 1999:92:183-185).
Wessely's assertions in his current article are of particular interest because they provide such clear illustration of his cognitive biases, for example:
"CFS illustrates the gap that lies between physical health/illness on the one hand and mental health/illness on the other": all life-destroying diseases affect both physical and mental health, not just ME/CFS.
"CFS is a multi-factorial illness": Wessely does not know this, since the cause remains unknown.
"To understand why some people do not get better as the months and years go by, one has to look at behavioural and psychological factors": this is nothing more than Wessely's assumption; people do not recover from multiple sclerosis or from motor neurone disease, so it is telling that he makes an exception only in the case of one particular classified neurological disorder (ME/CFS): why do so, unless it is as a face-saving measure because for the last 25 years the Wessely School have rigidly and unscientifically conflated psychiatric fatigue with ME/CFS?
"The illness is then a complicated mixture of predisposition, precipitation, and perpetuation": Wessely states this as though it were proven fact, but it is unproven and his inability to recognise this demonstrates a fundamental misunderstanding of the nature of scientific knowledge.
"A landmark trial on the management of CFS, known as the PACE Trial, was published recently in The Lancet….Two treatments, graded exercise and CBT, clearly made a difference, although they were certainly not 'magic bullets': not only were the interventions used in the PACE Trial very far from being magic bullets, the Chief Principal Investigator himself described them as being "only moderately effective".
"For those who appreciate these things, the trial is a thing of beauty": for those who appreciate these things, the PACE Trial -- which cost £5 million -- has been described as a travesty of science and a tragedy for patients; the conclusions were flawed; the primary outcome measures were dropped; ratings that would qualify a participant as sufficiently impaired to enter the trial were deemed by the Principal Investigators (PIs) to be "within the normal range" when recorded on completion of the trial; there were significant conflicts of interest in that all three PIs work for the insurance industry (whose managers insist that claimants undertake a course of CBT and GET -- called "rehabilitation" -- which, if people are too ill to do so or if they know from their own experience that it makes worse and therefore decline, payments are stopped on the basis that claimants do not to want to get better); the PIs intentionally studied a heterogeneous population and it was conceded only after publication of the results in The Lancet that the Investigators did not purport to be studying ME; there was a failure to control the trial; there was downgrading of what constituted serious adverse events; there were many changes to the entry criteria; data was not reported and objective outcome measures were dropped; methods of scoring were changed so as to produce minimally better results, and the results were blatantly misreported in The Lancet (see http://www.meactionuk.org.uk/COMPLAINT-to-Lancet-re-PACE.htm and see also http://www.meactionuk.org.uk/Normal-fatigue.htm ).
"We now have two treatments that we can recommend with confidence to our patients. However, the story does not quite end there. Patient groups rejected the trial out of hand, and the internet was abuzz with abuse and allegations. The main reason for this depressing reaction was the stigma that attaches to disorders perceived (rightly or wrongly) to be psychiatric in origin": the reason people with ME/CFS reject CBT and GET is because they do not work, but Wessely refuses to accept this, so he here provides an explanation already shown by his own research to be incorrect.
He has previously written: "CFS sufferers are also usually portrayed as hostile to psychological explanation, mental illness, and psychiatry in general….This study aims to investigate attitudes of CFS patients to psychiatric illness (and) a comparison group of patients with rheumatoid arthritis (RA) was chosen….We began with the following hypotheses: CFS patients have more negative attitudes to mental illness…(represented by the perceived stigma of psychiatric illness)…(and) failure to identify emotional states (alexithymia) contributes to denial of the role of psychiatric disorders in the aetiology of CFS….Contrary to our hypotheses and the media accounts of CFS, we found no evidence that CFS patients are characterized by particularly hostile attitudes to mental distress….Our study also failed to demonstrate any overall differences in personality traits that may underlie negative attitudes to mental illness or psychiatry….The… alexithymia scores found in the CFS compared with the RA patients were contrary to our original hypothesis….There was no difference between CFS and RA patients in hostility to mental illness….This study provides no evidence to support the anti-psychiatry tone that is so striking in the popular literature on CFS" (Personality and Social Attitudes in Chronic Fatigue Syndrome. Barbara Wood and Simon Wessely; J Psychsom Res 1999:47:4:385-397).
"If one obtained identical results to the PACE trial, but this time with anti-viral drugs, the reaction would have been totally different. This is exactly what did happen when a very small trial of a drug that modulates the immune system (and which has some nasty side effects) was greeted with acclaim from the same sources that tried to discredit the PACE trial, which tested interventions with an impeccable safety record": GET for people with ME does not have an impeccable safety record. Indeed, there is abundant evidence from numerous surveys by ME/CFS charities of almost 5,000 patients that in such patients CBT is ineffective and that GET is unacceptable and sometimes positively harmful.
Those surveys include one sponsored jointly by the ME Association and Action for ME ("Report on a Survey of Members of Local ME Groups". Dr Lesley Cooper, 2000). Cooper found that "Graded exercise was felt to be the treatment that made more people worse than any other" and that it had actually harmed patients
Another survey of 2,338 ME/CFS sufferers ("Severely Neglected: M.E. in the UK") was carried out in 2001 by Action for ME; its preliminary report stated: "Graded exercise was reported to be the treatment that had made most people worse"; in the final report, this was changed to stating that graded exercise had made 50% of patients worse
The 25% ME Group for the Severely Affected carried out a further survey in 2004 which found that 93% of respondents found GET to be unhelpful, with 82% reporting that their condition was made worse (http://www.25megroup.org/Group%20Leaflets/Group%20reports/March%202004%20Severe%20ME%20Analysis%20Report.doc).
In 2005, a report ("Our Needs, Our Lives") published by The Young ME Sufferers Trust found that 88% had been made worse by exercise (http://www.tymestrust.org/pdfs/ourneedsourlives.pdf).
In June 2007, through Section 16b funding from the Scottish Government, Action for ME produced a report "Scotland ME/CFS Scoping Exercise Report", which found that 74.42% were made worse by GET.
In 2008, Action for ME published another survey of over 2,760 patients ("M.E. 2008: What progress?") which found that one third had been made worse by GET and that at their worst, 88% were bed/housebound, being unable to shower, bathe or wash themselves, and that 15% were unable to eat unaided. The Press Release of 12th May was unambiguous: "Survey finds recommended treatment makes one in three people worse" (http://www.afme.org.uk/news.asp?newsid=355).
In 2009, the Norfolk and Suffolk ME Patient Survey of 225 respondents stated: "Respondents found the least helpful and most harmful interventions were Graded Exercise Therapy and Cognitive Behavioural Therapy" (http://www.norfolkandsuffolk.me.uk/surveylink.html ).
The International Association of CFS/ME recently published an article by Tom Kindlon (Bulletin of the IACFS/ME: 2011:19(2):59-111: Reporting Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) that details the high rates of adverse reactions to exercise, as well as dissecting the PACE Trial in relation to the heterogeneity of subjects, the tracking of adverse events and the lack of objective outcome measures.
As Ed Lewisohn correctly points out in correspondence relating to the Frenchay Hospital's clinic at Bristol: "You refer to 'Frenchay Hospital's specialist chronic fatigue, or ME clinic', but ME is an incurable neurological condition and cannot be synonymous with chronic fatigue. Chronic fatigue syndrome is treated by psychiatrists with graded exercise therapy, but if exercise makes (it) better, then that condition is not ME….But many patients with ME are also sent to chronic fatigue centres and receive the same treatment: they are then, shockingly, made more ill" (http://www.thisisbristol.co.uk/chronic-fatigue-syndrome/story-14243686-detail/story.html ).
There is thus an abundance of empirical evidence that GET can result in high rates of adverse effects.
Why is it that the Wessely School, who claim to be so committed to evidence-based medicine (EBM), are permitted to continue to disregard the evidence that proves them to be wrong about the nature of ME and about the efficacy of GET in those suffering from it?
The answer may be because, like so many of the Wessely School myths, EBM does not actually exist.
In 2009 Bruce Charlton, Professor of Theoretical Medicine at the University of Birmingham, clarified the facts in relation to EBM: "It is obvious that EBM was from its very inception a Zombie science….A Zombie science does not perform any scientific function, so it is invulnerable to scientific critique since it is sustained purely by the continuous pumping of funds….The massive success of EBM is that it has rationalised the takeover of UK clinical medicine by politicians and managers….Zombie science is not driven by the scientific search for truth (and it is) kept moving for so long as it serves the purpose of its funders….EBM embraced a top-down and coercive power structure to impose EBM-defined 'best evidence' on clinical practice, whether clinical scientists or doctors agreed that the evidence was best or not….Expertise was arbitrarily redefined (and) virtue redefined as submission to EBM recommendations, so the job of physician was at a stroke transformed into one based upon absolute obedience to the instructions of EBM-utilising managers. Indeed, since too many UK doctors were found to be disobedient to their managers, in the NHS this has led to a progressive long-term strategy of the replacing doctors by more-controllable nurses, who are now the first contact for patients in many primary and specialist health service situations…. EBM was not a real science, indeed, it wasn't any kind of science at all (and) it was not adopted by scientists but by politicians, government officials, managers, and biostatisticians….When the UK government understood that what was being proposed was a perfect rationale for re-moulding medicine into exactly the shape they had always wanted it, the NHS hierarchy were falling over each other in their haste to establish this new orthodoxy in management, medical education and in founding new government institutions such as NICE….Suddenly, the Zombie science of EBM was everywhere in the UK…unhampered by inconveniences such as truthfulness or integrity…it was being practised by many individuals…who lacked…any training and experience in clinical medicine and who certainly did not provide direct patient care….Here was a doctrine which advocated rejecting and replacing with itself the whole model of medical science and practice of the past. It advocated a new model of health service provision, new principles for research funding, a new basis for medical education. And the evidence for this? Well, none. Not one particle. 'Evidence-based' medicine was based on zero evidence (but it) was proclaimed Messiah with the backing of serious amounts of UK state funding…to create a fairly-realsitic Zombie of pseudo-science….Nowadays, EBM means whatever the political and managerial hierarchy of the health service want it to mean for the purpose in hand" (Zombie science of Evidence-Based Medicine. Bruce G Charlton. Journal of Evaluation in Clinical Practice 2009:15:930-934).
EBM, however, has proved invaluable to the Wessely School in the perpetuation of their own myths about and management of ME/CFS, to the advantage of both the state and the insurance industry.
Despite the relentless determination of the Wessely School to claim ME/CFS as a functional somatoform disorder (in his latest article, Wessely reiterates his claim that: "the greater the number of symptoms, the more likely the patient was to develop a mood or anxiety disorder"), medical science is at last ensuring that the Wessely era is coming to an end.
Whilst XMRV is now thought to be a laboratory contaminant (and the triumphant glee of those who rejoiced at this is to be greatly deplored), the role of a retrovirus has not yet been resolved: indeed, Dr Ian Lipkin of Columbia University and chief virus-hunter for the NIH was reported on the Wall Street Journal blog on 27th December 2011 by Amy Dockser Marcus to have said that all the scientists and doctors involved in the NIH study, including the authors of the retracted PNAS and Science papers, "are committed to completing this study because none of us believes that the issue of retroviral infection in CFS/ME is resolved".
Retrovirology apart, there is now undeniable evidence of multi-system damage in ME/CFS, including inflammation of the blood vessels, hypoperfusion of the brain, delayed recovery of muscles after exercise, dysfunction of the immune and neuroendocrine systems, and evidence of marked abnormalities in gene expression profiling.
Professor Nancy Klimas is to head a new Institute for Neuroimmune Medicine (specifically ME/CFS) at Nova Southeastern University: she will be providing cutting edge research and education of health care professionals, combined with care of patients; she will focus on systems biology, connecting neuro-imaging experts with scientists researching inflammation and genomics/proteomics, as well as collaborating with experts in neurotoxicology.
There is also the work of Dr Jose Montoya's Chronic Illness Initiative at Stanford; the husband and wife team of Drs Light at the University of Utah; Dr Derek Enlander's Chronic Fatigue Initiative with a very large budget for research at Mount Sinai, as well as the Public Health and Neuroimmunology Unit (PHANU) at Bond University in Australia (http://forums.phoenixrising.me/content.php?519), plus the committed work of Professors Mark VanNess and Christopher Snell at the University of the Pacific, all of which disprove the beliefs of the Wessely School that ME/CFS is a behavioural disorder.
Furthermore, the UK Medical Research Council has finally recognised the need for biomedical research into ME/CFS and is funding £1.6 million for research into aspects including autonomic dysfunction, aberrant mitochrondrial and cytokine production in skeletal muscles, and immune system dysfunction.
As clinical psychologist Dr Dorothy Rowe pointed out in 1993: "People who know absolutely that they are right are very dangerous" (The Observer, 14th November 1993), but who paid any attention? Father Cormac Rigby did: "The greatest enemies of truth are those who think they have a monopoly of truth" (The Lord be with you; Family Publications, Oxford, 2004).
Wednesday, December 28, 2011
For those of us who still believe in "innocent until proven guilty," a legal defense fund has been set up for Dr. Mikovits:
Mikovits Legal Fund 2031 Jamestown Way, Oxnard, CA 93035 or donate online at
and for questions or well wishes, please send to: [email protected]
Monday, December 26, 2011
Second XMRV-CFS Paper Pulled
Another shoe drops as authors retract PNAS chronic fatigue syndrome-virus paper
Authors retract paper on detection of murine leukemia virus-releated
sequences in CFS patients
Scholars Retract Another Study Linking Virus to Fatigue Syndrome
The Lo-Alter team's findings have come under scrutiny as possibly due to contaminants associated with common laboratory reagents. Phylogenetic analysis conducted by Katzourakis et al. and other groups suggest the sequences identified by Lo et al. in samples from CFS patients collected 15 years apart were not consistent with evolutionary change and were likely due to contamination of the samples with 22RV1, a prostate cancer cell line. The work by Katzourakis is cited in the retraction notice by the authors, although they also state, "there has been no evidence of contamination using sensitive mouse mitochondrial DNA or IAP assays or in testing coded samples…"
Sunday, December 25, 2011
Neurobiology underlying fibromyalgia symptoms.
Ceko M, Bushnell MC, Gracely RH.
Alan Edwards Centre for Research on Pain, McGill University, 3640
University Street, Room M19, Montreal, QC, H2A 1C1, Canada.
Fibromyalgia is characterized by chronic widespread pain, clinical
symptoms that include cognitive and sleep disturbances, and other
abnormalities such as increased sensitivity to painful stimuli,
increased sensitivity to multiple sensory modalities, and altered pain
Here we relate experimental findings of fibromyalgia symptoms to
anatomical and functional brain changes. Neuroimaging studies show
augmented sensory processing in pain-related areas, which, together
with gray matter decreases and neurochemical abnormalities in areas
related to pain modulation, supports the psychophysical evidence of
altered pain perception and inhibition.
Gray matter decreases in areas related to emotional decision making
and working memory suggest that cognitive disturbances could be
related to brain alterations.
Altered levels of neurotransmitters involved in sleep regulation link
disordered sleep to neurochemical abnormalities.
Thus, current evidence supports the view that at least some fibromyalgia symptoms are associated with brain dysfunctions or
alterations, giving the long-held "it is all in your head" view of the disorder a new meaning.
What Do the Psychophysical, Cognitive, and Neuroimaging Studies Tell
Us about the Neurobiology Underlying FM Symptoms?
The wealth of experimental evidence showing that FM patients are
hypersensitive to painful stimuli, as well as unpleasant stimuli from
other sensory modalities, in conjunction with functional brain imaging
data showing increased stimulus-evoked activation throughout
nociceptive pathways, shows that the defining symptom of FM—increased
pain—is in fact real and not just a response bias of the patients. The
finding that perception is increased in multiple modalities speaks
against the hypothesis that FM pain is due to an upregulation of
peripheral nociceptive processes. Further, psychophysical evidence
that descending modulatory systems are altered in FM patients supports
the opposing idea that FM symptoms are at least in part caused by
alterations in CNS processing of the pain signal, including a
dysregulation of pain modulatory systems. Nevertheless, the apparent
dysregulation within these systems could be caused and/or perpetuated
by a tonic activation related to the presence of ongoing widespread
pain, so that the systems are saturated and cannot regulate further in
response to external stimuli.
Since similar descending control systems, including attentional and
emotional regulatory circuitry, affect multiple sensory modalities
[113–119], a dysfunction (or saturation) in these systems could lead
to the hypersensitivity in multiple sensory modalities. FM patients
show reduced habituation to nonpainful tactile stimuli and increased
cortical response to intense auditory stimuli, both of which have been
linked to deficient inhibition of incoming sensory stimuli [120, 121].
Also in support of the idea of a central dysregulation or saturation
of pain modulation are changes in the opioid and dopamine
neurotransmitter systems, both known to be involved in hedonic
Finally, the findings that FM patients not only perceive themselves to
have altered memory and concentration ("fibrofog"), but also in fact
perform poorly on multiple cognitive tests, even when depression is
excluded as a contributing factor, suggest that there are alterations
in brain function. The anatomical brain imaging studies that show
reductions in gray matter in frontal regions important for cognitive
function further indicate that this common symptom of FM is based on
altered brain function. Together, the experimental evidence provides
strong support for the idea that FM symptoms are related to
dysfunctions in the central nervous system. The cause of these changes
cannot be deduced from the available evidence, as it is correlational
in nature. Did long-term ongoing pain cause the changes or did the
changes cause the pain? Without a relevant animal model or long-term
longitudinal studies, we cannot answer these questions.
Nevertheless, we can at least say that fibromyalgia is real and that it is associated with multiple changes in the brain.
PMID: 22135739 [PubMed - in process]
The full study can be found here:
some assumptions are tricky.
Misinterpretations of bodily symptoms as being depression or anxiety,
especially in diseases (and psychiatric disorders) lacking diagnostic
testing, may confound the results of studies and inflate estimates of
psychiatric co-morbidities. There is also always the danger of mixing
people without a disease in with people with a disease - which also
confounds study results.
As well, many doctors may assume psychiatric comorbidity instead of
asking the patient. Treatments are only efficacious if there is something to treat and assuming a psychiatric co-morbidity where none exist has the potential to create iatrogenic harm.
On the other hand, if a disease process involves the brain it may
create psychiatric problems such as in some seen in Lyme associated
disorders. There is much that remains unknown. Whether a virologist or
a psychiatrist if all you have is a hammer everything looks like a
Fibromyalgia: Mind-Body Disorder
Question:"I am seeing more and more patients come to my office saying
they have fibromyalgia. How should I conceptualize them? Do they have
a body disease, or a mind disease?"
Rakesh Jain, MD, MPH: The answer to your excellent question is - yes,
you guessed it, both! To consider many disorders as Mind-Body
Disorders is not just "politically correct," it is actually
scientifically highly accurate to do so, and it also helps shape, for
the better, our therapeutic offerings.
Mind-Body Disorders have been the focus of our work for many years,
and the four of us—Drs. Draud, Maletic, Raison, and myself—who
participate in this Community Forum on a rotating basis have been
deeply and positively affected by this changing paradigm. We have
become firmly convinced, based on both our experiences and the huge
amount of literature out there, that this Mind-Body approach is both
accurate and highly therapeutically beneficial to our patients.
Nothing exemplifies this crucial point better than the example of
Fibromyalgia is a disorder that until recently was described as a
disorder with widespread, unexplained pain only, and therefore thought
only to be a "body" disorder. You can easily see why this mistake was
made, right? The thinking was, "The patient's body hurts – well then,
of course it's a body disorder! Why drag the poor innocent brain and
mind into it?"
This mistake was so widespread that the 1990 American College of
Rheumatology criteria for fibromyalgia did indeed entirely focus on
the body and its pain.1 And that's it. It completely ignored several
facts, including the shockingly high rates of depression, anxiety,
insomnia, obesity, and cognitive difficulties that these unfortunate
patients suffered right alongside the pain.2-7The simplistic
explanation was, "They have all these problems, wouldn't you too be
depressed, anxious, etc if you had chronic pain?"
Well, the only problem with this simplistic explanation is that it's
not accurate. Don't you hate it when hard data and cold facts kill all
of our previous theories?! Multiple epidemiological studies show that
poor physical health, anxiety, depression, and insomnia can actually
precede the development of fibromyalgia.8-12 This, along with recent
neurobiological findings (we will discuss these shortly) then forces
you and me to confront a more complex, but ultimately more integrative
view of fibromyalgia – that it is actually a true Mind-Body Disorder.
The evidence to support this new Mind-Body paradigm is so striking
that the American College of Rheumatology's proposed revised criteria
for fibromyalgia actually now incorporates "mind" symptoms such as
depression and unrefreshing sleep into the diagnostic criteria. Such
true progress in a relatively short time is to be celebrated by
clinicians all over!2,13,14 True progress in conceptualizing this
disorder as a Mind-Body Disorder has been made.
At this point, I sincerely hope I have whetted your appetite to
examine some seriously impressive research studies. I will say, and
stand by it too, that the evidence for Mind-Body disruption in
fibromyalgia is so strong that no other explanation for this disorder
will work. For example, we know that even though it is body pain these
patients report, the clearest evidence for malfunction appears to be
at the level of the dorsal column of the spinal cord.15,16 Here,
evidence points to poor pain modulation being a key disruption,
thereby leading to the excessive pain perception.17,18 But the story
does not end here. We also have striking evidence pointing to cerebral
cortex disruption (both anatomic and functional) in fibromyalgia
afflicted patients, with high quality evidence from volumetric MRIs
and functional MRIs all suggesting one thing: the pathology is as much
in the brain as it is in the body.19-21
Let's look at the smoking gun evidence that now implicates and
explains the enormously high psychiatric burden these patients endure.
The brain areas I discussed above (anterior cingulate cortex, medical
prefrontal cortex, to name just a few) are also involved with stress,
mood, anxiety, and sleep regulation. Now you can see why we
conceptualize many disorders, including fibromyalgia, as Mind-Body
What clinical implications arise from this emerging Mind-Body view?
This question deserves attention from us as well. Let's first examine
the errors that have been made because we initially did not use a
Mind-Body approach with fibromyalgia. By solely focusing on pain
alone, we used to treat this condition solely with analgesics, and
that led to suboptimum outcomes. Now that the field utilizes a
Mind-Body treatment approach, things are improving. We now have 3
FDA-approved medications (pregabalin,22 duloxetine,?23 and
milnacipran24) that have the ability to modulate neurotransmitters in
both the spinal column and the brain. We also have integrated
non-pharmacological treatment modalities (such as yoga, physical
exercise, cognitive-behavioral therapies) that are all genuinely
Mind-Body in their approach to helping the patient.25-32This progress
has come about truly as a result of the emergence of the Mind-Body
approach to understanding and treating the condition. (By the way,
using this Mind-Body paradigm in explaining disorders to patients and
their families has been a very successful psycho-educational technique
in my practice.)
I suspect this change to the Mind-Body paradigm will become standard
for more and more disorders with the passage of time. I truly believe
that we, the forward-looking clinicians, should rush to embrace this
model as it appears to offer both the best explanation, as well as the
best outcomes for our patients.
—Rakesh Jain, MD, MPH
medications and or supplements for long stretches of time your doctor
should be monitoring your blood and organ function on a regular basis.
If your doctor is not doing this and is not willing to do this then it
may be time to find another doctor if you have that option. Or you may
wish to discuss other individualized treatment options. Everything
has drawbacks/side-effects regardless of whether it is a drug, a
supplement, an artificial device, surgery or even inappropriately
applied exercise or CBT. Evaluating and re-evaluating therapies on an
individualized basis is important no matter what the therapy is.
NSAID Dangers in Fibromyalgia & Chronic Fatigue Syndrome
By Adrienne Dellwo, About.com Guide
Do you take anti-inflammatories on a regular basis? A lot of people
withfibromyalgia and chronic fatigue syndrome do. We don't know of any
special dangers we face from them, but because our conditions are
chronic, many of us take them for decades.
Because we often take medications associated with more high-profile
side effects, such as narcotics and antidepressants, it's easy to
forget that non-steroidal anti-inflammatories (NSAIDs) can be
dangerous. That goes for over-the-counter meds -- Advil, Motrin
(ibuprofen), Aleve (naproxen) -- as well as prescription ones. Here's
a story shared by a reader here:
"I took [NSAIDs] for 25 years and in 2008, they almost killed me. My
kidneys were failing and my liver enzymes were high and I had fatty
liver. For 3 months I was flat on my back and could only eat a few
bites a day and forced a few swallows of water and was in terrible
pain. .... I finally found out it was the NSAIDs and stopped taking
them and the kidneys and liver healed. Watch for any problems with the
NSAIDs." - Char
Char's story makes me really grateful for my primary doctor, who keeps
a close eye on my kidney and liver function. A couple of years ago, my
liver enzymes were really high, which put me at risk for fatty liver
and cirrhosis. That scared me! In response, I weaned off of the
prescription NSAID I'd been taking for years. When we checked a few
months later, the levels were much closer to normal.
It wasn't easy for me to go without daily NSAIDs. Fibromyalgia isn't
linked to inflammation (except for possibly in the fascia), but my
autoimmune thyroid condition is. My rheumatologist also thinks I have
a rare condition that causes my body to hold on to inflammation. (Some
cases of chronic fatigue syndrome involve inflammation, as do many of
our overlapping conditions.)
As expected, not taking NSAIDs did make me puff up. To counter that, I
increased my Omega-3 and rhodiola supplements and worked to get more
anti-inflammatory foods into my regular diet. My doctor also referred
me to massage to help me through the transition.
I do still take NSAIDs from time to time, but not on a daily basis,
and usually only when I have an injury or when my thyroid condition
flares. We're continuing to watch my levels, and so far, I'm doing
Of course, NSAIDs aren't the only drugs that can be hard on our liver
and kidneys. Narcotics, antidepressants, anti-seizure drugs, Tylenol
(acetaminophen) ... all of them can damage the liver and/or kidneys,
depending on how they are processed. Any of us who are taking
medications long term need to be aware of their impact on our overall
Saturday, December 24, 2011
The retraction of Lombardi et al by Science is not the end of the story. Negative studies looking at only XMRV are not relevant. Because XMRV is gone, Dr. Coffin and other scientists cannot go beyond their data as they have done and say that HGRVs do not cause CFS and by extension other human disorders. I counsel these scientists to not exclude other evidence which I have to believe they are fully aware of and will repeat below.
As a physician I am used to looking for as much evidence, from as many aspects as possible before excluding a diagnosis. This includes clinical evidence; after all we are not just test tubes. For example, the classic laboratory tests for B12 deficiency can be negative and yet the patient can respond to B12 administration. In this latter case the penalty for dismissing the diagnosis prematurely would be brain and spinal cord damage for the patient. As physicians, we know that there are indeed false positive lab findings but also, and just as importantly, false negative results. The textbook picture exists only in the textbook.
The first chapter of our story was written 30 years ago from three independent laboratories, including Robert Gallo's at the NIH. Lest the scientists forget this, the studies proved the association of MLRVs and human disease.
The second chapter is mine. As you know, I tested positive in Dr. Mikovits laboratory for antibodies to MLRVs. As you know, both my leukemia and my CFS have responded to ARVs. If I had listened to Dr. Coffin's advice to not take ARVs, I would have lost at least 18 months of life. Dr. Coffin and Science have seen my results. The only comment Dr. Coffin made was that it had to represent "selective toxicity" which as an Oncologist with 40 years' experience, I can confidently exclude.
Bruce Albert of Science never commented but relies heavily on Dr. Coffin's judgment. I presented my data at a peer-reviewed Hematological Malignancy conference at MD Anderson Cancer Institute in 2010 and it was well received. including by the physician that is considered the premier researcher in my leukemia, Dr. Kanti Rai. I am just one patient, but I am a typical patient and I am told the association of HIV and AIDS was initially made with data from only a few patients.
So where does that leave us? Research will continue. We still have some scientists with enough courage and wisdom not to abandon the quest. There is a virus, or viruses and these will be found. This story will never end, despite Dr. Coffin and Science. The viruses are likely to be involved in many more disease processes and the world will be a better, or at least healthier place, when they are tamed.
Michael Snyderman, MD
Friday, December 23, 2011
Clinic opens after $1 million donation from Doctor Enlander's patients
By MOLLY MULDOON, IrishCentral Staff Writer
Published Friday, December 23, 2011, 8:13 AMUpdated Friday, December
23, 2011, 8:13 AM
An Irish doctor has launched a specialized research clinic in New York
for chronic fatigue syndrome (CFS) at the Mt. Sinai Hospital in
"I believe that an independent organization such as ours, which is not
funded by the government or answerable to the government, can be the
leader in new research," said Dr. Enlander.
The Mt. Sinai research team includes a geneticist, an immunologist and
a virologist. The center was established as a result of a $1 million
private donation from one of Dr Enlander's patients.
"I am very proud of it, we have got terrific people on board," Dr
Enlander told the Irish Voice.
"This is a very important center, it is the only ME/CFS center
attached to a major medical school," he added.
Dr Enlander has been a long-time advocate of the debilitating illness,
which he says many doctors misdiagnose.
"This is not a psychological disease," he notes, adding, "It's a
Born in Belfast, Enlander entered medical school at the age of 17.
"I wanted to be a doctor since I was five years old," he recalls.
He originally came to the U.S. in the sixties when he was offered a
fellowship to study at Stanford University Medical School.
"They gave me a faculty position in New York after Stanford," he said.
A faculty member of Mount Sinai Medical School, Dr Enlander is an
attending physician at Mount Sinai Medical Center in New York.
According to the Enlander's diagnosis, ME/CFS (myalgic
encephalomyelitis/chronic fatigue syndrome), is a debilitating and
complex disorder characterized by profound fatigue that is not
improved by bed rest and that may be worsened by physical or mental
Symptoms include fatigue, loss of memory or concentration, unexplained
muscle pain, and extreme exhaustion. It is most prevalent among women
in their 40s and 50s.
The doctor's interest in the condition began while on vacation in
Ireland almost two decades ago when an old school friend was suffering
"He told me he felt terrible and it and it spurred my interest," he recalls.
Two decades later, the Irish doctor has established himself as leading
profession in the illness, having conducted extensive research.
Up to 75 percent of Dr Enlander's patients are female between the ages of 18-52.
"This is not just ordinary tiredness, this is a debilitative disease," he noted.
With patients travelling from England, Ireland, Peru, France,
Bulgaria, and Romania, there is a great demand for his specialty.
"Patients have travelled from all over the world to see us," he noted.
The definite cause of CFS has not yet been identified, but the New
York based doctor's research has led him to believe that the disorder
is connected to the immune system.
"We believe that CGS is an immune system dysfunction," said Enlander,
"People used to think patients were imagining that they were sick as
all their blood tests were normal, doctors didn't pay as much
attention," he notes.
"The longer they have had it, the longer it takes to recover," he said.
The Belfast born doctor offers various treatment plans for the
illness. The Manhattan research facility is working with Hemispherx
Biopharma, a biopharmaceutical company, based in Philadelphia, to
examine the potential of the drug Ampligen, as a treatment for CFS.
Worldwide, 17 million people suffer from the syndrome, including at
least one million Americans, according to the New York Times.
For more information log onto www.enlander.com.
Read more: http://www.irishcentral.com/news/Irish-doctor-opens-new-chronic-fatigue-syndrome-clinic-in-NYC-136017443.html#ixzz1hNjiLK8I
Thursday, December 22, 2011
Pacing is a strategy which helps patients with ME/CFS limit exertion-related increases in symptomatology.
Pacing is appropriate for those who operating near or at their maximum level of functioning, and for individuals with neurological and immunological abnormalities.
Pacing may be offered as part of an individualized, multi-component management programme.
Read More: http://informahealthcare.com/doi/abs/10.3109/09638288.2011.635746
Pacing is a strategy which helps patients with ME/CFS limit exertion-related increases in symptomatology.
Pacing is appropriate for those who operating near or at their maximum level of functioning, and for individuals with neurological and immunological abnormalities.
Pacing may be offered as part of an individualized, multi-component management programme.
Read More: http://informahealthcare.com/doi/abs/10.3109/09638288.2011.635746
Wednesday, December 21, 2011
Monday, December 19, 2011
is a psychiatric disorder, with a symptom of a disease. Disorders can
be concurrent with any disease, but they are not a symptom. A symptom
is any morbid phenomenon or departure from the normal in structure,
function, or sensation, experienced by the patient and indicative of
disease. Depression for example, can be experienced separately from
Chronic Fatigue Syndrome vs. Depression: One Doctor's View
By Adrienne Dellwo, About.com Guide December 17, 2011
For decades, people with chronic fatigue syndrome (ME/CFS) have
battled the misconception that they were "just depressed." Many
doctors and a large chunk of the general public believe that myth - in
spite of a wealth of research showing numerous physiological
abnormalities across multiple systems.
In a recent comment here, a doctor (obviously one of the good ones!)
left a comment that really rung true with me and I think is the best
description I've ever seen of the difference in mentality between
depression and ME/CFS:
"In my years of practice I have seen hundreds of pain sufferers with
depressed mood, but only a couple of patients with true clinical
depression. One of the features of true depression is anergy or the
lack of desire to do anything (it is very difficult to put this in
words). Another feature of clinical depression is "social apathy" or
having no desire to participate in social activities. These features
are exceedingly rare in people suffering from all types of chronic
pain and/or ME. Indeed, ME sufferers uniformly have an unabashed
yearning to be able to DO things, to participate in life!" - Doc
I really think the doctor summed it up perfectly. In the 4 years I've
been hearing personal stories about ME/CFS, I've come across a lot of
people who say they miss the things they used to do, that it hurts
them to stay home when everyone else is off having fun, or perhaps
that they've given up trying to participate because they pay so dearly
afterward. However, I just don't hear people say that they don't want
to do things anymore.
Certainly, some people with ME/CFS become depressed. That's true of
every single chronic, debilitating illness out there. When illness
hits you out of the blue, derails your life, takes away myriad things
that you love and that provide you with a sense of worth, and leaves
you miserable and disabled ... um, yeah. It's depressing! Depression
is a major issue in cancer and no one blames the tumors on depression.
Likewise, it's being falsely implicated in ME/CFS. The same logic
applies to fibromyalgia.
I've seen the difference first hand...
Read the entire article here:
Sunday, December 18, 2011
Whittemore Peterson Institute vows to get past setbacks
Written by Lenita Powers
9:01 PM, Dec. 17, 2011
The Whittemore Peterson Institute for Neuro-Immune Disease in Reno
made headlines around the world in 2009 when news spread that its
researchers had discovered XMRV, a new retrovirus that might lead to
breakthroughs in the treatment of chronic fatigue syndrome and other
Two years later, aspirations of Reno becoming the mecca of a medical
breakthrough that could lead to treatment for chronic fatigue, an
illness that affects an estimated 17 million people worldwide,
evaporated when the research was discredited.
But the latest blow came this year when Dr. Judy Mikovits, the
Whittemore Peterson Institute's lead researcher behind the discovery
of XMRV, was fired in September for "insubordination and insolence."
In November, she was arrested on felony charges for allegedly
enlisting a fellow researcher to steal research notebooks and other
proprietary materials from the institute.
Annette Whittemore, president and founder of the institute, calls the
discredited research and Mikovits' arrest "a bump in the road" that
will not stop the institute's commitment to finding the cause and, she
hopes, a cure for chronic fatigue syndrome.
"The whole issue, until it is resolved, has a lot of people confused
and wondering whether we will be going forward and whether the federal
government is still going to be committed," she said, referring to
federal research grants and other funding. "There is more federal
funding for this disease than ever, and they're deeply committed."
Two current grants from the National Institutes of Health totaling
about $660,000 were made to the WPI, not to Mikovits, Whittemore said,
so those funds will remain with the institution.
More research under way
The WPI is continuing its research into the underlying causes of
neuroimmune diseases, including finalizing two research projects
involving gamma retroviruses and several studies related to the innate
"We're as committed as ever," Whittemore said. "Ultimately, this
institution is looking for the right answers, and nothing else
matters. So we are going to continue to do the good work and find the
answers to the best of our ability and make sure others can reproduce
and confirm that good work."
Meanwhile, the implosion of the institute's research with XMRV and the
firing of Mikovits has frustrated chronic fatigue syndrome patients.
"I was cautiously optimistic at beginning," said 73-year-old Penny
McCracken, a Fallon resident who has struggled with the illness since
"I'm just kind of resigned now," she said. "It's like, 'Oo-ha, here we
go again.' We've seen promising things fall apart before."
Whittemore is keenly aware of the disappointment, anger and even
mistrust voiced by people with chronic fatigue syndrome who have
commented on WPI's website, blogs and other sites on the Internet. In
a recent interview at the institute's office, she recently addressed
those comments as well as what she said was the real reason Mikovits
At the nearly two-hour interview, Whittemore was joined by Vincent
Lombardi, who has replaced Mikovits as the WPI's lead researcher.
Whittemore refuted claims being made on the Internet that Mikovits was
fired because the Whittemore family was trying to make money from
tests being conducted to detect XMRV in patients with chronic fatigue,
but Mikovits opposed the $400 to $650 cost for the tests as being too
Whittemore said WPI did not receive funds from the tests, and she said
the comment by one person on the Web who called the Whittemores greedy
was "very hurtful. Our family has given millions of dollars over the
last 40 years in support of charitable organizations, including WPI,"
VIPdx, the Reno laboratory that conducted the tests, is a privately
owned laboratory and is not affiliated with WPI, Whittemore said.
VIPdx did pay to license the use the technology from WPI to do the
testing, but that money was used by WPI to help fund its research.
And, despite news reports to the contrary, Mikovits was not fired
because she refused to share her research cell lines with other WPI
scientists, Whittemore and Lombardi said.
"In fact, those cell lines weren't shared," Lombardi said. "They
belonged to me, and she took them."
Lombardi said he had asked Japanese researchers who had built a cell
line to share it with him.
"When you publish research using a cell line you have developed, then
you're kind of obligated to share it with anybody who wants to use it,
and they said they would be happy to do that," he said.
Lombardi said the package with the cell line has his name on it, but
it apparently was sent to Mikovits' laboratory.
"She took them and never told me they came. When I called FedEx to
track them down, I found out that she had them. I asked her for them
back, and she said 'no' when they weren't even hers. So I talked to
Whittemore said she confronted Mikovits, who refused to return the
cell line to Lombardi, so she fired her for insubordination.
"And what she did interfered with (Lombardi's) ability to complete his
study," Whittemore said.
Petitioners support Mikovits
Mikovits, who is facing a civil lawsuit and criminal charges filed in
Washoe District Court, could not be reached for comment. Her lawyer,
Scott Freeman, also declined to discuss his client's case.
And researchers who had worked with her at the National Cancer
Institute or were listed as co-researchers on the XMRV article
published in Science refused to return telephone calls or hung up when
they were contacted by the Reno Gazette-Journal.
However, Orlando, Fla., resident Patricia Carter has created an online
petition in support of Mikovits that garnered about 380 signatures,
which Carter said would be sent to the U.S. Senate and the Whittemore
Peterson Institute. The petition calls for the institute to "treat
Mikovits fairly," return to her any research material that was hers
and refrain from taking any legal or other action that would
"intentionally damage Dr. Judy Mikovits' reputation of credibility."
However, Whittemore said Mikovits had signed a contract stating that
all research material belongs to the institute.
Peterson's new center
Earlier this year, a new research player came onboard in search for a
cause and treatment for neuroimmune diseases.
Dr. Daniel Peterson, the doctor who treated hundreds of Chronic
Fatigue Patients during an outbreak in Incline Village in the 1980s,
resigned from the Whittemore Peterson Institute that bears his name
and opened his own nonprofit research foundation in Incline Village.
Neither Peterson nor the director of the Simmaron Research Inc.
returned repeated telephone calls, but the research foundation's
website cites its mission as "playing a key role in bringing science
to the clinician to better diagnose, treat and manage patients" who
have chronic fatigue syndrome and myalgic encephalomyelitis.
Simmaron Research is working in collaboration with Sonya Marshall and
colleagues at the Bond University of Australia and Konnie Knox with
the Wisconsin Viral Research Group.
K. Kimberly McCleary, president of the Chronic Fatigue and Immune
Dysfunction Syndrome Association of America, said the high-profile
split with Mikovits at the Whittemore Peterson Institute, the
investigation by Science into the XMRV research paper and ensuing
legal actions "are of deep concern" to many of those in the patient
and scientific communities.
"Because of the hope that XMRV raised for better care, Dr. Mikovits
and the WPI have both attracted considerable support that is now being
tested as details of civil and criminal charges are made public,"
McCleary said. "We remain concerned for the well-being of all who are
affected by this dispute and hope that the various investigations will
yield an equitable resolution."
She said her organization will continue to focus on research to
improve the diagnosis and treatment of chronic fatigue syndrome, "and
efforts to end the life-altering disability, stigma and isolation CFS
For 17-year-old Rebecca Ghusn of Reno, who suffers from chronic
fatigue syndrome, the failure to link XMRV to her illness is just
another false lead in the scientific hunt to find a cause and a cure.
"You always hope something will happen when they find a lead, but they
had lots of leads, so this is just one step forward and two steps
back," she said. "And I think the whole XMRV thing was blown out of
proportion, but, yes, it was disappointing."
UNR research untainted
The WPI is not part of the University of Nevada, Reno, but the
institute's office and laboratories are housed in UNR's Center for
Molecular Medicine, a state-of-the-art facility that opened August
2010 and to which the Whittemores donated an undisclosed amount of
But the widely reported fact that the XMRV research has been
discredited and the lawsuits pending against Mikovits that have now
enveloped WPI won't impugn the credibility of the research being
conducted by the university's scientists, said Marc Johnson, UNR's
"The Whittemore Peterson Institute is located on our campus, although
it is independent of the university," he said. "The institute is in
the midst of a challenging time, and the university is noted in many
media reports as the location of the institute. However, this
geographic relationship does not detract from or even relate to the
outstanding caliber of work being done by our university researchers."
Johnson said Annette and Harvey Whittemore have been good friends of
the university and have made significant contributions to the
community and state.
"We wish them well in their scientific endeavors," he said.
Saturday, December 17, 2011
"If you have access to a swimming pool through your community, YMCA, or health club, consider water-based exercises, such as water aerobics classes. Water removes the pressure of gravity and supports your body while providing a little bit of strengthening resistance. Immersion in water can also be very good for the circulatory system.
"And remember: The most important step of all is the very first one. Just get started, and you can modify your routine from there."
Germans found that Vitamin D increases the immune system by 3-5 times and is better than any vaccine at helping the immune system beat the h5n1 (bird flu) virus. Watch the video. The Canadian is a socially progressive and not-for-profit national newspaper, with an international readership. We provide an alternative to the for-profit commercial focused media, which often censors vital information and perspective of potential interest to the diverse Canadian public, and other peoples internationally.
* New Report - Vitamin D Better Than Vaccines At Preventing Flu
Oliver Gillie, The Times
Friday, December 16, 2011
SITES AND USE IN NEWSLETTERS. PLEASE TWEET AND RE-TWEET ON TWITTER.
Whitehaven News Letters.
Following the publication of a letter about M.E. in the Whitehaven News
(8 December 2011), we have received a very kind offer of help, from a
reader, Joyce, to visit or shop for an M.E sufferer in the locality.
Since Joyce is herself an MCS (multiple chemical sensitivity) sufferer,
who remains well as long as she does not come into contact with
synthetic fragrances and especially VOCs (volatile organic compounds)
emitted from clothes treated by perfumed laundry products, she can only
be of assistance if the M.E. sufferer lives in a chemically free home,
Please contact [email protected] and we shall be
happy to introduce you.
We are publishing this internationally, especially in the M.E. Community
support groups, with permission to forward and re post, in order that
this good example may be followed to help reduce the social isolation
faced by so many people with this dreadfully disabling illness.
[email protected] org
Dr John H Greensmith
ME Community Trust. org
Thursday, December 15, 2011
reprinted in LOST magazine from his collection, "In the Shadow of Memory."
LOST will soon cease publication but is paying tribute to the 10 most
accessed pieces, including our friend Floyd's.
Gray Area: Thinking With a Damaged Brain
My entire brain, the organ by which my very consciousness is controlled,
was reorganized one day ten years ago. I went to sleep here and woke up
there; the place looked the same but nothing in it worked the way it used to
by Floyd Skloot
I used to be able to think. My brain's circuits were all connected and I
had spark, a quickness of mind that let me function well in the world. There
were no problems with numbers or abstract reasoning; I could find the right
word, could hold a thought in mind, match faces with names, converse
coherently in crowded hallways, learn new tasks. I had a memory and an intuition
that I could trust.
All that changed on December 7, 1988, when I contracted a virus that
targeted my brain. A decade later, my cane and odd gait are the most visible
evidence of damage. But most of the damage is hidden. My cerebral cortex, the
gray matter that M.I.T. neuroscientist Steven Pinker likens to "a large
sheet of two-dimensional tissue that has been wadded up to fit inside the
spherical skull," has been riddled with tiny perforations. This sheet and the
thinking it governs are now porous. Invisible to the naked eye, but readily
seen through brain imaging technology, are areas of scar tissue that
constrict blood flow. Anatomic holes, the lesions in my gray matter, appear as a
scatter of white spots like bubbles or a ghostly pattern of potshots. Their
effect is dramatic; I am like the brain-damaged patient described by
neuroscientist V.S. Ramachandran in his book Phantoms in the Brain: "parts of
her had forever vanished, lost in patches of permanently atrophied brain
tissue." More hidden still are lesions in my Self, fissures in the thought
process that result from this damage to my brain. When the brain changes, the
mind changes — these lesions have altered who I am.
"When a disease process hits the brain," writes Dartmouth psychiatry
professor Michael Gazzaniga in Mind Matters, "the loss of nerve cells is easy to
detect." Neurologists have a host of clinical tests that let them observe
what a brain-damaged patient can and cannot do. They stroke his sole to test
for a spinal reflex known as Babinski's sign or have a him stand with feet
together and eyes closed to see if the ability to maintain posture is
compromised. They ask him to repeat a set of seven random digits forward and
four in reverse order, to spell "world" backwards, to remember three specific
words such as "barn" and "handsome" and "job" after a spell of unrelated
conversation. A new laboratory technique, positron emission tomography, uses
radioactively labeled oxygen or glucose that essentially lights up
specific and different areas of the brain being used when a person speaks words or
sees words or hears words, revealing the organic location for areas of
behavioral malfunction. Another new technique, functional magnetic resonance
imaging, allows increases in brain blood flow generated by certain actions
to be measured. The resulting computer-generated pictures, eerily colorful
relief maps of the brain's lunar topology, pinpoint hidden damage zones.
But I do not need a sophisticated and expensive high-tech test to know what
my damaged brain looks like. People living with such injuries know
intimately that things are awry. They see it in activities of daily living, in the
way simple tasks become unmanageable. This morning, preparing oatmeal for
my wife Beverly, I carefully measured out one-third cup of oats and poured
them onto the pan's lid rather than into the bowl. In its absence, a
reliably functioning brain is something I can almost feel viscerally. The zip of
connection, the shock of axon-to-axon information flow across a synapse, is
not simply a textbook affair for me. Sometimes I see my brain as a scalded
pudding, with fluky dark spots here and there through its dense layers and
small scoops missing. Sometimes I see it as an eviscerated old TV console,
wires all disconnected and misconnected, tubes blown, dust in the crevices.
Some of this personal, low-tech evidence is apparent in basic functions
like walking, which for me requires intense concentration, as does maintaining
balance and even breathing if I am tired. It is apparent in activities
requiring the processing of certain fundamental information. For example, no
matter how many times I have been shown how to do it, I cannot assemble our
vacuum cleaner or our poultry shears or the attachments for our
hand-cranked pasta maker. At my writing desk, I finish a note and place the pen in my
half-full mug of tea rather than in its holder, which quite obviously teems
with other pens. I struggle to figure out how a pillow goes into a
pillowcase. I cannot properly adjust Beverly's stereo receiver in order to listen
to the radio; it has been and remains useful to me only in its present
setting as a CD player. These are all public, easily discernible malfunctions.
However, it is in the utterly private sphere that I most acutely experience
how changed I am. Ramachandran compares this to harboring a zombie,
playing host to a completely nonconscious being somewhere inside yourself. For
me, being brain damaged also has a physical, conscious component. Alone with
my ideas and dreams and feelings, turned inward by the isolation and
timelessness of chronic illness, I face a kind of ongoing mental vertigo in which
thoughts teeter and topple into those fissures of cognition I mentioned
earlier. I lose my way. I spend a lot of time staring into space, probably
with my jaw drooping, as my concentration fragments and my focus dissolves.
Thought itself has become a gray area, a matter of blurred edges and lost
distinctions, with little that is sharp about it. This is not the way I used
In their fascinating study, Brain Repair, an international trio of
neuroscientists — Donald G. Stein from America, Simon Brailowsky from Mexico, and
Bruno Will from France — report that after injury "both cortical and
subcortical structures undergo dramatic changes in the pattern of blood flow and
neural activity, even those structures that do not appear to be directly
or primarily connected with the zone of injury." From this observation, they
conclude that "the entire brain — not just the region around the area of
damage — reorganizes in response to brain injury." The implications of this
are staggering; my entire brain, the organ by which my very consciousness is
controlled, was reorganized one day ten years ago. I went to sleep here
and woke up there; the place looked the same but nothing in it worked the
way it used to.
If Descartes was correct, and to Think is to Be, then what happens when I
cannot think, or at least cannot think as I did, cannot think well enough to
function in a job or in the world? Who am I?
You should hear me talk. I often come to a complete stop in mid-sentence,
unable to find a word I need, and this silence is an apt reflection of the
impulse blockage occurring in my brain. Sitting next to Beverly as she
drives our pickup truck through Portland traffic at 6:00 p.m., I say "We should
have gone for pizza to avoid this blood … " and cannot not go on. I hear
myself; I know I was about to say "blood tower traffic" instead of "rush hour
traffic." Or I manifest staggered speech patterns — which feels like
speaking with a limp — as I attempt to locate an elusive word. "I went to the …
hospital yesterday for some … tests because my head … hurt." Or I blunder
on, consumed by a feeling that something is going wrong, as when I put
fresh grounds into the empty carafe instead of the filter basket on my coffee
maker, put eye drops in my nose, or spray the cleaning mist into my face
instead of onto the shower walls. So at the dinner table I might say "Pass
the sawdust" instead of "pass the rice," knowing even as it happens that I am
saying something inappropriate. I might start a conversation about
"Winston Salem's new CD" instead of Wynton Marsalis's or announce that "the shore
is breaking" when I mean to say "the shower is leaking." There is nothing
smooth or unified any more about the process by which I communicate; it is
dis-integrated and unpredictably awkward. My brain has suddenly become like
an old man's. Neurologist David Goldblatt has developed a table that
correlates cognitive decline in age-associated memory impairment and traumatic
brain injury, and the parallels are remarkable. Not gradually, the way such
changes occur naturally, but overnight, I was geezered.
It is not just about words. I am also "dyscalculic," struggling with the
math required to halve a recipe or to figure out how many more pages are left
in a book I'm reading. If we are on E. 82nd and Third in Manhattan,
staying with my childhood friend Larry Salander for the week, it is very
difficult for me to compute how far away The Gotham Book Mart is over on W. 47th
between Fifth and Sixth, though I spent much of my childhood in the city.
Because it is a place where I still try to operate normally, the kitchen is
an ideal neurological observatory. After putting the leftover chicken in a
plastic bag, I stick it back in the oven instead of the refrigerator. I
put the freshly cleaned pan in the refrigerator, which is how I figure out
that I must have put the chicken someplace else because it's missing. I pick
up a chef's knife by its blade. I cut off an eighth of a giant white onion
and then try to stuff the remainder into a recycled 16-ounce yogurt
container that might just hold the small portion I set aside. I assemble
ingredients for a vinaigrette dressing, pouring the oil into an old olive jar,
adding balsamic vinegar, mustard, a touch of fresh lemon juice, and spices. Then
I screw the lid on upside-down and shake vigorously, spewing the contents
everywhere. I stack the newspaper in the wood stove for recycling. I walk
the garbage up our 200-yard long driveway and try to put it in the mailbox
instead of the trash container.
At home is one thing; when I perform these gaffes in public, the effect is
often humiliating. I can be a spectacle. In a music store last fall, I was
seeking an instruction book for Beverly, who wanted to relearn how to play
her old recorder. She informed me that there were several kinds of
recorders; it was important to buy exactly the right category of book since
instructions for a soprano recorder would do her no good while learning on an
alto. I made my way up to the counter and nodded when the saleswoman asked what
I wanted. Nothing came out of my mouth, but I did manage to gesture over
my right shoulder like an umpire signaling an out. I knew I was in trouble,
but forged ahead anyway, saying "Where are the books for sombrero
reporters?" Last summer in Manhattan, I routinely exited the subway stations and
led Beverly in the wrong direction, no matter which way we intended to go.
She kept saying things like "I think west is that way, sweetie," while I
confidently and mistakenly headed east, into the glare of the morning sun, or
"Isn't that the river?" as I led her away from our riverside destination.
Recently, in downtown Portland on a warm November morning, I stopped at the
corner of 10th and Burnside, one of the busiest crossings in the city,
carefully checked the traffic light (red) and the traffic lanes (bus coming),
and started to walk into the street. A muttering transient standing beside me
on his way to Powell's Books, where he was going to trade in his overnight
haul of tomes for cash, grabbed my shoulder just in time.
At home or not at home, it ultimately makes no difference. The sensation of
"dysfunctional mentation" is like being caught in a spiral of lostness.
Outside the house, I operate with sporadic success, often not knowing where I
am or where I'm going or what I'm doing. Inside the house, the same
feelings often apply and I find myself standing on the top of the staircase
wondering why I am going down. Even inside my head there is a feeling of being
lost, thoughts that go nowhere, emptiness where I expect to find words or
ideas, dreams I never remember.
Back in the fall, when it was Beverly's birthday, at least I did remember
to go to the music store. More often, I forget what I am after within
seconds of beginning the search. As she gets dressed for work, Beverly will tell
me what she wants packed for lunch and I will forget her menu by the time I
get up the 14 stairs. Now I write her order down like a waiter. Sometimes
I think I should carry a pen and paper at all times. In the midst of
preparing a salad, I stop to walk the four paces over to the little desk where we
keep our shopping list and forget "tomatoes" by the time I get there. So I
should also have paper handy everywhere. Between looking up a phone number
and dialing it, I forget the sequence. I need the whole phone book on my
speed dial system.
Though they appear without warning, these snafus are no longer strange to
me. I know where they come from. As Dr. Richard M. Restak notes in The
Modular Brain, "a common error frequently resulting from brain damage involves
producing a semantically related word instead of the correct response." But
these paraphasias and neologisms, my "expressive aphasias," and my
dyscalculas and my failures to process — the rapids of confusion through which I
feel myself flailing — though common for me and others with brain damage, are
more than Symptoms to me. They are also more than what neurologists like
to call "Deficits," the word of choice when describing impairment or
incapacity of neurological function, as Oliver Sacks explains in his introduction
to The Man Who Mistook His Wife for a Hat. These "deficits" have been
incorporated into my very being, my consciousness. They are now part of my
repertoire. Deficits imply losses; I have to know how to see them as gains.
Practitioners of neuroscience call the damage caused by trauma, stroke, or
disease an "insult to the brain." So pervasive is this language that the
states of Georgia, Kentucky, Minnesota and others incorporate the phrase
"insult to the brain" in their statutory definitions of traumatic brain injury
for disability determinations. Such insults, according to the Brain Injury
Association of Utah, "may produce a diminished or altered state of
consciousness, which results in an impairment of cognitive abilities or physical
functioning." The death of one Miles Dethmuffen, frontman and founding member
of the Boston rock band Dethmuffen, was attributed in news reports to "an
alcoholic insult to the brain." The language used is so cool. There is this
sentence from the website NeuroAdvance.com: "When there is an insult to
the brain, some of the cells die." Yes.
Insult is an exquisitely zany word for the catastrophic neurological event
it is meant to describe. In current usage, of course, "insult" generally
refers to an offensive remark or action, an affront, a violation of mannerly
conduct. To insult is to treat with gross insensitivity, insolence, or
contemptuous rudeness. The medical meaning, however, as with so many other
medical words and phrases, is different, older, linked to a sense of the word
that is some two or three centuries out of date. "Insult" comes from the
Latin compound verb insultare, which means "to jump on" and is also the root
word for "assault" and "assail." It's a word that connotes aggressive
physical abuse, an attack. Originally, it suggested leaping upon the prostrate
body of a foe, which may be how its link to contemptuous action was forged.
Though "an insult to the brain" (a blow to the head, a metal shard through
the skull, a stroke, a viral "attack") is a kind of assault, I am curious
about the way contempt has found its way into the matter. Contempt was
always part of the meaning of "insult" and now it is primary to the meaning.
Certainly a virus is not acting contemptuously when it targets the brain;
neither is the pavement nor steering wheel nor falling wrench nor clot of blood
nor most other agents of "insult." But I think society at large, medical
scientists, insurers, legislators, and the person-on-the-street do feel a
kind of contempt for the brain damaged with their comical way of walking,
their odd patterns of speech or ways in which neurological damage is
expressed, their apparent stupidity, their abnormality. The damage done to a brain
seems to evoke disdain in those who observe it and shame or disgrace in
those who experience it — I know I refer to a feeling of humiliation when I
expose my neurologically induced aberrant behaviors in public.
Poet Peter Davison has noticed the resonant irony of the phrase "an insult
to the brain" and made use of it in his poem, "The Obituary Writer."
Thinking about the suicide of John Berryman, the heavily-addicted poet whose
long-expected death in 1972 followed years of public behavior symptomatic of
brain damage, Davison writes that "his hullabaloos/of falling-down
drunkenness were an insult to the brain." In this poem, toying with the meaning of
the phrase, Davison suggests that Berryman's drinking may have been an insult
to his brain, technically speaking, but that watching him was, for a
friend, another kind of brain insult. He has grasped the fatuousness of the
phrase as a medical term, its inherent judgment of contempt, and made use of it
for its poetic ambiguity.
But I have become enamored of the idea that my brain has been insulted by a
virus. I used it as motivation. There is a long tradition of avenging
insults through duels or counter-insults, through litigation, through the
public humiliation of the original insult. So I write. I avenge myself on an
insult that was meant, it feels, to silence me by compromising my word-finding
capacity, my ability to concentrate and remember, to spell or
conceptualize, to express myself, to think.
The duel is fought over and over. I have developed certain habits that
enable me to work — a team of seconds, to elaborate this metaphor of a duel. I
must be willing to write slowly, to skip or leave blank spaces where I
cannot find words that I seek, compose in fragments and without an overall
ordering principle or imposed form. I explore and make discoveries in my
writing now, never quite sure where I am going but willing to let things ride and
discover later how they all fit together. Every time I finish an essay or
poem or piece of fiction, it feels as though I have faced down the insult.
In his book Creating Mind, Harvard neurobiologist John E. Dowling says "the
cerebral cortex of the human brain, the seat of higher neural function —
perception, memory, language, and intelligence — is far more developed than
is the cerebral cortex of any other vertebrate." Our gray matter is what
makes us human. Dowling goes on to say that "because of the added neural
cells and cortical development in the human brain, new facets of mind emerge."
Like the fractured facet of a gemstone or crystal, like a crack in the
facet of a bone, a chipped facet of mind corrupts the whole, and this is what
an insult to the brain does.
Though people long believed, with Aristotle, that the mind was located
within the heart, the link between brain and mind is by now a basic fact of
cognitive science. Like countless others, I am living proof of it. Indeed, it
is by studying the behavior of brain-damaged patients like me that medical
science first learned, for example, that the brain is modular, with
specific areas responsible for specific functions, or that functions on one side
of the body are controlled by areas on the opposite side of the brain. "The
odd behavior of these patients," says V.S. Ramachandran, speaking of the
brain-damaged, "can help us solve the mystery of how various parts of the
brain create a useful representation of the external world and generate the
illusion of 'self' that endures in space and time." Unfortunately, there is
ample opportunity for observation since, according to the Brain Injury
Association, more than two million Americans suffer traumatic brain injury every
year, a total that does not include damage by disease.
"Change the brain, change the person," says Richard Restak in The Modular
Brain. But how, exactly? No one has yet explained the way a brain produces
what we think of as consciousness. How does the firing of electrical impulse
across a synapse produce love, math, nightmare, theology, appetite? Stated
more traditionally, how do brain and mind interact? Bookstore shelves are
now filled with books, like Steven Pinker's brilliant 1997 study How the
Mind Works, which attempt to explain how a three and a half pound organ that
is the consistency of Jell-O makes us see, think, feel, choose, and act.
"The mind is not the brain," Pinker says, "but what the brain does."
And what the brain does, according to Pinker, "is information processing,
or computation." We think we think with our brain. But in doing its job of
creating consciousness, the brain actually relies upon a vast network of
systems and is connected to everything — eyes, ears, skin, limbs, nerves. As
Dowling so dourly puts it, our mental function, our mind — memory, feelings,
emotions, awareness, understanding, creativity — "is an emergent property
of brain function." In other words, "what we refer to as mind is a natural
consequence of complex and higher neural processing."
The key word is "processing." We actually think with our whole body. The
brain, however, takes what is shipped to it, crunches the data, and sends
back instructions. It converts, it generates results. Or, when damaged, does
not. There is nothing wrong with my sensory receptors, for instance. I see
quite well. I can hear and smell, my speech mechanisms (tongue, lips,
nerves) are intact. My skin remains sensitive. But it's in putting things
together that I fail. Messages get garbled, blocked, missed. There is, it
sometimes seems, a lot of static when I try to think, and this is the gray area
where nothing is clear any longer.
Neurons, the brain's nerve cells, are designed to process information. They
"receive, integrate and transmit," as Dowling says, receiving input from
dendrites and transmitting output along axons, sending messages to one
another across chemical passages called synapses. When there are lesions like
the ones that riddle my gray matter, processing is compromised. Not only
that: certain cells have simply died and with them the receiving, integrating,
and transmitting functions they performed.
My mind does not make connections because, in essence, some of my brain's
connectors have been broken or frayed. I simply have less to work with and
it is no surprise that my IQ dropped measurably in the aftermath of my
illness. Failing to make connections, on both the physical and metaphysical
levels, is distressing. It is very difficult for me to "free-associate;" my
stream of consciousness does not absorb runoff or feeder streams well, but
rushes headlong instead. Mental activity that should follow a distinct pattern
does not, and, indeed, I experience my thought process as subject to
random misfirings. I do not feel in control of my intelligence. Saying "pass me
the tracks" when I intended to say "pass me the gravy" is a nifty example.
Was it because gravy sounds like grooves which led to tracks, or because my
tendency to spill gravy leaves tracks on my clothes? A misfire, a glitch
in the gray area that thought has become for me, and as a result my ability
to express myself is compromised. My very nature seems to have altered.
I am also easily overloaded. I cannot read the menu or converse in a
crowded, noisy restaurant. I get exhausted at Portland Trailblazers basketball
games, with all the visual and aural imagery, all the manufactured commotion,
so I stopped going nine years ago. My hands are scarred from burns and
cuts that occurred when I tried to cook and converse at the same time. I
cannot drive in traffic, especially in our standard transmission pickup truck. I
cannot talk about, say, the fiction of Thomas Hardy while I drive; I need
to be given directions in small doses rather than all at once, and need
those directions to be given precisely at the time I must make the required
turn. This is, as Richard Restak explains, because driving and talking about
Hardy, or driving and processing information about where to turn, are
handled by different parts of the brain and my brain's parts have trouble
I used to write accompanied by soft jazz, but now the least pattern of
noises distracts me and shatters concentration. My entire writing process, in
fact, has been transformed as I learned to work with my newly configured
brain and its strange snags. I have become an avid note taker, a jotter of
random thoughts that might or might not find their way together or amount to
anything, a writer of bursts instead of steady work. A slight interruption —
the movement of my cat across my window view, the call of a hawk, a spell
of coughing — will not just make me lose my train of thought, it will leave
me at the station for the rest of the day.
I have just finished reading a new book about Muhammad Ali, King of the
World, written by David Remnick. I anticipated identifying a bit with Ali, now
suffering from Parkinson's Disease, who shows so strikingly what brain
damage can do, stripped as he is of so many of the functions — speech,
movement, spontaneity — that once characterized him. But it was reading about
Floyd Patterson that got me.
Patterson was a childhood hero of mine. Not only did we share a rare first
name, we lived in neighboring towns — he was in Rockville Center, on Long
Island, while I was five minutes away in Long Beach, just across the bridge.
I was nine when he beat Archie Moore to take the heavyweight championship
belt, almost 12 when he lost it to Ingemar Johannson, and almost 13 when he
so memorably won it back. The image of Johannson's left leg quivering as
he lay unconscious on the mat is one of those vivid memories that endures
(because, apparently, it is stored in a different part of the brain than
other, less momentous memories). Floyd, like me, was small of stature in his
world, was shy and vulnerable, and I was powerfully drawn to him.
During his 64 professional fights, his long amateur career, his many rounds
of sparring to prepare for fights, Patterson absorbed a tremendous amount
of damage to his brain. Now in his sixties, his ability to think is
devastated. Testifying in court earlier this year in his capacity as head of the
New York State Athletic Commission, Patterson "generally seemed lost." He
could not remember the names of his fellow commissioners, his phone number or
secretary's name or lawyer's name. He could not remember the year of his
greatest fight, against Archie Moore, or "the most basic rules of boxing
(the size of the ring, the number of rounds in a championship fight)." He kept
responding to questions by saying "it's hard to think when I'm tired."
Finally, admitting "I'm lost," he said "sometimes I can't even remember my
wife's name, and I've been married 32, 33 years." He added again that it
was hard for him to think when he was tired. "Sometimes, I can't even
remember my own name."
People often ask if I will ever "get better." In part, I think what they
wonder about is whether the brain can heal itself. Will I be able, either
suddenly or gradually, to think as I once did? Will I toss aside the cane, be
free of symptoms, have all the functions governed by my brain restored to
smooth service, rejoin the world of work and long-distance running? The
question tends to catch me by surprise because I believe I have stopped asking
The conventional wisdom has long been that brains do not repair themselves.
Other body tissue, other kinds of cells, are replaced after damage, but
"when brain cells are lost because of injury or disease," John Dowling wrote
as recently as 1998, "they are not replaced." We have, he says, as many
brain cells at age one as we will ever have. This has been a fundamental tenet
of neuroscience, yet it has also long been clear that people do recover —
fully or in part — from brain injury. Some stroke victims relearn to walk
and talk, feeling returns in once-numbed limbs. Children, especially
children, recover and show no lasting ill effects from catastrophic injuries or
coma-inducing bouts of meningitis.
So brain cells do not get replaced or repaired, but brain-damaged people
occasionally do regain function. In a sense, then, the brain heals, but its
cells do not.
In Confronting Traumatic Brain Injury, Texas bioethicist William J.
Winslade says "Scientists still don't understand how the brain heals itself." He
adds that although "until recently, neuroscientists thought that much of the
loss of capabilities due to brain damage was irreversible," patients
recover spontaneously and rehabilitation programs "can restore cognitive and
functional skills and emotional and experiential capacity, at least in part."
There are in general five theories about the way people might recover
function lost to brain damage. One suggests that we do not need all our brain
because we only use a small part of it to function. Another is that some
brain tissue can be made to take over functions lost to damage elsewhere.
Connected is the idea that the brain has a backup mechanism in place allowing
cells to take over like understudies. Rehabilitation can teach people new
ways to perform some old tasks, bypassing the whole damaged area altogether.
And finally, there is the theory that in time, and after the chemical shock
of the original injury, things return to normal and we just get better.
It is probably true that, for me, a few of these healing phenomena have
taken place. I have, for instance, gotten more adept at tying my shoes, taking
a shower, driving for short periods. With careful preparation, I can
appear in public to read from my work or attend a party. I have developed
techniques to slow my interactions with people down or to incorporate my mistakes
into a longer-term process of communications or composition. I may not be
very good in spontaneous situations, but given time to craft my responses I
can sometimes do well. But I still can't think.
A recent development promises to up the ante in the game of recovery from
brain damage. The New York Times reported in October of 1998 that "adult
humans can generate new brain cells." A team at the Salk Institute for
Biological Studies in La Jolla, California, observed new growth in cells of the
hippocampus, which controls learning and memory in the brain. The team's
leader. Dr. Fred Gage, expressed the usual cautions; more time is needed to
"learn whether new cell creation can be put to work" and under what
conditions. But the findings were deemed both "interesting" and "important."
There is only one sensible response to news like this. It has no personal
meaning to me. Clinical use of the finding lies so far in the future as to
be useless, even if regenerating cells could restore my lost functions. Best
not to think about this sort of thing.
Because, in fact, the question of whether I will ever get better is
meaningless. To continue looking outside for a cure, a "magic bullet," some
combination of therapies and treatments and chemicals to restore what I have
lost is to miss the point altogether. Certainly if a safe, effective way
existed to resurrect dead cells, or generate replacements, and if this somehow
guaranteed that I would flash back or flash forward to "be the person I was,"
it would be tempting to try.
But how would that be? Would the memories that have vanished reappear? Not
likely. Would I be like the man, blind for decades, who had sight restored
and could not handle the experience of vision, could not make sense of a
world he could see? I am, in fact, who I am now. I have changed. I have
learned to live and live richly as I am now. Slowed down, softer, more heedful
of all that I see and hear and feel, more removed from the hubbub, more
internal. I have made certain decisions, such as moving from the city to a
remote rural hilltop in the middle of acres of forest, that have turned out to
be good for my health and even my soul. I have gained the love of a woman
who knew me before I got sick and likes me much better now. Certainly I want
to be well. I miss being able to think clearly and sharply, to function in
the world, to move with grace. I miss the feeling of coherence or
integrity that comes with a functional brain. I feel old before my time.
In many important respects, then, I have already gotten better. I continue
to learn new ways of living with a damaged brain. I continue to make
progress, to avenge the insult, to see my way around the gray area. But no, I am
not going to be the man I was. In this, I am hardly alone.
Reprinted from In the Shadow of Memory (University of Nebraska Press, 2003)
Original art courtesy Rob Grom.
This article originally appeared in Issue 3, February 2006.