What the Heck are They Talking About: Neurological CFS

"I used to be able to think..."

A brain just like mine:

Whether the assault is by car accident or viral assault - the result is brain damage: sometimes permanent. There is substantial organic research in this area, as well as the role of infectious triggers on the central nervous system and immune system specifically. The biological role of entroviruses is also substantial and connected to biomedical research clearly connecting the neurological disorder of ME/CFS (ICD 10 G93.3) with these viral triggers.

Obstacles to further research:  lack of funding, insurance politics and the repetition of unproven and tangential psychiatric speculation regarding the biopsychosocial role in "fatigue."

"He has suffered brain damage, caused by an undetermined virus that targeted his brain, but he clearly remembers his old way of thinking. He has written a book called In the Shadow of Memory, about the damage done to his brain and the process of rebuilding his life.

Skloot reads from In The Shadow of Memory: "I used to be able to think," the book begins. Now, his memory and abstract reasoning abilities are extremely diminished. He finds himself doing things like saying "blood tower" when he means "rush hour" or putting coffee beans in the carafe instead of the filter basket.

He continues reading, "Sometimes I see my brain as a scalded pudding, with fluky dark spots here and there through its dense layers, and small scoops missing. Sometimes I see it as an eviscerated old TV console, wires all disconnected and misconnected, tubes blown, dust in the crevices."

To make any sense at all, Skloot says he needs to avoid all distractions. During the interview, he has his eyes closed so he doesn't see the studio engineer, his wife, or his open book.

This need to limit outside stimuli is one of the reasons he moved from downtown Portland to the country -- he needed to be in a place where things are slow.

Skloot says his neurological condition is not all bad. It has given him a crash course in the essentials of life -- because he has no choice, he has learned to live in the moment and seek harmony, rather than mastery.

His writing process, too, has completely changed -- it took him over eight years to write the book -- but he finds he has become looser and more open to discovery, and, in many ways, he appreciates the slower pace of his life."

Floyd Skloot

Marit Haahr
The Infinite Mind: How We Think
Week of September 27, 2004

In previously published works, Floyd Skloot refers to his diagnosis of ME/CFS, however, in The Shadow of Memroy, he simply eliminated "fatigue aka the 'F' word" from the discussion. By simply reframing this neuroimmune disorder using more specific and biomedically accurate terms, gained a much wider audience garnering respect instead of curt dismissal.

See my post on using the "F" word.

A journalist's brain on encephalopathy

I began my journalism career in central California where being socked in with heavy, pea soup fog on

Salvador Dalí. The Persistence of Memory.
1931. Oil on canvas, 9 1/2 x 13" (24.1 x 33 cm).
January and February days kept us supplied
with  multi-car accident pile-ups on the freeways and unfortunately, fatalities.

I always drove to work using back roads it was safer. There were days the fog was so thick I drove at five m.p.h. with the driver’s

side door open so I could see the yellow line next to my car because I sure couldn’t see it looking over the hood.

And I wasn’t the only one sticking to side roads. Truckers who weren’t familiar with the area did it too, often at high speeds in an attempt to make up lost time.

I always drove with my windows down no matter how cold. I could hear vehicles before I could see them and it saved my life a number of times at four-way stops.

There would be clear stretches, but you could be back in grey cotton batting in a heartbeat. Having brain damage is like that.

Like most things the end of my journalistic career was more of a fizzle than a bang. I simply started losing my mind. Not insanity mind you, just the slow insidious process of brain damage. 

There is no known cure and the specialist I see says I may never recover my mind at my former level. Can you say bummer? Can you say tears, profanity, and why me? Can you say of all the things I’ve lost I miss my mind the most?

As anyone medically diagnosed with the neurological disorder ME/CFS and fibromyalgia knows just the 24/7/365 relentless grind of pain and exhaustion is enough to bring most anyone to their knees. But, like countless other lives, mine didn't play out quite so simply.

As a single parent, getting three kids off to school in the mornings was all I could manage between the morphine level pain and the never-ending profound bone-crushing exhaustion. Some mornings just didn’t lend themselves to more than a quick skim through the paper, which is akin to suicide to an assigning editor.

I had no idea I had a neurological disorder, but I could feel my mind slipping in small ways.

I lost focus. One of the things I love most about journalism is the variety and learning new ideas, but it wasn’t helping me to stay focused on the matters at hand. (read How squiggles and colored brain maps may change how we view ME/CFS and Fibromyalgia - Life on Seven Brain Cells a day.)

So many times I realized I’d missed whole conversations, conversations I was supposed to be monitoring, because my mind had taken off down an interesting line of thought. I would pinch myself endlessly trying to keep my concentration in the here and now. For those of you old enough to remember the cartoon, Family Circus, my mind map looked like one of “Billy’s” black dash paths through the neighborhood.

I began losing the names of things. The heavier the exhaustion, the worse it was. The neurological term for this pathology is aphasia, more specifically anomia. I ended up talking around things (circumlocution) because I couldn’t remember the word “table,” or the name of the publisher, or the name of the staff member who was covering the subject at hand.  Everything became a thingy and still is. I would substitute words like saying sausage when I meant salad.

You can only pass off so many things with a senior moment joke. I tried writing in notebooks, but would realize I hadn’t understood enough of what was being said to write down anything coherent. Or I would being having a “good day,” and could pretend that this wasn’t happening so I didn’t need to write it down. After all, I had an excellent memory. The operative word here is had.

I would go into meetings with a clear idea of everything I would be expected to cover and come up completely blank when called upon. I knew it, but I couldn’t remember it or figure out how to say it. This lovely little quirk is called expressive aphasia. How to convince the managing editor and executive editor you are clueless moron in one easy step. It was humiliating to say the least.

Other times problems cropped up simply because most editors knew their own beat very well, but I was expected to know everyone’ in the newsroom’s beat and so saying to me, well what about the “school” story didn’t help me much. I usually knew of 12 “school” stories in the works and needed more of a clue. Playing charades is not the best way to present yourself as a professional. Need I say more?

I’d be late because I could no longer find my way around in a city that I knew well. It is too scary to recount the number of times I went one way up a one-way street straight into oncoming traffic. I feel like a cat over due by two or three lives.

Numbers lost their meaning. And I’m not talking about the infamous “journalists can’t count” joke. Although I didn’t know it then, what I have is a rare disorder called adult-onset acalculia, meaning I’ve lost the ability to perform simple problems of arithmetic.

I couldn’t count money so I just handed over the largest bill I had and hoped it covered whatever I was purchasing. In the newsroom it meant that I assigned people to the wrong story on the wrong day, forgot to give enough travel time between assignments, the list was endless and highly upsetting to co-workers. I was frustrated, scared, angry about the anger and overwhelmed.

Oh yes, there is more in the little goody bag of this neurological disorder. I have what is known as pathological orthographic dsygraphia, meaning I cannot spell words with irregular spellings, not to mention merrily mixing and matching homophones as if there is know difference. Writing is no longer a process of minutes or even hours. Try weeks and months.

As essayist Floyd Skloot, who also has ME/CFS, puts it in his seminal book, The Shadow of Memory, if I lose my train of thought I end up stuck at the train station for the day, the week or maybe months. So the impossible takes a little longer. Life goes as life goes, and no one asked me, or you for that matter.

For me, journalism isn’t a job it is a calling. Permanently disabled by the capriciousness of this neurological disorder, it is no longer my living, but you cannot quench a passion with illness.

When French artist Henri Matisse was stricken with cancer in 1941 he kept painting from his wheelchair and towards the end he produced colorful paper cut collages. I can't do even this, even though I have an art degree. I have constructional apraxia which is the inability to assemble, build, draw, or copy  accurately. But, I can look and enjoy and appreciate. I can enjoy the talent of others.

So life does go on, and different doesn't have to mean unhappy. Most days I simply accept reality and just keep pedalling my trike, working around the impossible.

Bet you were wondering why this blog has a few spatters of blood where I overturned, but more often, I hope, there are little black rubber tracks where I popped a wheelie.

Live, love, laugh for life is short.

These exerpts from reviews of Floyd Skloot's book, "In the Shadow of Memory" fit like a glove. Although as individuals, we come from very different backgrounds, the problems caused by this immune-neurological disorder level the playing field of life.

FROM THE PUBLISHER
In December 1988, Floyd Skloot was stricken by a virus that targeted his brain. The resulting damage left him totally disabled and utterly changed. In the Shadow of Memory is a candid memoir of living with a brain and a mind that have suddenly been shattered -- an intimate picture of what it is like to find oneself possessed of a ravaged memory, unstable balance, and wholesale changes in both cognitive and emotional powers...

Publishers Weekly -

In this remarkable collection of essays, part of the American Lives series (edited by Tobias Wolff), Skloot (Night-Side: Chronic Fatigue Syndrome and the Illness Experience) conveys what it is like to live with a damaged brain. In 1988, Skloot was beset by a virus that left him with brain lesions (static dementia) that dramatically affected his ability to think. (Because of this condition, each piece here took one to two years to complete and was constructed laboriously in small periods of time.) He often cannot find an appropriate word and may say, for example, "pass the sawdust" instead of "pass the rice." He forgets faces, names, directions and how to perform simple tasks, and suffers from loss of balance...The author also details, without self-pity, how he was subjected by the Social Security Administration to a series of tests to prove that his illness was organically based and his disability status legitimate..."

(I'm now in the fourth year of my battle to win disability based on my oh so organic disorder. My medical file is about five inches thick with all the documentation the SSDI requires.)

I also like Kara Swanson's book, "I'll Carry the Fork." When she notes, "The curious thing about the crash that ended my life is that I lived through it," if you change crash to CFS you have a book that parallels some of the problems of the neuro-immune-disorder ME/CFS. 

Brain Problems in ME/CFS:Is There a Simple Explanation?

By: Dr EG Dowsett, MB ChB, DipBact   

THE “TOO MANY SYMPTOMS” SYNDROME

It may be that people with ME/CFS are so commonly and unfairly accused of hypochondriasis because they have too many symptoms to permit credibility. 

Alternatively, the casual observer may not have had time to listen, does not understand brain function or finds neurological research boring because it seems incomprehensible.  This is a tragedy for all concerned. 

The sick person faces cruel disbelief, the casual observer seems unkind and the research worker lacks recognition for a fascinating and important study which might produce an adequate research grant.

HEART-SINK PATIENTS

ME/CFS is primarily a NEUROLOGICAL illness which may or may not be accompanied by complications affecting skeletal and cardiac muscle, liver, endocrine and lymphoid organs. 

Whilst most of these can be accepted by the average television viewer as interesting and understandable parts of routine medical and veterinary practice, the problem of belief pertains to the neurological background and its attribution to psychological causes in humans, if not in animals. 

We therefore have to revise our scanty knowledge of brain function and its variation in disease before making a hasty judgment.  Obstacles in the way of improving our knowledge (which is essential for doctors as well as for sufferers) include the fact that the brain is an enclosed organ, sequestered from the rest of the body, devoid of visible movement and not readily accessible for investigation without invasive, expensive or scarce equipment. 

For centuries philosophers and physicians have debated its functions, the earliest suggestions ranging from the casket of the soul to a device for cooling the blood.  Yet, despite four hundred years of technological progress since the invention of the microscope and the current status of molecular biology, biochemistry and brain imaging, we still encounter well educated people prepared to manupulate their observations according to their beliefs. As a result, we have 2 separate camps in modern society - those who do and those who do not “believe” in ME/CFS. 

Unfortunate sufferers, who have no choice of listeners to their myriad symptoms, gain the inevitable reputation of being “heart-sink patients” - an appellation referring only to the doctor’s sinking heart at the sight of a large medical file and the prospect of too frequent clinic attendances.  Recently a group of research psychiatrists active in supporting a psychological origin for ME/CFS has been awarded a generous grant of  $190,000 to relieve the NHS of “heart-sink “ problems by the same route [1].

USING OUR EYES - ANATOMICAL INVESTIGATION OF THE BRAIN AND ITS EFFECT UPON “BELIEF”

Apart from organisms which are permanently static and do not require a brain to reorganise purposeful movement, all animated creatures have a brain with the same basic structure. 

Although its component parts vary greatly in size and proportion in adaptation to the lifestyles of different species, the ground plans invariably include a thick stalk (BRAIN STEM) tapering below to a tap-root like extension (the SPINAL CORD from which a number of paired SPINAL NERVES emerge) and bearing the above, two hemispherical outgrowths (the cerebrum or CEREBRAL HEMISPHERES) covered by a convoluted sheath of uninsulated nerve fibres (the CEREBRAL CORTEX, an extension of the brain’s GREY MATTER).

Two similar outgrowths (the little brain  or CEREBELLUM) are borne at the base of the brain stem.  Although some specific functions can be ascribed to special anatomical sites (eg SPEECH to the CEREBAL CORTEX, lying below the left temple) there are intricate nerve fibre connections to “association areas” such as the PRE-FRONTAL CORTEX, which enable the brain to function as a whole and may permit connected and undamaged nerve cells to restore or take over some function of others, lost because of accident, stroke or infection.

Naked eye examination of the brain at post-mortem, which could reveal scar tissue in Multiple Sclerosis, for example, is unlikely to disclose damage affecting function in ME/CFS, where the changes are more subtle. 

Investigations require the use of radio-imaging in life (eg. SPECT scans) [2]. or of molecular techniques to amplify viral genetic material (by PCR) [3] at post-mortem. 

Though deaths from complications such as heart or pancreatic failure, may be officially recorded [4], the lack of attribution to ME/CFS as the underlying disease, encourages insurance companies to “believe” that it is a benign illness and deny pension rights. 

It is a sad fact that the generosity of many sufferers wishing to donate organs for research is not matched by funding for appropriate scientific investigation.

CAN ANALAGOUS STUDIES OF THE BRAIN IN POLIOMYELITIS LEND CREDIBILITY TO SUFFERERS FROM ME/CFS ?

Using light microscopy and the available histological techniques for studying post mortem material from patients in 1948, BODIAN [5] demonstrated that the main impact of polio virus infection was upon the BRAIN STEM, an area through which almost every important neurological message must pass.

A more recent development has been the re-discovery in 1982, of the post-polio syndrome (first recorded in 1875) indicating that survivors of acute polio virus infection, despite apparent stability for some 40 years, may present with new symptoms of incapacitating fatigue, muscle pain and cognitive disturbance, often indistinguishable clinically from ME/CFS. 

A remarkable series of research papers from 1983 onwards by BRUNO and colleagues [6], using modern investigational techniques in both illnesses, provides strong supportive evidence of similar abnormalities of brain function leading to movement disturbances, anomalies of hormone and neurotransmitter function and of the electrical and chemical activity of the brain (suggesting a central cause for fatigue) as well as of cognitive function. 

These studies, which link the seemingly bizarre and unconnected symptoms reported by sufferers, should not only revolutionise preconceptions about patients previously considered to be hypochondriacal but encourage them to keep a careful record of all symptoms which can be used as evidence at social benefit tribunals.

HOW DOES THE BRAIN PROCESS INFORMATION?

The brain has often been likened to a computer.  However there are fundamental differences in its essential function of processing, comparing and storing information.  This is highly developed in humans, making us uniquely creative and better adapted to our environment than any animal. 

The brain, relies upon specialised cells designed for the reception and transmission of information (nerve cells or NEURONS) which are always electrically active, registering either a low voltage RESTING POTENTIAL or, after rearrangement of positively and negatively charge ions within and without the insulated CELL MEMBRANE, capable of generating a  higher voltage ACTION POTENTIAL down its main nerve fibre (AXON). 

At the axon tip, chemical transmission (via NEUROTRANSMITTERS, released from the axon) bridges the gap (SYNAPSE) between axon and the receptors (DENDRITES) of the receiving cell.  These are spider like outgrowths from the cell body which are simultaneously in contact with axons transmitting from other neurons. 

Unlike a computer, which can be switched on and off and is programmed to give set answers to a single question, the chemical transmitter bridging the synapse introduces a variability into the on-going message and “NEURONAL PLASTICITY” into the receiving/transmitting network. 

It has been shown that similar modifications in response may be induced by virus infection [7] and that a change in behaviour may be the only indication of this subtle effect. 

The brain contains some 100 billion neurons connected to some 10,000 relay stations and this enormous electrical activity creates a massive need for energy, using up 20% of the entire body’s demand for oxygen and glucose. 

Recent studies of the brain stem by SPECT scan, indicate hypoperfusion and low metabolic activity in subjects with ME/CFS. It is worrying that so many of these patients still smoke and adopt “sugar free” diets, further diminishing supplies of oxygen and glucose.

In order to avoid slowing down the incoming electrical impulses, chemical transmitters must be removed rapidly from the synapse and returned to cell metabolism. 

However, many drugs are designed to inhibit this process (eg. selective serotonin re-uptake inhibitors such as PROZAC).  Despite the manufacturer’s disclaimer and the belief of the patient in chemically manipulated happiness, such drugs can impair the natural production of neurotransmitters and lead to recurrence of the very symptoms for which they have been prescribed [8]. 

Most ME/CFS patients realise that, in view of their pre-existing brain dysfunction, potentially addictive drugs are better avoided unless used, as advised in the British National Formulary, only for brief periods.

MOVEMENT DISORDERS

The brain is continuously bombarded by incoming signals each of which, after information processing and co-ordination, will initiate an appropriate muscular response (however small). 

However, there is no single “movement centre” and incoming signals will either be directed via the brain stem to the spinal cord, undergoing processing on the way from specialised centres such as the cerebellum (the brain’s autopilot) or the THALAMUS and BASAL GANGLIA beneath the cerebral hemispheres, all of which act as subsidiary control areas, relieving higher motor centres in the cerebral cortex for more intricate muscular action. 

Thus, semi automatic movements (eg swimming) co-ordination of movement with visual and sensory input, determination of balance and the mediation of individual limb movements, will pursue a devious pathway, while direct connection is made between the higher motor cortex and muscles requiring exceptionally fine co-ordination such as those of the hand, face and mouth - an arrangement appropriate to the evolutionary tool making, and communication skills of humans. 

Such muscles are allotted an especially large share of the motor cortex and, when a motor impulse reaches the nerve end plate eg. in finger muscles, it is allocated to a few individual fibres rather than being spread over large areas, as in the leg. 

Modern research indicates disturbed metabolism in many areas essential to motor control in the brain stem of patients with ME/CFS, the majority of whom have evidence of incoordinated muscle twitching after slight exertion.

Difficulty with balance and with fine motor control, is often overlooked in medical assessments (especially in children). If patients can be persuaded to send a handwritten letter or children to produce a school notebook, evidence of a marked deterioration in fine motor control compared with previous proficiency or a deterioration in handwriting from one page to the next, can be a valuable aid to diagnosis.

SENSORY DISTURBANCE AND PAIN

The human brain possesses a degree of skill in parallel processing not yet matched by modern computers.  Of the five senses (touch, vision, hearing, taste and smell) all pursue devious pathways to various sites in the cerebral cortex for interpretation as well as being linked in parallel processing. 

Thus, an individual watching television while eating, if examined by SPECT Scan, would demonstrate several areas of the brain simultaneously activated by touch, taste and smell, possibly co-ordinated with vision and hearing.

Since vision can only be interpreted in the visual cortex, any damage in the intermediary pathway involving the THALAMUS, for example, will lead to visual disturbance despite a normally functioning eye while distortions of taste and smell may arise from disturbance in the same or adjacent areas of the mid brain through which the signal has passed for interpretation in the SOMATOSENSORY CORTEX.

It is not unusual for subjects suffering from ME/CFS to complain of distortions in taste or smell and to ascribe these to allergy while auditory and visual hallucinations may be experienced by individuals where certain neurotransmitters (such as dopamine) are produced in excess. 

It is important that these patients should record and report seemingly inexplicable symptoms of this type without fear of being disbelieved.  Aberrations of touch, pain, pressure and temperature sensation, initially transmitted from skin receptors, are common in ME/CFS and many patients suffer severely from a generalised pain syndrome which may arise from damage to the Thalamus. 

There is no specific pain centre in the brain but the sensation of pain is normally controlled by natural production of neurotransmitters such as enkephalin which, like synthetic opiods, does not so much remove the pain as render the sufferer indifferent to it. 

Pain control is difficult in ME/CFS and, if simple measures do not work, it has to be remembered that prolonged use of morphine analogues may reduce natural production of enkephalin. 

Acupuncture acts to increase local enkephalin production and, together with pleasurable activities which can “gate” pain sensation temporarily, as well as intermittent use of appropriate drugs, these patients may be made more comfortable.  However, referral to a specialist pain clinic is often necessary.

HORMONE DISTURBANCE

Hypothalamic function is often disturbed in ME/CFS.  The HYPOTHALAMUS is a central relay station for collecting and integrating signals from diverse sources (including the THALAMUS, LIMBIC SYSTEM and RETICULAR ACTIVATING SYSTEM in the brain stem and mid brain) and for producing hormones which affect kidney function and lactation before funneling them into the dependent PITUITARY GLAND, as well as inhibiting or promoting the release of pituitary hormones. 

In this fashion it has a major influence on specific reaction to stress, thyroid function, weight, appetite and control of glucose metabolism, as well as regulation of female sex hormones and the circardian sleep/temperature rhythm. 

Most of these hormones are neither difficult nor expensive to measure and there is no case for self medication with thyroid hormones (for example) without accurate laboratory monitoring. 

Children and adolescents suffer more severely than adults from symptoms of sleep and appetite disturbance as well as from difficulty with emotional control.  They should be relieved of school stress as far as possible until their condition stabilises [9].  Unfortunately, because of the hormone dependance of this illness, it is more common and more severe in females in the childbearing years and almost three times as common as in men, who have a more stable hormone profile throughout life.

THE GROWTH OF THE BRAIN, DEVELOPMENT OF MEMORY AND EFFECT UPON EDUCATION

A child’s brain, at birth, is no larger than that of Ancient Man and must grow rapidly in the 18 months before the skull bones close to adapt to modern life.  Multiplication of neurons, whose axons reach out in random fashion, occurs initially but, unlike a computer, neuronal connections are not irrefutably fixed and can adapt in later life. 

Neurons which do not achieve connection within the increasingly complex network, die off.  In childhood, it is a case of “use it or lose it” and a baby born with a squint will lose visual perception in the “lazy eye” unless nerve connections are made before the age of 5 years. 

From 11 to 16 years, when the multiplication of new neurons ceases, there is a 5% increase in brain size following which, growth in the complexity of neuronal networks proceeds throughout life. Although young people are quicker to learn, an adult gains in experience and judgement well into healthy old age. 

These facts underline not only the importance of play and human communication in childhood, but also the devastating effect of educational disadvantage, in the peak learning years of puberty and adolescence, suffered by young people with ME/CFS. 

At this stage of neuronal growth and increasing complexity of nerve pathways, language function, for example, may never be laid down.  Studies of identical twins indicate that experience and memory capacity has a more dramatic effect on neuronal growth and complexity of connections than genetic inheritance.

A good memory demands normal functioning of almost all areas of the cerebral cortex, the basal nerve centres of the mid brain (eg the THALAMUS and HIPPOCAMPUS) and their interconnecting pathways through the brain stem. 

Fluctuations of the metabolic activity in these areas (often made worse by physical and mental exhaustion) have been reported in SPECT SCANS of patients with ME/CFS [2], the vast majority of whom complain of difficulty with short term memory, though higher intellectual functions are usually preserved.

Normal functioning of the Temporal lobe and other areas of the cerebral cortex is required for:

Short Term Memory, laid down, for example, by uninterrupted repetition of telephone numbers and lasting for ½ hour.  It is not “hard wired” by further processing  to link with other memories, and resembles the free floating unassociated thoughts characteristic of dreaming and certain abnormal mental states.

        Memory for Simple Facts, unrelated to time and space.

Implicit Memory, for automatic sequential repetitive movements appropriate to driving or sports.  Sufferers from ME/CFS may experience some of these problems and be well advised to carry shopping lists, limit long distance driving and seek alternative hobbies.

Normal functioning of the entire cerebral cortex is required for:

Memory for Events, personal and unique to an individual.

Explicit Memory, which fixes special and personal events in time and space.

Temporary Memory Storage for two years or more in a “scaffolding” of nerve connections in the mid brain.

Long Term Memory Storage. Memories are retained as increasing experience modifies the nerve connections and, although it is still not quite clear how long term storage is finally accomplished, it depends upon a series of overlapping nerve circuits involving the entire cerebral cortex.

A good memory is the corner stone of the human mind and deprivation of special educational provision in their most formative years is the greatest disability inflicted on young people with ME/CFS [2].

SUMMARY

Patients with ME/CFS cannot be compared with a programmed robot.  Damage to vital brain centres (albeit temporary in some cases) may lead to a wide range of apparently unconnected and bizarre symptoms. These are invariably exacerbated by physical exhaustion and mental stress, leading to misinterpretation by the casual observer. 

Time taken to listen and to examine carefully (aided by a simple scoring chart to assess severity) will do much to prevent patients, who are so often courageous and uncomplaining despite serious disability, from the final indignity of becoming a statistic in “Heart-sink” research.

REFERENCES

[1] ILLMAN, JOHN. GPs to blame for problem patients.  The Observer 28.12.97; 13

[2] COSTA DC, TANNOCK C, BROSTOFF J.  Brainstem perfusion is impaired in patients with CFS. Quarterly Journal of Medicine. 1995; 88: 767-773

[3] MCGARRY F. et al. Enterovirus in Chronic Fatigue Syndrome. Annals of Internal Medicine. 1994; 120: 972-973

[4] BRAME. Forget me not. ME Today. 1997; 6: 30-34

[5] BODIAN D. Histopathological basis of clinical findings in poliomyelitis. American Journal of medicine. 1949; 6: 563-578

[6] BRUNO RL, FRICK NM, CREANGE SJ. et al. A brain model for post viral fatigue syndrome.  BRAME, ME Today. 1997; 5: 18-21

[7] DE LA TORRE. MALLORY M. BROT M. Viral persistence in neurons alters synaptic plasticity and cognition functions without destruction of brain cells.  Virology. 1996; 220:508-515.

[8] POWER A. Drug treatment of depression. British Medical Journal 1998; 316: 307-308.

[9] DOWSETT EG, COLBY J. Long term sickness absence due to ME/CFS in UK schools Journal of Chronic Fatigue Syndrome. 1997; 3(2): 29-42.
I am deeply indebted to the following authors upon whose work this entire paper is based:

GREENFIELD SUSAN (a) Journey to the Centre of the Brain.  Royal Institution of Great Britain Christmas Lecture, BBC Education 1994. (b) The Human Brain  -  a guided tour. London Wiedenfeld & Nicholson. 1997

BRUNO RL, CREANGE S, FRICK N.M. Parallels between Post-Polio Fatigue and Chronic Fatigue Syndrome - A common pathophysiology? American Journal of Medicine 1998 (in press)

How squiggles and colored brain maps may change how we view CFS and Fibromyalgia

Of all the things I’ve lost, I miss my mind the most!

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Ever find yourself trying to start your car from the passenger seat? Maybe you spend your day walking in endless circles trying to remember where you were going and why. Or maybe you just stare at your child’s math homework in panic because you can’t do the calculations either. Worse yet, the other day you had to hand the store clerk your cash so that they could count out the correct amount because you could not figure it out for the life of you. Has the concept of multi-tasking become a joke?

Hmmm, what could it be?  Depression, personality disorder, maybe Alzheimer’s?  No, you probably don’t have Alzheimer’s and it has nothing to do with your mental health either.  What you are experiencing are some very common cognitive dysfunctions, which are part and parcel of Fibromyalgia and Chronic Fatigue Syndrome. The medical term for what is happening is encephalopathy.

This is brain damage. Before you panic, CFS researchers currently classify it as one of the reversible encephalopathies although they have yet to come up with a cure.

How do researchers know it is encephalopathy? And how do you personally obtain objective medical evidence of this?

As there is a great deal of heavy-duty research and scads of unpronounceable terms related to following testing, I’m going to try to stick with the “cliff notes” version for this column.

The key to understanding and quantifying this baffling constellation of symptoms is a quantitative EEG (qEEG) also known as brain mapping. Generally, EEGs detect electrical changes associated with epilepsy, sleep disturbances, and metabolic or structural encephalopathies.

Essentially, an EEG is the recording of electrical patterns at the surface of the scalp that primarily reflect cortical electrical activity or "brainwaves." A quantitative EEG (qEEG) is the digital reading of an EEG. Instead of squiggly lines on paper, a computer image is then generated. The advantage of brain mapping is that the brain waves can be sampled much more frequently (usually 128 or 256 samples per second) and then compared to a normative database. Whew! Say that ten times fast.

Basically, there are four types of brain waves: beta, alpha, theta, and delta.

Beta waves (16-40 Hz or higher) are fast, spiky waves seen when the healthy subject is alert and thinking with focused attention. Alpha waves aren’t quite as fast as beta (8-13 Hz), but they are seen in healthy subjects who are awake but not engaged in substantial mental activity.

In healthy subjects, the brain uses 13Hz (high alpha or low beta) for "active" intelligence. Information processing occurs at a higher frequency approximately 40 Hz.

Theta waves (4-7 Hg) are slower and more rolling and in healthy subjects seen either in deep meditation states (high theta) or in the beginning stages of drowsiness and sleep. Delta waves (1-4 Hz) are extremely slow waves normally found only in deep sleep and coma states in adults.

VERY IMPORTANT!  RED LIGHT ALERT! The presence of Delta waves in waking adults is pathological and a clinical sign of brain dysfunction and damage.

And a growing body of research shows that patients with Chronic Fatigue Syndrome and Fibromyalgia have these in spades nor is it random. Research shows a distinct pattern of abnormally slow brain wave activity that is virtually unique to CFS, as well as the patterns found in Fibromyalgia. It is this pattern that substantially cripples cognitive function, particularly in the domains of attention, focus, executive function and memory.

These documented patterns of abnormalities in electrical relationships amongst various areas of brain are made by comparing the patients eyes closed recording with a normative database in addition to the added component of functional testing. This "Functional" qEEG testing includes recording under cognitive challenges, allowing for the examination of the brain's “cognitive” responses to reading, listening, math or other cognitive demands.

A number of neurophysiologists believe that some of this damage can be reversed by the use of neurotherapy, a treatment that helps the patient recognize the patterns and redirect brain waves. Results however show considerable variations. The greatest success is, and isn’t this always the case, with those patients more moderate symptoms.

Whether you need objective testing of cognitive dysfunction to back up a disability claim or you want to be tested to determine the suitability of neurotherapy for your individual circumstances, qEEG is a promising field.

Even as I write this, an SSDI judge has ruled that the results of my qEEG testing will be the basis he uses for deciding whether my claim for SSDI disability will be denied or not. My entire life hangs in the balance dependent on pretty pictures from a computer.  In my book, that makes qEEG testing both relevant and critical.

Other sources of information:

http://www.arthritis.org/communities/Chapters/UTI/Archives/FM_Connect/Brain_Mapping_and_Neurofeedback.asp

http://www.cfsdoc.org/eeg.htm

http://www.snr-jnt.org/journalnt/vol7/jntvol7.htm

http://start.eegspectrum.com/Newsletter/dec2002.htm

http://www.cinda.org/support/pamphlets/Preston2.pdf

http://www.cfids.org/archives/2003/2003-1-article07.asp