About the CRISP Database and this Web site
          This website was designed to assist persons seeking information concerning recent and current government funded research related to CFIDS,Chronic Fatigue Immune Dysfunction Syndrome, also known as CFS, Chronic Fatigue Syndrome, and ME, Myalgic encephelomelitis; and FM, Fibromyalgia; and Related Disorders (GWS, EI, MCS, etc.).

          As such, the majority of the Research Abstracts contained herein have been obtained via the CRISP Data base.

          C.R.I.S.P. stands for Computer Retrieval of Information on Scientific Projects, a government searchable database of federally funded biomedical research projects. Most of the research falls within the broad category of Extramural projects, grants, contracts and cooperative agreements conducted primarily by universities, hospitals, and other research institutions, and funded by the National Institutes of Health (NIH) and other government agencies.

          A relatively small number of research grants are funded by the Center for Disease Control and Prevention(CDC), the Food and Drug Administration(FDA), the Health Resources and Services Administration(HRSA), and the Agency for Health Care Policy and Research(AHCPR). Crisp also contains information on the Intramural programs of the NIH and the FDA. Users, including the public, can use the CRISP interface to search for scientific concepts, emerging trends and techniques, or identify specific projects and/or investigators.

          The CRISP Website is located at: www-commons.cit.nih.gov/crisp/

          The scope of our Website is limited to recent and current CFIDS related government funded research.

          The information provided on this website is in abstract form and thus not intended to be exhaustive. The accuracy of the government's CRISP data base is assumed.

          For further information not provided on the abstract, and for in-progress or completed study outcomes, please directly contact the Primary Investigator (PI) as listed on the specific abstract you are researching.

          The National Institutes of Health (NIH), homepage has a section for looking up employees. That website is located at: www.nih.gov

          To find the dollar amount of the Grant allocated per each specific study, please return to the Index click on Information on Funding and follow the instructions provided.

          For further help, you may wish to contact a computer specialist at the CRISP Information Resources Section at commons@od.nih.gov or return to the Index click on Information on Funding and use the contact information provided.

          It is our sincere hope that this Website helps patients, advocates, and researchers alike narrow the focus of their search for federally funded CFIDS related scientific projects.

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MOTOR CONTROL IN CHRONIC FATIGUE SYNDROME

Grant Number: 5R01AI034250-06
PI Name: STARR, ARNOLD
PI Title: PROFESSOR OF NEUROLOGY
Project Title: MOTOR CONTROL IN CHRONIC FATIGUE SYNDROME

Abstract: DESCRIPTION: (Adapted from Investigator's Abstract) Results from the prior grant period using electrophysiological recordings support the hypothesis that patients with CFS have a disorder of central motor control. Moreover, recent studies by others using transcranial magnetic stimulation also point to the central auditory pathway as being abnormal in CFS. The patients in our studies showed slowed reaction times in tasks requiring rapid responses and impaired brain activities accompanying motor response preparation. Transcranial magnetic stimulation has demonstrated a premature reduction of motor cortical output in CFS accompanying sustained motor activities. Our goals in the proposed new project are to define the time course of altered motor cortical function in CFS before and after a period of exercise-induced fatigue. The specificity of the abnormalities for CFS will be tested by comparison with a group of patients with clinical depression. The methods of study utilize neurophysiological recordings of slow brain potentials accompanying several different types of response preparation and transcranial magnetic stimulation of motor cortex to measure the extent of reduction of central motor drive.

Thesaurus Terms: chronic fatigue syndrome, motor cortex, neuromuscular function, neuromuscular system, neurophysiology, neuroregulation, stimulus /response action potential, aerobic exercise, brain electrical activity, rest, stimulus interval clinical research, human subject, interview, magnetic field, neuropsychological test

Institution: UNIVERSITY OF CALIFORNIA IRVINE
Fiscal Year: 1999
Department: NEUROLOGY
Project Start: 01-APR-1993
Project End: 31-AUG-2001
ICD: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
IRG: ZRG5

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INHIBITED FUNCTIONAL BRAIN ACTIVITY IN FIBROMYALGIA
Grant Number: 5P60AR20614-230018
PI Name: BRADLEY, LAURENCE A.
PI Title:
Project Title: INHIBITED FUNCTIONAL BRAIN ACTIVITY IN FIBROMYLAGIA

Abstract:
We propose two studies with the aim of better understanding the role of inhibited functional brain activity (assessed by regional cerebral blood flow [rCBF]) and abnormal pain perception in the etiopathogenesis of fibromyalgia (FM). To accomplish this aim, we will test six hypotheses based on an etiopathogenetic model of FM developed in our laboratory. Specifically, we wish to determine whether:

(a) functional brain activity in the thalamus and caudate nucleus during resting conditions and behavioral indices of pain perception reliably distinguish FM patients from patient with chronic fatigue syndrome (CFS) or major depression and healthy controls; and

(b) FM patients differ from the three comparison groups with respect to changes in functional brain activity in the thalamus, caudate nucleus, appropriate somatosensory cortices, and anterior cyngulate gyrus upon exposure to painful dolorimeter stimulation.

We will recruit (a) 30 patients with primary FM by American College of Rheumatology (ACR) criteria; (b) 30 patients with CFS by Centers for Disease Control criteria who are pain-free and do not meet ACR criteria for FM; (c) 30 patients with current major depression who are pain-free and do not meet criteria for other current psychiatric diagnoses or criteria for FM or CFS; and (d) 30 healthy controls who are pain-free and do not meet criteria for FM or CFS. Patients will be recruited from appropriate UAB outpatient clinics and controls will be recruited from the Birmingham community. All subjects will be right-handed women.

We propose to measure (a) pain thresholds for dolorimeter stimulation of 5 paired ACR tender points as well as behavioral indices of sensory discrimination ability and response bias; (b) rCBF using single photon emission computed tomographic (SPECT) imaging; and (c) responses to questionnaire measures of anxiety, depression, and pain as well as a structured psychiatric interview. The proposed studies represent an advance in the study of FM since they include the use of an experimental manipulation as well as correlational studies to evaluate an etiopathogenetic model of FM.

The results also will help us to better understand the mechanisms responsible for inhibited functional brain activity observed in FM patients during resting conditions.

Thesaurus Terms:
blood flow, cerebral circulation, fibromyalgia, pain, pathologic process, sensory discrimination, chronic fatigue syndrome, major depression, musculoskeletal disorder, pain threshold, rest, sensory mechanism, sensory threshold, behavioral /social science research tag, clinical research, functional magnetic resonance imaging, human subject, interview, psychological test, psychometrics, questionnaire, sensory disorder diagnosis, single photon emission computed tomography, statistics / biometry

Institution: UNIVERSITY OF ALABAMA AT BIRMINGHAM
UAB STATION
BIRMINGHAM, AL 35294
Fiscal Year: 2000
Department: MEDICINE
Project Start: 20-SEP-77
Project End: 31-DEC-01
ICD: NAT INST OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES
IRG: AMS

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MECHANISMS OF IMMUNOLOGICALLY MEDIATED FATIGUE

Grant Number: 5R01AI035110-07
PI Name: PETERSON, PHILIP K.
PI Title:
Project Title: MECHANISMS OF IMMUNOLOGICALLY MEDIATED FATIGUE

Abstract: Fatigue is a common clinical manifestation of infectious and autoimmune diseases; it is also the chief complaint of patients with chronic fatigue syndrome (CFS). Cytokines, which are produced during immune activation, have been hypothesized to affect brain cell function resulting in fatigue. The work proposed, which is potentially relevant to und erstanding CFS, will test the cytokine hypothesis of immunologically mediated chronic fatigue using recently developed murine models of whole cell Corynebacterium parvum antigen inoculation. The specific aims of this research proposal are to: (1) characterize a murine model of immunologically mediated chronic fatigue (Specific Aim 1); (2) evaluate the association between selected cytokine expression in splenic and brain tissues of mice and chronic fatigue development (Specific Aim 2); and (3) investigate the effects of drugs known to inhibit cytokine production on immunologically mediated chronic fatigue (Specific Aim 3). For these studies, fatigue will be quantified by measuring the degree and duration of reduction in spontaneous daily running activity on an exercise wheel following whole cell C. parvum antigen inoculation in C57BL/6 female mice. Serum cytokine levels (interleukin [IL]-1, IL-6, transforming growth factor-beta, interferon-alpha, and tumor necrosis factor-alpha) and cytokine mRNA expression in splenic and brain tissues of inoculated mice will be correlated with the development of chronic fatigue. Treatment of mice which display immunologically mediated chronic fatigue with drugs known to inhibit cytokine expression will be performed to assess their impact on development of chronic fatigue and their therapeutic potential in disorders involving immunologically mediated fatigue. These studies will enhance our understanding of the pathophysiology of immunologically mediated fatigue and will foster the development of new treatment strategies, particularly for patients with CFS.

Thesaurus Terms: chronic fatigue syndrome, cytokine, disease /disorder model, immunopathology, model design /development Corynebacterium, bacterial antigen, brain cell, exercise, gene expression, interferon alpha, interleukin 1, interleukin 6, messenger RNA, pathologic process, spleen, transforming growth factor, tumor necrosis factor alpha RNase protection assay, female, immunocytochemistry, laboratory mouse, monoclonal antibody

Institution: MINNEAPOLIS MEDICAL RESEARCH FDN, INC.
Fiscal Year: 2001
Department:
Project Start: 01-AUG-1994
Project End: 30-JUN-2002
ICD: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
IRG: ZRG5

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HPA AXIS DYSREGULATION IN FIBROMYALGIA
Grant Number: 5M01RR00042-381009
PI Name: BETZ, A L.
PI Title:
Project Title: HPA AXIS DYSREGULATION IN FIBROMYALGIA

Abstract:
Patients with Fibromyalgia (FM) and Chronic Fatigue Syndrome (CFS) display disturbances in hypothalamic-pituitary-adrenal (HPA) axis function that suggest failure of central regulatory mechanisms. We will characterize the basal, spontaneous secretory characteristics and stimulated activity of the HPA axis in patients with FM and CFS, compared to a matched population of healthy volunteers.

Thesaurus Terms:
chronic fatigue syndrome, fibromyalgia, hormone regulation / control mechanism, hypothalamic pituitary adrenal axis, neurobiology clinical research, human subject

Institution: UNIVERSITY OF MICHIGAN AT ANN ARBOR
ANN ARBOR, MI 48109
Fiscal Year: 1998
Department: NONE
Project Start: 01-DEC-77
Project End: 30-NOV-00
ICD: NATIONAL CENTER FOR RESEARCH RESOURCES
IRG: CLR


Grant Number: 5R01AR43148-05
PI Name: CROFFORD, LESLIE J.
PI Title:
Project Title: HPA AXIS DYSREGULATON IN FIBROMYALGIA

Abstract:
DESCRIPTION: (Adapted from the Investigator's Application): Fibromyalgia (FM) and chronic fatigue syndrome (CFS) share many clinical features; however, we believe the difference in the dominant symptomatic manifestations, pain in FM and fatigue in CFS, reflect divergence of their biological phenotype. The onset and course of both syndromes appear to be influenced by physical or emotional stress. The physiologic response to stress is characterized by activation of the hypothalamic-pituitary-adrenal (HPA) axis. Ongoing studies of the HPA axis have uncovered perturbations of the pulsatile and circadian architecture of pituitary-adrenal secretion that may yield clues to the biologic divergence between FM and CFS. The findings in FM suggest psychophysiological arousal, while those in CFS suggest hypoarousal. Both syndromes are also characterized by non-restorative sleep, which is likely to be related, in a bi-directional manner, to the observed HPA axis disturbances. Analysis of the relationships between neuroendocrine secretory patterns and sleep-wake physiology provides a means to test the functional integrity of neural systems responsible for circadian rhythmicity, sleep regulation and hormonal release.

The specific hypotheses to be tested in this proposal are:

a) HPA axis abnormalities in FM and CFS are mediated centrally at the level of the hypothalamus through failure of integration of neurochemical systems controlling basal and stimulated hormone secretion,

b) a relationship exists between mechanisms controlling sleep and HPA axis activity, such that correlations between neuroendocrine and sleep parameters will be present, and

c) although abnormal HPA axis activity occurs in both FM and CFS, there are distinctions in the central inputs to the axis resulting in psychophysiological arousal in FM patients and hypoarousal in patients with CFS that may be revealed by close examination of specific components of the HPA axis and provocative testing of sleep architecture.

The applicants propose to measure the dynamic pulsatile and circadian characteristics of the basal pituitary adrenal rhythm in FM and CFS patients under the influence of metyrapone, to inhibit glucocorticoid negative feedback and emphasize divergence in the central components of the HPA axis. they will examine the effects of the exogenously administered pituitary corticotroph secretagogues on pituitary-adrenal response in the study groups. They wll analyze sleep regulation and correlate sleep parameters with neuroendocrine hormone secretion. The results of these studies should further our understanding of the role of the HPA axis in the pathogenesis and clinical expression of FM and CFS, enlarge our understanding of the relationship between these two syndromes, and in so doing, make the informed development of reasonable diagnostic approaches and treatment interventions more likely.

Thesaurus Terms:
chronic fatigue syndrome, fibromyalgia, hormone regulation /control mechanism, hypothalamic pituitary adrenal axis, pathologic process, adrenocorticotropic hormone, arginine vasopressin, arousal, circadian rhythm, corticotropin releasing factor, endocrine disorder, melatonin, metyrapone, psychophysiology, secretion, sleep deprivation, blood chemistry, clinical research, human subject, urinalysis

Institution: UNIVERSITY OF MICHIGAN AT ANN ARBOR
ANN ARBOR, MI 48109
Fiscal Year: 1999
Department: INTERNAL MEDICINE
Project Start: 30-SEP-94
Project End: 31-AUG-01
ICD: NAT INST OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES
IRG: ZRG5

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COGNITIVE AND NEUROCHEMICAL FUNCTION IN FIBROMYALGIA

Grant Number: 5P60AR020557-230085
PI Name: PARK, DENISE
PI Title:
Project Title: COGNITIVE AND NEUROCHEMICAL FUNCTION IN FIBROMYALGIA

Abstract: Fibromyalgia (FM) is a rheumatic disorder characterized by the presence of widespread musculoskeletal pain and the presence of tender points. Other symptoms, including fatigue, sleep disturbance, and neuropsychological complaints, contribute significantly to the morbidity associated with FM. One of the most prominent complaints in patients with FM is impaired cognitive ability. The notion that cognitive deficits are fundamental to FM is impaired cognitive ability. The notion that cognitive deficits are fundamental to FM has some credibility, as there is growing evidence that there are subtle but important cognitive deficits associated with Chronic Fatigue Syndrome (CFS), a related disorder, that cannot be explained by psychiatric symptoms. It is possible that cognitive defects in FM patients could result from single or multiple central nervous system perturbations associated with FM. In the present proposal, we will correlate cognitive function of FM patients with measures of neuroendocrine function. A basic thesis advanced is that FM patients may have both cognitive and neuroendocrine function similar to that of controls subjects who are 20 to 30 years older. Indeed, cognitive testing in patients with CFS reveals changes similar to those seen in subjects of advanced chronological age. In two experiments, FM patients will be compared to age-and education- matched controls, as well as to education-matched older adults. Neuroendocrine function will be measured as well, as will depression, pain, fatigue, and beliefs about memory function. This approach permits us to determine whether there are differences in cognitive function of fibromyalgia patients from others, and whether cognitive agins is a good model for understanding the cognitive effects of FM. In addition and perhaps more importantly, the integration of a cognitive approach with a neuroendocrine approach will allow us to determine what mechanisms account for the cognitive differences--neurochemical, psychiatric, or experience pain and fatigue. Knowing the mechanisms underlying observed cognitive deficits, rather than merely demonstrating that there are deficits, has important implications for treatment of the disorder as well as for understanding its etiology.

Thesaurus Terms: aging, cognition disorder, fibromyalgia, neurochemistry, neuroendocrine system age difference, attention, chronic fatigue syndrome, hypothalamic pituitary adrenal axis, memory clinical research, human old age (65+), human subject

Institution: UNIVERSITY OF MICHIGAN AT ANN ARBOR
Fiscal Year: 2001
Department:
Project Start:
Project End:
ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES
IRG:

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