Monday, June 30, 2008

Dr. Katrina Berne on why CFS is not psychiatric

Dr. Katrina Berne is a licensed clinical psychologist.  She has had CFS since 1985 with secondary FMS, and specializes in treating patients with CFS/FMS.  Obviously, as a patient and a psychologist, she knows whereof she speaks, and how to differentiate physical illness from psychiatric conditions.

"The medical profession often views depression or inability to cope productively with stress as the cause of any symptom for which a physiological cause is not evident. Psychiatry becomes a convenient dumping ground for those with unexplained illness. However, indiscriminate attribution of symptoms to psychological factors is inappropriate.

"... The notion that we cannot handle life, fabricate symptoms, or develop illnesses in order to receive special attention is ludicrous. Attribution of illness to such conscious or unconscious motivation is inaccurate, unfair and insulting. Phrases such as ‘can’t manage stress’ and ‘mind over matter’ add insult to illness. ... Some CFS/FMS patients experience little or no depression.

"Numerous chronic disorders share common features, including symptoms and abnormalities. The similarities are remarkable ... Skeptics who dismiss CFS, FMS ... imply that poorly understood conditions do not deserve the respect afforded ‘testable’ illnesses. This practice lifts a burden from disinterested physicians and blames – even traumatizes – sufferers.

"Double standards allow medical doctors to diagnose psychiatric illness ... in the absence of a known physiological cause, but do not typically allow the psychiatrist or psychologist who rules out emotional causes to rule in physiologic illness. That is, acceptable practice allows a physician to say ‘It is all in your head’ but how often does a psychiatrist or psychologist say ‘Nothing is wrong with your head, the illness is in your body’? ... Illnesses such as MS, rheumatoid arthritis, polio, HIV/AIDS, stomach ulcers and diabetes were once considered to be of psychiatric origin. When markers or diagnostic tests were developed, the diagnoses shifted to ‘real’ illnesses, those of the body. History repeats itself.

"...The history of psychiatric disorders in the CFS/FMS population is similar to that in the general population. ... Depression does not cause these syndromes and is not present in all cases; however, many patients are given a psychiatric diagnosis when a physiological diagnosis is not apparent. Overlapping symptoms ...and simple ignorance causes confusion between CFS/FMS and depression.

"The rate of depression is not necessarily higher in patients with the most severe symptoms. ... Nonantidepressant medications common in CFS/FMS treatment are not effective in treating [depression].

"Psychological tests are frequently used to ‘rule in’ depression and other psychiatric disorders; however, they cannot distinguish between a test-taker’s medical and psychological disorders. One who endorses numerous physical complaints is likely to be labeled depressed. ‘Results in ill populations may be falsely elevated for psychological disorders’ (Jason, Richman, et al. 1997).

"...When ‘neurological’ items were removed from the test and the tests were rescored, all scores dropped to within the normal range, that is, no elevations remained. This finding provides evidence that neurological dysfunction rather than psychopathology accounts for the typical CFS profile.

"CFS and FMS share common factors with somatoform disorders – multiple symptoms, lack of consistent lab findings ... but are excluded from this category by symptom prevalence, age, suddenness of onset, lack of prevalent personality disorders, and exercise and alcohol intolerance.

"The term functional somatic syndromes refers to suffering in the absence of specific medical findings. This term is often inappropriately applied to poorly understood illnesses such as CFS, FMS ... FSS disorders are framed with circular reasoning: ‘You think you have a serious illness but you don’t because we have no specific test for it.’ The alleged secondary gains of illness are typically absent, yet patients are accused ...

"... a diagnosis of FSS more often provides a convenient way to dismiss patients’ symptomatic complaints whose cause is unknown. The absence of diagnostic tests for many known disorders creates fertile ground for physicians who view any difficult-to-diagnose disorder as imagined illness. However an illness that defies current scientific knowledge is still an illness.

"... Although multiple symptoms are seen in somatization disorder, symptom clusters typical of CFS and FMS are not found in this group, nor is sudden onset, which often characterizes CFS/FMS.

"... Many diseases are labeled psychiatric or 'stress' disorders until causal agents or illness markers are identified, at which time they graduate to the status of legitimized, genuine illness."

* * *

One of the things that was used in the early days of CFS to prove that patients were not merely hypochondriacs was the ability of patients who did not know any other patients to recite the exact same symptoms as the others.

One doctor accused me of being a hypochondriac because I showed up in his office in response to my husband reading a magazine article that described the symptoms I'd been having -- now that we recognized it as a serious condition that wouldn't go away on its own, we wanted medical help, but the doctor chose to believe the symptoms showed up only after I'd read the article (I wasn't well enough to read the article myself, so how could that be?). 

The next doctor observed that I could not be a hypochondriac, because I was describing accurately symptoms that were NOT in the article, or in any other published article for the general public.  The only way I could know what the next dozen symptoms on the list were (not just the half dozen in the article) was if, in fact, I had those symptoms.  He had no difficulty giving me the correct diagnosis.  I wasn't just picking symptoms at random, I was describing the same symptoms as every other patient; the odds of doing that by chance are astronomical.

Psych consultants have repeatedly stated that they find nothing to support a depression diagnosis.  They know the difference between medical illness and depression, and I'm not saying the right things to convince them I'm depressed; I'm describing only those symptoms of depression that overlap with symptoms of the flu, and then I'm describing other symptoms that are definitely physical, because they're not seen in depression.  Yet, the unanimous vote of the psychs that I'm physically ill has not prevented me from having a series of MDs contradict them by giving a psychiatric diagnosis that the psych experts themselves refuse to support.

As each piece of the puzzle falls into place, I get abnormal blood tests, etc., it's that much more damning evidence that those who think the problem is purely psychiatric are wrong.  When I had the same symptoms that are now being blamed on mydivorce DURING the marriage, they were blamed on being married and I was told they'd go away if I got a divorce.  That doctor refused to listen that the symptoms started BEFORE the marriage.  (We've heard the same story from other women: those who are single are told they don't like being single and the problems will go away if they get married, and those who are married are told the cure is a divorce, and some are married/divorced/married/divorced and have the symptoms no matter what their marital status.)

My chiropractor gave me a "diagnostic profile test", and rather than just relying on the computer's numbers, he reviewed the actual answers.  While the computer flagged me as depressed, he noted that everything I'd marked in that section was also cross-referenced in a physiological section of the profile; none of my answers in the depression category were to questions that would only point to depression -- the same questions were in the categories for chronic pain and other physical problems.  Just like Dr. Berne's rescoring of the tests after removing the "neurological" questions proved the problem was neurological rather than psychiatric.

There's already more than adequate evidence that CFS is a physical illness, not a psychiatric one.  Eventually, that evidence will become common knowledge, and those who have made erroneous psychiatric diagnoses and refused to accept the reality will be ostracized as uninformed and behind the times.

As Dr. Yunus has said "it's not the patients who are disturbed ... it's the doctors."  They can't open their minds enough to accept the reality that CFS is, as patients have described, post-viral, and that the symptoms, while seeming disjointed to a PCP, made perfect sense to a neurologist, who instantly recognized the pattern.

FIRST REPORTS FROM “VIRUSES IN CFS” CONFERENCE

Yet more nails in the coffin of the psychiatric lobby. Perhaps with more publicity like this, we can finally get the necessary differentiation between post-viral CFS and all those psych conditions they like to lump in with us so they don’t have to admit that CFS is a physical illness with a purely physical cause, and not "stress", "emotional trauma", or the ever-present "delicate hothouse flowers unable to cope with real life". (No "delicate hothouse flower" could possibly put up with the BS that CFS patients deal with on a daily basis, from verbal abuse to false accusations to the constant pain.)

 

http://www.hhv-6foundation.org/

HHV-6 FOUNDATION NEWS

Conference Report

The 6th International Conference on HHV-6 & 7 and satellite conference on Viruses in CFS held in Baltimore June 19- 23rd were very successful, with over 230 scientists and clinicians in attendance. We were also pleased to welcome representatives from five drug companies and half-dozen diagnostic companies who are exploring therapeutic options and new diagnostic assays.

Among the highlights:

International Conference on HHV-6 & 7:

Kazuhiro Kondo, MD, PhD, of the Jikei University Medical School in Tokyo identified a novel human herpesvirus-6 (HHV-6) protein present in Chronic Fatigue Syndrome (CFS) patients but not healthy controls that may contribute to psychological symptoms often associated with that and other disorders. http://www.hhv-6foundation.org/PRKondo_PFS.pdf

Italian researchers, professors Arnoldo Caruso of the University of Brescia and Dario Di Luca of the University of Ferrara presented data suggesting that human HHV-6 infects and persists in a dormant state in endothelial cells, the cells lining blood vessels, and that the latency protein U94 causes these cells to lose their ability to grow, to form new blood vessels, and to take part in healing processes. This finding has potential consequences for both cardiac disease and tumor control. http://www.hhv-6foundation.org/U94DiLuca.pdf

Danish scientists Professor Per Hollsberg, MD and his PhD student Vanda Lauridsen Turcanova from the University of Aarhus In Denmark demonstrated that HHV-6 activates endogenous retrovirus HERV-K18 with possible consequences for autoimmunity. Viral infections are known to worsen autoimmune conditions. http://www.hhv-6foundation.org/PRK18retrovirus.pdf

Dr. Jose Montoya, an infectious disease specialist at Stanford University, released preliminary findings on his double-blind placebo-controlled antiviral trial of Valcyte for a subset of patients displaying high antibody levels to human HHV-6 and Epstein-Barr virus (EBV). Statistically significant cognitive improvement was noted in the Multidemensional Fatigue Inventory (MFI-20) Mental Fatigue subscale and on patient self-reported of cognitive functioning, but there was not a significant result on the overall MFI-20 index. Data from treadmill testing, cytokine analysis, gene expression and other viral markers is still pending and will be announced at a later date.

Symposium on Viruses in CFS & Post-viral Fatigue:

Brigitte Huber, PhD, of the Tufts University School of Medicine presented evidence at a medical conference that suggested a reactivated ancient retrovirus embedded in the human genome may be active in chronic fatigue syndrome (CFS) and multiple sclerosis (MS) patients. Dr. Huber found that both MS and CFS patients (whose illness had been triggered by infectious mononucleosis) were at a higher relative risk for containing a HERV-K18 variant known to be particularly potent at inducing superantigen activity. Superantigens are proteins that are able to induce a strong undifferentiated T-cell response believed to impair the regulation of the immune system over time.

(~jvr: because the hyperlink on this site doesn't work, I repost this text below for the sake of completeness)

Birgitta Evengard, MD from the Karolinska Institute reported that 33 twin pairs discordant for CFS, the twins had higher median EBV Early Antigen antibody levels than matched controls. VCA and EBNA antibodies did not differ between the two groups. The median HHV-6 Antibody levels did not differ between patients and controls. The data on both is preliminary since only two dilutions were done. No data was supplied on whether there was a subset of patients with significantly elevated antibody levels to HHV-6.

OTHER NEWS IN HHV-6:

* HHV-6A was associated with rhomboencephalitis in immunocompetent children, characterized by new onset seizures, ataxia and opsoclonus-myoclonus. (Crawford 2007)

* HHV-6 was found in79% of lymph nodes from Hodgkin's Lymphoma patients (Lacroix, 2007) compared to EBV in 62%.

* HHV-6B was associated with post-transplant acute limbic encephalitis, characterized by anterograde amnesia, syndrome of inappropriate antidiuretic hormone secretion and temporal lobe abnormalities. (Seeley 2007)

* HHV-6 antibody titers were elevated in army recruits six to 12 months previous to diagnosis with schizophrenia (Niebuhr, 2007)

* HHV-6 was frequently found in the gastroduodenal mucosa of transplant and immunocompetent patients with gastroenteritis; 94% of transplant recipients with biliary complications had HHV-6 or CMV in the duodenal mucosa. (Halme 2008)

* Two thirds of resections from patients with refractory mesial temporal lobe epilepsy (MTLE) were found to have very high levels HHV-6B infection (Fotheringham, 2007); chronic viral infection may alter glutamate transport to cause seizures. (Fotheringham b, 2007) `

````````````````

*Retrovirus & ME/CFS, MS and Autoimmunity*; Help ME Circle, 24 June 2008

http://www.marketwire.com/mw/release.do?id=871774

SOURCE: HHV-6 Foundation

Jun 23, 2008 10:00 ET

Ancient Retrovirus May Contribute to Chronic Fatigue Syndrome, Multiple Sclerosis and Autoimmunity

Smoldering Infections of Two Common Viruses EBV and HHV-6 Cause Inherited Retrovirus Genes to Activate

BALTIMORE, MD--(Marketwire - June 23, 2008) -

Brigitte Huber, PhD, of the Tufts University School of Medicine, presented evidence at a medical conference that suggested that a reactivated ancient retrovirus embedded in the human genome may be active in chronic fatigue syndrome (CFS) and multiple sclerosis (MS) patients. Danish scientists at the same conference suggested that the activation of this retrovirus, dormant in healthy individuals, could be the reason why autoimmune conditions worsen with viral infections.

Chronic Fatigue Syndrome and Multiple Sclerosis Patients at Increased Risk From the Effects of HERV-K18 Activation

"Patients with profoundly fatiguing diseases such as MS and CFS may be particularly susceptible to HERV-K18 activation," said Dr. Huber. The announcement was made at the International Symposium on Viruses in CFS and Post-Viral Fatigue, a satellite conference of the 6th International Conference on HHV-6 & 7. Using an SNP-based genotyping method, Dr. Huber found that both MS and CFS patients (whose illness had been triggered by infectious mononucleosis) were at a higher relative risk for containing HERV-K18 variants known to induce superantigen activity. Superantigens are proteins that are able to induce a strong undifferentiated T-cell response believed to deplete the immune system over time.

Viral activity and/or immune activation has been shown to trigger HERV-K18 activity. Both Epstein-Barr virus infection (infectious mononucleosis) and interferon-alpha administration are associated with HERV-K18 activity. "HHV-6 activates HERV-K18 as well," said Danish investigator Per Hollsberg, MD and professor from the University of Aarhus In Denmark. His PhD student Vanda Lauridsen Turcanova presented this data at the same conference. "Furthermore, this retrovirus activation may have important consequences for autoimmunity," he added.

HERV-K18 activation may be the endpoint of an HHV6/EBV interferon pathway operating in both MS and CFS. HHV-6 is being investigated as a co-factor in both diseases. Other retroviruses, HERV-H and HERV-W, have been implicated in MS by other researchers. Over 75% of MS patients meet the criteria for CFS. Fatigue is often the most disabling symptom for MS patients. The two diseases also share characteristics such as grey matter atrophy, impaired cerebral glucose metabolism, autonomic nervous system activity and altered patterns of brain activity.

Dr. Huber's study suggests that endogenous retroviral activation in CFS and MS could produce some of the symptoms associated with both diseases. She has received a National Institutes of Health (NIH) grant to study these issues. Per Hollsberg has done extensive research on the role of EBV and HHV-6 in multiple sclerosis.

 

 

The HHV-6 Foundation

The HHV-6 Foundation encourages scientific exchanges and provides grants to researchers seeking to increase our understanding of HHV-6 infection in a wide array of central nervous system disorders. Daram Ablashi, the co-discoverer of the HHV-6 virus, is the Foundation's Scientific Director.

Contact: Kristin Loomis Executive Director HHV-6 Foundation Santa Barbara, CA 805-969-1174

http://www.hhv-6foundation.org/  

- - - -

Tom's first impressions of the HHV-6 Foundation's Satellite Conference are now posted on the RESCIND site. Since most newsletters will probably be geared toward the research itself, we decided to do a "fly on the wall perspective" of the conference. We'll have more musings on the conference as we are able. And as always, if you haven't signed the petition, please do so!

Tom & Jerry

http://www.rescindinc.org/  

Does ANYONE clean any more?

Doesn’t anyone in this town clean?

A friend stopped by this morning and noticed a pile of stuff on my couch. I explained it away as a cleaning lady who saw me momentarily toss something there so that I could use two hands for something else, and my setting something there for a minute was interpreted as permission to use the couch for permanent storage. He nodded; once one of his cleaning ladies saw him put something on the kitchen table that wasn’t dinner, she also decided it was easier to pile things on the table than to put them where they belong.  In other words "you won't mind me putting things there, because you put stuff there yourself."

He confirmed having the same problems with his cleaners: just like mine, when you tell them "put this in the closet", they act like they don’t understand English, and look for somewhere else to put it so that you’ll put it away yourself. But when you refuse to pay them for not doing what they were hired to do, suddenly they speak fluent English, including the phrase "pay up or I’ll sue you for fraud". (Though they don’t do so well with the legal term "quantum meruit", i.e., paying what the job is actually worth.)

His also have only wanted to dust and mop, and not do any serious cleaning. He also had one who considered it "cleaning" to move things from Point A to Point B this week, and from Point B to Point A next week, without ever wiping them down in the process.

After reassuring me that I’m not the only person in town who can’t find a good cleaner, verifying the same experience I’ve had (most don’t clean and those few who do clean are flaky and can’t remember to show up unless you call to remind them "tomorrow’s Tuesday, and you need to come clean my house"), we concluded that there is not a single cleaning lady in this town who is both a good cleaner and a reliable employee who’ll show up every week without fail.

So, I’ll put the call out here – if there is anyone in the Sacramento area who is willing to do more than just dust, who really cleans, who does 3 hours work for 3 hours pay, and can guarantee that she’ll show up every time, I know a lot of people in town who are looking for a good, reliable cleaner. Impress me, and I will give them your phone number. Between us, we can probably network you into working 5 days a week. I can’t speak for them, but I have no problem with paying a lot more than minimum wage for a job that’s done right. But you’re not going to convince me that I owe you 4 hours pay for a job that I know from experience can be completed in under 1 hour; if it took you 4 hours to do only that one task, that tells me that as soon as I stopped watching, you stopped working.

Although years of being forced to use hired cleaners instead of being able to do it myself might lead you to believe otherwise, I like my house CLEAN. Don’t assume that because it’s a mess when you come in the first time you’re here to clean that it’s OK to leave it a mess ... a lot of that mess was created by cleaners who put things on the nearest flat surface instead of back in the cupboard. You were hired to clean, not just to dust the clutter and spray a little Pine-Sol thinking the scent will fool me into thinking the house was properly cleaned. I can see for myself that you just boxed things up instead of putting them away, and the first time I open the fridge and find something with fur still sitting on the shelf, I’ll know you didn’t actually clean the fridge in the manner in which you were instructed to do the job.

My kitchen is logically organized, all the canned goods here, all the pots there, all the towels in this drawer – there is absolutely no excuse to say "I put it all in a box for you to put away yourself because I couldn’t figure out where to put it." Similarly, my dresser is logically organized, but I’ve had people tell me that they can’t figure out that the underwear goes with the underwear, the socks go with the other socks, the T-shirts go in the drawer with the million other T-shirts. (Not "I can’t make the million-and-one-th T-shirt fit in there because there’s no more room", but that she can’t deduce from what’s already in the drawers which half-empty drawer the socks go in ... so she just piled the laundry on the dining room table, messing up what had been a clean dining room, for me to put away later.) Either these people have a sub-moron IQ that they can’t figure out underwear goes in the drawer with the other underwear or they’re too lazy to work, and the easiest way to avoid working is to pretend you’re too stupid to do anything without being led by the hand through the steps, i.e., make the employer do the job herself under the guise of teaching you.  (The prizewinner in that category is the one who had to be taught every 3 days how to load the dishwasher.  And 3 days later had to be shown again.  And 3 days later had to be shown again.  Because if you put the dishes in sideways, you can call the bottom rack "full" after just 6 plates.  If you put them in ||||||, after 6 dinner plates there's still room for 6 soup bowls, 6 sandwich plates, and 2 pots, requiring you to bend down 14 more times.)

I have a disabled friend in another part of the state who, thank God, has been deemed "officially disabled" by the government, and thus gets her cleaners at no cost to her. Apparently, they are paid quite a bit less than I pay my cleaners (I’ve been paying $15-20/hour, and I think the government pays $9/hour ... I’m sure someone will correct meif I’m wrong), but because she is in a wheelchair (which I am not), they understand that she is disabled and that they cannot leave the chores for her to do, because she can’t do them. And because if they don’t do the laundry, put away the groceries, etc., she will call the government agency who sent them, complain that someone has to come and do these tasks, and they’ll get in trouble with someone far more powerful than a single disabled lady. One private agency told me that if I was not happy with what the cleaner did, I would have to take it up with her directly, but then refused to give me her phone number so that I could. Needless to say, when she was told by the boss that I wanted the work done that I had paid for, she wasn’t going to call me and get chewed out, so I paid $80 and got absolutely nothing for it.

Unfortunately, to get into the same government program that sends cleaners to my friend, I either have to convince the judge that it is possible to be legally disabled without being in a wheelchair, or turn 65. And since I’ve been fighting for nearly a decade with this judge’s perception that if I can get to his courtroom for one hour once every other year, I can get a job 8 hours every day, I’m thinking I’ll qualify by turning 65 before I’m deemed "officially disabled".

Sleep Disturbance and Fibromyalgia

Sleep disturbances in fibromyalgia syndrome: Relationship to pain and depression.

Arthritis Rheum. 2008 Jun 24;59(7):961_967. [Epub ahead of print]

Bigatti SM, Hernandez AM, Cronan TA, Rand KL.

Indiana University~Purdue University Indianapolis, Indiana.

PMID: 18576297

 

OBJECTIVE: This study is an examination of sleep, pain, depression, and physical functioning at baseline and 1_year followup among patients with fibromyalgia syndrome (FMS). Although it is clear that these symptoms are prevalent among FMS patients and that they are related, the direction of the relationship is unclear. We sought to identify and report sleep problems in this population and to examine their relationship to pain, depression, and physical functioning.

METHODS: Patients diagnosed with fibromyalgia were recruited from a Southern California health maintenance organization and evaluated according to American College of Rheumatology criteria in the research laboratory. Six hundred patients completed the baseline assessment and 492 completed the 1_year assessment. Measures included the Center for Epidemiologic Studies Depression Scale, the McGill Pain Questionnaire, the Pittsburgh Sleep Quality Index, and the Fibromyalgia Impact Questionnaire.

RESULTS: The majority of the sample (96% at baseline and 94.7% at 1 year) scored within the range of problem sleepers. Path analyses examined the impact of baseline values on 1_year values for each of the 4 variables. No variable of interest predicted sleep, sleep predicted pain (beta = 0.13), pain predicted physical functioning (beta = _0.13), and physical functioning predicted depression (beta = _0.10).

CONCLUSION: These findings highlight the high prevalence of sleep problems in this population and suggest that they play a critical role in exacerbating FMS symptoms. Furthermore, they support limited existing findings that sleep predicts subsequent pain in this population, but also extend the literature, suggesting that sleep may be related to depression through pain and physical functioning.

* * *

I had constant pain until I got my Sleep Number bed. By the end of the first week, I considered my fibromyalgia cured -- it no longer hurt just to exist. The fibro test points do still hurt when someone presses on them, so technically I still have fibro, but being able to sleep more than 2 hours before waking up in pain has had a big effect on my ability to function the next day. (And the time available to function, because I'm not spending a huge chunk of the day in a hot bath trying to ease the pain enough to be able to concentrate.)

Just like with CFS, fixing the quality of sleep is the first step in fixing fibromyalgia. A lot can be achieved by getting enough sleep to let the body start healing itself.

Sunday, June 29, 2008

Dr. John responds to Suzi Walker and Dr. Hilary

Letter here   http://www.mefreeforall.org/2008-Apr-Jun.448.0.html#c3698

in response to a "Celeb" M.E. sufferer, Suzi Walker, in which resident Dr
Hilary Jones says that M.E. "usually disappears within a few years on its
own"

(link  http://www.mefreeforall.org/M-E-in-the-News.107.0.html   to the
"Fabulous" Mag supplement of The News of the World, 29 June 2008 below my
signature)

(Someone might like to make the point that Suzi has been ill for 9 years).

I'm sure there are plenty of you out there who are living proof to the
contrary.

If you would like to tell Dr Hilary Jones so, the News of the World letters
e-mail address is  your.letters@notw.co.uk

Only short letters stand a chance.

Cheers
John
drjohngreensmith@mefreeforall.org


*Your Letters - News of the World*.

As far as I know, there are no statistics exclusively for people with M.E. (*Myalgic Encephalomyelitis*), which have not been distorted by adding in other patients, with a variety of illnesses, in which chronic fatigue is said to be a symptom and calling them all ME/CFS.  It may be this proportion of CFS patients who "usually improve with time" (*'I was so exhausted I couldn't move' , Suzi Walker, On the couch with Dr Hilary, Fabulous Mag, News of the World, 29 June 2008*), leaving the erroneous impression that M.E. "usually disappears within a few years on its own."

We won't know for sure until a thorough epidemiological study has been done
but, already, we can count hundreds of thousands of heads, who have remained
ill for decades, which proves Dr Hilary Jones's assertion very unlikely
indeed.

Yours sincerely
drjohngreensmith@mefreeforall.org
Dr John H Greensmith
ME Free For All. org

http://www.fabulousmag.co.uk/health/index.php

'I was so exhausted I couldn't move' (On the couch with Dr Hilary Jones:
Suzi Walker, Fabulous Mag, News of the World, 29 June 2008)


Every week a celeb asks our fabulous doctor for a diagnosis. This week it's
TV presenter Suzi Walker, 36

Some days I wake up feeling exhausted.

My head feels cloudy, my joints hurt and the smallest decision has me in
tears.

I feel so weak I can't even climb the stairs.

I have Myalgic Encephalopathy (ME), or Chronic Fatigue Syndrome.

For years I didn't know what was wrong with me, and at one point I felt so
awful, I thought it was cancer.

My symptoms began nine years ago, after my daughter Sophie was born.

I contracted post natal pre-eclampsia, and within hours of her birth, I had
a fit and went into a coma.

When I woke two days later I felt weak, and I continued to feel lethargic
and achy.

Four years later my GP finally diagnosed ME but said there was no cure,
which was devastating.

Over the years I've spent thousands of pounds looking for my own 'cure', from vitamin injections to faith healers, but nothing has worked.

Stress is a trigger so I try not to get too anxious.

I also try to eat well, but it can be hard if I'm feeling dreadful.

I once got so thin that I was hospitalised and had to be tube fed.

Overdoing it at the gym can cause a bad attack of fatigue.

Is there anything I can do to keep symptoms at bay?

Suzi is raising awareness for the charities Action for ME (Afme.org.uk) and
ME Research UK (Meresearch.org.uk).


DR HILARY'S DIAGNOSIS

In its mildest form, ME causes physical weakness, extreme tiredness,
emotional and psychological distress, sleep disturbance and depression.

At its worst, it is totally disabling, making people bed-bound and dependent
on others.

Although there is no 'cure', it usually improves with time and there are
things you can do that can help.

First, graded exercises with realistic goals and plenty of rest in-between
builds stamina.

Then cut out caffeine and alcohol and take extra magnesium and omega-3 fatty
acid supplements.

An anti-inflammatory tablet like ibuprofen can ease joint and muscle pains
and headaches, while talking therapy and antidepressants can lift mood.

The good news is that ME usually disappears within a few years on its own.

But in the meantime, joining a local support group and learning how to
handle stress effectively can make a world of difference.


(c) 2008 News Group Newspapers Ltd.

* * *

There are ways to improve post-viral CFS (which is not the same as psychiatric fatigue), but those ways do NOT include exercise.  Suzi is right, a trip to the gym will make you feel worse ... if you have CFS rather than depression -- depressives feel energized after exercising.  Dr. Hilary is wrong in saying that graded exercise is helpful.  Obviously, we don't recommend that anyone lie in bed doing nothing if they are capable of doing a few things for themselves, but Dr. Cheney has always been quite clear that aerobic exercise is dangerous for CFS patients -- do some stretches/yoga/resistance exercises to prevent your muscles turning to jelly, but nothing strenuous.  I can "mosey", but I can't walk at a normal speed.  If I allow 30 minutes to walk the 6 blocks to the grocery, I return home tired and needing to sit down, but if I try to walk the 6 blocks in 10 minutes, I return home exhausted and needing to go to bed the rest of the day.

There are many ways to differentiate depression and CFS -- Dr. Bell's book lists some of them, Dr. Berne's book has a two-page chart -- but the easiest is to gauge the patient's physical reaction to aerobic exercise.  A hallmark symptom of CFS is exercise intolerance, also called post-exertional malaise.  Unlike all those blood tests that will come up normal, this test costs nothing, and will give you a foolproof answer.

Some patients with CFS develop depression as a reaction to having their former lifestyle ripped away from them, just as some cancer patients and MS patients and amputees develop depression as a result of the lifestyle changes imposed on them.  Anti-depressants and counseling can help the depression, but they won't cure the CFS any more than they will cure cancer, MS or grow a new limb for an amputee.  Again, if the patient has tried several anti-depressants and still isn't feeling better, that's a pretty good sign that the problem isn't depression, it's CFS.

Talking to a friend who is a retired psychiatric nurse makes me feel better (in the sense of feeling less isolated, spending 99% of my time at home, and most of that in bed or on the couch), but it does not miraculously make me feel well enough to go back to work.  In fact, having to concentrate on a phone conversation exhausts me enough to require a nap after I'm done talking to her.  She (like several other psych professionals I communicate with on a regular basis) has never told me "I think you need counseling, you sound depressed".  It's only the amateurs who try to tag the depression label on anyone who says they're tired and spend most of the day in bed.  The professionals know there's more to it than that -- someone who's depressed doesn't WANT to do anything, whereas someone with CFS wants to do it very much, but finds their body doesn't cooperate.

My first specialist told me the key is to improve the quality of sleep.  And, sure enough, after years of being handed one anti-depressant after another that didn't do a thing, when I finally got sleeping pills that put me to sleep 8 hours a night (instead of 2 hours), I startd to improve.  My immune system restarted and was able to start attacking the virus again.  I ran a 101 fever for 6 months (duration documented by the doctor's office), which is additional evidence that I have post-viral CFS, not a psychological problem.

Ibuprofen is an anti-inflammatory.  If you have inflammatory pain (e.g., arthritis), it will help.  But if you have the neurological pain from CFS/fibro, you can take Advil by the handful, and all it'll do is give you an ulcer ... it won't relieve your pain.  If you can get your doctor to prescribe something narcotic (I'm taking Tramadol), terrific.  If not, heat is your friend: hot bath, hot weather, heating pad.  Also, try FibroSoak/FibroRub from www.MtShastaNaturals.com

This response by Dr. Hilary shows the immense level of ignorance that CFS patients have to deal with -- doctors who blissfully prescribe precisely the things that make CFS worse, because they can't tell the difference between the symptom of chronic fatigue, psychiatric Fatigue Syndrome, and post-infectious Chronic Fatigue Syndrome (known in other English-speaking countries as Myalgic Encephalomyelitis). 

Too many of us go to doctors expecting to be cured, and instead wind up getting steadily worse while they play Blame The Patient.  Instead, the blame needs to be laid where it belongs: at the feet of doctors who think they know more than they do.

In the legal profession, we're trained to say "I don't know, but I can find out".  There's no shame in looking things up -- to the contrary, we can charge $100/hour for making sure that we're giving you the right answer.  Doctors, on the other hand, hate to say "I don't know".  They'd rather doom a patient to a lifetime of disability than admit there's something they need to look up.  I'm far more impressed by a doctor who does what it takes to make sure that I get the RIGHT diagnosis and the RIGHT treatment than one who goes for the easy answer, and then blames me when the wrong treatment, for the wrong disease, doesn't cure me.

Thursday, June 26, 2008

A doctor speaks out

"The best doctors are the ones who aren’t afraid to say ‘I don’t know’ or ‘I’m not sure.’ The most dangerous are the ones who think they know but don’t."

      – Anonymous oncologist, Santa Cruz CA

         Reader’s Digest 7/08

Every CFS patient can tell you horror stories about doctors "who think they know but don’t." I’m not alone in having dealt with a doctor who thought he recognized a couple of symptoms and gave me a wrong diagnosis based on that partial information.

What made that doctor especially dangerous was the fact that he thought he knew more than the specialists who’d already given me the correct diagnosis. He took it upon himself to overrule their expertise, to prescribe something the experts say doesn’t work for what I really have, and to blame the patient when treating what I don’t have didn’t cure me.

I told him at every appointment what the experts recommend, and at every appointment he came up with something else he wanted to try first. It became apparent that this was an ego game: he’s the doctor, I don’t have a medical degree. Even if the patient learned from experts in the field, she’s still not a doctor and therefore he doesn’t have to listen to anything she says about expert-recommended treatments. (Although we have patients who are medical professionals, and they also report their doctors playing Blame The Patient. See Dr. Ryll’s history of the Mercy San Juan Hospital epidemic, where CDC investigators concluded the doctors and nurses were "just too lazy to work.")

When the subject of the misdiagnosis came up after the fact, Dr. Thinks He Knows Everything’s explanation was "nothing you said made sense." And that comment made all the sense in the world ... the symptoms I described don’t make sense in the context of what he wanted to diagnose, and he didn’t know enough about CFS to make sense of them. They were specifically intended to not make sense for his desired diagnosis: I know what symptoms differentiate CFS from depression, and I make sure to recite those to be sure that I get the right diagnosis, so that a doctor who might be thinking depression stops short and thinks "that doesn’t make sense" and looks for another diagnosis that matches the symptoms. But, that requires the doctor to know what all the symptoms of depression are, and not just "tired and listless" (depression also requires an emotional component – crying, low self-esteem, thoughts of suicide – which I don’t have).

The very first doctor in 1987 who wanted to diagnose "hypochondriac female" insisted on a psych evaluation; a professor of counseling explained to us that without the required emotional involvement, the symptoms of depression/anxiety were the same as those of physical illness, and since I was running a fever, it would make more sense to him to refer my problem to an MD instead of a psychiatrist, because it sounded to him like I had the flu. In his professional opinion, nothing that was described sounded like a psychological problem. That doctor, too, didn’t want to hear that I had a clean psychiatric bill of health, and was in favor of sending me to as many shrinks as it took to get the opinion he wanted to hear.

As the Griffith/Zarrouf article posted earlier today says, the best diagnostic tool is a good history. They’re not popular among doctors because it takes time to take a good history, whereas you can slap an erroneous depression label on a patient as soon as she says "I’m tired". But "my symptoms started with a virus" will lead you along the path to CFS, as will inquiring into the patient’s emotional state, instead of taking the short-cut of assuming you know what she’s thinking: the circular reasoning that "if" the patient has depression, therefore the patient has the emotional symptoms of depression, and therefore, the patient must have depression, without ever asking the patient about those required emotional components. (As with any other debilitating illness, some patients develop depression as a result of being ill and unable to continue life as they knew it, but again, a good history will reveal that the patient was not depressed until after months of physical illness and reduced quality of life. In which case, anti-depressants can help the overlay of depression, though they won’t do a thing for the underlying physical illness, whether that’s CFS or cancer.)

I have respect for the doctor who told me "I don’t know much about CFS." I have respect for the doctor who told me "I’m not sure what to do for you, because there’s no magic pill." But I don’t have respect for doctors whose ego won’t allow them to say "I don’t know" or "I’m not sure" or "you’ve read a lot about this over the years since you were diagnosed, what do the experts say?"

My current doctor is not a CFS expert – it’s a full day’s journey to get to the nearest CFS expert and my health isn’t up to full days out of bed – but he’s open-minded enough to accept that I’m an intelligent, educated human being who can read English and tell the difference between snake oil and published research. If I bring him a research abstract or an article by one of the experts, he will discuss it with me; I know he’s not going to just write a prescription, we’re going to talk about the pros and cons, the potential side effects, but if I tell him "this expert says to try that pill" he’ll consider it, and not just dismiss it out of hand because it was my suggestion and not his own idea. And that’s really all I ask of a doctor: to admit that he can still learn a few things. Even the experts occasionally get together at conferences to learn from each other.

The problem is, the dangerous doctors will never admit to you or to themselves that they don’t know. They think they know, and therefore, they don’t think they need to seek outside expertise. If you ask them, they will tell you that they know about CFS; it takes time to see the proof that they don’t know as much as they think they do, and by then, the damage may be done.

I can never erase the erroneous comments in my medical records describing the fictional "long history of depression", the lie "never diagnosed by any doctor", the disparaging remarks that I "refuse to get better" so I don’t have to go back to work. The best I can do is to demand that anyone reviewing those records look at other records to try to find where anyone was prescribing all those anti-depressants I supposedly took non-stop for years and years, look at the proof that I was diagnosed with CFS by a CFS specialist in 1988 (and diagnosed again by rheumatologists in 2000, 2001, 2003, 2004...), and read the experts’ comments that support my stance that the reason I didn’t get better was because anti-depressants are totally useless for CFS.

At the time I was accused of not wanting to work, I had a business of my own and a second business started with a partner; what really doesn’t make sense is that accusation that I don’t want to work, because I’ve always either been looking for a job or running my own business. The real problem with work is that, without doctors addressing my actual disease, my health got worse and no one would hire someone who came into their office looking and acting deathly ill (one interviewer described me as "a worker’s comp claim waiting to happen" because the symptoms the doctor refused to see were so obvious to someone who was not in deep denial about the physical nature of my ailment).

As Dr. Katrina Berne writes, "Some problems are just not easily fixed, even when the motivation is strong." Most CFS patients have a strong motivation to get well and return to work, but the lack of proper medication means that their problem is not easily fixed. The lack of proper medication to fix the problem should not be blamed on the patient – it’s a direct result of the fact that many in the medical profession either don’t know or refuse to believe that CFS and depression are not the same thing, and the dearth of research funding resulting from CFS not being taken seriously. (According to Dorothy Wall, "In 2003, more than twenty years after the first CFS patients ... the total federal expenditure for CFS research – from both the NIH and CDC – was still a paltry $16 million. By contrast, according to its own documents, the NIH alone spent $99 million on multiple sclerosis in 2003, an illness affecting half as many people." Yet, the experts are clear that the level of disability in CFS is equivalent to the disability of MS, and therefore, it would seem fair that CFS should receive at least equal research funding.)

And as long as there are doctors who don’t know how to tell the difference between CFS and depression, yet insist on treating CFS patients anyway, there will be patients whose future health is in danger due to the doctor’s inability to say "I don’t know."

DON'T ASSUME IT'S DEPRESSION - PART 1

Figures and Tables at http://www.co-cure.org/Griffith.htm  

The Primary Care Companion to the Journal of Clinical Psychiatry Vol. 10, #2, pp. 120-128

March 2008

http://psychiatrist.com/pcc/

http://psychiatrist.com/pcc/abstracts/abstracts.asp?abstract=pcc100206.htm

A systematic review of Chronic Fatigue Syndrome:

Don't assume it's depression

James P. Griffith, M.D., F.A.C.P., and Fahd A. Zarrouf, M.D. - From the Internal Medicine/Psychiatry Residency Program, West Virginia University, Charleston. - Corresponding author and reprints: Fahd A. Zarrouf, M.D., Medicine/ Psychiatry Residency Program, West Virginia University, 501 Morris St., 4 West, Charleston, WV 25326 fahdzarrouf@hotmail.com  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Abstract

Objective

Chronic fatigue syndrome (CFS) is characterized by profound, debilitating fatigue and a combination of several other symptoms resulting in substantial reduction in occupational, personal, social, and educational status. CFS is often misdiagnosed as depression. The objective of this study was to evaluate and discuss different etiologies, approaches, and management strategies of CFS and to present ways to differentiate it from the fatigue symptom of depression.

Study Selection and Data Extraction

CFS definitions, etiologies, differential diagnoses (especially depression) and management strategies were extracted, reviewed, and summarized to meet the objectives of this article.

Data Synthesis

CFS is underdiagnosed in more than 80% of the people who have it; at the same time, it is often misdiagnosed as depression. Genetic, immunologic, infectious, metabolic, and neurologic etiologies were suggested to explain CFS. A biopsychosocial model was suggested for evaluating, managing, and differentiating CFS from depression.

Conclusions

Evaluating and managing chronic fatigue is a challenging situation for physicians, as it is a challenging and difficult condition for patients. A biopsychosocial approach in the evaluation and management is recommended. More studies about CFS manifestations, evaluation, and management are needed.

"She is depressed," her physician wrote when referring Ms. A, a 65-year-old married woman, for a psychiatric consult. "She has been feeling tired for more than a year and described being exhausted most of the time, with headaches, joint pain, and problems with her concentration and memory. Her fatigue is frustrating for her and for her family; she cannot function well even in the morning. She denied being depressed, and does not have any previous mental or medical illnesses. Every lab I checked was normal. I still think that she is hiding her depression and manifesting it with all these somatic complaints."

Prolonged fatigue is defined as self-reported, persistent fatigue of 1 month or longer.1 Chronic fatigue syndrome (previously known as myalgic encephalomyelitis2 or neurasthenia3) is characterized by profound, debilitating fatigue and a combination of symptoms resulting in substantial reduction in occupational, personal, social, and educational status1,2,4-7 (see Table 1). Diagnosis of the chronic fatigue syndrome (CFS) can be made only after alternate medical and psychiatric causes of chronic fatiguing illness have been excluded.

At least 1 million Americans have CFS,1,8 more than have lung cancer or multiple sclerosis; yet more than 80% go undiagnosed. In the primary care setting, the prevalence of CFS ranges from 3% to 20% and from 80% to 90% at the end of life.9,10 There are no ethnic or racial differences. Previous reports have mentioned a female:male ratio of 1.3:1,6 but a recent report by the U.S. Centers for Disease Control and Prevention (CDC) showed a female:male ratio of 4:1. It occurs most often in the 40- to 59-year age group and in the geriatric population.1,9,10

Although the concept of neurasthenia was introduced in 1869 by George Miller Beard,3 CFS was defined in 1988 by the CDC, and while more than 3000 research studies have been done in this field, there is still some debate about the existence of this syndrome.1,11,12 The uncertainty about its existence and the lack of a specific laboratory test or marker to identify it, associated with hesitancy about making a diagnosis without knowing exactly how to treat it, all act as barriers to the diagnosis and treatment of CFS by primary care practitioners and psychiatrists.

Unlike the uncertainty about its existence, there is strong certainty about the impact of CFS. CFS patients, by definition, are functionally impaired and as disabled as patients with multiple sclerosis, heart disease, end-stage renal disease, and similar chronic conditions. The annual economic impact of CFS in the United States is estimated to be $9.1 billion in lost productivity.1

DATA SOURCES

A MEDLINE search was conducted to identify existing information about CFS and depression using the headings chronic fatigue syndrome AND depression. The alternative terms major depressive disorder and mood disorder were also searched in conjunction with the term chronic fatigue syndrome. Additionally, MEDLINE was searched using the term chronic fatigue. All searches were limited to articles published within the last 10 years, in English. A total of 302 articles were identified by these searches. Also, the term chronic fatigue syndrome was searched by itself. This search was limited to articles published within the last 5 years, in English, and resulted in an additional 460 articles. Additional publications were identified by manually searching the reference lists of the articles from both searches.

FATIGUE ETIOLOGIES

CFS cannot be considered either physical or psychological but instead requires a biopsychosocial approach to the illness. Numerous studies have tried to pinpoint specific etiologies by considering the following fields.

Genetic Etiologies

CFS is sometimes seen in members of the same family,13,14 but there is no evidence that it is contagious; instead, there may be a familial predisposition or a genetic link. The concordance rate was higher in monozygotic than in dizygotic female twins for chronic fatigue.15 Hickie et al.16 evaluated genetic and environmental determinants of prolonged fatigue in a twin study and found 44% (95% CI=25% to 60%) of the genetic variance for fatigue was not shared by the other forms of psychological distress, and also found that environmental factors made negligible contributions to fatigue. On the other hand, Cho et al.17 found evidence of a partly genetic influence, but environmental effects continued to be predominant. Clearly, further research is needed to explore these possible relationships.

Immunologic Etiologies

Abnormal natural killer cell cytotoxicity,18 increase immune activation markers,19 greater numbers of CD16+/CD3- natural killer cells,20 and the presence of interferon in serum and cerebrospinal fluid in CFS patients21 have been identified. Staines22 suggested the loss of immunologic tolerance to vasoactive neuropeptides or their receptors following infection, other events, or de novo as a mechanism.

Infectious Etiologies

Possible infectious etiologies have generated the most interest among CFS researchers. It has been postulated that chronic fatigue is a continuum ranging from cases with chronic viremia on the one hand to instances of frank psychiatric illness on the other.23 Multiple infectious agents have been linked to CFS, including Borna disease virus,24,25 parvovirus B19,26,27 glandular fever,28 Enterovirus,29 human herpesviruses 4, 6, and 7,30-32 infectious mononucleosis,33 Nipah virus encephalitis,34 and Q fever.35

Infections have not only played important etiologic roles, but also have been considered predictors of better prognoses when compared to noninfectious CFS cases.36 Human herpesvirus 6 reactivation has been suggested as an objective biomarker for fatigue.30

Endocrinology/Metabolism Etiologies

Hypothalamic-pituitary-adrenal (HPA) axis abnormalities have been studied as potential biological tests to diagnose CFS. Studies have shown HPA hypoactivity and higher chronic adrenocorticotropic hormone (ACTH) autoantibody levels as significant pathologic factors in CFS.37-39 Also reduced area under the ACTH response curve in CFS patients undergoing insulin tolerance test was significantly associated with the duration of CFS symptoms (r=-0.592, p=.005) and the severity of fatigue symptomatology.40 Other studies have suggested upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome but not in those with primary depression.41 However, another study showed no etiologic role for deficiency in central opioids or the HPA axis in the symptoms of CFS.42 Other biological factors have been investigated and considered as biological markers in CFS, including low magnesium level,43 low arachidonic acid level, low L-carnitine level,25 serum dehydroepiandrosterone (DHEA) sulfate deficiency,44 and impairments of the 2',5'-oligoadenylate (2-5A) synthetase/RNase L pathway.45 Other studies showed no role of linoleic acid, eicosatrienoic acid (both p>.05),25 ferritin, vitamin B12, folate, or serum erythropoietin levels.46

Mental/Neurologic Etiologies

Psychosocial factors are frequently thought to contribute to fatigue. Rangel et al.13 found that CFSin childhood and adolescence is associated with higher levels of parental mental distress, emotional involvement, and family illness burden than those observed in association with juvenile rheumatoid arthritis, a chronic pediatric physical illness. Endicott14 described stressors including earlier mortality age and increased prevalence of cancer, autoimmune disorders, and CFS-like conditions in parents of psychiatric patients with CFS as compared to control groups. Thirty percent of the CFS patients and none of the controls reported dilemmas in the 3 months prior to the CFS onset in one study.47 History of abuse, particularly during childhood, may play a role in the development and perpetuation of chronic fatigue,48 and childhood trauma was associated with a 3- to 8-fold increased risk for CFS across different trauma types in one study.49 Sleep is also an interesting etiologic factor, as many patients with CFS have sleep disorders, and those with sleep disorders showed greater functional impairment independent of their psychiatric disorders.50-52

FATIGUE: DON'T ASSUME IT'S DEPRESSION

Fatigue is a part of a wide spectrum of diagnoses ranging from being a symptom in depression, anxiety, seasonal affective disorder,53 and multiple other diagnoses to being a full syndromal disorder in CFS, yet CFS goes undiagnosed in 80% of cases and is often misdiagnosed as depression. The Diagnostic and Statistical Manual of Mental Disorders doesn't list CFS as a diagnosis although the International Classification of Diseases, 10th Revision, does.12 In clinical practice, CFS presentations range from complicated cases associated with a psychotic state resulting in multiple murders in one case report54 to noncomplicated presentations with multiple psychiatric disorders, primarily depression.55 It is very important to understand the distinctive features between chronic fatigue and depressive disorder when evaluating a patient with a main complaint of fatigue. A full detailed history accompanied by questionnaire forms can be very helpful to differentiate CFS from major depressive disorder. There is still no specific test that can confidently differentiate between them. Multiple studies have tried to find distinctive factors and they are listed in Table 2.

EVALUATION OF FATIGUE

Diagnosing CFS can be challenging for health care professionals for many reasons; the most important one is finding fatiguein a large number of illnesses and disorders. We reviewed information available about evaluation of chronic fatigue and discuss it in 3 parts: history, exam, and diagnostic tests.

History and Differentials

Because CFS is a diagnosis of exclusion,1 a full detailed history is considered essential. The history should include a detailed account of the symptoms, the associated disability, the choice of coping strategies, and importantly, the patient's own understanding of his/her illness.65 Every patient should be carefully evaluated for certain medical, psychiatric, and neurologic diseases that can cause fatigue as the most prominent symptom (Table 3). Two of the important differential diagnoses are depression and fibromyalgia. Although it is difficult to differentiate CFS from fibromyalgia confidently depending on the history or other reported differences of cognitive dysfunction components or clinical pain measures,66,67 CFS and fibromyalgia commonly co-occur within the concept of central sensitivity syndromes or functional somatic syndromes.68 This co-occurring increases functional impairment when compared to CFS individuals alone.69,70 Some of the distinguishing features between CFS and fibromyalgia include evidence for triggering viral infection and lower level of serum acylcarnitine observed in CFS patients, which is lacking in the majority of patients with fibromyalgia;71 slower information-processing in CFS patients compared to impaired control of attention in fibromyalgia patients;66 and lacking of the characteristic diffuse soft tissue pain and pain on palpation in at least 11 of 18 paired tender points in CFS patients.

Exam

Every CFS evaluation should include a mental status examination to identify abnormalities in mood, intellectual function, memory, and personality. Particular attention should be directed toward current symptoms of depressive, anxious, self-destructive thoughts and observable signs such as psychomotor retardation.1 Although there is no definite physical finding, a full and thorough physical examination may be helpful in excluding other conditions. Multiple studies have suggested dysautonomia with greater increase in heart rate together with a more pronounced systolic blood pressure fall on standing in CFS patients compared to healthy individuals.46, 72 Other studies found no statistically significant differences in either heart rate or galvanic skin resistance both during a normal day and before, during, and after exercise testing.73

Tests

The CDC has recommended the following initial screening tests when evaluating patients with CFS: urinalysis, total protein, glucose, C-reactive protein, phosphorus, electrolyte, complete blood count with leukocyte differential, alkaline phosphatase, creatinine, blood urea nitrogen, albumin, antinuclear antibody and rheumatoid factor, globulin, calcium, alanine aminotransferase or aspartate transaminase serum level, and thyroid function tests (thyroid stimulating hormone and free T4).1 Further tests or referral to specialists may be indicated to confirm or exclude a diagnosis that better explains the fatigue state or to follow up on results of the initial screening tests.

Multiple other studies have tried to find biomarkers or radiological markers for CFS. Erythrocyte sedimentation rate was normal in all 23 CFS patients in one study.74 Another study found that concentrations of C-reactive protein, beta_2-microglobulin, and neopterin were higher in patients with CFS (p=<.01).75 On the other hand, a study by Swanink et al.76 found that complete blood cell count, serum chemistry panel, C-reactive protein, and serologic tests were not different in 88 patients with CFS when compared to a control group. A potential role for DHEA in CFS, both therapeutically and as a diagnostic tool, was suggested in one study.64

Magnetic resonance imaging studies have been inconsistent, with some of them suggesting larger ventricular volumes.77-84 Functional magnetic resonance was more promising, as it showed quantitative and qualitative differences in activation of the working memory network,85 attenuation of the responsiveness to stimuli not directly related to the fatigue-inducing tasks,86 utilization of more extensive regions of the network associated with the verbal working memory system,87 impaired functioning and reduced gray-matter volume in the bilateral prefrontal cortex,88 and inactive ventral anterior cingulate after making an error.89

Single-photon emission computed tomography (SPECT) and brain electrical activity mapping scans were promising in one study,90 and SPECT scans showed more abnormalities than did magnetic resonance scans in one study (p<.025).91 Siessmeier et al.92 detected abnormalities in 18-fluorodeoxyglucose positron emission tomography in approximately half the CFS patients examined, but found that no specific pattern for CFS could be identified. Positron emission tomography showed an alteration of the serotonergic system in the rostral anterior cingulate in one study, which was suggested as an etiology.93 Recently, Puri94 described the application of proton neurospectroscopy and 31-phosphorus neurospectroscopy in chronic fatigue syndrome. It is essential to mention that evidence to date does not support routine use of the imaging modalities discussed above in evaluating potential CFS patients.

Finally, it is important to remember that a good history is more important than any available test to diagnose CFS and differentiate it from depression. The algorithm shown in Figure 1, which is based on the CDC recommendations and the results of the studies reviewed, is suggested for evaluating chronic fatigue.

Don't Assume It's Depression (Part 2)

MANAGEMENT OF FATIGUE

It is important to manage fatigue in the context of each patient suffering with it. Treatment of CFS, with its various major clinical and functional impacts, should be associated with a "biopsychosocial model" of management. Educating patients about their diagnoses is crucial. Physicians should emphasize distinction among factors that may have predisposed patients to develop, trigger, or perpetuate the illness.65 Progressive muscular rehabilitation, combined with behavioral and cognitive treatment, and appropriate choice of medications are essential parts of therapy.8

We will review the major concepts of CFS management and the evidence behind them.

Supportive and Symptomatic Treatment

Educating patients about CFS and validating their illness experience in addition to establishing a working alliance are the initial steps in the treatment.1,65 Direct the treatment toward the most problematic symptoms, as prioritized by the patient,1 and other illness-perpetuating factors.65 Encourage a well-balanced diet, and discuss with patients their nutritional habits. Advice about preventing over- and under-activity is essential. "Start low and go slow" is the correct advice for activities and exercise, the same as for using medications. Gear activities toward improving function in areas that are of greatest importance in achieving activities of daily living and remain open-minded about alternative therapies (electroacupuncture was helpful in one study95) and discuss them with your patients when appropriate.1 Consider referring or asking for consults and discuss that with patients early in the treatment.

Cognitive Behavioral Therapy

The short-term studies of cognitive behavioral therapy (CBT) in CFS have shown improvement in function and symptom management, especially in conjunction with other treatment modalities and in comparison to relaxation controls.96-99 Reports about good outcome following CBT ranged from 70%99 to none or even worsening of the symptoms.100 CBT was effective in treating symptoms of fatigue, mood, and physical fitness, but no improvement in cognitive function or quality of life was noticed in one study.101 Other studies showed limited effect on pain and fatigue.1 When treating CFS patients, the CBT therapist needs to be familiar with CFS, to be aware of the evidence for CFS as a biologically based disorder, and to validate the patient's experience of living with a misunderstood illness.

Exercise

CFS patients are very sensitive, and any treatment modality including exercise should start low and advance slowly. All exercises need to be followed by a rest period at a 1:3 ratio (i.e., 10 minutes of exercise: 30 minutes of rest). Review of the studies showed that exercise decreased the psychological stress102 and improved fatigue, functional capacity, and fitness significantly better than flexibility treatment,103 especially when associated with mood-enhancing, stress-reducing activities.104,105

Pharmacologic Treatment

Multiple studies have evaluated different treatment interventions, including recombinant erythropoietin, psychostimulants, corticosteroids, anti-inflammatory drugs, L-carnitine, and others.10,106 Antidepressants are the most common medications used in this regard; selegiline had a small but significant therapeutic effect independent of its antidepressant effect.107 Fluoxetine has been shown to improve overall symptoms and measures of immune function in one study,108 but failed in randomized, double-blind studies against placebo109 and graded exercise.110 Bupropion was effective for treatment of the fatigue and depressive symptoms associated with CFS in 9 fluoxetine-resistant patients111 and was also helpful in augmenting paroxetine in one case report.112 Venlafaxine was effective in 2 case reports.113 Moclobemide up to 600 mg a day for 6 weeks showed significant but small reductions in fatigue, depression, anxiety, and somatic amplification, as well as a modest overall improvement.114 Duloxetine may have a theoretical therapeutic benefit because of its characteristic of targeting pain. We could not find any study evaluating it in CFS patients. It is essential to mention that evidence to date does not support superiority of one medication over the others.

Other medications have been studied also. Clonidine enhanced both growth hormone (p=.028) and cortisol release (p=.021) and increased speed in the initial stage of a planning task (p=.023) only without affecting hormonal, physiologic, symptomatic, or neuropsychological measures.115 Low-dose hydrocortisone therapy caused increases in plasma leptin levels, with this biological response being more marked in those CFS subjects who showed a positive therapeutic response to hydrocortisone therapy.116 Essential fatty acid supplement rich in eicosapentaenoic acid was beneficial in a case report.117 Carnitine supplementation has been shown to reduce chronic inflammation and oxidative stress in hemodialysis patients and, in cancer patients, reduce fatigue and improve outcome.118 Treatment with modafinil was not beneficial in patients with CFS in one study.119

No therapeutic effects were found for natural killer cell stimulant,120 low-dose combination therapy of hydrocortisone and fludrocortisone,121 immunologic and antiviral substances, melatonin, or bright-light phototherapy.122

CONCLUSION

Evaluating and managing chronic fatigue is a challenging situation for physicians as it is a challenging and difficult condition for patients. A biopsychosocial approach in the evaluation and management is recommended. More studies about CFS manifestations, evaluation, and management are needed.

Drug names: bupropion (Wellbutrin and others), duloxetine (Cymbalta), clonidine (Catapres, Duraclon, and others), fluoxetine (Prozac and others), hydrocortisone (Cortef, Texacort, and others), modafinil (Provigil), paroxetine (Paxil, Pexeva, and others), selegiline (Eldepryl, Emsam, and others), venlafaxine (Effexor).

Tuesday, June 24, 2008

The case for inequality

Over the past few weeks, 600 people have gotten salmonella from tomatoes, and the government has launched an international search for the source of the infection.

Over the past 25 years, 1,000,000 Americans have gotten CFS, and the government seemingly could not care less.  Money designated for CFS research was used for something else, discovered, repaid, and then a second time used for something else!

Why does salmonella -- which is usually just a matter of a few days of digestive problems -- deserving of this multi-million-dollar investigation, while a disease that results in permanent disability has to beg for every research dollar?

The answer is clear to anyone who has read "Osler's Web" ...  one of the experts eventually realized "they don't WANT to find anything."  Finding proof that CFS exists would result in proof that CDC lied all along.

Monday, June 23, 2008

Self Help: Pacing

This week we begin a new eight-part series: "Pacing: What It Is and How to Do
It." The first article describes how to define your Energy Envelope.

Our website contains many articles on topics such as coping strategies, pacing
and support. In addition, there are patient success stories and information for
family and friends. In addition to our website, we offer self-help courses
online. Founded in 1998 as a 501(c)(3) non-profit organization, we have
conducted nearly 250 self-help courses and groups.

Bruce Campbell, Ph.D., Executive Director
CFIDS & Fibromyalgia Self-Help Program
www.cfidsselfhelp.org

* * *

Dr. Ellen Goudsmit (one of our many patients with the academic qualifications to also be an expert) has written extensively on pacing.  Some of those articles appear in this blog, others can readily be googled.

The key to pacing is that you never push yourself to the point that causes you to relapse.  Ideally, you would work for a short time, rest for 2-3 times that period (e.g., 20 minutes work/60 minutes rest) then work a little more.  By working in short increments, you never get over-tired, you're continually topping off your tank.

Obviously, there are times you can't do that -- grocery stores take a dim view of people napping in the aisles -- but I find that I feel better if I work in short bursts throughout the day, for a total of 2 hours, than if I work for 2 hours all at once. 

There's nothing that says you can't load the top rack of the dishwasher, take a nap, then load the bottom rack.  At my worst, on Day 1 I would strip the bed and load up the laundry basket; on Day 2 I'd carry the basket to the washer; on Day 3 I'd load the washer....  It took me a full week to do one load of laundry, but it was done, and I hadn't made myself worse.

I hope all CFS patients reading this blog take the opportunity to sign up for this series on pacing.  Research has shown that you won't accomplish more with pacing, you'll just feel better.  And the key with this disease is to avoid making yourself worse.  Stay well within your limits, and you may start to recover. 

I was able to work full-time for 12 years after diagnosis because of pacing: if I wasn't at work, I was resting.  I missed a lot of parties, festivals, plays, museum exhibitions, etc.,  because of my need to rest evenings and weekends, but I was able to put off the day when I had no choice but to swallow my pride and apply for SSDI benefits. 

Pain and Therapy

From acute musculoskeletal pain to chronic widespread pain and
fibromyalgia: Application of pain neurophysiology in manual therapy practice.

Man Ther. 2008 May 27. [Epub ahead of print]

Nijs J, Van Houdenhove B.

Department of Human Physiology, Faculty of Physical Education and
Physiotherapy, Vrije Universiteit Brussels, Belgium; Division of
Musculoskeletal Physiotherapy, Department of Health Care Sciences,
University College Antwerp, Van Aertselaerstraat 31, B-2170 Merksem, Belgium.

PMID: 18511329


During the past decade, scientific research has provided new insight
into the development from an acute, localised musculoskeletal
disorder towards chronic widespread pain/fibromyalgia (FM). Chronic
widespread pain/FM is characterised by sensitisation of central pain
pathways. An in-depth review of basic and clinical research was
performed to design a theoretical framework for manual therapy in
these patients.

It is explained that manual therapy might be able to influence the
process of chronicity in three different ways.

(I) In order to prevent chronicity in (sub)acute musculoskeletal
disorders, it seems crucial to limit the time course of afferent
stimulation of peripheral nociceptors.

(II) In the case of chronic widespread pain and established
sensitisation of central pain pathways, relatively minor
injuries/trauma at any locations are likely to sustain the process of
central sensitisation and should be treated appropriately with manual
therapy accounting for the decreased sensory threshold. Inappropriate
pain beliefs should be addressed and exercise interventions should
account for the process of central sensitisation.

(III) However, manual therapists ignoring the processes involved in the development and maintenance of chronic widespread pain/FM may
cause more harm then benefit to the patient
by triggering or
sustaining central sensitisation.

* * *

If you're looking for a massage therapist or a physical therapist, always ask about their familiarity with fibromyalgia or CFS before you sign on with them.  The wrong type of massage can cause more pain, and a personal trainer or physical therapist who believes "no pain, no gain" will likely push a CFS patient beyond her limits, which could result in permanent disability.

Your body is not normal and should not be treated in the normal manner, because it will react abnormally.  The therapist must be willing to stop when you say "ow" or "enough", because the best expert on what your body can handle is YOU. 

Restoration of ADA

ADA Restoration & a Potential Deal with the Business Community

Summary of Current Status on ADA Restoration

This is a key week for ADA Restoration. After thirteen weeks of negotiations with the business community, endless drafting and redrafting of legislative language, and numerous meetings and calls for internal vetting within our own community, we have potential deal language. This language can radically improve the legal outcomes of people with disabilities who have tried to bring employment discrimination cases but who have been turned away by the courts for almost ten years now.

Time is of the essence. In order to have any chance of passing this legislation in this Congress given the full Congressional calendar and the upcoming focus on the elections, we must know where we stand as we enter this holiday weekend to enable us to put things into motion early next week. For that reason, both the disability and business communities have agreed to come to a decision on whether or not we will accept and support the proposed deal language by close of business this Thursday, May 22.

Why do we need ADA Restoration?

Almost eighteen years ago, Congress passed and President H.W. Bush signed the Americans with Disabilities Act (ADA), a civil rights law promising freedom and equality for people with disabilities in public transportation, businesses, public programs and services, and the workplace. Borrowing the definition of disability from Section 504 of the Rehabilitation Act, Congress intended the ADA to stop employers from making employment decisions based on a person's current, past, or perceived disability.

Under current law, the ADA defines an individual with a disability as an individual with a physical or mental impairment that substantially limits a major life activity, an individual with a history of such an impairment, or an individual who is regarded or perceived as having such an impairment.

Unfortunately, since 1999, the courts have dramatically scaled back the ADA definition to the point where it bears little resemblance to the robust civil rights law that Congress passed in 1990. In a series of Supreme Court cases, the Court decided that the use of medication, prosthetics, hearing aids, auxiliary devices, etc. must be considered when a court is determining if someone is protected under the law. That means that people with all kinds of disabilities who enjoy greater independence (including the ability to work) on account of medication, hearing aids, specific diets, prosthetics, etc., are often no longer protected under the ADA because the courts view their limitations as no longer substantial "enough." Courts have even denied ADA protection to those whose employers have freely admitted that they terminated the individuals because of their disabilities!

The ADA was meant to be just like other civil rights laws that address employment discrimination - when someone experiences discrimination because of disability, the sole focus of the legal case should be on whether the actions of the employer were unlawful. However, the Courts have created an extra hoop for people with disabilities to challenge an employer's actions. First, people with disabilities must "prove" their disability by providing highly personal and often wholly irrelevant information about their lives. Only if they have satisfied this difficult standard are they then permitted to present the facts of the discrimination they encountered. Increasingly, fewer and fewer people are able to get to this point.

Instead of following Congress's clear intention that the definition of "disability" in the ADA be interpreted broadly, the Supreme Court decided to ignore Congressional intent and directed that the definition of disability needed to be interpreted narrowly. As a result, there have been hundreds of court cases with bizarre and devastating outcomes -- with the courts siding with employers rather than individuals facing discrimination more than 90% of the time. People with epilepsy, muscular dystrophy, multiple sclerosis, diabetes, cancer, HIV, intellectual disabilities (formerly known as "mental retardation"), hearing loss, major depression, PTSD, bipolar disorder, and many other disabilities are consistently being told that they are not "disabled enough" and therefore not protected by the ADA.

By watering down civil rights protections for people with disabilities, the courts have created an unacceptable U-turn in the progress that people with disabilities have made to date. Courts have made it legal for an employer to say "You are not welcome here" to people with disabilities who have skills and who want to work.

We knew we needed to act.

What have we done to fix these problems?

In 2004, the National Council on Disability (NCD), the same independent federal agency that drafted the original ADA, published a report entitled "Righting the ADA", which harshly criticized the Supreme Court decisions referenced above. In its recommendations, NCD included proposed legislative language to remedy the problems created by the Courts' narrow interpretations of the definition of disability in the ADA.

While the devastation created by the courts was obvious to everyone, there was widespread concern within the community that "opening" the ADA up for legislative fixes would result in opponents of the law would attempting to water down other protections. For several years, internal discussions within the community revolved around when and how to best address the damage done by the courts.

Then, in September of 2006, after much discussion with the community and using the NCD report language as a basis, then House Judiciary Committee Chairman Jim Sensenbrenner and House Minority Whip Steny Hoyer introduced H.R. 6258, the ADA Restoration Act of 2006. While the legislation did not receive any action, advocates used its introduction to strategize for the next Congress.

A short time later, on July 26, 2007, the 17th anniversary of the signing of the original ADA, Congressman Sensenbrenner and now Majority Leader Hoyer introduced H.R. 3195, the ADA Restoration Act of 2007 (the companion bill, S. 1881, was introduced in the Senate on the same day by Sens. Tom Harkin and Arlen Specter). Due to the tireless efforts of disability advocates, there were 143 original co-sponsors in the House on the day of the bill's introduction. That number has since risen to 245 co-sponsors.

Why did we even enter into negotiations with the business community in the first place?

At the same time that the disability community has been visiting the offices of Members of Congress to urge co-sponsorship and support of ADA Restoration, members of the business community were also hard at work, delivering a message to many of the same offices that the legislation goes "too far" and would hurt businesses.

Concerned that Members of Congress who are sympathetic to the business community's interests would attempt to alter or amend the legislation in damaging ways, including some of the bill's own co-sponsors, Congressional champions of the bill, including Majority Leader Steny Hoyer, encouraged the disability community to meet with the business community to discuss the legislation in the hope that mutually agreed-upon language would emerge. The understanding and goal of both sides was to attempt to craft language that could be mutually defended through the entire legislative process to increase the likelihood of successful passage of a "clean" bill - one free of amendments or other unforeseen changes - in the House and Senate during this year.

Since February 19, 2008, the disability community, with leadership from the American Association of People with Disabilities (AAPD), the National Council on Independent Living (NCIL), the Bazelon Center on Mental Health Law, the National Disability Rights Network (NDRN), and the Epilepsy Foundation, has been in negotiations with the business community around the legislative language. . These groups have met with the understan.ding that, if a deal is reached, both sides will defend the deal and that if any minor clarifications or amendments are put forward during the legislative process, both sides must agree to them.

How does the proposed deal change the ADA?

The proposed deal language:

a.. Requires that the definition of disability be interpreted broadly;

b.. Prohibits courts from considering the effects of medication, prosthetics, hearing aids, etc. when determining whether a person meets the ADA's definition of disability;

c.. Defines "disability" as any actual, past, or perceived physical or mental impairment that "substantially limits a major life activity" and then defines this phrase to mean "materially restricts a major life activity;"

d.. Includes a broad definitional section listing a wide range of major life activities that is intended to restore coverage for many of the groups who have been interpreted out of the ADA by the courts, and

e.. Includes a broad "regarded as" prong that will provide civil rights protection to anyone who is adversely treated based on a physical or mental impairment

The proposed deal provides examples of "major life activities" in its definition section which helps to set the record straight where the courts have wrongly interpreted the term narrowly in the past. The non-exhaustive list includes but is not limited to: "caring for oneself, seeing, hearing, eating, sleeping, walking, standing, lifting, bending, speaking, breathing, learning, reading, concentrating, thinking, communicating, and working." The language also includes a list of "major bodily functions" as part of the definition of "major life activities."

In addition, the proposed deal language expressly rejects the Supreme Court cases which have created the mess which we seek to remedy. It also makes clear that for someone whose disability is episodic (such as with epilepsy) or in remission (such as with cancer), for purposes of establishing their eligibility for the ADA's protections, they are to be considered when their disabilities are active, meaning they will not be shut out of protections if they are discriminated against because of their disabilities simply because they are not currently experiencing the symptoms associated with their disabilities in their active state.

Under the proposed deal, people with a wide range of conditions like epilepsy, diabetes, depression, cancer, and muscular dystrophy will be able to come into the scope of the law's protection through a number of avenues. They can come in under a much broader "regarded as" prong, they can come in under a reconfigured first prong that includes the operation of important bodily functions as part of the definition of major life activities. And, probably most importantly, they can come in under the clarification that their conditions are to be assessed in the absence of any mitigating measures for purposes of deciding if they are substantially limited in a major life activity. For people with episodic conditions, the deal language also makes it clear that their conditions are to be assessed when their conditions are manifesting themselves, not when they are dormant or in remission. In sum, the proposed deal gives people with a wide range of disabilities many more tools for asserting their civil rights protections than they have under current law.

In summary, under the deal language, if a person is discriminated against because of an actual, past, or perceived physical or mental impairment, regardless of severity (except for transitory and minor impairments like the common cold or flu), s/he is eligible for protection under the ADA but not for a reasonable accommodation. However, if a person requests a reasonable accommodation and is materially restricted in a major life activity, s/he would be eligible for a reasonable accommodation.

How does the proposed deal help the disability community?

Right now, all across America, a multitude of people with a wide range of disabilities are denied their civil rights protections on account of the Supreme Court's narrow interpretation of what was intended to be our great civil rights law. As referenced earlier, more than 90% of the time, courts throw out the legal cases of people with disabilities before they even have a chance to prove the facts of discrimination because the courts decide that they are not "disabled enough" to warrant the law's protections in the first place. If we don't pass ADA Restoration legislation, it is not clear how much further the courts will go in narrowing the scope of the ADA's protected class. Any person with a disability who is able to work and live independently is at risk of being found not disabled "enough" for civil rights protections in the workplace given the decisions that we have seen in the federal courts.

In fact, just days after one of the Supreme Court's devastating ADA decisions, cases of disability employment discrimination- some of which involved employers who openly admitted to discriminating on the basis of disability - were thrown out of court because of the Supreme Court's decision. Disability advocates around the country have for years reported the "chilling effect" of the Supreme Court's decisions on efforts to bring disability employment discrimination cases, with lawyers often telling them that there is little hope in winning such cases.

Given the current political climate, the proposed deal language gives us our best shot at fixing the definition of "disability" under the ADA in this Congress and restoring the civil rights of people from across our community who have been told they don't have any rights. Advocates at NCIL, AAPD and others who have worked on this legislation are not convinced that we will do better in the next Congress, in part because the business community's views will be taken seriously by many Democrats and Republicans in any Congress.

The deal language is in line with the goal of ADA Restoration, which is to restore Congress' intent under the ADA by shifting the focus from whether a person is "truly" disabled, to whether the person was treated unfairly on the basis of disability - whether actual, past, or perceived.

What happens if we accept the deal?

If the disability community agrees to this deal language, we will work closely with our Congressional champions to move quickly to pass the revised legislation in the House of Representatives and the Senate. Our goal is to have the legislation passed by this Congress and signed by President Bush before October.

Please direct any questions, comments, or concerns to Anne Sommers at AAPDanne@earthlink.net .

* * *

I am one of many people who employers and VocRehab consider "too disabled to work", but the courts consider "not bad enough to qualify as 'disabled'."  People who fall into the cracks are denied the help they need -- Social Services acknowledges that I clearly need assistance, but the law says they can't give it to me because I'm not officially "disabled"; you have to be either "disabled" or over 65 to qualify for In Home Support Services, and it looks like I'll get it by virtue of turning 65 long before any judge agrees with VocRehab that I'm not employable due to disability.

On the one side, a judge ruling on ADA-required accommodations said that a CFS patient who required "work when able" was too disabled to work.  On the other side, judges ruling on Disability applications have repeatedly stated that a CFS patient who can "work when able" is not disabled because they can occasionally work.

My SSDI judge has repeatedly said that "with your qualifications and experience, anyone should be happy to hire you and make any necessary accommodations."  Yet, when I talked to an attorney with ADA expertise about getting the accommodations I needed in order to be able to work, he gave me a list of cases to read that make it clear that the accommodations I need are far beyond what employers are required to give me.  In the current "bottom line first and foremost" business climate, it's not likely I'll find an employer willing to go above and beyond what the law mandates, so I remain too disabled to use ADA to get a job, but apparently not disabled enough to get SSDI benefits. 

Text of ADA Restoration Bill

The proposed deal language follows below:

A BILL

To restore the intent and protections of the Americans with Disabilities Act of 1990. Be it enacted by the Senate and House of Representatives of the United States of America in Congress assembled,

SECTION 1. SHORT TITLE. This Act may be cited as the 'ADA Restoration Act of 2008'.

SEC. 2. FINDINGS AND PURPOSES. (a) Findings- Congress finds that-

(1) in enacting the Americans with Disabilities Act of 1990 (ADA), Congress intended that the Act 'establish a clear and comprehensive prohibition of discrimination on the basis of disability' and provide broad coverage;

(2) in enacting the ADA, Congress recognized that physical and mental disabilities in no way diminish a person's right to fully participate in all aspects of society, but that people with physical or mental disabilities are frequently precluded from doing so because of prejudice, antiquated attitudes, or the failure to remove societal and institutional barriers;

(3) while Congress expected that the definition of disability under the ADA would be interpreted consistently with how courts had applied the definition of handicap under the Rehabilitation Act of 1973, that expectation has not been fulfilled;

(4) the holdings of the Supreme Court in Sutton v. United Airlines, Inc., 527 U.S. 471 (1999), Murphy v. United Parcel Service, Inc., 527 U.S. 516 (1999), Albertson's, Inc. v. Kirkingburg, 527 U.S. 555 (1999), and Toyota Motor Manufacturing, Kentucky, Inc. v. Williams, 534 U.S. 184 (2002) have narrowed the broad scope of protection intended to be afforded by the ADA, thus eliminating protection for many individuals whom Congress intended to protect; and

(5) as a result of these Supreme Court cases, lower courts have incorrectly found in individual cases that people with a range of substantially limiting impairments are not people with disabilities.

(b) Purpose- The purposes of this Act are-

(1) to carry out the ADA's objectives of providing 'a clear and comprehensive national mandate for the elimination of discrimination' and 'clear, strong, consistent, enforceable standards addressing discrimination' by reinstating a broad scope of protection to be available under the ADA;

(2) to reject the requirement enunciated by the Supreme Court in Sutton v. United Airlines, Inc., 527 U.S. 471 (1999), Murphy v. United Parcel Service, Inc., 527 U.S. 516 (1999), and Albertson's, Inc. v. Kirkingburg, 527 U.S. 555 (1999), that whether an impairment substantially limits a major life activity is to be determined with reference to the ameliorative effects of mitigating measures;

(3) to reject the Supreme Court's reasoning in Sutton v. United Airlines, Inc., 527 U.S. 471 (1999) with regard to coverage under the third prong of the definition of disability and to reinstate the reasoning of the Supreme Court in School Board of Nassau County v. Arline, 480 U.S. 273 (1987) which set forth a broad view of the third prong of the definition of handicap under the Rehabilitation Act of 1973;

(4) to reject the standards enunciated by the Supreme Court in Toyota Motor Manufacturing, Kentucky, Inc. v. Williams, 534 U.S. 184 (2002), that the terms 'substantially' and 'major' in the definition of disability under the ADA 'need to be interpreted strictly to create a demanding standard for qualifying as disabled,' and that to be substantially limited in performing a major life activity under the ADA 'an individual must have an impairment that prevents or severely restricts the individual from doing activities that are of central importance to most people's daily lives'; and

(5) to provide a new definition of "substantially limits" to indicate that Congress intends to depart from the strict and demanding standard applied by the Supreme Court in Toyota Motor Manufacturing, Kentucky, Inc. v. Williams and by numerous lower courts.

SEC. 3. CODIFIED FINDINGS. Section 2(a) of the Americans with Disabilities Act of 1990 (42 U.S.C. 12101) is amended-

(1) by amending paragraph (1) to read as follows:

'(1) physical or mental disabilities in no way diminish a person's right to fully participate in all aspects of society, yet many people with physical or mental disabilities have been precluded from doing so because of discrimination; others who have a record of a disability or are regarded as having a disability also have been subjected to discrimination;'

(2) by striking paragraph (7).

SEC. 4. DISABILITY DEFINED.

Section 3 (42 U.S.C. §§12102) is amended:

By revising subsection (2) to read as follows:

(2) Disability -- The term "disability" means -

(A) a physical or mental impairment that substantially limits a major life activity;

(B) a record of an impairment that falls under (A); or

(C) being regarded as having an impairment that falls under (A) or (B).

By inserting after subsection (2) the following new subsections:

(3) Substantially Limits -

The term "substantially limits a major life activity" means materially restricts a major life activity.

(4) Major Life Activities -

a) Non-Exhaustive List of Major Life Activities -- Major life activities include, but are not limited to, caring for oneself, seeing, hearing, eating, sleeping, walking, standing, lifting, bending, speaking, breathing, learning, reading, concentrating, thinking, communicating and working. b) Major Bodily Functions -- A major life activity also includes the operation of a major bodily function. Major bodily functions include, but are not limited to, functions of the immune system, normal cell growth, digestive, bowel, bladder, neurological/brain, respiratory, circulatory, endocrine and reproductive functions.

(5) Regarded as -

(a) In General -- Subject to subsection (b), an individual meets the requirement of "being regarded as having an impairment that falls under (a)-(b)" if the individual establishes that he or she has been subjected to an action prohibited under this Act because of an actual or perceived physical or mental impairment, whether or not the impairment actually substantially limits a major life activity or whether or not the individual actually has the perceived impairment.

(b) Transitory and Minor Impairments -- This subsection shall not apply to transitory and minor impairments where "transitory" means an impairment with an actual or expected duration of six months or less.

(c) Reasonable Accommodation -- An employer is not required to provide a reasonable accommodation to an individual who meets the definition of disability solely under 2(C).

(6) Standards for Applying the Definition of Disability -

(A) To achieve the remedial purposes of this Act, the definition of "disability" shall be construed broadly.

(B) An impairment that materially restricts one major life activity need not limit other major life activities in order to be considered a disability.

(C) An impairment that is episodic or in remission is a disability if it would materially restrict a major life activity when active.

(D) (a) When determining whether an impairment materially restricts a major life activity, such determination shall be made without regard to the ameliorative effects of mitigating measures such as:

(i) medication, medical supplies, equipment or appliances, low vision devices (which do not include ordinary eyeglasses or contact lenses, as defined in (b)), prosthetics including limbs and devices, hearing aids and cochlear implants or other implantable hearing devices, mobility devices, or oxygen therapy equipment and supplies; (ii) use of assistive technology; (iii) reasonable accommodations or auxiliary aids or services; or (iv) learned behavioral or adaptive neurological modifications.

(b) The term "ordinary eye glasses or contact lenses" means lenses that are designed to fully correct visual acuity or eliminate refractive error.

(c) Low vision devices are devices that magnify, enhance, or otherwise augment a visual image.

(E) The ameliorative effects of the mitigating measures of ordinary eyeglasses or contact lenses shall be considered in determining whether an impairment materially restricts a major life activity.

(F) Nothing in this Act alters the standards for determining eligibility for benefits under state worker's compensation laws or under state and federal disability benefit programs.

SEC. 5. DISCRIMINATION ON THE BASIS OF DISABILITY.

(a) Section 102 of the Americans with Disabilities Act of 1990 (42 U.S.C. 12112) is amended--

(1) in subsection (a), by striking `with a disability because of the disability of such individual' and inserting `on the basis of disability'; and

(2) in subsection (b) - (A) in the matter preceding paragraph (1), by striking `discriminate' and inserting `discriminate against a qualified individual on the basis of disability'; and

(B) by adding at the end the following:

(8) Notwithstanding any other provision of law, using qualification standards, employment tests, or other selection criteria based on an individual's uncorrected vision or unaided hearing under this Act unless the standard, test, or other selection criteria, as used by the covered entity, is shown to be job-related for the position in question and consistent with business necessity.

(b) Section 101(8) is amended -

(1) in the paragraph heading, by striking "With a Disability"; and (2) by striking "with a disability" after "individual" both places it appears.

SEC. 6. RULE OF CONSTRUCTION REGARDING REGULATORY AUTHORITY.

Title V of the Americans with Disabilities Act of 1990 (42 U.S.C. 12201) is amended by adding at the end the following:

SEC. 515. RULE OF CONSTRUCTION REGARDING REGULATORY AUTHORITY.

The authority to issue regulations granted to the Equal Employment Opportunity Commission, the Attorney General, and the Secretary of Transportation under this Act, includes the authority to issue regulations implementing the definitions contained in section 3.

SEC. 7. EFFECTIVE DATE

This Act shall become effective on January 1, 2009.