VIROLOGY/MICROBIOLOGY 

Ablashi, DV., Eastman, HB., Owen, CB., Roman, MM., Friedman, J., Zabriskie, JB., Peterson, DL., Pearson, GR and Whitman, JE. Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. Journal of Clinical Virology, 2000, 16, 3, 179-191.

Human herpes virus-6 (HHV-6) is a ubiquitous virus. Infection usually occurs in childhood and then becomes latent. HHV-6 reactivation has been shown to play a role in the pathogenesis of AIDS and several other diseases. The aim of this study was to determine what role HHV-6 infection or reactivation plays in the pathogenesis of multiple sclerosis (MS) and CFS.

The subjects were 21 patients with MS (of whom 6 were in remission) and 35 patients with CFS (CDC criteria '94, with 27 having "severe disease"). The results were compared with those of 28 healthy blood donors (HD) and 20 people with other neurological disorders (OND). HHV-6 IgG and IgM antibody levels were measured and peripheral blood mononuclear cells (PBMCs) were analysed for the presence of HHV-6 using a short term culture assay.

In both MS and CFS patients, higher levels of HHV-6 IgM antibody and elevated levels of IgG antibody were found when compared to healthy controls. Over 70% of the MS patients studied had IgM antibodies against HHV-6 compared to 57.1% of the CFS group, 15% of the healthy donors and 20% of the OND group. Moreover, 54% of CFS patients exhibited antibody to HHV-6 IgM early protein (p41/38) compared to only 8.0% of the HD group. Elevated IgG antibody titers were detected in both the MS and the CFS patients.  There was evidence of a higher frequency of HHV-6 infection in MS patients with progressive or relapsing disease when compared to patients in remission.

PBMCs from the MS, CFS and HD groups were analysed in a short term culture assay in order to detect HHV-6 antigen expressing cells and to characterize the viral isolates obtained as either Variant A or B. Fifty-four per cent of MS patients had HHV-6 early and late antigen producing cells and 87% of HHV-6 isolates were Variant B. Isolates from CFS patients were predominately Variant A (70%) while those from the healthy donors were predominately Variant B (67%).

Persistent HHV-6 infection was found in the two CFS patients tested over a period of 2.5 years and HHV-6 specific cellular immune responses were detected in PBMCs from ten CFS patients.

Aside from the increased levels of HHV-6 antibody and HHV-6 DNA, the researchers also detected a decrease in cellular immune responses. "These data suggest that HHV-6 reactivation plays a role in the pathogenesis of these disorders." Moreover, the elevation in late viral protein IgG suggests that "reactivated virus may be stimulating the immune system." Finally, IgM antibody to p41/38  "could be clinically useful to assess viral reactivation, viral persistence or primary infection."

IMMUNOLOGY

De Meirleir, K., Bisbal, C., Campine, I., De Becker, P., Salehzada, T., Demettre, E and Lebleu, BA.  37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome.  American Journal of Medicine, 2000, 108, 2, 99-105.

Recent studies have revealed abnormalities in the ribonuclease L pathway in PBMCs of patients with CFS. The researchers conducted a blinded study to detect possible differences in the distribution of 2-5A binding proteins in the cells of patients with CFS and controls.

The sample comprised 57 patients with CFS (CDC criteria '88 and '94) and 53 control subjects (28 healthy subjects and 25 patients with depression or fibromyalgia). A radioactive probe was used to label 2-5A binding proteins in unfractionated PBMC extracts and to compare their distribution in the three groups.

A 37 kDa (kilodaltons) 2-5A binding polypeptide was found in 88% of the CFS patients compared with 28% of the controls (p<0.01). When present, the amount of 37 kDa protein was very low in the control groups. When expressed as the ratio of the 37 kDa protein to the (normal) 80 kDa protein, 72% of the patients with CFS had a ratio >0.05, compared with 11% of the healthy subjects and none of the patients with fibromyalgia or depression.

"The presence of a 37 kDa 2-5A binding protein in extracts of peripheral blood mononuclear cells may distinguish patients with chronic fatigue syndrome from healthy subjects and those suffering from other diseases."

With editorials by Komaroff, commenting on the significance of the findings (p. 169-171) and Manu, emphasising the arguments supporting the CBT explanation (p. 172-173).

• [Ed. note: The editorial by Manu contains a misleading interpretation of the research by Sharpe et al (1992) and ignores psychiatric research which is inconsistent with his views.]

Kavelaars, A., Kuis, W., Knook, L., Sinnema, G and Heijnen, CJ. Disturbed neuroendocrine-immune interactions in chronic fatigue syndrome. Journal of Clinical Endocrinology and Metabolism, 2000, 85, 2, 692-696.

The present study was designed to investigate the interaction between neuroendocrine mediators and the immune system in CFS. The researchers examined the sensitivity of the immune system to the glucocorticoid agonist dexamethasone and the β2-adrenergic agonist terbutaline in 15 adolescent girls with CFS (CDC criteria '94, mean age 15.8 years) and 14 age- and gender-matched controls. Mean duration of disease was 21.8 months (range 6-48 months).

In the absence of dexamethasone, there was a greater response to stimulation of the T-cells by phytohemagglutinin (PHA) in the CFS group compared to the controls. "Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients."  The addition of dexamethasone to the blood samples resulted in the reduction of T-cell proliferation, which was less pronounced in CFS patients as compared with the controls.

There were no group differences in baseline levels of tumour necrosis factor-α (TNF-α). After stimulation with lipopolysaccaride (LPA) to induce monocyte cytokine production, the β2-adrenergic receptor agonist terbutaline was added to the blood samples. Terbutaline inhibits TNF-α production and enhances interleukin-10 production by monocytes. The results showed that the capacity of terbutaline to regulate the production of these two cytokines was reduced in patients with CFS.

There were no differences in the levels of baseline or CRH-induced cortisol and ACTH between CFS patients and controls. Baseline noradrenaline was similar in the two groups, although baseline adrenaline levels were significantly higher in the patients with CFS.

The researchers concluded that CFS is accompanied by a relative resistance of the immune system to regulation by the neuroendocrine system. They suggest CFS that should be viewed as a disease of deficient neuroendocrineimmune communication, possibly the result of psychological stress (based on a study of the effects of bereavement) and a precipitating event (e.g. viral infection).

PHYSIOLOGY, NEUROPHYSIOLOGY AND NEUROENDOCRINOLOGY

Cleare, AJ., Sookdeo, SS., Jones, J., O'Keane, V and Miell, JP. Integrity of the growth hormone/insulin-like growth factor system is maintained in patients with chronic fatigue syndrome.  Journal of Clinical Endocrinology and Metabolism,  2000, 85, 4, 1433-1439.

Karas, B., Grubb, BP., Boehm, K and Kip, K. The postural orthostatic tachycardia syndrome. A potentially treatable cause of chronic fatigue, exercise intolerance, and cognitive impairment in adolescents. PACE-Pacing and Clinical Electrophysiology, 2000, 23, 3, 344-351.

BIOCHEMISTRY AND BIOLOGY

McGregor, NR., Dunstan, RH., Donohoe, M., Roberts, TR., Butt, HL., Watkins, JA., Murdoch, RN and Taylor, WG. Assessment of plasma fatty acids and sterols in sudden and gradual-onset chronic fatigue syndrome patients. Journal of Nutritional and Environmental Medicine, 2000, 10, 13-23.

A study was undertaken in 60 people with CFS (CDC criteria '88) and 39 age and gender-matched non-CFS controls to determine whether the patients had characteristic lipid profiles which may be indicative of specific viruses or cytokine responses. Plasma saponified lipid products were assessed using capillary gas chromatography-mass spectrometry (GC-MS) to measure qualitative changes in plasma lipid profiles.

Twenty of the CFS patients reported an acute viral-like infection at onset whereas the remaining 40 reported a gradual onset.  None of the sudden-onset patients had evidence of a current common viral infection.

The lipid profiles between the CFS group and controls were significantly different with the primary discriminatory features for the former including a decreased relative abundance of trans-9-octadecenoic acid (elaidic acid), a decreased concentration of plasma total cholesterol and a decrease in the ratio of trans-9-octadecenoic acid: octadecanoic acid. However, there were no associations or changes in the relative abundances or ratios reported to be good indicators of either viral infection or cytokine responses. Nevertheless, the decrease in cholesterol levels may be indicative of some pathogenic challenge.

Analysis of sudden versus gradual onset cases revealed different lipid profiles. Indeed, 25 lipid ratios were different when comparing the sudden-onset group with the controls, but there was only one abnormal ratio differentiating the gradual-onset cases and controls. Thus there was a greater disturbance in lipid homeostasis in the sudden-onset group compared with the gradual-onset group. The sudden-onset group also showed a change in the important post-viral associated lipid ratio, the cis-9-octadecanoic acid: cis-9, 12-octadecadienoic acid (i.e. olieic acid: linoleic acid, p<.003), but no other previously reported viral or cytokine associated ratios were found to be altered.

The data suggest that viral infections may influence the development of CFS in certain patients. The changes in lipid homeostasis may reflect common long-term sequelae to single or multiple pathogen-induced modifications in lipid homeostasis and may represent the culmination of several infectious challenges and environmental influences (including toxic chemical insults). The changes do not appear to be a response to current infections.

PATHOLOGY

Richards, RS, Roberts, TK., Mathers, D., Dunstan, RH., McGregor, NR and Butt, HL. Erythrocyte morphology in rheumatoid arthritis and chronic fatigue syndrome: a preliminary study. Journal of Chronic Fatigue Syndrome, 2000, 6, 23-35.

Erythrocyte deformability and erythrocyte membrane stability are dependent on the erythrocyte cytoskeleton and its relationship with the contents of the cell. Certain internal occurrences such as oxidation of sulphydryl groups on the membrane cytoskeleton or the haemoglobin molecule could alter this relationship and as a consequence, alter the membrane properties and the shape of the cell. It is thus conceivable that in conditions where there is a potential increase in the generation of free radicals, erythrocyte shape could be altered. This study investigated the possibility that predictable shape changes occur in erythrocytes from patients with rheumatoid arthritis (RA), a condition associated with free radical damage, and in CFS.

Patients with CFS could be divided into two groups based on their erythrocyte morphology. Seven out of the 11 patients (Oxford/CDC criteria '88) had a higher percentage of stomatocytes (early and late cup forms) than the healthy controls (n=16).  There was no difference between the CFS group and the patients with RA (n=15) or controls in terms of blood viscosity. RA was associated with an increase in leptocytes (flat cells), possibly due to free radical oxidation.

Richards, RS., Roberts, TK., Mathers, D., Dunstan, RH., McGregor, NR and Butt, HL. Investigation of erythrocyte oxidative damage in rheumatoid arthritis and chronic fatigue syndrome.  Journal of Chronic Fatigue Syndrome, 2000, 6, 1, 37-46.

It has been proposed that while carrying out their role of free  radical scavenging, erythrocytes are damaged by oxidation, leading to shape changes and increased rigidity. To look for evidence of oxidative damage in vivo, erythrocytes were assessed for reduced glutathione (GSH), malondialdehyde (MDA), methaemoglobin (metHb) and 2,3-diphosphoglyceric acid (2,3-DPG) in patients suffering from RA (n=37), CFS (Oxford/CDC criteria '88, n=33) and healthy controls (n=27). Full blood counts, serum vitamin B12, erythrocyte folate, serum ferritin, serum iron, serum iron binding capacity and erythrocyte magnesium were also performed on all samples.

Patients with RA had increased 2,3-DPG, GSH and metHb when compared with the control group as well as the expected decreased haemoglobin, haematocrit and serum iron. There was evidence of oxidative damage in CFS with 2,3-DPG metHb and MDA increased in this group. An increase in GSH could also be demonstrated in a subgroup of the CFS patients (n=18) compared to controls.  The damage may explain the shape changes (presumably accompanied by increased rigidity) that have been reported in erythrocytes in patients suffering from CFS and suggests a role for free radicals in the pathogenesis of CFS. (Erythrocyte magnesium levels were similar to the controls).

PSYCHOLOGY, NEUROPSYCHOLOGY AND PSYCHIATRY

Friedberg, F., Dechene, L., McKenzie, MJ and Fontanetta, R. Symptom patterns in long-duration chronic fatigue syndrome. Journal of Psychosomatic Research, 2000, 48, 1, 59-68.

This cross-sectional self-report study compared groups with long-duration CFS (median = 18 years; n=258) and short-duration CFS (median = 3 years; n=28) to a group of healthy significant others (n=79) on symptomatic, neurocognitive and psychological variables. Data were gathered from a 574-item postal questionnaire, which included a fatigue scale (Krupp et al 1989), the Brief Symptom Inventory, the Illness Management Questionnaire and a measure of functional status.

A principal-components analysis of the CFS symptom data yielded a three-factor solution: cognitive problems; flu-like symptoms; and neurologic symptoms. Compared with the short-duration CFS group, the long-duration group had significantly higher CFS symptom severity scores (p<0.04), largely attributable to increased cognitive difficulties.

A subgroup comparison of subjects ill for <3 years versus those ill 4-7 years suggested that denial coping strategies were more likely in those participants with the shorter illness duration but there were no group differences with regard to fatigue, depression (CES-D), allergies, stress, social support, coping strategies or functional status.  Both CFS groups differed from the healthy controls in terms of the number of (lifetime) comorbid disorders, such as chemical sensitivity (CS), fibromyalgia, major depression and cardiac arrhythmias.

Eighty-seven per cent reported prolonged fatigue after exercise. Participants with CFS most often endorsed immune/viral abnormalities and persistent stress as important perceived causes of their illness.

The pattern of comorbid disorders in the CFS groups was consistent with the hypersensitivity and viral reactivation hypotheses. The viral model suggests that the exacerbating influence of stress on CFS symptoms may be the result of stress-triggered herpes virus activation. The weak correlations between psychological (stress and depression) measures and allergy and CS symptom scores suggest that emotional factors cannot fully explain the high levels of symptomatology.

• [Ed. note: The vast majority of subjects were physician-diagnosed but a few self-diagnosed cases were included as well. It is not clear how many patients met CDC criteria '94.]

Jason, LA., Fennell, PA., Taylor, RR., Fricano, G and Halpert, JA. An empirical verification of the Fennell phases of the CFS illness. Journal of Chronic Fatigue Syndrome, 2000, 6, 1, 47-56.

Neerinckx, E., Van Houdenhove, B., Lysens, R., Vertommen, H and Onghena P.   Attributions in chronic fatigue syndrome and fibromyalgia syndrome in tertiary care. Journal of Rheumatology, 2000, 27, 4, 1051-1055.

Prins, JB and Bleijenberg, G. Cognitive behavior therapy for chronic fatigue syndrome: a case study.  Journal of Behavior Therapy and Experimental Psychiatry, 1999, 30, 4, 325-339.

Case study of a 26 year old woman who had developed tiredness, myalgia and hypersomnia following a number of stressful events, including an examination, her move from East Germany to Holland and the death of her father back home.  She felt guilty about her absence during her father's illness and this, her perfectionist personality and her tendency to push herself, may have contributed to her fatigue.

She completed 22 sessions of CBT aimed at challenging her unhelpful cognitions. It was initially accompanied by advice regarding pacing.  ("She was instructed to stop with daily activities as soon as fatigue comes up or increases.") Once her fatigue had lessened, she was advised to build up her activities gradually and to consider a return to work.

The treatment was successful in reducing her fatigue, depression and pain. She also returned to work (around 5 hours per day). There was no change in her views about the cause of her illness.

EPIDEMIOLOGY

Jordan, KM., Ayers, PM., Jahn, SC., Taylor, KK., Huang, C-F, Richman, J and Jason, LA. Prevalence of fatigue and chronic fatigue syndrome-like illness in children and adolescents. Journal of Chronic Fatigue Syndrome, 2000, 6, 1, 3-21.

A community-based screening of over 12,000 households in Chicago was conducted in order to determine the prevalence of fatigue and CFS-like illness in a sample of 5- to 17-year olds.

Information was collected from an adult in the family. Over 4% of the youngsters had reported experiencing fatigue and 2.05% were diagnosed with CFS-like illness (modified CDC criteria '94). Adolescents had a slightly higher rate of CFS-like illness (2.91%) than children aged 5-12 (1.96%). Those with CFS-like illness were almost evenly divided between male (47.5%) and female (52.5%). Youngsters of Latino origin had the highest representation in the CFS-like group.

Amongst adults in the survey, 1.4% were diagnosed with a CFS-like illness (Jason et al. In press).

Rangel, L., Garralda, ME., Levin, M and Roberts, H.  The course of severe chronic fatigue syndrome in childhood.  Journal of the Royal Society of Medicine, 2000, 93, 128-133.

This study reported interview data on 25 children and adolescents with CFS (Oxford criteria). The interviews were conducted a mean of 45.5 months following illness onset. Triggers of the illness were mainly infectious, with 7 cases following glandular fever. At its worst, the condition had been very severe, leading to prolonged bed rest and school absence in two-thirds. However, at follow-up, two-thirds had recovered to some extent and the mean illness duration was 38 months. No one developed other medical conditions.

Recovery (n=17) was associated with high socio-economic status, physical triggers and start of illness in the autumn term (mean age at onset was 11.7 years). Emotional problems were not linked to outcome. Symptoms other than fatigue included headaches, disrupted night sleep, muscle pains/discomfort and concentration problems. Twelve per cent had major depression, 40% a depressive disorder.

Complicating factors in terms of the interpretation of data were premorbid fatigue (12%) as well as pre-existing aches and pains (28%) and behaviour problems and mood changes (16%).

The authors note that in many children, the onset coincided with the transfer to secondary school, a recognised source of stress requiring both physical and psychological adaptation. Many parents appreciated the support from paediatricians at the tertiary centre.

Zhang, QW., Natelson, BH., Ottenweller, JE., Servatius, RJ., Nelson, JJ., De Luca, J., Tiersky, L and Lange, G. Chronic fatigue syndrome beginning suddenly occurs seasonally over the year. Chronobiology International, 2000, 17, 1, 95-99.

This study assessed 69 patients with CFS (CDC criteria '88 and '94) whose condition was on the more severe side of the illness spectrum, and who all reported sudden illness onset with sore throat, fatigue/malaise, and diffuse achiness developing over no longer than a 2-day period.

The date of illness onset was distinctly non-random. It peaked from November through January and was at its lowest from April through May. These data support the hypothesis that an infectious illness can trigger the onset of CFS. If CFS were a psychiatric disorder related to symptom amplification, one would expect onset to occur randomly over the calendar year. However, while the trigger may be infectious, the variables responsible for maintaining the illness remain unclear.

REVIEWS

Buskila, D.  Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Current Opinion in Rheumatology, 2000, 12, 113-123.

Chaudhuri, A., Watson, WS., Pearn, J and Behan, PO. The symptoms of chronic fatigue syndrome are related to abnormal ion channel function.  Medical Hypotheses, 2000, 54, 1, 59-63.

Pall, ML. Elevated, sustained peroxynitrite levels as the cause of chronic fatigue syndrome. Medical Hypotheses, 2000, 54, 1, 115-125.

Swenson, TS. Chronic fatigue syndrome. Journal of Rehabilitation, 2000, 66, 1, 37-42.

MEETING ABSTRACTS

Neerinckx, ER., Vingerhoets, A and Van Houdenhove, B. Daily hassles reported by chronic fatigue and fibromyalgia syndrome patients in tertiary care: a qualitative and quantitative analysis. Psychosomatic Medicine, 2000, 62, 1, 109, no. 1468.

This study assessed daily hassles during the past two months. The samples comprised patients with 177 CFS (not defined) and fibromyalgia (FM), 26 patients with MS and 26 patients with RA. Pain and fatigue were evaluated with visual analogue scales.

The CFS/FM patients reported significantly more daily hassles than the comparison groups (p<.01) and the impact of these stressors were experienced as significantly more burdening. There were weak (but significant) correlations between the number of daily problems and depression, fatigue and anxiety. The nature of daily hassles were focused on dissatisfaction with oneself, lack of social recognition and insecurity in the CFS/FM patients but not in the comparison groups.

Van Houdenhove, B and Neerinckx, ER. Victimization in fibromyalgia and chronic fatigue syndrome in tertiary care: a controlled study on prevalence and characteristics. Psychosomatic Medicine, 2000, 62, 1, 148, nr 1467.

This study investigated victimization in 95 patients with CFS/FM (not defined), and compared the results with people suffering from MS and RA.

The general prevalence rates of victimization was significantly higher in the CFS/FM group compared to the controls.   There were also significant differences in terms of emotional neglect, emotional abuse and physical abuse between the three groups. The family of origin and partner were the most important perpetrators.  There were no differences between the CFS and FM patients.

Rangel, L., Garralda, E., Levin, M and Roberts, H. Personality in adolescents with chronic fatigue syndrome. European Child & Adolescent Psychiatry, 2000, 9, 1, 39-45.

Repka-Ramirez, S., Naranch, K., Park, YJ., Velarde, A and Baraniuk, JN. IgE levels in chronic fatigue and control subjects. Journal of Allergy and Clinical Immunology, 2000, 104, 1 (pt 2), S359, 1058.

A study of 95 patients with CFS and 109 non-CFS control subjects indicated that IgE was higher in subjects with positive allergy skin tests, regardless of whether they had CFS.

MISCELLANEOUS

Byrne, E. Aetiological considerations on some conditions in the  borderlands of neurology: chronic fatigue syndrome, pan allergy syndrome and repetitive strain injury - a personal view. Journal of Clinical Neuroscience,  2000, 7, 1, 9-12.

Gilbert, RB., Kaan, R., Lipkin, DH and Lepp, M. Chronic fatigue: syndrome or disease? Journal of American Medical Association, 2000, 283, 6, 744. Plus reply, p. 744-745.

Letter relating to a book review by Ehrlich (ibid, 1999, 282, 1095). The authors note some of the problems associated with the current definition of CFS and how it affects diagnosis.

In his reply, Ehrlich states that "legitimizing the symptoms as a disease construct serves no one, especially the patient, and is intellectually and fiscally impoverishing."  He also implies that diagnosis invariably misleads patients into thinking that "they are doomed to continued suffering and disability."

• [Ed. note: Ehrlich describes Wessely, Hotopf and Sharpe as psychiatrists and psychologists. In fact, all three are psychiatrists. There is no evidence that the correct diagnosis of CFS has a detrimental effect on the majority of patients.]

Lee, S., Yu, H., Wing, Y., Chan, C., Lee, AM., Lee, DTS., Chen, CN., Lin, KM and Weiss, MG. Psychiatric morbidity and illness experience of primary care patients with chronic fatigue in Hong Kong. American Journal of Psychiatry, 2000, 157, 3, 380-384.

Marcovitch, H.  Chronic fatigue in adolescents. Journal of the Royal College of Physicians of London, 2000, 34, 1, 21-23.

Moore, L.  Chronic fatigue syndrome: all in the mind? An occupational therapy perspective. British Journal of Occupational Therapy, 2000, 63, 4, 163-170.

Study of 20 occupational therapists revealed that many had a neutral, client-centred approach.

Myers, C and Wilks, D. Comparison of Euroqol EQ-5D and SF-36 in patients with chronic fatigue syndrome. Quality of Life Research, 1999, 8, 9-16.

Steven, ID., McGrath, B., Qureshi, F., Wong, C, Chern, I and Pearn-Rowe, B.  General practitioners' beliefs, attitudes and reported actions towards chronic fatigue syndrome. Australian Family Physician, 2000, 29, 1, 80-85.

A random sample of 2090 Australian GPs were surveyed in 1995. Of these, 77% responded. Criteria used by the GPs to diagnose CFS included chronic fatigue lasting >6 months, failure to recover energy after rest, generalised myalgia and poor concentration. Individual counselling was the most frequently used treatment. Only 14% used 'graduated mobilisation'. Forty-six per cent believed that CFS was a distinct entity (particularly female and younger GPs), while 27% did not believe that CFS was a distinct entity.  Of these, 70% reported that the most likely cause of chronic fatigue was depression.

Swenson, TS. Chronic fatigue syndrome. Journal of Rehabilitation, 2000, 66, 1, 37.

Takahashi, Y., Ohta, S., Sano, A., Kuroda, Y., Kaji, Y., Matsuki, M and Matsuo, M. Does severe nutcracker phenomenon cause pediatric chronic fatigue? Clinical Nephrology, 2000, 53, 3, 174-181.

Tomoda, A., Miike, T., Yamada, E., Honda, H., Moroi, T., Ogawa, M., Ohtani, Y and Morishita, S. Chronic fatigue syndrome in childhood. Brain & Development, 2000, 22, 1, 60-64.

Treib, J., Grauer, MT., Haass, A., Langenbach, J., Holzer, G and  Woessner, R. Chronic fatigue syndrome in patients with Lyme borreliosis. European Neurology, 2000, 43, 2, 107-109.

Various. Letters responding to Marcovitch. British Medical Journal, 2000, 230, 1004.

Letter by Pheby criticising Marcovitch (BMJ, 1999, 319, 1376) and comments from Wessely, supporting him.

• [Ed. note: A letter by Goudsmit challenging misleading information in the response by Wessely was published by the EBMJ.]

White, KP., Speechley, M., Harth, M and Ostbye, T. Co-existence of chronic fatigue syndrome with fibromyalgia syndrome in the general population - a controlled study. Scandinavian Journal of Rheumatology, 2000, 29, 1, 44-51.

ARTICLES ON OTHER DISORDERS

Bruno, RL.  Paralytic vs. "nonparalytic" polio. Distinction without a difference? American Journal of Physical Medicine & Rehabilitation, 2000, 79, 1, 4-12.

Nonparalytic polio (NPP) is commonly thought to be synonymous with "abortive polio," in which the poliovirus neither entered the central nervous system (CNS) nor damaged neurons. Described are two epidemic illnesses - "The Summer Grippe" and Iceland Disease - apparently caused by a low virulence but neuropathic type 2 polio-virus. Clinicians should be aware that NPP, and possibly even poliovirus-induced "minor illnesses" can be associated with acute CNS damage and late-onset muscle weakness and fatigue.

• [Ed. note: Iceland Disease (ID) and NPP were distinct entities. Differences include the high incidence of sensory changes in ID, febrile relapses with new tissues infected and peripheral nerve involvement (cf. Ramsay 1988) and Hardtke, EF., Journal of the Indiana State Medical Association, 1955, 48, 3, 245-250).]

Eaton, KK., Anthony, HM., Birtwistle, S., Downing, D., Freed, DLJ., McLaren Howard, J., Maberly, DJ., Mansfield, JR., Myhill, S and Radcliffe, MJ. Multiple chemical sensitivity: recognition and management. A document on the health effects of everyday chemical exposures and their implications. Journal of Nutritional & Environmental Medicine, 2000, 10, 39-84.

Review of research into MCS.

Iriarte, J., Subira, ML., de Castro, P.  Modalities of fatigue in multiple sclerosis: correlation with clinical and biological factors.  Multiple Sclerosis, 2000, 6, 2, 124-130.

The researchers suggest that fatigue is a complex symptom which can occur in three different forms (asthenia, fatigability and worsening of other symptoms with effort). The goal of this study was to assess if there is a specific mechanism for each type of fatigue.

The sample comprised 155 patients with clinically definite MS. Fatigue was measured using the Fatigue Descriptive Scale (FDS) and the Fatigue Severity Scale (FSS). Also studied were treatment, depression, anxiety, sleep and cellular immune status.

Fatigue was a symptom in 76% of patients; 22% described it as asthenia (fatigue at rest); 72% as fatigability (fatigue during or after with exercise), and 6% as a worsening of other symptoms (e.g. blurred vision, unsteadiness etc). Discriminant analysis of the data showed that some of the immunoactivation parameters were associated with asthenia (p<0.001) while pyramidal tract involvement was associated with fatigability (p<0.001). Sleep disorders, anxiety and depression were linked with fatigue in a few patients.

Fatigue in MS seems to be a heterogeneous entity. Certain immunoactivation parameters correlate with the presence of asthenia while pyramidal involvement is associated with fatigability.

Correction

The reference to the letter by K. Cleminger (in Annals of Internal Medicine, 2000, 132, 327) should have read: "since when was 'enough' a suitable quantification to pass peer review?"

This issue was compiled by Dr. EM Goudsmit, Dr. A. Macintyre and Mrs S. Howes. We gratefully acknowledge the help and support from Dr. C. Shepherd, M. Sullivan, Mr. D. Axford and AbilityNet. Sources used include ISI Current Contents, ISI Personal Alert, Co-Cure and Medline. This Medical Update is funded by donations.

Disclosure

This publication aims to provide factually accurate and reliable information on chronic fatigue syndromes to clinicians and researchers around the world. It is envisaged as a supplement to the British Library Quarterly Medline Updates. Articles or reports which in the editors' opinion make a significant contribution to the literature, or which are interesting in other ways, will be summarised. Other publications are listed and readers are directed to the British Library's Update for the authors' abstracts.

None of the editors work for or receive payment from pharmaceutical companies as this may undermine editorial independence and objectivity. Summaries are written by qualified health care professionals and checked for accuracy and fairness by experienced physicians, all of whom are specialists in this field. Editorial notes are primarily aimed at identifying and correcting erroneous or misleading information, and occasionally may alert readers to relevant facts which might further aid their understanding of the subject in question.

Our sole motivation is a desire to provide reliable information, although we also wish to make colleagues aware of biased and prejudiced publications which undermine the scientific process and may cause harm to patients. Articles including personal opinions, e.g. as in the book reviews, will be clearly marked.

E-mail:

ellengoudsmit@hotmail.com or david.axford@virgin.net

Copyright EM. Goudsmit 2000. ©
Psychologist/Archivist, London.
All rights reserved. This article may not be reproduced without
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