title: The relationship between neurally mediated hypotension and the chronic fatigue syndrome.
abstract: OBJECTIVE
  To compare the clinical symptoms and response evoked by upright tilt-table testing in healthy individuals and in a sample of those satisfying strict criteria for chronic fatigue syndrome.
  
  
  METHODS
  Case-comparison study with mean (SD) follow-up of 24 (5) weeks.
  
  
  METHODS
  Tertiary care hospital.
  
  
  METHODS
  A sample of 23 patients with chronic fatigue syndrome (five men and 18 women; mean age, 34 years), each of whom fulfilled the strict diagnostic criteria of the Centers for Disease Control and Prevention, was recruited from regional chronic fatigue support groups and from the investigators' clinical practices. There were 14 healthy controls (four men and 10 women; mean age, 36 years).
  
  
  METHODS
  Each subject completed a symptom questionnaire and underwent a three-stage upright tilt-table test (stage 1, 45 minutes at 70 degrees tilt; stage 2, 15 minutes at 70 degrees tilt with 1 to 2 micrograms/min of isoproterenol; and stage 3, 10 minutes at 70 degrees with 3 to 4 micrograms/min of isoproterenol). Patients were offered therapy with fludrocortisone, beta-adrenergic blocking agents, and disopyramide, alone or in combination, directed at neurally mediated hypotension.
  
  
  METHODS
  Response to upright tilt and scores on symptom questionnaires prior to and during follow-up.
  
  
  RESULTS
  An abnormal response to upright tilt was observed in 22 of 23 patients with chronic fatigue syndrome vs four of 14 controls (P < .001). Seventy percent of chronic fatigue syndrome patients, but no controls, had an abnormal response during stage 1 (P < .001). Nine patients reported complete or nearly complete resolution of chronic fatigue syndrome symptoms after therapy directed at neurally mediated hypotension.
  
  
  CONCLUSIONS
  We conclude that chronic fatigue syndrome is associated with neurally mediated hypotension and that its symptoms may be improved in a subset of patients by therapy directed at this abnormal cardiovascular reflex.
authors.affiliation: Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md, USA.
authors.forename: I
authors.initials: I
authors.lastname: Bou-Holaigah
authors.forename: P C
authors.initials: PC
authors.lastname: Rowe
authors.forename: J
authors.initials: J
authors.lastname: Kan
authors.forename: H
authors.initials: H
authors.lastname: Calkins
mesh_terms: D000293:Adolescent; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D004206:Disopyramide / Q000627:therapeutic use; D015673:Fatigue Syndrome, Chronic / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005438:Fludrocortisone / Q000627:therapeutic use; D006439:Hemodynamics; D006801:Humans; D007024:Hypotension, Orthostatic / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012982:Sodium, Dietary; D013575:Syncope / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D018667:Tilt-Table Test
chemical_list: D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D000893:Anti-Inflammatory Agents; D012982:Sodium, Dietary; D004206:Disopyramide; D005438:Fludrocortisone