Tag: letter

Myalgic encephalomyelitis

Note: This letter appeared in the British Journal of General  Practice in April 1990.

 

Sir, During the past few months the Myalgic Encephalomyelitis Association has initiated a determined effort to find a cure for this devastating disease. A scientific and medical advisory panel has been formed under the chairmanship of Professor James Mowbray of St Mary’s Hospital Medical School, and in order to fund much needed research the Breakthrough Trust has been established and is already attracting money.

The scientific and medical advisory panel is anxious to stimulate new thought on research into the causes of myalgic encephalomyelitis, its possible treatments and, most important of all, research into finding a cure. Because of the complexities of the disease members of the panel would welcome new ideas and requests for grants from a wide variety of disciplines. Any such applications should be sent to me at the Myalgic Encephalomyelitis Association.

STEPHEN POWELL

Myalgic Encephalomyelitis Association

PO Box 8, Stanford le Hope

Essex SS17 8EX

 

Source:  S Powell. Myalgic encephalomyelitis. Br J Gen Pract. 1990 Apr; 40(333): 170. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371257/

 

Myalgic encephalomyelitis

Note: This letter appeared in the Journal of the Royal Society of Medicine in March 1990.

 

We accept that Martin Lev (November 1989 JRSM, p 693) is correct to point out that the anxiety and depression noted in patients labelled as suffering from ‘ME’ are the consequence of ‘underlying organic processes’. The demonstration of hyperventilation in the overwhelming majority of these patients (Rosen SD, King JC, Nixon PGF, unpublished results), provides a clear metabolic reason for the anxiety (1-3). ‘Depression’ is a predictable reaction to the inability to make and sustain effort due in part to the ease of acidosis of muscle cells depleted of buffer base reserves(4).

We agree with Sargant(5), that the sufferers from the late stages of effort syndrome, who have nothing to gain from their ill health and much to lose, are among the most gifted and energetic of people, and consequently the most upset about the frustration caused by loss of performance.

~S D ROSEN Cardiac Registrar

~J C KING Honorary Head Occupational Therapist (Research)

~P G F NIXON Consultant Cardiologist Charing Cross Hospital London

 

 References

1 Lewis T, et al. Breathlessness in soldiers suffering from irritable heart. Br Med J 14 October 1916:517-19

2 Lum LC. The syndrome of chronic habitual hyperventilation. In: Hill OW, ed. Modern trends in psychosomatic medicine, vol. 3. London: Butterworths, 1976: 196-230

3 Groen JJ. The measurement of emotion and arousal in the clinical physiological laboratory and in medical practice. In: Levi L, ed. The emotions: their parameters and measurement. New York: Raven Press, 1975:727-46

4 Rosen SD, King JC, Nixon PGF. Magnetic resonance muscle studies. J R Soc Med 1988;81:676-7 5 Sargant W. Battle for the mind Aphysiology ofconversion and brain-washing. London: Heinemann 1957

 

Source:  Rosen, SD, King, JC, Nixon, PGF. Myalgic encephalomyelitis. Journal of the Royal Society of Medicine Volume 83 March 1990.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292587/

 

Management of post-viral fatigue syndrome

Note: This letter appeared in the February 1990 issue of the British Journal of General Practice. The letter was written in response to an article, “Patient management of post-viral fatigue syndrome,” written by Dr. Ho-Yen, in which he advised that patients rest. You can read the article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371214/

 

Management of the post-viral fatigue syndrome Sir, We read with interest Dr Ho-Yen’s thoughtful paper on the management of the post-viral fatigue syndrome (January Journal, p.37) and welcome the renewed interest in practical management. Dr HoYen’s article is written in response to our previous paper on the subject, (1) and although there are differences between the two approaches, we must first point out the considerable areas of agreement between us, perhaps no more so than the emphasis on the role of the general practitioner, and of the crucial importance of a healthy doctor-patient relationship.

Many of the apparent differences between our approach and that of Dr HoYen are, as he states, due to sample differences. Our experience is based on patients with chronic illness seen in specialist neurological settings with a mean illness duration of five years.(2 )Dr Ho-Yen is familiar with patients with shorter illness durations, referred for a microbiological opinion. Many of the strategies advocated by Dr Ho-Yen are therefore designed for those in whom spontaneous recovery can still be anticipated. However, what about when such recovery has not occurred? In the two largest samples to date others have noted ‘an alarming tendency to chronicity (1,3) and it has been alleged that ‘most of the cases seen do not improve, give up their work and become permanent invalids’.(4) The current therapeutic approach for these patients is obviously unsatisfactory.

How does such chronicity develop? Dr Ho-Yen criticizes the first stage of the model we proposed to explain such chronicity, and points out that far from initially adopting forced inactivity after a viral infection, many chronic sufferers did the opposite, and tried to exercise away the fatigue. We accept his observation. Dr HoYen’s comments do indeed coincide with our own clinical impressions: many patients report initially adopting such strategies, and find that these are unsatisfactory, leading to a rapid recurrence of symptoms. However, we suggest this is an even more convincing explanation of the remainder of the model we propose Simple operant conditioning suggests that such a powerful experience of failure will lead to persistent avoidance, perhaps when the original need for it is no longer present. We also suggest that early and repeated exposure to uncontrollable, aversive and mysterious symptoms, such as the profound muscle pain that characterizes the syndrome, is another potent cause of the demoralization and helplessness so frequently found (Powell R, Wessely S, manuscript submitted for publication) and may in turn explain the high rates of mood disorder that have been observed in several studies.

We do, however, disagree that the management we advocate is to ‘get out and exercise’. This is a common misconception. Cognitive behavioural therapy is not exercise therapy, and we are not physiotherapists. It is true that in the later stages of treatment patients are encouraged to increase their activity (which must ultimately be the aim of any treatment) but therapy does not involve the simple prescription of set amounts of exercise. Instead, treatment is based on mutually agreed targets, which are themselves jointly chosen as being some activity that the patient wishes to undertake, but has avoided. In practice this may simply be brushing one’s teeth, or sitting out of bed to eat a meal. The behaviour is chosen solely on the basis of avoidance; the physiological and ergonomic consequences of such activity are irrelevant. The aim is to introduce predictability, and the return of self-control and self efficacy, not to restore muscle power. Furthermore, the other important component of our approach to management is an awareness of emotional disorders, and a recognition that these may need treatment in their own right.

We agree that the management we advocate is neither new nor unique. Almost identical management is now the treatment of choice for chronic pain (5) and fibromyalgia. (6) The latter is particularly relevant, since it is increasingly accepted that fibromyalgia may indeed be the same condition as post-viral fatigue.(7) Furthermore, it is difficult to think of a pathological mechanism by which gradual increased activity could be harmful, (8’9) even in the minority of patients with clear cut neuromuscular pathology.

The final decision must be based on evidence. We have already announced preliminary details of a pilot evaluation of cognitive behavioural therapy (Wessely S, et al, abstract presented at the scientific meeting of the Royal College of Psychiatrists, London, 25 September 1989). Our conclusion was that the advice currently offered to these patients may not be accurate, and that the current therapeutic nihilism in this condition may be unduly pessimistic.

In summary, the differences between our approach and that of Dr Ho-Yen may be less marked than at first sight. Given the difference in our samples and clinical experience, one might summarize by saying that whereas Dr Ho-Yen correctly emphasizes the dangers of doing too much, too early in the natural history of the condition, we emphasize the equally damaging consequences of doing too little, too late. The most appropriate strategy depends upon the stage of the illness reached by the patient.

~SIMON WESSELY , ANTHONY DAVID Institute of Psychiatry De Crespigny Park London SE5 8AF

~SUE BUTLER, TRUDIE CHALDER National Hospital for Nervous Diseases Queen Square London WC1N 3BG

References

  1. Wessely S, David A, Butler S, Chalder T. The management of chronic post-viral fatigue syndrome. J R Coll Gen Pract 1989; 39: 26-29.
  2. Wessely S, Powell R. Fatigue syndromes: a comparison of chronic ‘postviral’ fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry 1989; 52: 940-948.
  3. Smith D. Myalgic encephalomyelitis. In: 1989 Members’ reference book. London: Sabrecrown Publishing, 1989: 247-250.
  4. Behan P, Behan W. The postviral fatigue syndrome. CRC Crit Rev Neurobiol 1988; 42: 157-158.
  5. Pither C. Treatment of persistent pain. Br Med J 1989; 299: 1239.
  6. Yunus M. Diagnosis, etiology and management of fibromyalgia syndrome: an update. Comp Ther 1988; 14: 8-20.
  7. Goldenberg D. Fibromyalgia and other chronic fatigue syndromes: is there evidence for chronic viral disease? Semin Arthritis Rheum 1988; 18: 111-120.
  8. Vignos P. Physical models of rehabilitation in neuromuscular disease. Muscle Nerve 1981; 6: 323-338.
  9. Milner-Brown S, Miller R. Muscle strengthening through high-resistance weight training in patients with neuromuscular disorders. Arch Phys Med Rehabil 1988; 69; 14-19

 

Source: Wessely S, David A, Butler S, Chalder T. Management of post-viral fatigue syndrome. Br J Gen Pract. 1990 Feb;40(331):82-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371151/pdf/brjgenprac00083-0040.pdf

 

Chronic fatigue syndrome

Note: This letter appeared in the February 15, 1989 edition of the Canadian Medical Association Journal in response to Dr. Ray Holland’s letter of August 1, 1988 . You can read Dr. Holland’s letter as well as Dr. Salit’s response here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268060/?page=1 and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268061/

 

A useful supplement to the letters about chronic fatigue syndrome from Drs. Ray G.L. Holland (Can Med Assoc J 1988; 139: 198-199) and Irving E. Salit (ibid: 199) might be the working case definition of this syndrome proposed by Holmes and colleagues,(1) of the US Centers for Disease Control.

Holmes and colleagues have suggested that a case of chronic fatigue syndrome must fulfill two major criteria: that it consist of persistent or relapsing debilitating fatigue of new onset that has reduced the patient’s activity level to below 50% of normal for at least 6 months and that other clinical conditions that may produce similar symptoms have been excluded by thorough evaluation.

In addition, there must be 6 or more of 11 minor features (mild fever, sore throat, painful neck or axillary lymph nodes, generalized muscle weakness, myalgia, easy fatigability, headaches, migratory arthralgia, neuropsychologic complaints, sleep disturbances and rapid onset of the main symptom complex), along with 2 or more of 3 physical findings (low-grade fever, nonexudative pharyngitis, and palpable or tender neck or axillary lymph nodes).

We have found that many people with this clinical picture have concomitant food and chemical sensitivities and may have an intracellular magnesium deficiency in spite of normal serum levels.(2) This is probably the result of the inordinate amount of this essential mineral that they spill in their urine. The generalized aching and muscle tightness these patients experience can frequently be eased by appropriate magnesium (and calcium) supplementation, presumably because of the reduction of neuromuscular irritability.

We were therefore greatly surprised to learn in a later letter from Dr. Holland (ibid: 706) that “it would be nontherapeutic to offer such a patient empathy” and that we must not condone a belief in a “nonexistent disease”.

These statements are difficult to reconcile with the immunologic abnormalities,(3,5) disorders of muscle metabolism (5) and abnormal results of muscle biopsy (5) found in such patients. Specific flow cytometric measurements of lymphocyte dysfunction may prove to be a means of characterizing and diagnosing this syndrome.(6)

Holland, who reminds us of the dictum “Primum non nocere”, should take his own advice to heart. We are only beginning to unravel the secrets of this debilitating condition, which is very likely caused by a combination of triggering factors, including infective and environmental influences.

This condition, called myalgic encephalomyelitis in Britain, is most certainly not psychosomatic, in spite of the frequently associated emotional turmoil.

Most normal healthy people will react “emotionally” when their finances, lifestyle and health are shattered by a debilitating condition, and they may well respond to a sympathetic approach to their total well-being.

~Gerald H. Ross, MD, CCFP, Fellow in environmental medicine

~Jean A. Monro, MB, BS, LRCP, MRCS, Medical director Breakspear Hospital for Allergy and Environmental Medicine Abbots Langley, England

 

References

  1. Holmes GP, Kaplan JE, Gantz NM et al: Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-389
  2. Rea WJ, Johnson AR, Smiley RE et al: Magnesium deficiency in patients with chemical sensitivity. Clin Ecol 1986; 4:17-20
  3. Tosato G, Straus SE, Werner H et al: Characteristic T cell dysfunction in patients with chronic active EpsteinBarr virus infection (chronic infectious mononucleosis). J Immunol 1985; 134:3082-3088
  4. Kuis W, Roord JJ, Zegers BJM et al: Heterogeneity of immune defects in three children with a chronic active Epstein-Barr virus infection. J Clin Immunol 1985; 5: 377-385
  5. Behan PO, Behan WMH, Bell EJ: The postviral fatigue syndrome – an analysis of the findings in 50 cases. J Infect 1985; 10: 211-222
  6. Johnson TS, Gratzner HG, Steinbach T et al: Flow cytometric measurement of lymphocyte immune function in chronic fatigue syndrome patients. Presented at 22nd scientific session, American Academy of Environmental Medicine, Lake Tahoe, Nev, Oct 22-25, 1988

Source: Gerald H. Ross and Jean A. Monro. Chronic fatigue syndrome. CMAJ. 1989 Feb 15; 140(4): 361. PMCID: PMC1268650 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268650/?page=1

 

“Virus of the year”?

Note: This letter by Dr. Ray Holland, published in the Canadian Medical Association Journal on August 1, 1988, generated several responses. Dr. Salit’s response appears below. 

 

There appears to be a scarcity of information in medical and psychiatric journals (although not in the lay press) on what was initially termed the Epstein-Barr syndrome but was later renamed chronic fatigue syndrome because it can be caused by infective agents other than the Epstein-Barr virus (EBV). For example, the last article on the subject in CMAJ appeared in 1985.(1) There the syndrome, consisting of fatigue, depression, myalgia, muscle weakness, headaches and paresthesia, was named sporadic postinfectious neuromyasthenia (PIN), a term preferable to chronic fatigue syndrome because it is not ambiguous and because the condition can be of both infectious and psychologic origin.

Presumably the condition was named chronic fatigue syndrome because fatigue is the main presenting symptom, but in psychologic depression fatigue can also be the main manifestation. It is unfortunate, therefore, that the American Medical Association appears to have adopted such an ambiguous term while lamenting that the lack of a definitive diagnosis leaves both patients and health care providers frustrated.(2)

To confuse matters further, the media have labelled the condition chronic fatigue in overachievers or Yuppie flu. In fact, traditional psychiatrists have for some timed called chronic fatigue in overachievers anhedonia (inability to experience pleasure), which, if untreated, may lead to fatigue, depression and the other symptoms mentioned.

While the clinical picture may be ambiguous, the serologic findings may be more so, even when interpreted along with the clinical findings, because those exposed to EBV may have positive serologic results but no chronic sequelae, in much the same way as most people exposed to tuberculosis have subclinical infection. How high does the antibody titre have to be for a definite diagnosis of chronic fatigue syndrome in those who were apparently well before the acute viral attack, even if one excludes those with a previous psychiatric history, as Salit did? One must suspect that a high antibody titre that does not correlate with the clinical findings implies a psychologic origin, as does a low antibody titre. However, it appears that many patients who are told that they have positive but inconclusive serologic results of testing for EBV are choosing to believe that they have the disease. The local medical laboratory has informed me that there is not even a range of titres for EBV but that patients must find their own range by correlating values with how they feel! The media seem to infer that cases with negative results of EBV testing either have not been diagnosed because of lack of the necessary technology or have been misdiagnosed, because there is no mention that the cause may be psychologic.

Such a state of affairs is only too likely in today’s society, in which people are actually healthier than ever before but are more disease conscious and in which the media have a lively interest in medical matters. Rather than an epidemic of the disease, there appears to be an epidemic of the diagnosis, such that EBV should be named “virus of the year”.

May primum non nocere prevail as high-tech medicine continues to advance, at an alarming rate.

~Ray G.L. Holland, MD, FRCPC Box 458 Port Colbome, Ont.

References

  1. Salit IE: Sporadic postinfectious neuromyasthenia. Can Med Assoc J 1985; 133: 659-663
  2. Straus SE: EB or not EB – that is the question [E]. JAMA 1987; 257: 2335- 2336

 

[Dr. Salit responds:]

I too believe that the lack of information in medical journals on PIN [postinfectious neuromyasthenia] is a problem. There appears to be confusion about the condition among physicians, granting agencies and medical journals; they are unable to neatly classify the ailment into a nosologic category. The comment has been that the illness is “too vague” or “ill-defined”. This translates into an inability to have studies related to this subject published. Indeed, last year CMAJ rejected my article on immunologic aberrations in PIN, citing similar reasons.

The term chronic fatigue syndrome (1) was probably chosen by US investigators because it is a generic term. In 1985 these investigators thought that the illness was due to EBV; hence the common designation chronic EBV infection.(2) At that time I felt that the illness was induced by many etiologic agents, so I used the term PIN.(3) Most investigators in this area have come around to this way of thinking but have chosen not to use the term PIN.

Dr. Holland indicates that this disease has been acknowledged by psychiatrists in the past under other designations. Indeed, very similar illnesses have been known to different specialists by different names for decades. I have suggested a unifying hypothesis concerning a common pathophysiologic mechanism.(4)

EBV serologic findings have been the most confusing diagnostic aspect of this illness. Some patients after typical acute infectious mononucleosis have a form of chronic mononucleosis that symptomatically resembles PIN.(5) The serologic findings strongly suggest chronic active EBV infection. However, in most cases of PIN the illness probably did not start with acute infectious mononucleosis, and the patients probably do not have continuing active EBV infection. Using a sensitive DNA probe we found that PIN patients were not excreting EBV.(6) Furthermore, there is such extensive overlap between PIN patients and healthy controls that EBV serologic findings cannot be used to make the diagnosis.(7) It is also likely that such patients have moderately elevated titres of antibodies to a variety of other antigens. Most adults in Canada have EBV antibodies from a prior infection. Too often a diagnosis of chronic EBV infection is made on the basis of certain symptoms and the findings of any EBV antibody. This is inappropriate.

Holland says that “there appears to be an epidemic of the diagnosis”. What has become very apparent to me is that there are a large number of people in the community with illnesses that might be included under the rubric PIN. Physicians argue about the existence of this disease, but it is clear to me that PIN patients have an illness (or a deviation from a normal state of health). Despite the fact that we do not understand the disease process that results in this illness, the patients still require appropriate medical care, consisting of empathy, an acknowledgement that they are ill, reassurance that there is an absence of a more severe disease and, finally, guidelines on how best to manage the condition.(4’8’9)

I do not think that primum non nocere should prevail, although I can accept secundum non nocere. First we should show some understanding and compassion.

~ Irving E. Salit, MD, FRCPC Division of Infectious Diseases Toronto General Hospital Toronto, Ont.

References

  1. Holmes GP, Kaplan JE, Gantz NM et al: Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-389
  2. Jones JF, Ray CG, Minnich LL et al: Evidence for active Epstein-Barr virus infection in patients with persistent, unexplained illnesses: elevated antiearly antigen antibodies. Ann Intern Med 1985; 102: 1-7 3. Salit IE: Sporadic postinfectious neuromyasthenia. Can Med Assoc J 1985; 133: 659-663
  3. Idem: Chronic EBV infections (postinfectious neuromyasthenia). Med North Am 1987; 10: 1944-1950
  4. Straus SE: The chronic mononucleosis syndrome. J Infect Dis 1988; 157: 405- 412
  5. Salit IE, Diaz-Mitoma F, Walmsley S et al: Absence of Epstein-Barr virus excretion in post-infectious neuromyopathies. Presented at the American Society for Microbiology annual meeting, Miami Beach, May 9, 1988
  6. Buchwald D, Sullivan JL, Komaroff AL: Frequency of “chronic active Epstein-Barr virus infection” in a general medical practice. JAMA 1987; 257: 2303-2307
  7. Salit IE: Post-infectious fatigue. Can Fam Physician 1987; 133: 1217-1219 9. Taerk GS, Toner B, Salit IE et al: Depression in patients with neuromyasthemia. Int J Psychiatry Med 1987; 17: 49-56

 

Source: R G Holland. “Virus of the year”? CMAJ. 1988 Aug 1; 139(3): 198–199. PMCID: PMC1268060 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268060/?page=1 and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268061/

 

Chronic fatigue syndrome

I was surprised that CMAJ published the letter from Drs. Gerald H. Ross and Jean A. Monro (Can Med Assoc J 1989; 140: 361) supporting such a vague, descriptive and unscientific term as “chronic fatigue syndrome”. As a practising psychiatrist I have attempted to emphasize that there are also primary psychologic causes of chronic fatigue such as depression and panic disorder (ibid: 361, 364); thus, it is more prudent to consider the relative causes of chronic fatigue than to create a “syndrome” that imposes a diagnostic life sentence of an incurable disease.

That a minuscule percentage of cases of chronic fatigue are due to chronic mononucleosis, other chronic infections and chemical sensitivity is not disputed. What is disputed is the number so diagnosed, particularly now that panic disorder – a primarily psychologic condition that causes chronic fatigue but is more amenable to treatment (antidepressant medication and dynamic insight-oriented psychotherapy) – appears to be reaching epidemic proportions. (1) Therefore, at the risk of considerable ideologic unpopularity, it would seem, I must repeat: “Primum non nocere.”

The statement by Ross and Monro that magnesium deficiency is associated with chemical sensitivity means just that and only that.

Ross and Monro’s six references are not definitive enough, the possible exception being the article of Tosato and colleagues (2) if – and only if – the chronic infectious mononucleosis referred to in the title was confirmed by serologic evidence of an acute attack. (3)

Ross and Monro display psychologic “sympathy” with “empathy” and quote me as referring to the term “psychosomatic” when I used the term “psychologic”.

“Syndromes” like “chronic fatigue syndrome” lessen the burden of introspection. In reverence to the “father” of nosology, Thomas Sydenham, and the “father” of psychiatry, Sigmund Freud, I must state, as a traditionally oriented psychiatrist, that it is nontherapeutic to condone self-defeating behaviour.

~Ray Holland, MD, FRCPC Box 458 Port Colborne, Ont.

References

1. Introduction. In Summary Proceedings of “Panic Disorder – Relative Merits of Pharmacotherapy and Psychotherapy” (satellite symposium of 1988 American Psychiatric Association annual meeting), Medical Group, Mississauga, Ont, 1988
2. Tosato G, Straus SE, Werner H et al: Characteristic T cell dysfunction in patients with chronic active EpsteinBarr virus infection (chronic infectious mononucleosis). J Immunol 1985; 134:3082-3088
3. Evans AS: A virus for all seasons.Buffalo Phys Biomed Sci 1988; 22 (2):14-15

 

Source: R Holland. Chronic fatigue syndrome. CMAJ. 1989 May 1; 140(9): 1016. PMCID: PMC1268972
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268972/pdf/cmaj00190-0022b.pdf

 

Chronic fatigue syndrome

Note: This letter was written in response to a letter published in the Canadian Medical Association Journal on May 1, 1989. You can read Holland’s letter here:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1268972/pdf/cmaj00190-0022b.pdf

 

It is regrettable that the publication of an earlier letter from one of us (G.H.R.) and Dr. Jean A. Monro (Can Med Assocj 1989; 140: 361) generated surprise (and apparent disapproval of CMAJ’s action) on the part of Dr. Ray Holland (ibid 1016).

In expressing his disagreement with the use of the term “chronic fatigue syndrome” Holland also appears to be at odds with the US Centers for Disease Control (CDC), whose case definition for this condition (1) was the main point of the earlier letter. We have no disagreement with Holland that “there are also primary psychologic causes of chronic fatigue”. However, the CDC case definition specifically calls for the exclusion of clinical conditions, including psychiatric disease, that may produce similar symptoms.

The whole issue of what triggers psychologic symptoms or illness, however, is an important related matter. Holland reports, quite rightly, that panic disorder appears to be increasingly common. As physicians we have been led to assume that panic disorder has a psychologic origin rather than identifiable extrinsic causes. At the Environmental Health Center – Dallas we have confirmed that panic attacks and other emotional responses may be reproducibly triggered by double-blind testing for sensitivities to foods, inhalants and chemicals. (2)

Similar behavioural effects have been seen in pesticide poisoning (3) and with exposure to other environmental toxins. (4) Specifically, panic attacks have been cited in the psychiatric literature as being triggered by solvent exposure. (5’6)

Being unable to find physical diagnoses for chronic fatigue does not necessarily mean that psychologic illness is the cause. It may simply be that our understanding of the factors precipitating the illness is far from complete. Medical history teaches us that once physical causes for “psychologic” symptoms are discovered the condition moves, as if by magic, from the psychiatric to the medical realm. A good example of this is the relief of behavioural symptoms by correction of thiamin (7) or cobalamin (8) deficiency.

It is our experience that a substantial percentage of chronic fatigue cases (not a minuscule percentage, as Holland suggests) may arise from or be worsened by adverse reactions to components of the patient’s total environment, such as food, inhalants and chemicals.

~Gerald H. Ross, MD, CCFP Fellow in environmental medicine

~William J. Rea, MD, FACS, FAAEM Medical director

~Alfred R. Johnson, DO, FAAEM Environmental Health Center – Dallas; Dallas, Texas

References

1. Holmes GP, Kaplan JE, Gantz NM et al: Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-389
2. King DS: Can allergic exposure provoke psychological symptoms? A double-blind test. Biol Psychiatry 1981; 16:3-19
3. Rea Wl, Butler JR, Laseter JL et al: Pesticides and brain function changes in a controlled environment. Clin Ecol 1984; 2:145-150
4. Fein GG, Schwartz PM, Jacobson SW et al: Environmental toxins and behavioral development: a new role for psychological research. Am Psychologist 1983; 38: 1188-1197
5. Dager SR, Holland JP, Cowley DS et al: Panic disorder precipitated by exposure to organic solvents in the work place. Am I Psychiatry 1987; 144:1056-1058
6. Lindstrom K, Ruhimake H, Hamminen K: Occupational solvent exposure and neuropsychiatric disorders. Scand J Work Environ Health 1984; 10: 321-323
7. McLaren DS: Clinical manifestations of nutritional disorders. In Shils ME, Young VR (eds): Modem Nutrition in Health and Disease, Lea and Febiger, Philadelphia, 1988: 733-745
8. Lindenbaum J, Healton EB, Savage DG, et al: Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N EnglJ Med 1988; 318: 1720-1729

 

Source: G H Ross, W J Rea, and A R Johnson. Chronic fatigue syndrome. CMAJ. 1989 Jul 1; 141(1): 11–12. PMCID: PMC1269261  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1269261/

 

Epidemic myalgic encephalomyelitis

The letter below, “Epidemic myalgic encephalomyelitis,” was published in the British Medical Journal in 1978. In it, the authors maintain that ME is an organic illness that exists as a distinct clinical entity with recognizable signs and symptoms. The authors propose that the cause may be “a persistent viral infection.”

 

Epidemic myalgic encephalomyelitis

Outbreaks of the paralytic disease known as epidemic myalgic encephalomyelitis have puzzled doctors all over the world in the past 30 years. One of the best known of these epidemics was that at the Royal Free Hospital in London in 1955, which affected more than 300 people. (1) Most outbreaks tend to occur in the summer, young adults are predominantly affected, and the incidence is higher in women. The evidence suggests that infection is spread by personal contact, and young hospital personnel seem particularly at risk. The features common to every epidemic include headache, unusual muscular pains (which may be severe), lymphadenopathy-often of the posterior cervical lymph nodes-and low-grade fever.(2, 3) In a minority of cases frank neurological signs can be detected by careful clinical examination: there may be nystagmus, diplopia, myoclonus, bulbar weakness, motor weakness, increased or decreased tendon reflexes, disturbances of the sphincters, and extensor plantar responses.(2-7) Fasciculations, cranial nerve lesions, and extrapyramidal signs have also been reported. Most patients complain of paraesthesiae, and sensory loss is common.”(4) One characteristic feature of the disease is exhaustion, any effort producing generalised fatigue. Often there are psychiatric abnormalities, especially emotional lability and lack of concentration.(1- 3, 4) The clinical outcome may take any of three courses: some patients recover completely, some follow a relapsing course, and some are permanently incapacitated.(3)

At a symposium held recently at the Royal Society of Medicine to discuss the disease and plan research there was clear agreement that myalgic encephalomyelitis is a distinct nosological entity. Other terms that have been used to describe the disease were rejected as unsatisfactory for various reasons: the cardinal clinical features show that the disorder is an encephalomyelitis; “Iceland disease” is not specific enough; and “neuromyasthenia” suggests a relation to myasthenia gravis whereas the muscle fatigability is different, as are the electrophysiological findings.(8) Indeed, the exhaustion and tiredness are similar to that described by patients with multiple sclerosis.(9) From the patient’s point of view the designation benign is also misleading, since the illness may be devastating. Originally the term was used because no deaths had been recorded from myalgic encephalomyelitis. Two patients who had had the disease have now been examined post mortem: one was found to have multiple sclerosis. The adjective epidemic is correct, since most cases occur in an epidemic, but the disease may be endemic, and sporadic cases may occur. (10-12)

Some authors have attempted to dismiss this disease as hysterical, (13) but the evidence now makes such a tenet unacceptable. Some purely psychiatric symptoms may well occur, particularly in patients entering the chronic phase. No doubt, too, in an epidemic some hysterical persons will simulate the symptoms of the disease. Nevertheless, the organic basis is clear-from the finding that the putative agent can be transferred to monkeys(14); the detection of an increased urinary output of creatine2 (15); the persistent finding of abnormal lymphocytes in the peripheral blood of some patients (16); the presence of lymphocytes and an increased protein concentration in the cerebrospinal fluid of occasional patients (3); and the neurological findings. At this symposium more evidence was produced to support the organic nature of the disease. Increased serum concentrations of lactic dehydrogenases and transaminases have been found in several patients examined during the acute attack. In a recent outbreak in London immunological studies showed a high incidence of serum anticomplementary activity and the presence of ill-defined aggregates on electron microscopy of acute-phase sera.(17) A perplexing finding, suggesting the possibility of a persistent virus infection, was the ability of lymphocytes from patients to proliferate and survive in vitro for up to 19 weeks. The results of electroencephalographic studies were also stated to be abnormal, confirming other reports. (10)

We still know nothing about the nature and cause of epidemic myalgic encephalomyelitis, but outbreaks are still occurring. Future epidemics should be studied by a collaborative team of neurologists, epidemiologists, virologists, and immunologists. Its findings would be important not only for the study of epidemic myalgic encephalomyelitis but also for other neurological disorders, including multiple sclerosis.

1 British Medical Journal, 1957, 2, 895.

2 White, D N, and Burtch, R B, Neurology, 1954, 4, 506.

3 Acheson, E D, American Journal of Medicine, 1959, 26, 569.

4 Gilliam, A G, Epidemiological Study of an Epidemic, Public Health Bulletin, No 240. US Public Health Service, Washington, 1938.

5 Acheson, E D, Lancet, 1955, 2, 394.

6 Pellew, R A A, Medical Journal of Australia, 1951, 1, 944.

7 Hill, R C J, South African Medical Journal, 1955, 29, 344.

8 Richardson, A T, Annals of Physical Medicine, 1956, 3, 81.

9 McAlpine, D, Compston, N D, and Lumsden, C E, Multiple Sclerosis, chap 5. Edinburgh and London, Livingstone, 1955. ”

10 Ramsay, A M, and O’Sullivan, E, Lancet, 1956, 1, 761.

11 Jelinek, J E, Lancet, 1956, 2, 494.

12 Ramsay, A M, Lancet, 1957, 2, 1196.

13 McEvedey, C P, and Beard, A W, British Medical Journal, 1970, 1, 7.

14 Pellew, R A A, and Miles, J A R, Medical Journal of Australia, 1955, 2, 480.

15 Albrecht, R M, Oliver, V L, and Poskanzer, D C, Journal of the American Medical Association, 1964, 187, 904.

16 Wallis, A L, MD Thesis, Edinburgh University, 1957.

17 Dillon, M J, et al, British Medical Journal, 1974, 1, 301.

 

Source: BRITISH MEDICAL JOURNAL 3 JUNE 1978 1436-1437

You can read and download a PDF file of the letter at:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1604957/?page=1