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Index to Abstracts from AACFS Conference October 1998


Abstracts of Papers Presented at
The Bi-Annual Research Conference of the
American Association for
Chronic Fatigue Syndrome (AACFS)

October 10-11, 1998 -- Cambridge, Massachusetts

Poster Session 6: Physiology

Co-chairs: Wilhemina Behan, M.D., and Benjamin Natelson, M.D.
October 10, 1998, 5:30-6:00 pm

1. Postural Orthostatic Tachycardia And Chronic Fatigue: a distinct subset of Neurally-Mediated Syncope in adolescents
Mark E. Alexander. M.D.. Charles Berde, M.D, Ph.D., John Triedman, M.D., Robert Sundel, M.D., J. Philip Saul, M.D.
2. Working capacity measured by bicycle testing in CFS and fibromyalgia patients
P. De Becker, E. Joos, I. Campine, E. Van Steenberge, J. Roeykens, A. Leys, K. De Meirleir
3. Respiratory symptoms and lung function testing in Chronic Fatigue Syndrome (CFS) patients
P. De Becker. I.Campine, E. Van Steenberge, M. Noppen, A. Leysl, K. De Meirleir
4. No evidence for elevated Substance P levels in cerebrospinal fluid of patients with CFS
Evengård B, Nilsson CG, Lindh G, Lindquist L, Eneroth P, Fredrikson S, Terenius L, Henriksson KG
5. Upregulation of Ca2+ ion channels in patients with CFS
Gow JW, McGill M, Behan WMH, Simpson K and Behan PO
6. Association of intracranial abnormalities between rCBF and acetyl-carnitine uptake in patients with CFS studied by PET
Hirohiko Kuratsune, Kouzi Yamaguti, Gudrun Lindh, Birgitta Evengård, Takashi Machii, Kiyoshi Matsumura, Bengt Långström, Yuzuru Kanakura, Teruo Kitani and Yasuyoshi Watanabe
7. Heterogeneity of symptom, onset and biochemical profiles in "defined" CFS patients
McGregor NR, Hoskin L, Dunstan RH, Clifton Bligh P, Butt HL, Fulcher G, Roberts TK, Dunsmore J, Zerbes M, Klineberg IJ
8. Exercise overtraining as a possible risk factor for Chronic Fatigue Syndrome
J.P. Montalván, M.S. C.S.C.S., Paul H. Levine, M.D.
9. Measurement of postural stability in patients with Chronic Fatigue Syndrome
Paul L and Wood L
10. The electroencephalogram as a diagnostic marker for Chronic Fatigue Syndrome (CFS)
Myra Preston, Ph.D. and Charles W. Lapp, M.D.
11. Brain SPET in Chronic Fatigue Syndrome
D. Di Giuda, G. De Rossi, D.Racciatti. A. Barberio, E. Pizzigallo
12. Neurally-Mediated Hypotension and Chronic Fatigue Syndrome: preliminary results
A. Sisto, P. Lanzillotta, A. Ceccornancini, P. Di Palma, D. Racciatti, G. Abate and E. Pizzigallo


Postural Orthostatic Tachycardia And Chronic Fatigue: a distinct subset of Neurally-Mediated Syncope in adolescents

Authors: Mark E. Alexander M.D., Charles Berde, M.D, Ph.D., John K. Triedman, M.D., Robert Sundel, M.D., J. Philip Saul, M.D.
Departments of Cardiology, Anesthesia and Medicine, Children's Hospital, Boston, MA

Background: Some patients with chronic fatigue syndrome (CFS) have findings of neurally-mediated syncope. We report initial results of evaluation and therapy in 26 adolescents (18 females, mean 15.7 ± 2.4 yrs) with > 6 months of debilitating symptoms including fatigue, orthostatic intolerance and multiple somatic symptoms. Head up tilt (HUD) was performed at 600 for 12 minutes. Ten patients underwent concomitant Doppler monitoring of middle cerebral artery blood flow velocity (CBFV). Hemodynamic responses were compared with 20 patients with isolated syncope (SYNC), 12 who had CBFV monitoring.

Results: Initial supine HR, systolic and diastolic BP, and CBFV were similar for the two groups. Compared to SYNC patients, CFS patients had greater increases of HR, higher maximum HR, larger decreases in CBFV, but unchanged BP during the first 3 minutes of HUT (figure). Overall, 6/26 (23%) of CFS patients had syncope, compared with 5/20 (25%, p = ns), while 15/26 (58%) of CFS patients had postural orthostatic tachycardia (POTS) with greater than 40 bpm increase in HR, compared with 4/20 (20%) of the SYNC group. While the supine response to isoproterenol was comparable, CFS patients had higher heart rates with early tilt (153 ± 18.6) compared with syncope patients (125 ± 33.1). Therapy for orthostatic intolerance in the CFS group improved reported well-being, on a 0-10 scale, from 3.9 ± 1.6 to 8 ± 1.7 (p < .001).

Conclusions: CFS patients have a distinct response to orthostatic stress, with excessive tachycardia and decreased CBFV early in HUT as well as an exaggerated response to isoproterenol infusion. Therapy directed at orthostatic incompetence appears to improve overall well-being. More precise physiologic studies are required to understand this group of patients.

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Working capacity measured by bicycle testing in CFS and fibromyalgia patients

Authors: P. De Becker, E. Joos, I. Campine, E. Van Steenberge, J. Roeykens, A. Leys, K. De Meirleir.

Objective: Chronic Fatigue Syndrome and fibromyalgia are clinically resembling disorders in which muscle pain, muscle weakness and intolerance to physical exertion are characteristic. The CDC-criteria for CFS require a reduction of at least 50 % in the ability to perform activities of daily living. The purpose of this study was to evaluate whether this disability could be objectivated.

Methods: 305 CFS-patients (252 female and 53 male) who fulfilled the 1988 CDC-criteria for CFS, 226 fibromyalgia patients (140 female and 86 male) and 308 healthy controls (208 female and 100 male) performed a maximal exercise test on a electrically braked bicycle ergometer, and continuous gas exchange measurements were made. The groups were matched for sex and age. The following parameters were measured: heart rate in rest, maximal heart rate (HR max), maximal work capacity (MCW) attained, MCW per kg of body weight (Watt max/kg), maximum oxygen uptake per kg body weight (VO2 max/kg), HR at RQ 1, Watt at RQ = 1, percentage of target heart rate.

Statistical analysis was performed using the Mann-Whitney test.

Results:
The main results were:

FEMALE

CFS

Fibromyalgia  

Control

HR max (bpm)

147* ± 23

152* ± 24

167 ± 17

W max/kg (Watt/kg)

1.42 ± 0.42

1.36 ± 0.45

2.90 ± 0.75

VO2max/kg (ml/min/kg-1)     

20.7 ± 8.2

19.4 ± 5.6

32.42 ± 7.36

MALE

CFS

Fibromyalgia  

Control

HR max (bpm)

157* ± 23

149* ±

169 ± 13

W max/kg (Watt/kg)

2.12* ± 0.72

1.69* ± 0.59

3.62 ± 0.48

VO2max/kg (ml/min/kg-1)      

28.4* ± 11.6

22.9* ± 6.6

39.22 ± 4.84

* = p > 0.01 compared to Control population

Conclusion: CFS and fibromyalgia patients have a working capacity that is at least 40% lower compared to controls, which objectively proves their physical disability.

The majority of patients achieved the anaerobic threshold, but not 85% of THR (data not shown). We postulate that this is due to a severe muscle weakness, and not to deconditioning.

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Respiratory symptoms and lung function testing in Chronic Fatigue Syndrome (CFS) patients

Authors: P. De Becker, I. Campine, E. Van Steenberge, M. Noppen, A. Leysl, K. De Meirleir

Objective: The purpose of this study is to report the prevalence of respiratory symptoms in a cohort of CFS patients and to assess the usefulness and importance of pulmonary function testing in the clinical management of these patients.

Methods: A sample of 55 consecutive CFS patients, who met the CDC (1988) and Fukuda (1994) criteria, were recruited from a university-based fatigue clinic in Brussels, Belgium. The following respiratory symptoms were observed in 46 of these patients (9 CFS patients did not present any respiratory symptoms at all): cough (19/55), medical history of allergy (8/55), new onset of allergy (16/55), chest tightness (6/55) and the major respiratory complaint appeared to be a pronounced exercise induced dyspnea (39/55).

A control group consisted of a community based sample of 39 age-and sex-matched individuals, not seeking medical care, and specifically denying any CFS related symptoms. Furthermore, they did not present any respiratory symptoms. Only 10 subjects showed a medical history of allergy (2 penicillin, 8 hayfever/house dust).

All patients and controls underwent a standardized pulmonary function testing, measuring following parameters: forced vital capacity (FVC), forced expiratory volume in one second (FEV1), functional residual capacity (FRC), residual volume (RV), vital capacity (VC) and total lung capacity (TLC).

In all CFS patients, a histamine broncho-provocation test was additionally performed to determine the presence of bronchial hyper-responsiveness (defined as PD20 his < 2 mg histamine).

Statistical analysis was performed using descriptive statistics and a nonparametric Mann-Whitney test.

Results: Compared to controls (A), CFS patients (B) do not show a significant difference in TLC (mean ± SD, A: 5.94 L ± 1.04 L; B: 5.72 L ± 1.005; p = 0.37). However, we found a significant difference between both groups in VC (A: 4.74 L ± 0.90 L; B: 4.255 ± 0.849; p < 0.01) and in RV (A: 1.19 L ± 0.33 L; B :1.479 ± 0.494; p < 0.01). In 33/55 (60%) patients a marked bronchial hyper-responsiveness was present.

Conclusion: CFS patients show a significant decrease in VC, possibly due to a significant increase of RV. The incidence of bronchial hyper-responsiveness in this group is also remarkably high. These observations can, at least partially, explain the respiratory symptoms in these patients.

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No evidence for elevated Substance P levels in cerebrospinal fluid of patients with CFS

Evengård B, Nilsson CG, Lindh G, Lindquist L, Eneroth P, Fredrikson S, Terenius L, Henriksson KG.
Dept Infectious Disease, Unit for applied biochemistry clinical research center, Dept Neurology, Karolinska Insitutet at Huddinge University Hospital, Dept of Drug Dependence Research, Karolinska Hospital, Stockholm, and Neuromuscular Unit and Pain Clinic, University Hospital, Lirköping, Sweden

Background: Substance P (SP) is a neuropeptide involved in the neurotransmission of pain from periphery to the central nervous system. It has been reported that SP in the cerebrospinal fluid is markedly elevated in patients with Fibromyalgia. As Fibromyalgia and CFS are conditions which share some symptoms, we wanted to investigate the levels of SP in the cerebrospinal fluid of CFS patients.

Methods: Cerebrospinal fluid was obtained from 15 patients (9 women, average age 39.3 years) fulfilling CDC-criteria for CFS but not for Fibromyalgia. The sample was immediately centrifuged at +4°C for 10 min. at 1000g to remove cells. Rapid cooling was performed. The sample was stored in plastic cryogenic tubes and stored frozen at -70°C. An radioimmunoassay was used to analyze the sample. For comparison, cerebrospinal fluid drawn from 13 patients with cerebrovascular disease (7 women, average age 65 years) was treated and analyzed in the same manner. All samples were analyzed blindly.

Results: All values of SP of the CFS patients were within previously reported normal range of SP in cerebrospinal fluid. In the control group, 2 patients had slightly increased values.

Conclusion: The results support the notion that FM and CFS are different disorders in spite of overlapping symptomatology.

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Upregulation of Ca2+ ion channels in patients with CFS

Gow JW, McGill M, Behan WMH, Simpson K & Behan PO
Glasgow University Dept of Neurology, Southern General Hospital, Govan Rd, Glasgow 051 4TF, Scotland.

Objective: Chronic fatigue syndrome (CFS) is a clinical condition of unknown ætiologies and the specific abnormalities which explain the persistent fatigue and myalgia are unclear. Viruses, often implicated as initiators of CFS, affect cell membrane ion channels. For instance, HIV gp120 proteins can alter calcium flux through voltage-dependent calcium ion channels and picornavirus VP1 can mimic insect charybdotoxin and induce changes in Na/K monovalent cation channels. CFS also shows some similarity with ciguatera food poisoning, which is caused by toxins known to act on cell membrane ion channels. Excessive calcium influx leads to the depletion of energy reserves by activating Ca2+-ATPase and impairs mitochondrial oxidative phosphorylation. The aim of this study was to examine the expression of genes related to Ca2+ ion handling in the muscle of patients with CFS.

Methods: Skeletal muscle biopsy RNA was prepared by the AGPC method from 16 patients with CFS and 16 age and sex-matched healthy controls. We examined the levels of RNA encoding the sarcoplasmic reticulum Ca2+-ATPase (SERCA 1) and the a1 subunit of the dihydropyridine-sensitive (DHP) Ca2+ channel receptor. Two methods were employed in order to quantitate the RNA from the biopsies, including Southern blot analysis with oligonucleotide probe hybridisation and RT-PCR. The human actin gene was used as a baseline reference for each sample, and results were measured by densitometry.

Results: From independent multiple experiments, densitometric readings were analysed on the Herolab E.A.S.Y.Plus enhanced documentation system. The levels of the Ca2+-ATPase RNA and the DHP receptor RNA were increased compared with the control samples.

Conclusion: This data is indicative of an upregulation of expression of the skeletal muscle genes involved in Ca2+ handling in patients with CFS. We had previously also looked at the ryanodine receptor of the Ca2+ release channel of the sarcoplasmic reticulum and Na+/K+ ATPase, but had noted no difference in signal. The data presented here may suggest that abnormal Ca2+ flux is present in the skeletal muscle of patients with CFS and warrants further investigation.

This work was supported by the Barclay Trust and the ME Association.

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Association of intracranial abnormalities between rCBF and acetyl-carnitine uptake in patients with CFS studied by PET

Hirohiko Kuratsune¹:*, Kouzi Yamaguti¹*, Gudrun Lindh², Birgitta Evengård², Takashi Machii¹, Kiyoshi Matsumura*, Bengt Långström³, Yuzuru Kanakura¹, Teruo Kitani° and Yasuyoshi Watanabe*
¹Hematology and Oncology, Osaka Univ. Med. School., Osaka 565, Japan
²Department of Infectious Disease, Karolinska Inst., Huddinge Hospital, Stockholm, S-141 86, Sweden
*Osaka Bioscience Inst., Osaka 565, Japan
³Uppsala Univ. PET Centre, UAS, S751 85, Uppsala, Sweden
°Sakai Municipal Hospital, Osaka 590, Japan.

Recently, we found a serum acylcarnitine (ACR) deficiency in the vast majority of patients with chronic fatigue syndrome (CFS). There is a clear correlation between serum ACR concentrations and the levels of fatigue. More recently, we succeeded in synthesizing acetyl-L-carnitine labeled with 11C, and thus making it possible to study the dynamics of serum acylcarnitine. From our recent studies, it became clear that mammals have a certain regulatory system of serum acylcarnitine in the liver, and that serum acylcarnitine has a very important physiological role for the brain, that is, conveying an acetyl moiety into the brain.

Objective: To clarify whether or not the abnormality of acetyl-carnitine metabolism in the brain might be associated with the pathogenesis of CFS, we studied not only the uptake of acetyl-L-carnitine labeled with 11C into the brain (ACR uptake) but also regional cerebral blood flow (rCBF) in 8 patients with CFS and 8 age- and sex-matched controls in Sweden.

Methods: The rCBF was studied using a bolus of intravenous radioactively labeled water (H215O), and ACR uptake into the brain was studied using [2-11C] acetyl-L-carnitine. All of individual data were put into one model of standardized brain atlas, and we compared the rCBF and ACR uptake between the CFS group and the control group.

Results: The CFS group had a lot of brain regions where rCBF decreases. That is, very low levels of rCBF were found in a part of Brodmann 24(r), 33(r), 37(l), and low levels of rCBF were found in a part of Brodmann 9(l), 10(l), 11(l), 12(r,l), 13(r), 18(r,l), 19(r,l), 21(r,l), 22(r,l), 24(l), 32(r), 33(l), 36 (r,l), 37 (r), 38(r,l), 39(l), 43(l), 44(l), 47(r), insula (r,l), thalamus (r,l), putamen(r,l), hippocampus (r,l), parahippocampal regions (l), amygdala (l), N. caudatus (l), mesencephalus, pons and cerebellum. On the other hand, the reasons which showed lower ACR uptake in CFS group were restricted, and the main reason was Brodmann 24 (r,l). ACR uptake abnormalities were also found in Brodmann 9(l), 21(l), 22(r,l), 33(r,l), 36 (l), insula (l) and cerebellum, but they were frequently dissociated with rCBF abnormalities. There was no reason in CFS group which had higher levels of rCBF and ACR uptake compared to control group.

Conclusion: Intracranial abnormalities of ACR metabolism might be related to the pathogenesis of CFS, in addition to the rCBF abnormalities.

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Heterogeneity of symptom, onset and biochemical profiles in "defined" CFS patients

Authors: McGregor NR¹*, Hoskin L², Dunstan RH¹, Clifton Bligh P², Butt HL¹, Fulcher G², Roberts TK¹. Dunsmore J², Zerbes M¹, Klineberg IJ*
¹Collaborative Pain Research Unit, Department of Biological Sciences, The University of Newcastle, Callaghan, NSW 2308,Australia.
*Neurobiology Research Unit, Centre for Oral Health, Research University of Sydney, Westmead Hospital, Westmead, NSW 2084 Australia
²Department of Endocrinology, Royal North Shore Hospital, St Leonards, NSW, Australia.

Objective: To assess the symptom, biochemical and onset data of patients who comply with the CFS definitions to assess whether they are either homogeneous or heterogeneous. The CFS definition requires the exclusion of other known fatigue-related diseases and compliance with a primarily host-response associated symptom constellation.1,2 The patient set derived by this process is heterogeneous in their psychological presentation, and no single ætiological agent or event has been found using this definition.

Methods: Multiple regression analysis and clustering techniques were applied to several CFS study data sets to detect either homogeneity or heterogeneity of the patients symptoms, onset events, urinary amino and organic acid, and serum lipid profiles.

Results: CFS patients divided on the basis of host responses, infectious responses, sudden or gradual onset or type of onset, had different symptom and biochemical constellations. The disturbances of urinary amino and organic acid excretion could distinguish CFS patients from controls, but the events associated with fatigue or muscle pain, common to all CFS patients, were not selective for defined CFS. Common fatigue-associated host response changes could not be specifically associated with any onset event or psychological response. However alterations in the excretion of various metabolites could be associated with different onset, symptom and psychological response patterns. In a similar manner, the plasma fatty acids profile could differentiate defined CFS patients from control subjects but the differentiating patterns did not occur in all defined CFS patients. The lipid profiles associated with current viral infections, such as EBV, or post-EBV infection were not distinguishing factors for defined CFS. The major lipid changes distinguishing CFS patients from controls appear to be of genetic or acquired origin. Multiple regression and clustering techniques revealed 5 basic types of CFS lipid profiles, whilst the control group had a high degree of homogeneity. These CFS lipid changes are associated with known lipid disorders and provided evidence of heterogeneity.

Conclusion: The current CFS definitions either lack standardization and/or the CFS exclusion criteria are insufficient to determine all additional excludable fatigue disorders. The capacity to group currently defined CFS patients into subsets using objectively derived measurements, many of which may indicate known disease states, represents a major advance in CFS research.

References:
¹Holmes OP, Kaplan JE, Gantz NM, et al. Chronic fatigue syndrome: A working case definition. Ann Intern Med 1988; 108:387-389.
²Fukuda K, Straus SE, Hickie I, et al. The chronic fatigue syndrome: A comprehensive approach to its definition and study. Ann Intern Med 1994; 121:953-959.

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Exercise overtraining as a possible risk factor for Chronic Fatigue Syndrome

Authors: J.P. Montalván M.S. C.S.C.S., Fitness/Works LLC
Paul H. Levine, M.D., George Washington University School of Public Health and Health Services

Objective: To report case histories of Chronic Fatigue Syndrome (CF S) occurring in two female athletes who were overtraining, and to describe a possible mechanism.

Methods: Severe and acute-onset CFS was diagnosed in two female athletes involved in vigorous exercise programs at the onset of their symptoms. The athletes were suspected to have overtrained prior to their diagnosis of CFS. The athletes were interviewed regarding the onset of CFS, exercise history by type and duration, and concurrent symptoms related to CFS and overtraining. A literature search was performed and physiological and psychological mechanisms involved in overtraining were compared with immune abnormalities reported in CFS.

Both female athletes reported symptoms consistent with those associated with overtraining, including decreased athletic performance, increased stress, and depression prior to their diagnosis of CFS (Phys. Sports Med. 19(5):l 12-118, 1991). Both reported similar occurrences in athletes of their acquaintance who were also overtraining. While some research demonstrates moderate exercise improves immune function, some literature suggests a decline in immune function and responsiveness in overtrained endurance athletes. Furthermore, some clinicians and coaches believe muscular fatigue lowers resistance and is a predisposing factor to infectious disease (J Strength and Cond. Res. 8(4): 251-254, 1994).

Infection has been implicated as a possible cause of CFS, and possible risk factors for the development of CFS include history of depression, stress and exercise (Am. J Med. 100: 548-54, 1996). Given the immunoregulatory abnormalities believed present in CFS patients, overtraining may have contributed to the athletes' increased risk of infection. Furthermore, the athletes' overtraining symptoms may have increased their susceptibility to the development of CFS.

Conclusion: The occurrence of CFS in the two case histories evaluated and the report by MacDonald et al. of stress, depression and exercise as risk factors for CFS support the possibility that overtraining may be a risk factor for CFS. A more systematic study of athletes regarding this hypothesis is proposed.

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Measurement of postural stability in patients with Chronic Fatigue Syndrome

Authors: Paul L ¹ and Wood L.²,
¹Division of Physiotherapy and ²Department of Biological Science, Glasgow Caledonian University, Glasgow, Scotland.

Objective: Virtually all neuromusculoskeletal disorders may result in impaired balance. It is broadly estimated that between 30% and 70% of subjects with Chronic Fatigue Syndrome (CFS) suffer from dysequilibrium. Maintenance of balance requires visual, somatosensory and vestibular input, central processing of this information, and a co-ordinated motor response. Balance is not a static process. Continuous postural adjustments are necessary to keep the body upright even during quiet standing. These postural adjustments can be quantified by using a force plate to examine the movement of the body's centre of pressure. The aims of this study were:

  1. to compare measurements of balance between CFS subjects and controls,
  2. to investigate the effect of exercise on balance in subjects with CFS and controls.
Methods:Ten CFS subjects and ten sedentary age and sex-matched controls took part in the study. Postural stability was assessed using a Kistler force plate. Subjects stood on the Kistler force plate and the position of their Centre of Pressure (COP) was recorded at 250Hz. The movement of the COP in both the anteroposterior and mediolateral directions was recorded, as was the total excursion of the path of the COP. Each test lasted 25 seconds and was performed under eyes-opened and eyes-closed conditions. Balance assessment was performed before subjects completed a 15 minute steady-state exercise test. The exercise was carried out on a cycle ergometer, where subjects cycled at 90% of their predicted work rate at their anaerobic threshold based on age, sex and weight. Balance assessment was repeated immediately after the exercise, then at 20 minute intervals for the subsequent hour, and reassessed 24 hours later.

Results: Preliminary data analysis suggests that, in general, before exercise, postural stability was not significantly different between CFS subjects and controls. Unsurprisingly, for both groups, postural sway was greater under eyes-closed conditions. In both groups, CFS and control, it would appear that exercise did not alter postural stability when subjects stood with their eyes-opened. Under eyes-closed conditions, however, subjects with CFS had poorer balance following the exercise period. Balance was not adversely affected by exercise in the control group under eyes closed conditions.

Conclusions: Static balance, as assessed by the Kistler force plate, is not affected by CFS. It is known that static balance tests may not be sensitive enough to investigate minor dysequilibrium problems associated with some pathologies, therefore further study, in progress, aims to investigate more dynamic balance in CFS subjects. Exercise did not affect the balance of either CFS subjects or controls in eyes-opened conditions, however with eyes closed, CFS subjects exhibited greater postural instability. Further study is required, however, this finding may lend support to the anecdotal evidence that activity can exacerbate the symptoms of CFS.

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The electroencephalogram as a diagnostic marker for Chronic Fatigue Syndrome (CFS)

Authors:Myra Preston Ph.D. and Charles W. Lapp, M.D., Charlotte, North Carolina

Research efforts have failed to uncover a diagnostic marker for CFS. This study looks to the brain as the site of a possible diagnostic marker that would be sensitive and specific to the illness of CFS. The objective of this study is to differentiate CFS subjects from controls in a blinded fashion. To differentiate the two populations, we utilize an EEG pattern that was present in approximately 280 persons with CFS (PWCs), that we had previously studied in an unblinded fashion in the 24 months prior to this study. This brain abnormality was not present in other patient populations or controls.

Methods: We used a blinded protocol to collect raw EEG data in patients that met the CDC case definition of CFS. Controls were screened for current and/or potential exposure to health problems to insure that participants did not have prolonged fatigue or an acute illness.

Results: PWCs were correctly identified with 80% sensitivity and 82% specificity compared to healthy controls. Four files utilized as an internal positive control were selected with 100% consistency.

Conclusions: EEG data can be used to differentiate PWCs from controls with high sensitivity and specificity. The specific EEG signature seen in persons with CFS can be a diagnostic disorder for the disorder.

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Brain SPET in Chronic Fatigue Syndrome

Authors: D. Di Giuda,¹ G. De Rossi,¹ D. Racciatti,² A. Barberio,² E. Pizzigallo²
¹Nuclear Medicine Department, "A. Gemelli" Catholic University of Rome, Italy
² Clinic of Infectious Diseases, "G. D'Annunzio" University of Chieti

Objective: Chronic Fatigue Syndrome (CFS) is a severely disabling illness of uncertain ætiology, characterized by somatic and neuropsychiatric symptoms. At present, there is no clearly defined diagnostic test for the syndrome. This study was designed to investigate possible changes in the brain perfusion of patients with CFS.

Methods: Forty patients with suspected CFS underwent 99mTc-HMPAO SPET; 31 of them fulfilled the CFS diagnostic criteria of the Centers for Disease Control (CDC) of Atlanta. A 30 min examination with a brain-dedicated multicamera system was performed 10 mm after 925 Mbq 99mTc-HMPAO i.v. injection. A SPET analysis with a predefinite 26 ROI template yielded some semi-quantitative parameters.

Results: Regional brain perfusion impairment (mainly hypoperfusion) was found in 26 (83.9%) of 31 CFS patients, in comparison with 20 age-matched control subjects. In 8 (30.8%) of these 26 patients, a concurrent fibromyalgia syndrome was present. All patients had normal findings on MR images. On the basis of psychiatric tests, mood disorders (38.7%), personality abnormalities (29.3%) and other psychiatric disorders (22.0%) occurred in CFS patients. A total of 147 brain regions showed abnormal 99mTc-HMPAO uptake: 132 cortical and 15 subcortical areas. The most frequent abnormalities were found in the following middle-anterior cortical regions (with a low left hemisphere prevalence): anterior frontal (16), sylvian (16) and middle frontal (14) areas. In relation to associated psychiatric symptoms, the highest number of impaired regions was present in the personality abnormalities and in the group of other psychiatric disorders (71.2% and 61.4% of middle-anterior cortical areas hypoperfusion, respectively).

Conclusion: This study confirmed previous reports of brain perfusion impairment in CFS, providing objective evidence of CNS dysfunction. On the basis of our results, 99mTcHMPAO SPET seems to carefully assess cerebral perfusion abnormalities in CFS, simultaneously allowing a comparison with related psychiatric disorders. This may be useful in CFS prognosis and therapy planning.

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Neurally-Mediated Hypotension and Chronic Fatigue Syndrome: preliminary results

Authors: A. Sisto,¹ P. Lanzillotta,² A. Ceccomancini,¹ P. Di Paima,² D. Racciatti,¹ G. Abate² and E. Pizzigallo¹
¹Clinic of Infectious Diseases and
²Department of Gerontology, "G. D'Annunzio" University of Chieti, Italy

Chronic Fatigue Syndrome (CFS) is a clinical syndrome consisting primarily of fatigue and cognitive dysfunction. The etiology and pathogenesis of CFS remain unclear. Many authors report a correlation between CFS and dysfunction of the autonomic neurological system.

Objective: In this study, we evaluated the possible correlations between Chronic Fatigue Syndrome and neurally-mediated hypotension.

Methods: 10 patients satisfying the Centers for Disease Control criteria for the diagnosis of CFS were preliminarily enrolled. All subjects were evaluated with upright tilt-table test in a quiet room. Blood pressure was detected by "FINAPRES" (Ohmeda-Lousville, Colorado) and an electrocardiogram was continually performed by a monitor. After 10 mm supine, the patients were tilted upright to 600 for 45 min. If a positive response was not observed after 30 min., a sublingual tablet of nitroglycerin was administered. A positive response was defined as a decrease in blood pressure more than 60% of basal value, presyncope, or syncope.

All patients were evaluated for Valsava test and hand-grip test, also.

Results: All patients showed negative response after 30 min. on the tilt-table; 3 patients (30%) showed a positive response after sublingual administration of nitroglycerin. The Valsalva test and the hand-grip test in all subjects were negative.

Conclusions: Tilt-table test is an important system for the evaluation of neurally-mediated hypotension in patients with structurally normal heart. The association between CFS and neurally-mediated hypotension is reported. Our data suggest this correlation, but others' investigations seem to detect more of a pathogenetic mechanism of fatigue in subjects with neurally-mediated hypotension. Finally, neurally-mediated hypotension may be a possible cause of fatigue in patients with CFS.

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