Treatment – Page 19 – American ME and CFS Society

Cognitive behaviour therapy for the chronic fatigue syndrome. Good general care may offer as much benefit as cognitive behaviour therapy

Comment on: Cognitive behaviour therapy for the chronic fatigue syndrome: a randomized controlled trial. [BMJ. 1996]

EDITOR,-Successful outcomes have been reported from controlled clinical trials of an eclectic range of treatments-from immunotherapy to magnesium supplementation-for the chronic fatigue syndrome.’ Unpublished data suggest that equal success can be achieved with some forms of alternative therapy (for example, homoeopathy) when patients believe strongly in the approach. Most physicians, however, continue to view all such results with healthy scepticism. An equally cautious view needs to be taken when assessing Michael Sharpe and colleagues’ study of cognitive behaviour therapy.2 In a disorder that is almost certainly heterogeneous in nature, two important questions need to be answered before we can conclude that cognitive behaviour therapy is of value.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350899/pdf/bmj00539-0052b.pdf

Source: Shepherd C. Cognitive behaviour therapy for the chronic fatigue syndrome. Good general care may offer as much benefit as cognitive behaviour therapy. BMJ. 1996 Apr 27;312(7038):1096; author reply 1098. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350899/

Is neurally mediated hypotension an unrecognised cause of chronic fatigue?

Abstract:

Neurally mediated hypotension is now recognised as a common cause of otherwise unexplained recurrent syncope, but has not been reported in association with chronic fatigue. We describe seven consecutive non-syncopal adolescents with chronic post-exertional fatigue, four of whom satisfied strict criteria for chronic fatigue syndrome. Upright tilt-table testing induced significant hypotension in all seven (median systolic blood pressure 65 mm Hg, range 37-75), consistent with the physiology of neurally mediated hypotension. Four had prompt improvement in their chronic fatigue when treated with atenolol or disopyramide. These observations suggest an overlap in the symptoms of chronic fatigue syndrome and neurally mediated hypotension.

Comment in:

Is neurally mediated hypotension an unrecognised cause of chronic fatigue? [Lancet. 1995]

Source: Rowe PC, Bou-Holaigah I, Kan JS, Calkins H. Is neurally mediated hypotension an unrecognised cause of chronic fatigue? Lancet. 1995 Mar 11;345(8950):623-4. http://www.ncbi.nlm.nih.gov/pubmed/7898182

Chronic fatigue syndrome and fibromyalgia

Comment on: Population study of tender point counts and pain as evidence of fibromyalgia. [BMJ. 1994]

EDITOR,-The relation between muscle pain, tender points, the chronic fatigue syndrome, and fibromyalgia are complex, and simplistic answers are inappropriate. In their paper Peter Croft and colleagues extrapolate their results to make two statements that I believe to be incorrect.’

My conclusions are based on 100 consecutive patients seen at Raigmore Hospital NHS Trust, who fulfilled precise definitions of the chronic fatigue syndrome 2 or fibromyalgia.3 The importance of this definition of the syndrome is that it has the same three month cut off for length of illness as fibromyalgia.3 Of the 100 patients, 99 (74 women, 25 men) had the chronic fatigue syndrome and one (a woman) had fibromyalgia. Of the patients with the chronic fatigue syndrome, 63 had muscle pain and 28 had tender points on examination, 23 had both, and five had no muscle pain but tender points. These results do not support the authors’ statement that the reason why fibromyalgia is not more common in Britain has been the acceptability of the chronic fatigue syndrome as an alternative diagnosis.

The authors also say that it is “inappropriate to define an entity as fibromyalgia.” As a clinical virologist, I strongly disagree with this as the distribution and number of tender points in fibromyalgia are different from those in the chronic fatigue syndrome, and the management of the two conditions is different.4 Patients with the syndrome should be advised not to increase their activities gradually until they feel 80% of normal,5 whereas patients with fibromyalgia may benefit from a regimen of increasing activity.4

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2541601/pdf/bmj00468-0067b.pdf

Source: Ho-Yen DO. BMJ. Chronic fatigue syndrome and fibromyalgia. 1994 Dec 3;309(6967):1515. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2541601/

Chronic fatigue syndrome: a diagnostic challenge for the laboratory

Abstract:

OBJECTIVE: To review the literature and current research about the causes of chronic fatigue syndrome (CFS).

DATA SOURCES: Recent research articles about CFS and data gathered by the author.

STUDY SELECTION: Performed by the author.

DATA EXTRACTION: Performed by the author.

DATA SYNTHESIS: Chronic fatigue syndrome (CFS) is a disease of pain, excessive fatigue after minor exertion, cognitive difficulties, and other symptoms-all occurring in cycles. While its etiology is unclear, CFS is associated with abnormal results of immune system tests. There is no specific marker for the illness. Treatment is symptomatic, and the long-term outlook for recovery is good.

CONCLUSION: A rational, symptomatic approach to treating CFS patients can be made using the model developed at the author’s institution. Research into the causes of CFS must continue.

Source: Lanham RJ. Chronic fatigue syndrome: a diagnostic challenge for the laboratory. Clin Lab Sci. 1994 Sep-Oct;7(5):279-82. http://www.ncbi.nlm.nih.gov/pubmed/10150382

The etiology and possible treatment of chronic fatigue syndrome/fibromyalgia

Abstract:

It is suggested that chronic fatigue syndrome/fibromyalgia is caused by virus injury to the calcium channels leading to larger quantities than usual of calcium ions entering the striated muscle cells. Should this be true, then treatment with a calcium antagonist (CA) may possibly be of value.

Source: Lund-Olesen LH, Lund-Olesen K. The etiology and possible treatment of chronic fatigue syndrome/fibromyalgia. Med Hypotheses. 1994 Jul;43(1):55-8. http://www.ncbi.nlm.nih.gov/pubmed/7968720

Changes in the 2-5A synthetase/RNase L antiviral pathway in a controlled clinical trial with poly(I)-poly(C12U) in chronic fatigue syndrome

Abstract:

Latent 2′, 5′-oligoadenylate (2-5A) synthetase activity, bioactive 2-5A and RNase L activity were measured in extracts of peripheral blood mononuclear cells (PMBC) before and during a randomized, multicenter, placebo-controlled, double-blind study of poly(I)-poly(C12U) in individuals with chronic fatigue syndrome (CFS) as defined by the Centers for Disease Control and Prevention. The mean values for bioactive 2-5A and RNase L activity were significantly elevated at baseline compared to controls (p < .0001 and p = .001, respectively). In individuals that presented with elevated RNase L activity at baseline, therapy with poly(I)-poly(C12U) resulted in a significant decrease in both bioactive 2-5A and RNase L activity (p = .09 and p = .005, respectively). Decrease in RNase L activity in individuals treated with poly(I)-poly(C12U) correlated with cognitive improvement (p = .007). Poly(I)-poly(C12U) therapy resulted in a significant decrease in bioactive 2-5A and RNase L activity in agreement with clinical and neuropsychological improvements (Strayer DR, et al., Clin. Infectious Dis. 18:588-595, 1994). The results described show that poly(I)-poly(C12U) is a biologically active drug in CFS.

Source: Suhadolnik RJ, Reichenbach NL, Hitzges P, Adelson ME, Peterson DL, Cheney P, Salvato P, Thompson C, Loveless M, Müller WE, et al. Changes in the 2-5A synthetase/RNase L antiviral pathway in a controlled clinical trial with poly(I)-poly(C12U) in chronic fatigue syndrome. In Vivo. 1994 Jul-Aug;8(4):599-604. http://www.ncbi.nlm.nih.gov/pubmed/7893988

The treatment of chronic fatigue syndrome: science and speculation

Abstract:

The chronic fatigue syndrome (CFS) is a heterogeneous disorder characterized by fatigue, neuropsychiatric symptoms, and various other somatic complaints. Treatment studies to date reflect both the diversity of medical disciplines involved in the management of patients with CFS and the multiple pathophysiologic mechanisms proposed.

There have been few attempts to study integrated treatment programs, and although several controlled studies have been reported, no treatment has been shown clearly to result in long-term benefit in the majority of patients. Good clinical care integrating medical and psychologic concepts, together with symptomatic management, may prevent significant secondary impairment in the majority of patients.

Future treatment studies should examine differential response rates for possible subtypes of the disorder (eg, documented viral onset, concurrent clinical depression), evaluate the extent of any synergistic effects between therapies (ie, medical and psychologic), and employ a wide range of biologic and psychologic parameters as markers of treatment response.

Source: Wilson A, Hickie I, Lloyd A, Wakefield D. The treatment of chronic fatigue syndrome: science and speculation. Am J Med. 1994 Jun;96(6):544-50. http://www.ncbi.nlm.nih.gov/pubmed/8017453

Therapeutic guidelines in chronic fatigue syndrome

Abstract:

The treatment of CFS is not definitive up till now and it is limited both by ignorance of its causes and by different applicable operative case definitions. It has been etiopathologically related to infectious agents, neuromuscular illnesses, neuro-endocrinous-immunologic alterations and to different psychiatric disorders, particularly depressive disorders. Consequently, a great variety of therapeutic strategies have been tried, most of them with insufficient results. Among the medicamentous ones: immunity activator agents such as recombinant interleukin-2, nonspecific immunitary modulators such as seric gamma globulin, antivirus drugs such as acyclovir, muscular relaxants such as ciclobenzaprine, H2 receptor blockers and steroid and nonsteroid anti-inflammatory drugs such as ibuprofen, naproxen and fulbiprofen. Better results seem to have been obtained with antidepressants, and amfebutamone and serotonin-reuptake selective inhibitors are specially promising. Among the nonmedicamentous strategies, cognitive behavioural treatment can be effective and the so called “psychiatric management of the patient with CFS” has been proposed as a global, pragmatic, individualized, comprehensive approach which must be completed with other interdisciplinary interventions on the patient and his environment.

Source: Bertolín Guillén JM, Bedate Villar J. Therapeutic guidelines in chronic fatigue syndrome. Actas Luso Esp Neurol Psiquiatr Cienc Afines. 1994 May-Jun;22(3):127-30. [Article in Spanish] http://www.ncbi.nlm.nih.gov/pubmed/7484295

Upregulation of the 2-5A synthetase/RNase L antiviral pathway associated with chronic fatigue syndrome

Abstract:

Levels of 2′,5′-oligoadenylate (2-5A) synthetase, bioactive 2-5A, and RNase L were measured in extracts of peripheral blood mononuclear cells (PBMCs) from 15 individuals with chronic fatigue syndrome (CFS) before and during therapy with the biological response modifier poly(I).poly(C12U) and were compared with levels in healthy controls.

Patients differed significantly from controls in having a lower mean basal level of latent 2-5A synthetase (P < .0001), a higher pretreatment level of bioactive 2-5A (P = .002), and a higher level of pretherapy RNase L activity (P < .0001). PBMC extracts from 10 persons with CFS had a mean basal level of activated 2-5A synthetase higher than the corresponding control value (P = .009). All seven pretherapy PBMC extracts tested were positive for the replication of human herpesvirus 6 (HHV-6).

Therapy with poly(I).poly(C12U) resulted in a significant decrease in HHV-6 activity (P < .01) and in downregulation of the 2-5A synthetase/RNase L pathway in temporal association with clinical and neuropsychological improvement. The upregulated 2-5A pathway in CFS before therapy is consistent with an activated immune state and a role for persistent viral infection in the pathogenesis of CFS. The response to therapy suggests direct or indirect antiviral activity of poly(I).poly(C12U) in this situation.

Source: Suhadolnik RJ, Reichenbach NL, Hitzges P, Sobol RW, Peterson DL, Henry B, Ablashi DV, Müller WE, Schröder HC, Carter WA, et al. Upregulation of the 2-5A synthetase/RNase L antiviral pathway associated with chronic fatigue syndrome. Clin Infect Dis. 1994 Jan;18 Suppl 1:S96-104. http://www.ncbi.nlm.nih.gov/pubmed/8148461

A controlled clinical trial with a specifically configured RNA drug, poly(I).poly(C12U), in chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) is a physically debilitating illness associated with immunologic abnormalities, viral reactivation, and impairment of cognition.

In a randomized, multicenter, placebo-controlled, double-blind study of 92 patients meeting the CFS case definition of the Centers for Disease Control and Prevention, the response of several laboratory and clinical variables to an antiviral and immunomodulatory drug, poly(I).poly(C12U), was determined.

Measures of clinical response included Karnofsky performance score, a cognition scale derived from a self-administered instrument assessing symptomatology (SCL-90-R), an activities of daily living scale, and exercise treadmill performance.

After 24 weeks, patients receiving poly(I).poly(C12U) had higher scores for both global performance and perceived cognition than did patients receiving placebo. In particular, patients given poly(I).poly(C12U) had increased Karnofsky performance scores (P < .03), exhibited a greater ability to do work during exercise treadmill testing (P = .01), displayed an enhanced capacity to perform the activities of daily living (P < .04), had a reduced cognitive deficit (P = .05), and required less use of other medications (P < .05).

Source: Strayer DR, Carter WA, Brodsky I, Cheney P, Peterson D, Salvato P, Thompson C, Loveless M, Shapiro DE, Elsasser W, et al. A controlled clinical trial with a specifically configured RNA drug, poly(I).poly(C12U), in chronic fatigue syndrome. Clin Infect Dis. 1994 Jan;18 Suppl 1:S88-95. http://www.ncbi.nlm.nih.gov/pubmed/8148460