Tag: 1996

Cognitive behaviour therapy for the chronic fatigue syndrome. Evening primrose oil and magnesium have been shown to be effective

EDITOR,-In their paper on cognitive behaviour therapy for the chronic fatigue syndrome Michael Sharpe and colleagues state that many pharmacological treatments have been suggested but none are of proved value.1 Last year Lewith stated that the only two treatments that had been properly evaluated were evening primrose oil and magnesium by injection.2 Intramuscular magnesium supplements have been given to patients with low red cell magnesium in a double blind placebo controlled trial; myalgia and fatigue improved in about 70% of subjects.3 Evening primrose oil has been used to treat myalgic encephalomyelitis and is the only other treatment that has been adequately tested in a controlled trial. High doses in randomised controlled trials have been shown to have a significant effect in 70-80% of patients with myalgic encephalomyelitis or the chronic fatigue syndrome.4 I would be interested to hear Sharpe and colleagues’ comments about these papers.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350915/pdf/bmj00539-0052a.pdf

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

 

Source: Chilton SA. Cognitive behaviour therapy for the chronic fatigue syndrome. Evening primrose oil and magnesium have been shown to be effective. BMJ. 1996 Apr 27;312(7038):1096; author reply 1098. http://www.ncbi.nlm.nih.gov/pubmed/8616424

 

Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome

Abstract:

Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects.

Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscles (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150-3000 times the normal values.

By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripheral mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.

 

Source: Vecchiet L, Montanari G, Pizzigallo E, Iezzi S, de Bigontina P, Dragani L, Vecchiet J, Giamberardino MA. Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome. Neurosci Lett. 1996 Apr 19;208(2):117-20. http://www.ncbi.nlm.nih.gov/pubmed/8859904

 

Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome

Abstract:

1. Chronic fatigue syndrome is characterized by muscle fatigue and pain at rest, symptoms which are usually exacerbated with exercise. Although various studies have shown minor, non-specific morphological and biochemical changes in muscle of patients with chronic fatigue syndrome, no consistent defect has been identified. Some have suggested that an enteroviral infection in muscle may cause the chronic muscle fatigue seen in patients with chronic fatigue syndrome, with acute infection directly and irreversibly impairing mitochondrial function, and persistent infection depressing muscle protein synthesis and metabolism.

2. To clarify the involvement of enterovirus infection in chronic fatigue syndrome, muscle biopsies from a group of patients with chronic fatigue syndrome were examined for the presence of enteroviral RNA by reverse transcriptase-polymerase chain reaction techniques in relation to functional studies of muscle mitochondria and the muscle RNA/DNA ratio.

3. Fifty-eight percent of patients reported an uncharacterized ‘viral infection’ before the onset of their illness, but none of the muscle samples from 34 patients contained detectable amounts of enteroviral RNA. Muscle tissue had a general reduction in the RNA/DNA ratio and mitochondrial enzyme activities with no specific abnormality in the activity of enzymes encoded partially on the mitochondrial genome (cytochrome-c oxidase) or nuclear genome (citrate synthase, succinate reductase).

4. These data provide no evidence of an enteroviral infection in muscle of patients with chronic fatigue syndrome, although this does not exclude a role of enterovirus in initiating the disease process. The general reduction in RNA/DNA ratio and mitochondrial enzyme activities is consistent with a general reduction in habitual activity.

 

Source: McArdle A, McArdle F, Jackson MJ, Page SF, Fahal I, Edwards RH. Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome. Clin Sci (Lond). 1996 Apr;90(4):295-300. http://www.ncbi.nlm.nih.gov/pubmed/8777836

 

Randomized, double blind, controlled placebo-phase in trial of low dose phenelzine in the chronic fatigue syndrome

Abstract:

Because of the striking similarity of the clinical manifestations produced by use of the drug reserpine and seen in patients with the chronic fatigue syndrome (CFS), we theorized that CFS was a disorder of reduced central sympathetic drive. Because of the pharmacology of control of this central sympathetic system, we further postulated that CFS symptoms would respond quickly to low dose treatment with a monamine oxidase inhibitor. To test these hypotheses, we designed a randomized, double blind placebo controlled study using phenelzine.

No patient in the trial had a diagnosis of lifetime or current psychiatric disorder and none had depressed mood in the range of clinically depressed patients on a paper and pencil test of depression. Patients in the placebo group received placebo for 6 weeks while those in the drug treatment group were treated in three 2-week segments-placebo, 15 mg phenelzine every other day, and then 15 mg daily. This treatment regimen produced a significant pattern of improvement compared to worsening in 20 self report vehicles of CFS symptoms, illness severity, mood or functional status.

Thus the data support our hypothesis of reduced sympathetic drive, although an alternative hypothesis of pain alleviation is also possible. The study design also allowed us to evaluate patients for a placebo effect: no evidence for this was found, suggesting that CFS is not an illness due to patients’ being overly suggestible.

 

Source: Natelson BH, Cheu J, Pareja J, Ellis SP, Policastro T, Findley TW. Randomized, double blind, controlled placebo-phase in trial of low dose phenelzine in the chronic fatigue syndrome. Psychopharmacology (Berl). 1996 Apr;124(3):226-30. http://www.ncbi.nlm.nih.gov/pubmed/8740043

 

Preliminary determination of a molecular basis of chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS/ME) is a debilitating fatigue illness that has an unknown etiology. We studied 20 chronic fatigue syndrome (CFS) patients, who complied with the Oxford and American CDC definitions, and 45 non-CFS subjects.

Participants completed questionnaires, were clinically examined, and had first morning urine specimens collected, which were screened by gas chromatography-mass spectrometry for changes in metabolite excretion.

Multivariate analysis of the urinary metabolite profiles differed significantly in the CFS patients compared to the non-CFS patients (P < 0.004). The CFS patients had increases in aminohydroxy-N-methylpyrrolidine (P < 0.00003, referred to as chronic fatigue symptom urinary marker 1, or CFSUM1), tyrosine (P < 0.02), beta-alanine (P < 0.02), aconitic acid (P < 0.05), and succinic acid (P < 0.05) and reductions in an unidentified urinary metabolite, CFSUM2 (P < 0.0007), alanine (P < 0.005), and glutamic acid (P < 0.02). CFSUM1, beta-alanine, and CFSUM2 were found by discriminant function analysis to be the first, second, and third most important metabolites, respectively for discriminating between CFS and non-CFS subjects.

The abundances of CFSUM1 and beta-alanine were positively correlated with symptom incidence (P < 0.01 and P < 0.001, respectively), symptom severity, core CFS symptoms, and SCL-90-R somatization (P < 0.00001), suggesting a molecular basis for CFS.

 

Source: McGregor NR, Dunstan RH, Zerbes M, Butt HL, Roberts TK, Klineberg IJ. Preliminary determination of a molecular basis of chronic fatigue syndrome. Biochem Mol Med. 1996 Apr;57(2):73-80. http://www.ncbi.nlm.nih.gov/pubmed/8733884

 

Insulin-like growth factor-I (somatomedin C) levels in chronic fatigue syndrome and fibromyalgia

Abstract:

OBJECTIVE: Fibromyalgia (FM) and chronic fatigue syndrome (CFS) are similar conditions characterized by substantial fatigue, diffuse myalgias, sleep disturbances and a variety of other symptoms. Many patients with CFS meet strict criteria for FM. Recently, low insulin-like growth factor-I (IGF-I) levels have been demonstrated in patients with FM, suggesting that disruption of the growth hormone-IGF-I axis might explain the link between the muscle pain and poor sleep. Our goal was to determine whether IGF-I levels are decreased in CFS, and whether such findings are restricted to patients with concurrent FM.

METHODS: Radioimmunoassays were used to determine serum concentrations of IGF-I and its binding protein, (IGFBP-3). Subjects were 3 patients seen in a referral clinic for chronic fatigue: 15 patients with CFS, 15 who met criteria for both CFS and FM (CFS-FM), 27 with FM alone; and 15 healthy control (HC) subjects.

RESULTS: Patients and control subjects had similar demographic and clinical characteristics. No significant differences were observed among any of the 3 patient groups and control subjects in the mean concentration of either IGF-I or IGFBP-3. Likewise, the proportion of subjects with values above or below the laboratory’s reference range did not differ for IGF-I or IGFBP-3.

CONCLUSIONS: These findings suggest the disruption of the growth hormone-IGF-I axis previously demonstrated in FM patients is not evident in a referral population of patients with CFS, CFS-FM, or FM.

 

Source: Buchwald D, Umali J, Stene M. Insulin-like growth factor-I (somatomedin C) levels in chronic fatigue syndrome and fibromyalgia. J Rheumatol. 1996 Apr;23(4):739-42. http://www.ncbi.nlm.nih.gov/pubmed/8730136

 

Periodic K-alpha sleep EEG activity and periodic limb movements during sleep: comparisons of clinical features and sleep parameters

Abstract:

The K-alpha sleep electroencephalographic (EEG) phenomenon is characterized by periodic (approximately 20-40 seconds) K-complexes, immediately followed by alpha-EEG activity (7.5-11 Hz) of 0.5- to 5.0-second duration. A group of 14 subjects with the periodic K-alpha anomaly was found to have a similar distribution pattern of interevent intervals as compared with previously published data for sleep-related periodic limb movements during sleep (PLMS). Sleep parameters and somatic symptoms of 30 patients with K-alpha were compared with 30 patients with PLMS. The periodic K-alpha group was predominantly female, younger, exhibiting more slow-wave sleep, gastrointestinal symptoms and muscular complaints and fewer movement arousals on overnight polysomnography. The K-alpha group presented uniformly with complaints of unrefreshing sleep, often associated with fibromyalgia and chronic fatigue syndrome. The PLMS group was predominantly male, showed greater sleep disruption and presented with a variety of sleep-related symptoms.

 

Source: MacFarlane JG, Shahal B, Mously C, Moldofsky H. Periodic K-alpha sleep EEG activity and periodic limb movements during sleep: comparisons of clinical features and sleep parameters. Sleep. 1996 Apr;19(3):200-4. http://www.ncbi.nlm.nih.gov/pubmed/8723376

 

Chronic fatigue syndrome–also an insurance medicine problem

Abstract:

Not everybody who is chronically tired has a chronic fatigue syndrome. The diagnosis of the chronic fatigue syndrome is still a problem, and is becoming a problem in health insurance medicine too. There is a lack of knowledge concerning the causes, the diagnosis and the therapy of the chronic fatigue syndrome. And there is still the question if the chronic fatigue syndrome is an entity of its own. For these reasons we should apply the few facts we really know about the chronic fatigue syndrome. This is the working case definition of Kaplan et al. from 1988. Otherwise there will be done hundreds of expensive laboratory tests, which are useless for the patient and very costly for the health insurance companies.

 

Source: Hakimi R. Chronic fatigue syndrome–also an insurance medicine problem. Versicherungsmedizin. 1996 Apr 1;48(2):59-61. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/8659056

 

Expert assessment of chronic fatigue syndrome

Abstract:

The Chronic-Fatigue-Syndrome (CFS) has been first described in 1988 and has been also in Germany recently more frequently diagnosed. It is similar to a lot of other terms, especially to “neurasthenia”, which has been introduced 1869 from Beard and is now again content of ICD-10. CFS is defined by primary and secondary criteria, which are however largely subjective. There are no objective signs. It is unknown if this syndrome represents a disease entity of its own. The explanation is either exclusive organic based on immunological and virological findings or exclusive psychogenic as a special form of anxiety psychosis. Possibly are both factors involved as part of “psycho-neuro-immunology”. CFS is increased subject of medical certification. It has been tried to give a practical guidance to the assessment of CFS.

 

Source: Hausotter W. Expert assessment of chronic fatigue syndrome. Versicherungsmedizin. 1996 Apr 1;48(2):57-9. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/8659055

 

Chronic fatigue syndrome–psychiatric aspects

Abstract:

Diagnosis of the chronic fatigue syndrome depends on various somatic and psychopathological symptoms. Somatic symptoms of the syndrome have been subject of an extensive body of literature. In comparison, psychiatric aspects have caught relatively less attention.

Psychiatric aspects of etiological, diagnostic, and therapeutic concepts are essential for evaluation of the syndrome. Application of CDC-criteria to a well known disease does not solve the nosological problem, but may define the syndrome more accurately. In this respect, issues including psychiatric comorbidity and specificity of neuropathological symptoms are discussed.

Psychological variables seem to have a high predictor value for time course and outcome of the symptoms. Etiological concepts emphasize on biological or psychosocial factors. Alterations of biological parameters including immune functions, sleep regulation, and hypothalamic-pituary-adrenocortical function have been reported. The role of cultural factors has been discussed extensively. Somatic and psychological stress may result in the same clinical syndrome via psychoimmunological mechanisms. An integrated, interdisciplinary approach to further refine diagnostic criteria, understanding of etiology and development of adequate therapeutic measures seems necessary.

 

Source: Lemke MR. Chronic fatigue syndrome–psychiatric aspects. Fortschr Neurol Psychiatr. 1996 Apr;64(4):132-41. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/8655125