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Posted to Co-Cure Fri, 28 Jul 2000 00:51:42 -0400 by Drew Martin

Diagnosis of psychiatric disorder in clinical evaluation of CFS

Diagnosis of psychiatric disorder in clinical evaluation of chronic fatigue syndrome.
J R Soc Med 2000 Jun;93(6):310-2
Deale A, Wessely S

Abstract:
The overlap of symptoms in chronic fatigue syndrome (CFS) and psychiatric disorders such as depression can complicate diagnosis. Patients often complain that they are wrongly given a psychiatric label. We compared psychiatric diagnoses made by general practitioners and hospital doctors with diagnoses established according to research diagnostic criteria.

68 CFS patients referred to a hospital fatigue clinic were assessed, and psychiatric diagnoses were established by use of a standardized interview schedule designed to provide current and lifetime diagnoses. These were compared with psychiatric diagnoses previously given to patients.

Of the 31 patients who had previously received a psychiatric diagnosis 21 (68%) had been misdiagnosed: in most cases there was no evidence of any past or current psychiatric disorder. Of the 37 patients who had not previously received a psychiatric diagnosis 13 (35%) had a treatable psychiatric disorder in addition to CFS.

These findings highlight the difficulties of routine clinical evaluation of psychiatric disorder in CFS patients. We advise doctors to focus on subtle features that discriminate between disorders and to use a brief screening instrument such as the Hospital Anxiety and Depression Scale.

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Posted to Co-Cure Fri, 28 Jul 2000 00:48:01 -0400 by Drew Martin

The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome

The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome.
Am J Med Sci 2000 Jul;320(1):1-8
Streeten DH, Thomas D, Bell DS
Department of Medicine, State University of New York Health Science Center, Syracuse 13210, USA.

BACKGROUND: Orthostatic hypotension during upright tilt is an important physical disorder in patients with chronic fatigue syndrome. We have tested its occurrence during prolonged standing, whether it is correctable, and whether reduced circulating erythrocyte volume is present.

METHODS: Fifteen patients were randomly selected from a large population of patients with chronic fatigue syndrome, studied, and observed for several years (by DSB). Blood pressure (BP) and heart rate (HR) measured with Dinamap every minute for 30 minutes supine and 60 minutes standing were compared with these findings in 15 healthy age- and gender-matched control subjects and later during lower body compression with military antishock trousers (MAST). Plasma catecholamines and circulating erythrocyte and plasma volumes were also measured by isotopic dilution methods.

RESULTS: Abnormal findings in the patients included excessive orthostatic reductions in systolic (P < 0.001) and diastolic BP (P < 0.001) and excessive orthostatic tachycardia (P < 0.01), together with presyncopal symptoms in 11 of the 15 patients and in none of the control subjects after standing for 60 min. Lower body compression with the MAST restored all orthostatic measurements to normal and overcame presyncopal symptoms within 10 min. Circulating erythrocyte but not plasma volumes were subnormal in the 12 women (P < 0.01) and plasma norepinephrine concentration rose excessively after standing for 10 min.

CONCLUSION: Delayed orthostatic hypotension and/or tachycardia caused by excessive gravitational venous pooling, which is correctable with external lower-body compression, together with subnormal circulating erythrocyte volume, are very frequent, although not invariably demonstrable, findings in moderate to severe chronic fatigue syndrome. When present, they may be involved in its pathogenesis.

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Posted to Co-Cure Thu, 27 Jul 2000 20:47:08 -0400

Effects of sleep deprivation on neural circulatory control

Effects of sleep deprivation on neural circulatory control.
Authors: Kato M, Phillips BG, Sigurdsson G, Narkiewicz K, Pesek CA, Somers VK
Division of Clinical and Administrative Pharmacy, College of Pharmacy, University of Iowa, Iowa City, Iowa, USA.
Journal: Hypertension 2000;35(5):1173-5.
NLM citations: PMID: 10818083, UI: 20279957

In a study of 8 healthy subjects, the authors found sleep deprivation did not significantly effect heart rate, forearm vascular resistance, plasma catecholamines, or autonomic and hemodynamic responses to stressful stimuli. Sleep deprivation did result in increased resting blood pressure and decreased muscle sympathetic nerve activity.

Abstract

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Posted to Co-Cure Thu, 27 Jul 2000 18:29:36 -0400

NIH reports study on pain

[Moderator's Note: This may be of interest because of its implications for our understanding of FMS.]

ANIMAL MODEL SHOWS PAIN AND TISSUE INJURY IN NEWBORNS ALTERS NERVE CIRCUITRY AND REACTION TO PAIN LATER IN LIFE

Newborns who experience tissue injury and pain during critical periods of development may undergo a permanent rewiring of their nervous system that increases their sensitivity to pain later in life.

Working with an animal model, scientists at the National Institute of Dental and Craniofacial Research (NIDCR) have provided the first physical evidence that pain and inflammation in newborns alters the development of pain pathway circuitry, causing a stronger response to pain in adulthood. The study, which appears in the July 28 issue of "Science", calls attention to the need to assess the long- term effects of pain and tissue injury on human newborns.

"Although we have yet to directly link animal research findings to what happens in human infants, one is tempted to speculate that similar changes as those identified in the animals may occur in newborn humans exposed to pain and inflammation," said Dr. M. A. Ruda, principal investigator on the study and chief of NIDCR's Cellular Neuroscience Section.

Each year, more than 400,000 babies in the U.S. are born either prematurely or at a low birth weight. Of these, 25,000 are considered to be extremely premature--born at 27 weeks of gestation or less. While 10 or 15 years ago most of these micropreemies did not live, it is no longer unusual for them to survive, thanks to advances in medical technology. Yet these tiny babies face a host of problems. Not only are they confronted with the trauma of living in the outside world too soon, but available medical procedures used to keep them alive and monitor their progress may cause pain and tissue injury. Heel sticks to draw blood, the insertion of IV lines and nasogastric tubes, and the use of ventilators are some of the modern technologies and procedures that are both miraculous and difficult.

"A premature infant can be thought of as still in the fetal time of their life when the basic elements of brain development are occurring," explained Dr. Ruda. "Abnormal stimulation during these critical developmental time points may abnormally wire the brain."

There has been considerable debate over the existence of pain in newborns and its management. As late as the mid- 1980's, surgery was performed on infants without benefit of anesthesia, the belief being that even if babies did experience pain, they would forget about it. Since then, studies of the biological response to pain and the facial expressions of newborns during traumatic procedures document that they do indeed respond to pain. Today, pain from traumatic surgeries in newborns is carefully managed with anesthesia and analgesics.

Scientists have learned that by 24 weeks gestation, very immature pain transmission pathways are already in place. The development of these pathways continues postnatally. What newborns lack are fully developed and functional pain inhibitory systems. These typically develop several weeks after a full-term baby is born.

"Unlike other sensory modalities such as vision and hearing that require the input of sight and sound for their appropriate development, pain pathways normally develop in the absence of, or with little exposure to, painful stimulation. However, medical procedures shortly after birth can expose the nervous system to pain, the developmental effects of which we are just learning," said Dr. Ruda.

In their study, Dr. Ruda and her colleagues used newborn rat pups to explore the effect of tissue injury and pain on the development of pain pathways. An irritant was injected into the left hind paw of the pups to induce swelling. One group received the injection when they were 1 day old, an age equivalent to 24 weeks gestation in humans. A second group received the injection 14 days after birth, equivalent to adolescence in humans. Swelling and redness occurred shortly after the injection and persisted for 5-7 days in both groups.

When the animals were examined as adults, it was found that rats who received the left hind paw injection on day 1 had an increase in the density of nerve fibers on the left side of the dorsal horn, the layered structure in the spinal cord that propels pain signals up to the brain. Even at the level of individual nerve cells, the response to pain was increased. Spinal cord segments also exhibited an increase in pain input on the left neonatal treated side, including areas that normally would not be expected to display this. The picture was very different for the rats that received the injection on postnatal day 14. The patterns of nerve fibers in this group looked like those of normal rats. The researchers surmise that the critical time point responsible for a change in input had passed by day 14, so that neuronal circuits were not altered by the tissue injury and pain.

Adult rats that experienced left hind paw tissue injury and swelling on day 1 also reacted more strongly to pain as adults. When an irritant was injected into their left hind paw and the paw was exposed to heat, they were much quicker to withdraw it than normal rats. The changes that occurred because of tissue injury and pain are likely not limited to the spinal cord but could also involve higher centers of the brain that are part of pain pathways, suggest the researchers.

"Our study adds pain to the emerging list of early birth stimuli that we are discovering have a lifelong impact and suggests that further study is warranted to develop approaches to limit or prevent those effects," added Dr. Ruda.

Collaborating with Dr. Ruda on the study were Drs. Qing-Dong Ling, Andrea G. Hohmann, Yuan Bo Peng, and Toshiya Tachibana from the Cellular Neuroscience Section, Pain and Neurosensory Mechanisms Branch, NIDCR. The National Institute of Dental and Craniofacial Research is one of the federal National Institutes of Health, located in Bethesda, MD.

###

NATIONAL INSTITUTES OF HEALTH
National Institute of Dental and Craniofacial Research
NIH NEWS RELEASE
EMBARGOED FOR RELEASE
Thursday, July 27, 2000
2:00 p.m. EST

Contact:
Jody Dove
(301) 594-7558

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Posted to Co-Cure Wed, 26 Jul 2000 17:55:55 -0400 by Fred Springfield

Diagnostic Criteria of Myofascial Pain Caused by Trigger Points

Diagnostic Criteria of Myofascial Pain Caused by Trigger Points
Journal of Musculoskeletal Pain Vol.7, No. 1/2, 1999, pp. 111-120
David G. Simons

SUMMARY.
Objectives: To summarize the newly recognized pathophysiology of myofascial trigger points , to note three new and promising techniques for identifying TrPs, and to consider possible clinical diagnostic criteria in the light of the pathophysiology of MTrPs.

Nature of Trigger Points: The core features, of MTrPs are identified electrophysiologically by characteristic spontaneous electrical activity and histologically by contraction knots. Both phenomena apparently result from excessive release of the neurotransmitter acetylcholine from the nerve terminal of the motor endplate. This relationship identifies MTrPs as a neuromuscular disease.

Diagnostic Criteria: Three recently identified objective confirmatory findings of MTrPs include: the electromyographic recording and ultrasound imaging of local twitch responses, the spontaneous electrical activity of multiple active loci in the MTrP, and biopsies of MTrPs that show contraction knots and giant round muscle fibers. Many of the clinical characteristics of MTrPs can be accounted for by their pathophysiology.

Conclusion: The endplate dysfunction characteristic of MTrPs involves both the nerve terminal and the postjunctional muscle fiber. This relationship identifies MTrPs as a neuromuscular disease. Official diagnostic criteria should take this into consideration.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com.]

KEYWORDS. Trigger points, contraction knots, spontaneous electrical activity, diagnosis, neuromuscular endplates

INTRODUCTION

It is critical to reach agreement as to which findings are needed to establish the diagnosis of myofascial trigger points {MTrPs]. Published research studies concerning MTrPs have employed a variety of diagnostic criteria and often the criteria used for a study are poorly specified. This compromises: progress in MTrP research, reimbursement for the treatment of MTrPs, and the recognition MTrPs for medicolegal purposes. The lack of a scientifically credible etiology and an officially recognized set of diagnostic criteria are largely responsible for the generally meager initial training of physicians and therapists in this subject. The first half of this paper identifies a scientifically credible etiology, and the second half relates promising clinical diagnostic criteria to that etiology. The critically important process of reaching official consensus on a set of clinical diagnostic and research criteria began at the MYOPAIN ‘98 World Congress in Italy.

David G. Simons, MD, MS, DSc [Hon], is Clinical Professor, Department of Rehabilitation Medicine, Emory University, Atlanta, GA, and Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA.
Address correspondence to: David G. Simons, MD, 3176 Monticello Street, Coyington, GA 30014-3535 e-mail: D4Lsimons@aol.com).

© 1999 by The Haworth Press, Inc. All rights reserved.

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Posted to Co-Cure Wed, 26 Jul 2000 04:34:24 -0400 by Fred Springfield

Sleep Disturbance in Patients with Chronic Fatigue Syndrome and Chronic Fatigue

Sleep Disturbance in Patients with Chronic Fatigue Syndrome and Chronic Fatigue.
Journal of Chronic Fatigue Syndrome, Vol. 6 No. 2, 2000, pp. 37-43
Con Stough, PhD, MAPS
Giselle Withers, B App Sci, PG Dip (Health Psych)

ABSTRACT. To examine whether the identification of patients with Chronic Fatigue Syndrome can he made using more objective criteria than presently available (1), we compared 14 patients with Chronic Fatigue Syndrome and 12 patients with chronic fatigue (but who did not meet the criteria for Chronic Fatigue Syndrome) on sleep architecture, continuity, and sleep abnormalities from polysomnography recordings. No differences in sleep continuity or architecture were found between the two groups, except that patients with Chronic Fatigue Syndrome recorded significantly increased sleep latencies. There were no differences in the frequency of sleep disorders. Results indicated that apart from sleep latency, other sleep variables do not adequately differentiate patients with CFS from those with chronic fatigue and that other variables should be examined, which may validly diagnose patients with CFS.

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com.]

KEYWORDS. Alpha-delta wave sleep, rapid eye movement (REM) sleep, sleep architecture, periodic leg movements (PLM)

Con Stough and Giselle Withers are affiliated with Brain Sciences Institute, Swinburne University of Technology, Australia.
Address correspondence to: Con Stough, Brain Sciences Institute, Swinburne University of Technology, P.O. Box 218 Hawthorn, Victoria 3122, Australia (E-mail: cstough@swin.edu.au).
The authors wish to thank Dr. Michael Oldmeadow, Dr. Matthew Naughton and Dr. John Sweica of the Alfred Hospital, Melbourne, Australia for their kind assistance throughout the development of this project.

INTRODUCTION

Chronic Fatigue Syndrome (CFS) is an illness characterized by extreme fatigue and a combination of symptoms that feature self reported impairment of cognition and concentration, musculoskeletal pain, and sleep disturbances (1). These non-specific symptoms can make the syndrome difficult to objectively identify (2). According to the first case definition produced by the Center for Diseases Control in 1988 (3), a patient with CFS must satisfy two major criteria and 8 out of 11 minor symptom criteria. The first major criterion is the presence of a debilitating fatigue as a new symptom, persisting or relapsing for at least 6 months. The second major criterion is that other medical conditions that may produce similar symptoms must be excluded by thorough evaluation of patient medical history, physical examination and laboratory testing. The 11 minor symptoms include mild fever, sore throat, painful lymph nodes, unexplained generalized muscle weakness, muscle and joint pain, physical exertion after minimal exercise, generalised headaches, migratory arthralgia without joint swelling or redness, neuropsychologic complaints (i.e., depression, confusion, loss of short term memory and/or concentration), sleep disturbance, and that symptoms developed abruptly (over a few hours to a few days).

As yet there are no diagnostic tests available for CFS validation (1). Each patient may have a different combination and severity of symptoms, which tend to wax and wane over the course of the illness. The absence of a typical case profile of CFS, makes controlled research particularly difficult.

In the search for diagnostic markers of CFS, some research was directed towards identifying possible sleep patterns and sleep pathologies characteristic of these patients which may differentiate them from chronically fatigued patients without the syndrome. Whether sleep pathology can be adequately used to objectively differentiate patients with CFS from those with chronic fatigue is as yet unclear. The present paper replicates and extends a recent study (4) that has addressed this problem by investigating the role of sleep disorders in patients with CFS and chronic fatigue. The present study extends this recent study by examining, in addition, sleep continuity and architecture in these two groups. These variables may be important as significant effects for variables associated with sleep architecture and continuity between patients with CFS and normal healthy controls have been demonstrated (5). An investigation of these variables may prove useful in differentiating between CFS patients and non-CFS patients.

Journal of Chronic Fatigue Syndrome, Vol. 6(2) 2000
© 2000 by The Haworth Press, Inc. All rights reserved.

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Posted to Co-Cure Mon, 24 Jul 2000 23:15:54 -0700 by Melissa O'Toole

Nongastrointestinal Disorders in the Irritable Bowel Syndrome

Nongastrointestinal Disorders in the Irritable Bowel Syndrome.
Digestion 2000;62(1):66-72
Azpiroz F, Dapoigny M, Pace F, Muller-Lissner S, Coremans G, Whorwell P, Stockbrugger RW, Smout A
Digestive System Research Unit, Hospital General Vall d'Hebron, Barcelona, Spain.
PMID: 10899728

Abstract:
A large proportion of irritable bowel syndrome (IBS) patients also complain of other functional disorders, such as headache, noncardiac chest pain, low back pain, and dysuria. Some of these features, particularly headache, may have a negative influence on the outcome of IBS. In a large proportion of female IBS patients, sexual intercourse triggers the symptoms, and frequently IBS symptoms exacerbate during menses.

These gynecological-type symptoms often mislead the patients to the gynecological clinic, which may imply unnecessary investigations and inappropriate treatments.

The diagnostic criteria of the fibromyalgia syndrome include IBS, and hence, the apparent relationship of both syndromes is difficult to analyze. On the other hand, no convincing evidence has been produced to date to sustain an association between IBS and the chronic fatigue syndrome.

Copyright 2000 S. Karger AG, Basel

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Posted to Co-Cure Mon, 24 Jul 2000 01:45:05 -0400 by Fred Sprinbgfield

Comparative Study of Antidepressants and Herbal Psychotropic Drugs in a Mouse Model of Chronic Fatigue

Comparative Study of Antidepressants and Herbal Psychotropic Drugs in a Mouse Model of Chronic Fatigue
Journal of Chronic Fatigue Syndrome, Vol. 6 No. 2, 2000, pp. 23-35
Gurpreet Kaur and S.K. Kulkarni

ABSTRACT. This study examined the effects and comparative efficacy of various antidepressants and herbal psychotropic drugs in a mouse model of chronic fatigue. Animals were subjected daily to forced swimming (Porsolt’s forced swimming test) and the duration of the immobility period was recorded in 6-minute sessions on each day for 7 days. Chronic forced swimming resulted in significant increases in immobility time on day 7 as compared to day 1 in control mice.

Pretreatment with imipramine (10 mg/kg, i.p.), desipramine (10 mg/kg, i.p.), tranylcypromine (10 mg/kg, i.p.), alprazolam (0.5 mg/kg, i.p.), fluoxetine (10 mg/kg, i.p.) and melatonin (10 mg/kg, i.p.) produced significant decreases in immobility time as compared to control on each day.

Similar decreases in immobility periods were observed with herbal psychotropic preparations—Withania somnifera root extract (100 mg/kg, p.o.), BR-16A® (200 mg/kg, p.o.), siotone® granules (200 mg/kg, p.o.) and evening primrose oil (0.2 ml/20 g, p.o.). However, trazodone and idazoxan failed to modify the immobility times on all the days.

The present observations underscore the established use of antidepressants in providing symptomatic relief of fatigue in Chronic Fatigue Syndrome (CFS) patients and further reinforce the potential therapeutic usefulness of herbal psychotropic preparations in CFS patients.

KEYWORDS. Chronic Fatigue Syndrome, antidepressants, herbal psychotropic preparations, immobility time, mice

INTRODUCTION
Chronic Fatigue Syndrome (CFS) is a disorder of multifactorial etiology. It is a heterogeneous symptom complex characterized by an overwhelming sense of fatigue, neuropsychiatric symptoms (anxiety, depression), neuroimmunological disturbances (2), neuroendocrine abnormalities and various somatic complaints (1). Fatigue is the pivotal feature of the syndrome. Both the organic and psychiatric factors contribute to fatigue to an uncertain extent. CFS patients are also more prone to psychiatric disorders like anxiety and depression, which occur in about two-third of some groups of patients. Also, the subjects with pre-existing psychiatric problems are more likely to develop chronic fatigue after recurrent infections (3).

The conundrum of CFS is further compounded by the fact that its natural history and ultimate prognosis are unknown and that there is neither a diagnostic test nor an immediate effective treatment. Thus, the exact treatment still remains elusive. Although various classes of drugs have been studied for their effectiveness in CFS, no specific therapeutic agent is available. Yet among these, antidepressants appear to be promising agents and they already have been reported to be beneficial in providing symptomatic relief in such patients. Besides improving the depressive symptoms, these agents ameliorate sleep disturbances and emotional symptoms (4,5).

With the above point of view, the present study was designed to investigate the comparative effectiveness of antidepressants and herbal psychotropic drugs in a mouse model of chronic exposure to forced swimming. The anxiety level of the animals was also tested before and after subjecting them to the chronic forced swimming test.

__________________________

[ Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: mailto:getinfo@haworthpressinc.com .]

__________________________

Gurpreet Kaur and S. K. Kulkarni are affiliated with the Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160 014, India.
Address correspondence to: S. K. Kulkarni at the above address (E-mail: skk@i:punjabuniv.chd.nic.in ).

Journal of Chronic Fatigue Syndrome, Vol. 6(2) 2000
© 2000 by The Haworth Press, Inc. All rights reserved.

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Note: All abstract summaries, unless otherwise noted, were prepared by Margaret Bailey.


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