Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Cyclic Vomiting Syndrome

  • Author: Thangam Venkatesan, MD; Chief Editor: Carmen Cuffari, MD  more...
 
Updated: Mar 09, 2016
 

Background

Cyclic vomiting syndrome (CVS), first described in children by Samuel Gee in 1882, is a chronic functional disorder of unknown etiology that is characterized by paroxysmal, recurrent episodes of vomiting.

The pathophysiology is unknown (see Pathophysiology and Etiology), but data suggest a strong genetic component in children with CVS, with evidence of mitochondrial heteroplasmies that predispose to CVS and other related disorders (eg, migraine and chronic fatigue syndrome). Other theories include autonomic dysfunction and, possibly, corticotropin-releasing factor (CRF) because stress is known to be a trigger for these episodes. The possible role of cannabis in causing CVS has been examined, though it remains controversial.

CVS is characterized by recurrent, discrete, stereotypical episodes of rapid-fire vomiting between varying periods of completely normal health (see Presentation). This on-and-off stereotypical pattern of vomiting is nearly pathognomonic.

Because no biochemical markers for CVS have been identified, physicians must initially look for alarming symptoms and then tailor the subsequent workup accordingly (see Workup). Depending on the presenting symptoms and signs other than vomiting, different diagnostic approaches are recommended. In the absence of known pathophysiology, treatment of CVS remains empiric (see Treatment).

For ongoing support and information, families are encouraged to contact the Cyclic Vomiting Syndrome Association, which is an international voluntary organization that serves the needs of patients in the United States and Canada.

Next

Pathophysiology and Etiology

The etiology and pathophysiology of CVS are not known. However, studies have suggested several potential brain-gut mechanisms.

Migraine-related mechanisms have been proposed.[1, 2] In one study, patients with CVS have a significantly higher prevalence of family members with migraine headaches (82% vs 14% of control subjects with a chronic vomiting pattern). Furthermore, 28% of patients with CVS whose vomiting subsequently resolved developed migraine headaches. Approximately 80% of affected patients with family histories positive for migraine respond to antimigraine therapy.[1, 2]

Mitochondrial DNA (mtDNA) mutations may be involved in the pathogenesis of CVS. Boles et al demonstrated that 86% of children with CVS and neuromuscular disease had a history of migraines on the matrilineal side. In children with CVS, 2 mtDNA polymorphisms (16519T and 3010A) are expressed with a high degree of frequency and may serve as a surrogate marker for predisposition to the disease.[3]

The 16519T polymorphism is 6 times more common in pediatric CVS patients than in control populations.[4] The 3010A polymorphism increases the likelihood of CVS in subjects with 16519T by as much as 17 times. These mtDNA polymorphisms may account for the clustering of functional conditions and symptoms in the same individuals and families. One small (and possibly underpowered) study found that adult-onset CVS, unlike pediatric CVS, CVS is not associated with these polymorphisms, suggesting a degree of genetic distinction.[2]

Sympathetic hyperresponsiveness and autonomic dysfunction also appear to contribute to the pathogenesis of CVS.[5] Many associated symptoms, such as pallor, flushing, fever, lethargy, salivation, and diarrhea, are mediated by the autonomic nervous system.[6, 7, 8] Several studies support altered autonomic function in CVS.

Rashed et al[9] and To et al[10] demonstrated heightened sympathetic cardiovascular tone in patients with CVS. Kasawinah et al reported the successful use of dexmedetomidine, an alpha2-adrenergic agonist, to treat CVS.[11] In a small study involving 6 children with CVS, all patients had sympathetic autonomic dysfunction, affecting mainly the vasomotor and sudomotor systems. Symptoms developed during tilt testing in half of these patients, suggesting that these findings may play a role in the pathophysiology of CVS.[12]

To evaluate this association with autonomic dysfunction, a cross-sectional study was performed in which the Ohio dysautonomia (ODYSA) questionnaire was administered to 21 patients with CVS (3 children) and 46 patients with migraines.[13] The 2 patient groups had similar comorbid conditions, with fibromyalgia noted in 38% of subjects with CVS, orthostatic intolerance in 47% of subjects with CVS, functional dyspepsia in 9.5% of subjects with CVS, and complex regional pain syndrome in 24% of subjects with CVS.

The main limitation of this study was that the findings were not corroborated by means of either a physical examination or standard autonomic function testing.[13] However, the findings of orthostatic intolerance are of clinical significance because the use of pharmacologic therapy (eg, fludrocortisone and beta-blockers) may be considered in these patients.

In a prospective trial in adult CVS patients, Venkatesan et al found that most subjects with CVS (90%) had impairment of the sympathetic nervous system with postural tachycardia or sudomotor dysfunction while parasympathetic nerve function was intact.[14]

In this study, 17 (85%) of 20 adult CVS subjects and 2 (10%) of 20 control subjects had abnormalities on thermoregulatory sweat testing.[14] A total of 7 (35%) patients and 1 control subject had evidence of postural tachycardia with an increase of more than 30 beats/min in heart rate (HR) on standing. Of the subjects, 18 (90%) had abnormal sudomotor function, postural tachycardia, or both. The HR response to deep breathing was normal in 19 (95%) subjects with CVS and 18 (95%) controls.

The stress response, mediated by the hypothalamic-pituitary-adrenal (HPA) axis, can also potentially induce episodes of CVS. Infectious, psychological, and physical stressors are known triggers of episodes.[15, 16, 17, 18, 19] Sato et al documented increased levels of adrenocorticotropic hormone (ACTH) and cortisol, associated with extreme lethargy and hypertension, before the onset of vomiting.[20, 21, 22, 23] Furthermore, Taché showed that central CRF induced gastric stasis, emesis, or both in animals.[24]

Therefore, CRF may be a brain-gut mediator of CVS that directly connects stress and vomiting.[25] If this theory holds true, CRF receptor antagonists currently in development could theoretically ablate vomiting by blocking the CRF receptor’s vagally mediated actions.[26]

Cannabis use in CVS has received considerable attention. Chronic marijuana use has been associated with hot showers or compulsive hot water bathing and CVS, though a cause-and-effect relation has not been confirmed. The endocannabinoid system (ECS) consists of the ligands 2-AG and anandamide and the cannabinoid receptors CB1 and CB2. This system is thought to play a role in nausea and vomiting and in coping with stress.

There is considerable evidence that activation of central and peripheral CB1 cannabinoid receptors inhibits nausea and vomiting; conversely, both nausea and vomiting are frequent adverse effects accompanying CB1 receptor antagonist use in humans. These and other data strongly suggest that that tone of the ECS regulates nausea and vomiting; further studies are needed to explore this possibility more fully.[27, 28]

That CVS has a central component has been suggested by functional magnetic resonance imaging (MRI) studies using whole-brain seed-based analysis. Patients with CVS exhibited a distinct alteration in resting state functional connectivity involving connections from the cingulate and inferior frontal gyrus (IFG), a known neural correlate of nausea.[29]

In conclusion, the pathogenesis of CVS is likely to be multifactorial, with multiple genetic, autonomic, central, and environmental factors playing a role. Further studies are needed to elucidate the exact mechanisms underlying this disorder.

Previous
Next

Epidemiology

United States statistics

The true incidence and prevalence of CVS in the United States are unknown. In central Ohio, amid a predominantly white population, the prevalence of CVS in children (evaluated by the sole pediatric gastroenterology referral center) was 0.04%.[30]

International statistics

On the basis of limited epidemiologic data, Cullen and MacDonald estimated the prevalence of periodic vomiting in western Australia to be 2.3%.[6] Similarly, Abu-Arafeh and Russell observed a prevalence of 1.9% in school-aged children in Aberdeen, Scotland.[31] Both of these figures are derived from white populations and may not accurately reflect prevalence in all races or ethnic populations. In a study performed at KEM Hospital in Pune, India, CVS accounted for 0.5% of admissions to pediatric wards during 1998-2000.

In a population-based study from Ireland, the incidence of CVS was relatively high at 3.15 cases per 100,000 children. This incidence is comparable to those of other major GI diseases of childhood (eg, Crohn disease) in Ireland.[32]

Age-, sex-, and race-related demographics

The median age at onset is 4.8 years; however, CVS has been observed in infants as young as 6 days and in adults as old as 73 years.[1] The typical interval from onset of symptoms to diagnosis is 2.7 years.[1] In adults, the average age of onset is 21 years and the average age of evaluation for recurrent vomiting 34 years.[8] Females show a slight predominance over males (female-to-male ratio, 57:43). CVS occurs in all races but seems to affect whites disproportionately.

Previous
Next

Prognosis

Most published series indicate that CVS lasts an average of 2.5-5.5 years, resolving in late childhood or early adolescence. A few patients continue to be symptomatic through adulthood.

As early as 1898, clinicians observed that some patients went on to develop migraine headaches. That some children with CVS progress to abdominal migraines and then to migraine headaches implies that there may be a sequential progression of age-dependent manifestations of migraine.

A survey by Abu-Arafeh et al found the mean ages of children with CVS, abdominal migraines, and migraine headaches to be 5.3 years, 10.3 years, and 11.5 years, respectively.[31] This finding supports the developmental progression from vomiting to abdominal pain to headache. In unpublished data, Li and Hayes determined that nearly one third of patients develop migraines after resolution of CVS and predicted that nearly 75% would develop migraines by age 18 years.

A study of 31 patients with CVS by Hikita et al found that the median overall duration of the disorder was 66 months and that 44% of the patients seen for follow-up (25 patients) developed migraine. The authors also found abnormally high adrenocorticotropic hormone and antidiuretic hormone levels among the 25 patients for whom follow-up data were available. Significant correlations between attack duration and adrenocorticotropic hormone levels and attack duration and antidiuretic hormone levels were noted.[33]

Although patients are well about 90% of the time, CVS can be medically and socially disabling. More than 50% of patients require intravenous (IV) fluids, compared with less than 1% of patients with rotavirus gastroenteritis. The average annual cost of testing, treatment, and absenteeism totals $17,000. Children miss an average of 24 school days per year and often need home tutoring or, occasionally, home schooling. Additionally, because of its frequency during times of excitement, CVS has ruined many birthdays, holidays, and vacations.[30]

In adults, substantial morbidity is associated with CVS, perhaps because of lack of awareness and resultant delays in diagnosis. In a study of 41 CVS patients, Fleisher found that 32% were completely disabled at the time of diagnosis.[8] A total of 293 procedures were performed in the 41 patients, and none were indicative of organic etiology. In addition, 17 surgical procedures, including 10 cholecystectomies, appendectomies, exploratory laparotomies, a pyloroplasty, and a hysterectomy, were performed without any therapeutic benefit.

Adults and children with CVS also have multiple emergency department (ED) visits (see Table 1 below), and the diagnosis is often unrecognized.[34]

Table 1. Characteristics of Emergency Department Visits in Patients With Cyclic Vomiting Syndrome (Open Table in a new window)

Characteristic Adults



(n = 104)



Children



(n = 147)



Number of ED visits per patient with CVS (median) 15 (range, 1-200) 10 (range, 1-175)
Number of ED visits before diagnosis of CVS (median) 7 (range, 1-150) 5 (range, 0-65)
Diagnosis not made in ED 89 (93%) 119 (93%)
Diagnosis not recognized in ED in patients with established diagnosis of CVS 84 (88%) 97 (80%)
Number of different EDs visited (mean ± SD) 4.69 ± 4.72 2.6 ± 2.42
CVS = cyclic vomiting syndrome; ED = emergency department; SD = standard deviation.
Previous
 
 
Contributor Information and Disclosures
Author

Thangam Venkatesan, MD Associate Professor of Medicine, Fellowship Director, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical College of Wisconsin

Thangam Venkatesan, MD is a member of the following medical societies: American Gastroenterological Association, Indian Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

B UK Li, MD Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Medical College of Wisconsin; Attending Gastroenterologist, Director, Cyclic Vomiting Program, Children’s Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Chief Editor

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Acknowledgements

Jayant Deodhar, MD Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India

Disclosure: Nothing to disclose.

Seth Marcus, MD Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital, Northwestern University

Seth Marcus, MD is a member of the following medical societies: American Academy of Pediatrics and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Abhilasha Pandey, MBBS Froedtert Hospital, Medical College of Wisconsin

Disclosure: Nothing to disclose.

David A Piccoli, MD Chief of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine

David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Shikha Sundaram, MD Fellow, Department of Gastroenterology, Hepatology and Nutrition, Children's Memorial Hospital of Chicago and Northwestern University

Shikha Sundaram, MD is a member of the following medical societies: American Academy of Pediatrics and American Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
  1. Li BU, Misiewicz L. Cyclic Vomiting Syndrome: a brain-gut disorder. Gastroenterol Clin N Am. 2003. 32:997-1019. [Medline].

  2. Boles RG, Zaki EA, Lavenbarg T, et al. Are pediatric and adult-onset cyclic vomiting syndrome (CVS) biologically different conditions? Relationship of adult-onset CVS with the migraine and pediatric CVS-associated common mtDNA polymorphisms 16519T and 3010A. Neurogastroenterol Motil. 2009 Sep. 21(9):936-e72. [Medline].

  3. Venkatesan T, Zaki EA, Kumar N, Sengupta J, Ali M, Malik B, et al. Quantitative pedigree analysis and mitochondrial DNA sequence variants in adults with cyclic vomiting syndrome. BMC Gastroenterol. 2014 Oct 21. 14:181. [Medline].

  4. Zaki EA, Freilinger T, Klopstock T, et al. Two common mitochondrial DNA polymorphisms are highly associated with migraine headache and cyclic vomiting syndrome. Cephalalgia. 2009 Jul. 29(7):719-28. [Medline].

  5. Gordan N. Recurrent vomiting in childhood, especially of neurological origin. Dev Med Child Neurol. 1994 May. 36(5):463-7. [Medline].

  6. Cullen KJ, MacDonald WB. The periodic syndrome: its nature and prevalence. Med J Aust. 1963 Aug 3. 50(2):167-73. [Medline].

  7. Fleisher DR. The cyclic vomiting syndrome described. J Pediatr Gastroenterol Nutr. 1995. 21 Suppl 1:S1-5. [Medline].

  8. Fleisher DR, Gornowicz B, Adams K, Burch R, Feldman EJ. Cyclic Vomiting Syndrome in 41 adults: the illness, the patients, and problems of management. BMC Med. 2005 Dec 21. 3:20. [Medline]. [Full Text].

  9. Rashed H, Abell TL, Familoni BO, Cardoso S. Autonomic function in cyclic vomiting syndrome and classic migraine. Dig Dis Sci. 1999 Aug. 44(8 Suppl):74S-78S. [Medline].

  10. To J, Issenman RM, Kamath MV. Evaluation of neurocardiac signals in pediatric patients with cyclic vomiting syndrome through power spectral analysis of heart rate variability. J Pediatr. 1999 Sep. 135(3):363-6. [Medline].

  11. Khasawinah TA, Ramirez A, Berkenbosch JW, Tobias JD. Preliminary experience with dexmedetomidine in the treatment of cyclic vomiting syndrome. Am J Ther. 2003 Jul-Aug. 10(4):303-7. [Medline].

  12. Chelimsky TC, Chelimsky GG. Autonomic abnormalities in cyclic vomiting syndrome. J Pediatr Gastroenterol Nutr. 2007 Mar. 44(3):326-30. [Medline].

  13. Chelimsky G, Madan S, Alshekhlee A, Heller E, McNeeley K, Chelimsky T. A comparison of dysautonomias comorbid with cyclic vomiting syndrome and with migraine. Gastroenterol Res Pract. 2009. 2009:701019. [Medline]. [Full Text].

  14. Venkatesan T, Prieto T, Barboi A, Li B, Schroeder A, Hogan W. Autonomic nerve function in adults with cyclic vomiting syndrome: a prospective study. Neurogastroenterol Motil. 2010 Dec. 22(12):1303-7, e339. [Medline].

  15. Fleisher DR, Matar M. The cyclic vomiting syndrome: a report of 71 cases and literature review. J Pediatr Gastroenterol Nutr. 1993 Nov. 17(4):361-9. [Medline].

  16. Li BU, Fleisher DR. Cyclic vomiting syndrome: features to be explained by a pathophysiologic model. Dig Dis Sci. 1999 Aug. 44(8 Suppl):13S-18S. [Medline].

  17. Li BU, Murray RD, Heitlinger LA, et al. Is cyclic vomiting syndrome related to migraine?. J Pediatr. 1999 May. 134(5):567-72. [Medline].

  18. Smith CH. Recurrent vomiting in children: Its etiology and treatment. J Pediatr. 1937. 10:719-42.

  19. Withers GD, Silburn SR, Forbes DA. Precipitants and aetiology of cyclic vomiting syndrome. Acta Paediatr. 1998 Mar. 87(3):272-7. [Medline].

  20. Sato T. Prevalence of Syndrome of ACTH-ADH discharge in Japan. Clin Pediatr Endocrinol. 1993. 2:7-12.

  21. Sato T, Funahashi T, Mukai M, et al. Periodic ACTH discharge. J Pediatr. 1980 Aug. 97(2):221-5. [Medline].

  22. Sato T, Igarashi N, Minami S, et al. Recurrent attacks of vomiting, hypertension and psychotic depression: a syndrome of periodic catecholamine and prostaglandin discharge. Acta Endocrinol (Copenh). 1988 Feb. 117(2):189-97. [Medline].

  23. Sato T, Uchigata Y, Uwadana N, et al. A syndrome of periodic adrenocorticotropin and vasopressin discharge. J Clin Endocrinol Metab. 1982 Mar. 54(3):517-22. [Medline].

  24. Tache Y. Cyclic vomiting syndrome: the corticotropin-releasing-factor hypothesis. Dig Dis Sci. 1999 Aug. 44(8 Suppl):79S-86S. [Medline].

  25. Lee C, Sarna SK. Central regulation of gastric emptying of solid nutrient meals by corticotropin releasing factor. Neurogastroenterol Motil. 1997 Dec. 9(4):221-9. [Medline].

  26. Zobel AW, Nickel T, Kunzel HE, et al. Effects of the high affinity corticotrophin-releasing hormone receptor 1 antagonist R121919 in major depression: the first 20 patients treated. J Psychiatr Res. 2000. 34:171-81. [Medline].

  27. Parker LA, Rock EM, Limebeer CL. Regulation of nausea and vomiting by cannabinoids. Br J Pharmacol. 2011 Aug. 163(7):1411-22. [Medline]. [Full Text].

  28. Choukèr A, Kaufmann I, Kreth S, Hauer D, Feuerecker M, Thieme D. Motion sickness, stress and the endocannabinoid system. PLoS One. 2010. 5(5):e10752. [Medline].

  29. Erica A. Samuel, Arash Babaei, Anna Patel, Robert M. Siwiec, Mark Kern, Thangam Venkatesan, et al. Cyclic Vomiting Syndrome is Associated With Alterations of Brain Connectivity. Gastroenterology. May/2012. 142:S-552-S-553.

  30. Li BU, Balint JP. Cyclic vomiting syndrome: evolution in our understanding of a brain-gut disorder. Adv Pediatr. 2000. 47:117-60. [Medline].

  31. Abu-Arafeh I, Russell G. Prevalence and clinical features of abdominal migraine compared with those of migraine headache. Arch Dis Child. 1995 May. 72(5):413-7. [Medline]. [Full Text].

  32. Fitzpatrick E, Bourke B, Drumm B, Rowland M. The incidence of cyclic vomiting syndrome in children: population-based study. Am J Gastroenterol. 2008 Apr. 103(4):991-5; quiz 996. [Medline].

  33. Hikita T, Kodama H, Ogita K, Kaneko S, Nakamoto N, Mimaki M. Cyclic Vomiting Syndrome in Infants and Children: A Clinical Follow-Up Study. Pediatr Neurol. 2016 Jan 7. [Medline].

  34. Venkatesan T, Tarbell S, Adams K, McKanry J, Barribeau T, Beckmann K, et al. A survey of emergency department use in patients with cyclic vomiting syndrome. BMC Emerg Med. 2010 Feb 24. 10:4. [Medline]. [Full Text].

  35. [Guideline] Li BU, Lefevre F, Chelimsky GG, et al. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition consensus statement on the diagnosis and management of cyclic vomiting syndrome. J Pediatr Gastroenterol Nutr. 2008 Sep. 47(3):379-93. [Medline].

  36. Pfau BT, Li BU, Murray RD, et al. Differentiating cyclic from chronic vomiting patterns in children: quantitative criteria and diagnostic implications. Pediatrics. 1996 Mar. 97(3):364-8. [Medline].

  37. Hoyt CS, Stickler GB. A study of 44 children with the syndrome of recurrent (cyclic) vomiting. Pediatr. 1960. 25:775-80. [Medline].

  38. Li BU. Cyclic vomiting: the pattern and syndrome paradigm. J Pediatr Gastroenterol Nutr. 1995. 21 Suppl 1:S6-10. [Medline].

  39. Venkatasubramani N, Venkatesan T, Li BUK. Extreme Emesis: Cyclic Vomiting Syndrome. Practical Gastroenterology. September 2007. 31:21-34.

  40. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut. 2004 Nov. 53(11):1566-70. [Medline]. [Full Text].

  41. Donnino MW, Cocchi MN, Miller J, Fisher J. Cannabinoid hyperemesis: A case series. J Emerg Med. 2009 Sep 16. [Medline].

  42. Hejazi RA, Lavenbarg TH, Foran P, McCallum RW. Who are the non-responders to standard treatment with tricyclic antidepressant agents for cyclic vomiting syndrome in adults? A large single center experience. Aliment Pharmacol Ther. 2009 Oct 10. [Medline].

  43. Choung RS, Locke GR 3rd, Lee RM, Schleck CD, Zinsmeister AR, Talley NJ. Cyclic vomiting syndrome and functional vomiting in adults: association with cannabinoid use in males. Neurogastroenterol Motil. 2012 Jan. 24(1):20-6, e1. [Medline].

  44. Simonetto DA, Oxentenko AS, Herman ML, Szostek JH. Cannabinoid hyperemesis: a case series of 98 patients. Mayo Clin Proc. 2012 Feb. 87(2):114-9. [Medline].

  45. Wallace EA, Andrews SE, Garmany CL, Jelley MJ. Cannabinoid hyperemesis syndrome: literature review and proposed diagnosis and treatment algorithm. South Med J. 2011 Sep. 104(9):659-64. [Medline].

  46. Li BU, Murray RD, Heitlinger LA, et al. Heterogeneity of diagnoses presenting as cyclic vomiting. Pediatrics. 1998 Sep. 102(3 Pt 1):583-7. [Medline].

  47. Li BU. Cyclic vomiting syndrome and abdominal migraine: periodic syndromes with gastrointestinal symptoms. Int Semin Pediatr Gastroenterol Nutr. 2000. 9(3):1-8.

  48. Olson AD, Li BU. The diagnostic evaluation of children with cyclic vomiting: A cost-effectiveness assessment. Pediatr. 2002. 141:724-8. [Medline].

  49. Forbes D, Withers G. Prophylactic therapy in cyclic vomiting syndrome. J Pediatr Gastroenterol Nutr. 1995. 21 Suppl 1:S57-9. [Medline].

  50. Lee LY, Abbott L, Mahlangu B, Moodie SJ, Anderson S. The management of cyclic vomiting syndrome: a systematic review. Eur J Gastroenterol Hepatol. 2012 Sep. 24(9):1001-6. [Medline].

  51. Hejazi RA, McCallum RW. Cyclic vomiting syndrome: treatment options. Exp Brain Res. 2014 Aug. 232(8):2549-52. [Medline].

  52. Moses J, Keilman A, Worley S, Radhakrishnan K, Rothner AD, Parikh S. Approach to the diagnosis and treatment of cyclic vomiting syndrome: a large single-center experience with 106 patients. Pediatr Neurol. 2014 Jun. 50(6):569-73. [Medline].

  53. Ozdemir HH, Bulut S, Berilgen MS, Kapan O, Balduz M, Demir CF. Resistant cyclic vomiting syndrome successfully responding to chlorpromazine. Acta Medica (Hradec Kralove). 2014. 57(1):28-9. [Medline].

  54. Li BU. Cyclic vomiting syndrome: a pediatric Rorschach test. J Pediatr Gastroenterol Nutr. 1993 Nov. 17(4):351-3. [Medline].

  55. Li BU. Cyclic vomiting: new understanding of an old disorder. Contemp Pediatr. 1996. 13:48-62.

  56. Hejazi RA, Reddymasu SC, Namin F, Lavenbarg T, Foran P, McCallum RW. Efficacy of tricyclic antidepressant therapy in adults with cyclic vomiting syndrome: a two-year follow-up study. J Clin Gastroenterol. 2010 Jan. 44(1):18-21. [Medline].

  57. Boles RG, Lovett-Barr MR, Preston A, Li BU, Adams K. Treatment of cyclic vomiting syndrome with co-enzyme Q10 and amitriptyline, a retrospective study. BMC Neurol. 2010 Jan 28. 10:10. [Medline]. [Full Text].

  58. Boles RG. High degree of efficacy in the treatment of cyclic vomiting syndrome with combined co-enzyme Q10, L-carnitine and amitriptyline, a case series. BMC Neurol. 2011 Aug 16. 11:102. [Medline]. [Full Text].

  59. Clouse RE, Sayuk GS, Lustman PJ, Prakash C. Zonisamide or levetiracetam for adults with cyclic vomiting syndrome: a case series. Clin Gastroenterol Hepatol. 2007 Jan. 5(1):44-8. [Medline].

  60. Kumar N, Bashar Q, Reddy N, Sengupta J, Ananthakrishnan A, Schroeder A. Cyclic Vomiting Syndrome (CVS): is there a difference based on onset of symptoms - pediatric versus adult?. BMC Gastroenterol. 2012 May 28. 12(1):52. [Medline].

  61. Benson JM, Zorn SL, Book LS. Sumatriptan in the treatment of cyclic vomiting. Ann Pharmacother. 1995 Oct. 29(10):997-9. [Medline].

  62. Calhoun AH, Pruitt AP. Injectable sumatriptan for cyclic vomiting syndrome in adults: a case series. Headache. 2014 Oct. 54(9):1526-30. [Medline].

  63. King T, Gardell LR, Wang R, Vardanyan A, Ossipov MH, Malan TP Jr. Role of NK-1 neurotransmission in opioid-induced hyperalgesia. Pain. 2005 Aug. 116(3):276-88. [Medline].

  64. Vardanyan A, Wang R, Vanderah TW, Ossipov MH, Lai J, Porreca F. TRPV1 receptor in expression of opioid-induced hyperalgesia. J Pain. 2009 Mar. 10(3):243-52. [Medline].

  65. Tarbell SE, Li BU. Anxiety Measures Predict Health-Related Quality of Life in Children and Adolescents with Cyclic Vomiting Syndrome. J Pediatr. 2015 Sep. 167 (3):633-638.e1. [Medline].

 
Previous
Next
 
Cyclic versus chronic temporal patterns of recurrent vomiting. Number of emeses is plotted over 2-month period. Chronic pattern, represented by thin dashed line, has low grade on nearly daily basis (eg, gastroesophageal reflux). Cyclic pattern, represented by heavy solid line, involves high-intensity episodes intermittently once every several weeks (eg, cyclic vomiting syndrome).
Table 1. Characteristics of Emergency Department Visits in Patients With Cyclic Vomiting Syndrome
Characteristic Adults



(n = 104)



Children



(n = 147)



Number of ED visits per patient with CVS (median) 15 (range, 1-200) 10 (range, 1-175)
Number of ED visits before diagnosis of CVS (median) 7 (range, 1-150) 5 (range, 0-65)
Diagnosis not made in ED 89 (93%) 119 (93%)
Diagnosis not recognized in ED in patients with established diagnosis of CVS 84 (88%) 97 (80%)
Number of different EDs visited (mean ± SD) 4.69 ± 4.72 2.6 ± 2.42
CVS = cyclic vomiting syndrome; ED = emergency department; SD = standard deviation.
Table 2. Clinical Features in Adults and Children with Cyclic Vomiting Syndrome
Feature Children Adults
Age of onset 4.8 years (earliest, 6 days) 35 years (latest, 73 years)
Delay in diagnosis 2.6 years 8 years
Female-to-male ratio 57:43 17:24
Frequency Every 2-4 weeks Every 3 months
Duration (mean) 1-2 days (range, 1-10 days) 6 days (range, 1-21 days)
Periodicity 49% Not reported
Early morning onset 42% 50%
Stereotypical episodes 99% 85%
Prodrome 72%, 1.5 hours 93%
Symptoms Nausea, anorexia, pallor Nausea, epigastric pain
Recovery to oral feeding 6 hours 24 hours
Relieving factors Deep sleep Hot bath or shower (56%)
Precipitating factors Stress (47%), infection (31%) Menses (57%), anxiety
Comorbid conditions Anxiety Not reported
Interepisodic nausea < 6% 63%
Coalescence of episodes Few 50%
Vomiting 6 episodes/hr at peak, bile (81%) 8.5 episodes/hr
Systemic symptoms Pallor, salivation, listlessness Intense thirst (33%)
GI symptoms Anorexia, nausea, diarrhea, abdominal pain Abdominal pain, diarrhea
Neurologic symptoms Headache, photophobia, phonophobia, abdominal pain Irritability, confusion
Natural history =28% progress to migraine Not reported
Family history 82% 57%
Complications Dehydration, esophagitis Dehydration, esophagitis, laparotomy (18%)
Morbidity 14-25 days of missed school per year 32% completely disabled
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.