AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Cyclic vomiting syndrome (CVS) is a paroxysmal, especially severe, recurrent vomiting disorder of unknown etiology. It was first described by Gee in 1882. Because vomiting is a common index symptom attributable to various GI and extraintestinal disorders, this idiopathic syndrome remains poorly recognized. Consensus diagnostic criteria established in 1994 at the First International Scientific Symposium on CVS helped define the criteria needed to make this elusive diagnosis. At its core, CVS is characterized by a unique temporal pattern of recurrent, discrete, and stereotypical episodes of explosive vomiting that punctuate periods of completely normal health (Li, 1995).

Pathophysiology

The etiology, pathophysiology, and target organ in CVS remain unknown. With a flurry of research over the last decade, recent studies have proposed several potential brain-gut mechanisms. Support exists for migraine-related mechanisms, and 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 resolved subsequently developed migraine headaches. Finally, 80% of affected patients with family histories positive for migraine respond to antimigraine therapy (Li, 2003).

Mitochondrial DNA mutations may be involved in the pathogenesis of CVS. Boles et al have demonstrated that, among children with CVS and neuromuscular disease, 86% have maternal-side migraines. Boles and colleagues (1999; 2003) reported a large mitochondrial DNA deletion in a single child with CVS and they have identified additional mutations concentrated in the D-loop, a hypervariable locus of the control region, in other children with CVS. Children with mitochondrial myopathy, encephalopathy, lactacidosis, and stroke (MELAS) syndrome are known to have both severe migraines and episodic vomiting, as in CVS (Hirano, 1994). Several children with CVS, including 4 members of an Italian family, have recently been reported to have various mitochondrial mutations (Ito, 2001; Salpietro, 2003).

Sympathetic hyperresponsivity and autonomic dysfunction also appear to contribute to the pathogenesis of CVS (Gordan, 1994). Many associated symptoms, such as pallor, flushing, fever, lethargy, salivation, and diarrhea, are mediated by the autonomic nervous system (Cullen, 1963; Fleisher, 1993; Fleisher, 1995). Several studies support altered autonomic function in CVS. Rashed et al (1999) and To et al (1999) demonstrated a heightened sympathetic cardiovascular tone in patients with CVS. Kasawinah and colleagues (2003) reported the successful use of dexmedetomidine, an alpha-2 adrenergic agonist, to treat CVS.

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 (Fleisher, 1993; Smith, 1937; Withers, 1998; Li and Murray, 1999; Li and Fleisher, 1999). Sato and colleagues documented increased levels of adrenocorticotropic hormone (ACTH) and cortisol, associated with extreme lethargy and hypertension, before the onset of vomiting (Sato, 1993; Sato, 1980; Sato, 1982; Sato, 1988). Furthermore, Taché (1999) has definitively shown that central corticotropin-releasing factor (CRF) induces gastric stasis, emesis, or both in animals. Therefore, CRF may be a potential brain-gut mediator of CVS that directly connects stress and vomiting (Lee, 1997). If this theory holds true, CRF receptor antagonists, currently in development, could theoretically ablate the vomiting by blocking the CRF receptor's vagally-mediated actions (Zobel, 2000).

How these pathways fit together is still unclear. Li and Misiewicz have proposed that heightened neuronal excitability due to enhanced membrane ion permeability (ion channelopathy), mitochondrial energy deficits (due to dysfunction), or hormonal state (eg, menstrual periods) may be present. Both physical (infection) and psychologic stressors (excitement) can initiate a known cascade that releases hypothalamic CRF, the suspected neuroendocrine mediator, resulting in vomiting. Altered brainstem regulation of these autonomic signals may be the necessary abnormality that allows the dysautonomia to feed forward and become self-sustained for days on end (Li and Misiewicz, 2003).

Frequency

United States

The true incidence and prevalence of CVS 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% (Li and Balint, 2000).

International

Limited epidemiologic data by Cullen and MacDonald estimate the prevalence of periodic vomiting in western Australia to be 2.3% (Cullen, 1963). Similarly, Abu-Arafeh and Russell observed a prevalence of 1.9% in school-aged children in Aberdeen, Scotland (Abu-Arafeh, 1995). Both of these figures estimate the prevalence in white populations and may not reflect 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.

Mortality/Morbidity

Although patients are well approximately 90% of the time, CVS can be a medically and academically disabling disorder. More than 50% of affected patients require intravenous fluids, compared with less than 1% of patients with rotavirus gastroenteritis. The average annual cost of testing, treatment, and work absences totals US $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 (Li and Balint, 2000).

Race

CVS occurs in all races but seems to disproportionately affect whites.

Sex

Females show a slight predominance over males; the female-to-male ratio is 57:43 (Li and Kagalwalla, 2002).

Age

The median age at onset is 4.8 years, but CVS has been observed in infants as young as age 6 days and in adults as old as age 73 years (Li and Misiewicz, 2003). Typical delay in diagnosis from onset of symptoms is 2.7 years (Li and Misiewicz, 2003).

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

• Cyclic vomiting syndrome (CVS) is characterized by recurrent, discrete, stereotypical episodes of rapid-fire vomiting in between varying periods of completely normal health (see Consensus diagnostic criteria for CVS below). This on-and-off stereotypic pattern of vomiting is nearly pathognomonic of CVS. If a patient experiences any symptoms in between episodes, it implies either a misdiagnosis of CVS or a superimposed chronic vomiting disorder (eg, gastroesophageal reflux), which must be investigated further (Pfau, 1996).

• The Consensus diagnostic criteria for CVS (adapted from the International Scientific Symposium on Cyclic Vomiting Syndrome held at St. Bartholomew's Hospital, London, United Kingdom, in 1994) is as follows:

• • Essential criteria
  • • Recurrent, severe, discrete episodes of vomiting are reported.
    • Varying intervals of normal health between episodes are noted.
    • The vomiting episodes last from hours to days.
    • No apparent cause of vomiting is found, with negative laboratory, radiographic, and endoscopic test results.
  • Supportive criteria
  • • Vomiting pattern is stereotypical, and each episode is similar in terms of time of onset, intensity, duration, frequency, associated symptoms, and signs within an individual.
    • Vomiting pattern is self-limited, and episodes resolve spontaneously if left untreated.
    • Associated symptoms include nausea, abdominal pain, headache, motion sickness, photophobia, and lethargy.
    • Associated signs include fever, pallor, diarrhea, dehydration, excess salivation, and social withdrawal.
• The vomiting in CVS typically is much more severe and intermittent than that of gastroesophageal reflux.
• • When children with CVS were compared with children with chronic vomiting, children with CVS had a much higher peak rate of emeses per hour (12.6 vs 1.9) but far fewer episodes per month (1.5 vs 36) (Li and Misiewicz, 2003). A cutoff criteria of at least 4 emeses per hour at peak and fewer than 2 episodes per week was 92% sensitive and 100% specific for the final diagnosis of CVS (Pfau, 1996).
  • With a larger cohort, the median peak rate of emeses is still 6 times per hour (Li and Fleisher, 1999). Only Bacillus cereus food poisoning matches this high intensity of emesis (Li and Balint, 2000). This singularly severe vomiting (so-called cyclic vomiting pattern) typifies patients with CVS and helps point toward a disorder that is localized outside the GI tract.
  • Persons with the cyclic pattern (high-intensity, low-frequency) tend to have extraintestinal disorders (eg, neurologic, renal, metabolic, endocrine), whereas persons with a chronic vomiting pattern (low-grade, daily) tend to have upper GI injury such as gastroesophageal reflux and gastritis (Li and Balint, 2000).
• The emesis is often projectile (48%) and frequently contains bile (81%), mucous (72%), and blood (34%) (Li and Misiewicz, 2003). Hematemesis is more often due to retrograde herniation of the gastric cardia through the gastroesophageal junction (ie, prolapse gastropathy) than to a classic Mallory-Weiss tear (Li and Hayes, unpublished data, 1999; Shepherd, 1984).
• The "on-off" stereotypical pattern often begins with a half-hour prodrome of nausea and pallor. Vomiting peaks in the first hour and then begins to decline over the ensuing 4-8 hours, lasting a mean of 24 hours (median, 43 h). Episodes commonly occur in the early morning (2-4 am) or upon awakening (6-8 am). The recovery period from the end of vomiting to the point of being able to eat and play lasts a mere 5 hours. Despite the label cyclic, only one half of patients have a stable periodicity, and the rest have sporadic intervals (Li and Balint, 2000).
• Besides vomiting, patients may also experience other GI symptoms.
• • Abdominal pain is present in 80% of patients and may initially be severe enough to mimic acute abdomen and result in a laparotomy (Li and Fleisher, 1999). Patients may also have epigastric pain secondary to peptic injury of the esophagus.
  • Besides vomiting (100%), most patients experience retching (79%) and nausea (82%) (Li and Misiewicz, 2003). Most patients describe the nausea to be the most distressing symptom. It is unrelenting, completely unrelieved by vomiting, and disappears only when the child is asleep or the episode is over.
  • Many of the behavioral symptoms commonly observed in patients with CVS (eg, fetal positioning, social withdrawal, turning off lights and televisions) are attempts to lessen nausea (Li and Balint, 2000).
  • Approximately one third of patients also experience fever and/or diarrhea, complicating differentiation from gastroenteritis (Li and Hayes, unpublished data, 1999).
• Autonomic symptoms are also common, particularly lethargy (93%) and pallor (91%) (Li and Misiewicz, 2003). Lethargy may be profound, and patients may be unable to walk or talk or may appear comatose. Excess salivation (27%) can also be dramatic (Li and Misiewicz, 2003).
• Many patients with CVS have neurologic symptoms, which supports the relationship between migraines and CVS. Symptoms include headache (42%), photophobia (38%), phonophobia (30%), and vertigo (26%). Because fewer than one half of patients with CVS have classic migraine symptoms, this precludes using the symptoms as diagnostic criteria for a migraine variant (Li and Misiewicz, 2003).
• Approximately 68% of families are able to identify events that appear to precipitate a patient's episode (Cullen, 1963; Withers, 1998; Li and Fleisher, 1999; Hoyt, 1960).
• • The most common precipitating event is infection (41%), particularly chronic sinusitis (Li and Balint, 2000).
  • Psychological stresses (34%) and food products, including chocolate, cheese, and monosodium glutamate (MSG), rank close behind chronic sinusitis (Li and Balint, 2000). Positive excitement, such as birthdays, holidays, vacations, and school outings, appear to trigger more episodes than do negative stresses.
  • Others recognize physical exhaustion or lack of sleep (18%), atopic events (13%), motion sickness (9%), and menses (13%) as triggers (Li and Balint, 2000).
  • Many patients experience remission in the summer, when the number of infections and school stressors decline (Li, 1995).
• The terms CVS and abdominal migraine have often been used interchangeably because of overlap in clinical criteria. Indeed, the key criteria, except vomiting, in abdominal migraines are identical to those in CVS: recurrent, stereotypical, and severe episodes of abdominal pain; punctuating well periods; autonomic symptoms (eg, pallor, lethargy); and a family history of migraine headaches. Because 80% of children with CVS have abdominal pain, and 50% of those with abdominal pain vomit, many children can be diagnosed with either CVS or abdominal migraine. When both symptoms occur, the authors use the predominant or most consistent symptom as the primary label.
• The following 3 additional criteria help strengthen the diagnosis of CVS (Li and Balint, 2000):
• • Negative screening test results to exclude common GI, hepatobiliary, renal, metabolic, and endocrine disorders
  • Subsequent development of migraine headaches
  • A positive response to antimigraine medications

DIFFERENTIALS

Section 4 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
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• References

Other Problems to be Considered

Gastrointestinal disorders
Gastroesophageal reflux disease (peptic esophagitis)
Peptic disorders (gastritis, duodenitis, Helicobacter pylori infection)
Inflammatory bowel disease (Crohn disease, Ulcerative colitis)
Anatomic obstruction (malrotation with intermittent volvulus)
Hirschsprung disease
Intestinal pseudoobstruction
Cholelithiasis (gallbladder dyskinesia)
Choledochal cyst
Chronic appendicitis
Recurrent pancreatitis

Neurologic disorders
Abdominal migraine with vomiting
Migraine headaches with vomiting
Chronic sinusitis
Subtentorial neoplasm (cerebellar medulloblastoma, brainstem glioma)
Chiari malformation
Familial dysautonomia (Riley-Day syndrome)

Renal disorders
Acute hydronephrosis secondary to uteropelvic junction obstruction
Nephrolithiasis

Metabolic disorders
Disorders of fatty acid oxidation
Urea cycle defects
Mitochondriopathy
Acute intermittent porphyria

Endocrine disorders
Addison disease
Diabetes mellitus with ketoacidosis
Pheochromocytoma
Hyperemesis gravidum

Psychological disorders
Munchausen syndrome by proxy
Anxiety
Depression
Bulimia

Other
Pregnancy

WORKUP

Section 5 of 10  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• A heterogeneous group of disorders can mimic cyclic vomiting syndrome (CVS), and these disorders must be excluded with systematic laboratory and radiographic testing. An analysis by Li and colleagues (1998) demonstrated 3 main categories to consider in the differential diagnoses: gastrointestinal disorders, extraintestinal disorders, and idiopathic CVS.
• When evaluating for GI diseases, screening blood work should include a CBC count with differential, erythrocyte sedimentation rate (ESR), and levels of hepatic transaminases, pancreatic amylase, and lipase.
• Nonanatomic renal disease can be detected using serum BUN and creatinine tests, urinalysis, and urine calcium-to-creatinine ratio (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).
• Screening for multiple metabolic and endocrine disorders can be accomplished by assessing electrolytes, pH, glucose, lactic acid, ammonia, amino acids, ACTH, and antidiuretic hormone (ADH).
• Urinary ketones, organic acids, ester-to-free carnitine ratio, porphobilinogen, and aminolevulinic acid may also guide diagnosis in the correct direction (Li, Int Semin Pediatr Gastroenterol Nutr, 2000). These metabolic and endocrine tests must be obtained during the episode to detect intermittent disorders (eg, disorder of fatty acid oxidation) or heterozygote disorders (eg, partial ornithine transcarbamylase deficiency).
• Blood and urine tests must be obtained before starting intravenous fluids that contain glucose or other medical treatments.
• In a postmenarchal girl, the physician must consider a beta human chorionic gonadotropin (bhCG) test for pregnancy (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).

Imaging Studies

• When evaluating for GI diseases, an upper GI (UGI) with small-bowel followthrough (SBFT) radiography, esophagogastroduodenoscopy (EGD), abdominal ultrasonograph, or CT and gastric-emptying scans may provide definitive information (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).
• When evaluating for neurologic or otolaryngologic diseases, a sinus CT scan or brain MRI should be considered (Li, Int Semin Pediatr Gastroenterol Nutr, 2000). CT scans may not adequately visualize the subtentorial region.
• Obstructive renal disease can be revealed with renal ultrasonography or CT imaging (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).
• With a broad array of possible diagnoses and possible diagnostic approaches, an extensive evaluation may appear cumbersome. Recently, Olson and Li reported that UGI radiography followed by empiric antimigraine therapy for 2 months is the most cost-effective approach (US $1600) for the initial treatment of recurrent episodic vomiting in children (US $3020 for extensive diagnostic evaluation, and US $1830 for empiric treatment alone) (Olson and Li, 2002). Until prospective trials are conducted, the authors' current approach generally includes initial blood and urine screens, including metabolic screening and UGI at initial presentation.
• The presence of specific symptoms such as hematemesis, bilious vomiting, persistent headache, flank pain, acidosis, or uncharacteristically severe or atypical vomiting episodes should raise the clinician's index of suspicion of an underlying disorder and should warrant a prompt and more extensive or repeat evaluation (Olson and Li, 2002). The 4 tests with the highest yield include endoscopy, sinus radiography or CT imaging, small-bowel radiography, and head CT imaging or MRI (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).

Other Tests

• A psychological evaluation may reveal ongoing panic, anxiety, and eating disorders, and stress management may attenuate the stress triggers (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).

TREATMENT

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Medical Care

Pharmacologic therapy is used to prevent episodes of vomiting or to decrease their frequency. Other medications may be used to abort or attenuate episodes once they begin. Preventive medications are normally used in patients with more than a single episode of cyclic vomiting syndrome (CVS) per month. The mainstays of prophylactic therapy include cyproheptadine, amitriptyline, propranolol, phenobarbital, and erythromycin. When prophylactic agents fail or episodes occur infrequently, abortive agents such as ondansetron and sumatriptan may be used. If abortive therapy fails, supportive combinations such as ondansetron plus lorazepam or chlorpromazine plus diphenhydramine may attenuate an attack of cyclic vomiting in progress.

• In the absence of known pathophysiology, treatment of CVS remains empiric (Li and Fleisher, 1999; Forbes, 1995). The following 5 management strategies are used for CVS: avoidance of triggers, prophylactic pharmacotherapy, abortive therapy, supportive care during acute episodes, and family support (Li and Balint, 2000).
• In some instances, avoiding identified dietary triggers such as chocolate, cheese, and MSG can prevent episodes without the use of medication (Li and Balint, 2000). If psychological stressors trigger episodes, stress management techniques or benzodiazepine anxiolytics (lorazepam or diazepam) may help to abort attacks in the early stages. However, avoiding common triggers such as car rides and infection may be impractical or impossible. Interestingly, a 70% decrease in frequency of episodes (placebo effect) upon consultation and lifestyle changes without drug therapy has been noted (Fleisher, 1995).
• Daily prophylactic pharmacotherapy may be used to prevent episodes that occur more than once per month or if they are extremely severe and disabling, (eg, lasting >3 d) (Li, 1993; Li, 1996). Most of these drugs are non-GI medications such as antimigraine agents, anticonvulsants, neuroleptics, and prokinetic drugs. A family history positive for migraines predicts a high response rate (80%) to antimigraine medications; therefore, these agents are a logical first choice (Li and Balint, 2000).
• In an open-label experience, with efficacy defined as greater than 50% reduction in episode frequency or severity, propranolol, cyproheptadine, and amitriptyline were effective 57%, 39%, and 67% of the time, respectively (Li and Hayes, unpublished data, 1999; Pfau, 1996; Andersen, 1997). The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines recommend cyproheptadine as first-line therapy in children younger than 5 years. However, cyproheptadine can cause substantial weight gain because of an increase in appetite. Amitriptyline is the first-line choice in children older than 5 years and adolescents (Li and Balint, 2000). Phenobarbital demonstrated a 79% success rate in one open-label trial in children who did not have EEG changes (Gokhale, 1997). Erythromycin, a gastric prokinetic agent, demonstrated a 75% success rate in one open-label study (Vanderhoof, 1993).
• Recently, Winner et al reported a significant reduction (>75%) in days with migraine headaches in patients receiving topiramate compared with placebo (Winner, 2005). Topiramate is currently used anecdotally in patients with CVS. Another recent small therapeutic trial using L-carnitine reported reduced episode frequency and neurologic symptoms in patients with CVS (Van Calcar, 2002).
• Abortive agents may be taken at the onset of an attack to stop progression when prophylactic medication fails or is not taken because of the sporadic and infrequent occurrence of CVS episodes (<1/mo). These antinausea and antimigraine agents are best administered nasally, rectally, or parenterally, as they are not usually tolerated by mouth in the face of intractable emesis (Li, Int Semin Pediatr Gastroenterol Nutr, 2000). Sumatriptan, a 5-hydroxytryptamine receptor 1B/1D (5-HT_1B/1D) agonist used off-label, has a 46% efficacy rate when administered either intranasally or subcutaneously. The subcutaneous route has fallen out of favor because of a severe associated burning sensation in the chest and neck (Benson, 1995; Li and Hayes, 1999).
• Ondansetron, a 5-hydroxytryptamine receptor 3 (5-HT₃) antagonist, is a potent and effective antiemetic that acts on the chemoreceptor zone in the brainstem. In CVS, it is more effective at a higher dose of 0.3-0.4 mg/kg every 6 hours and is rendered more effective in severe episodes with use of a benzodiazepine or diphenhydramine as an adjunctive antinausea agent (Li and Misiewicz, 2003). High-dose intravenous ondansetron has a 59% efficacy rate and ameliorates, more often than aborts, episodes (Li and Kagawalla, 2002). Aprepitant, a promising tachykinin (NK-1)-receptor antagonist, is used for chemotherapy-induced emesis and could have benefit in CVS (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).
• When both prophylactic and abortive therapy fail, supportive care becomes an essential aspect of treatment during acute episodes. Intravenous glucose-containing fluids may diminish the severity of episodes by up to 42% (Li, Int Semin Pediatr Gastroenterol Nutr, 2000). Glucose may be the active ingredient by truncating the ketosis. However, the abdominal pain may be severe enough to require nonsteroid anti-inflammatory drugs (NSAIDs) or narcotics once a surgical abdomen has been excluded. Sedatives such as diphenhydramine, lorazepam, and chlorpromazine have been administered to permit sleep and to provide temporary respite from unrelenting nausea (Li, Int Semin Pediatr Gastroenterol Nutr, 2000). The combined use of lorazepam and ondansetron appears to be more effective than ondansetron alone.

MEDICATION

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Drug Category: Antiemetic agents

The CNS vomiting center (VC) may be stimulated directly by GI irritation, motion sickness, or vestibular neuritis. Increased activity of central neurotransmitters, such as dopamine in the chemoreceptor trigger zone (CTZ) or acetylcholine in the VC, appear to be major mediators of vomiting. An emetogenic episode may initiate the release of serotonin (5-HT) from enterochromaffin cells in the GI tract. 5-HT then binds to 5-HT₃ receptors that stimulate vagal neurons that transmit signals to the VC, resulting in nausea and vomiting. Pharmacologic agents are directed to the particular etiology or mechanism that stimulates the vomiting response.

FOLLOW-UP

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Deterrence/Prevention

• In some instances, avoiding identified dietary triggers such as chocolate, cheese, and MSG can prevent episodes without the use of medication (Li and Balint, 2000).
• If psychological stresses trigger episodes, stress management techniques or benzodiazepine anxiolytics (lorazepam or diazepam) may help abort attacks. However, avoiding common triggers such as car rides and infection may be impractical or impossible.
• Interestingly, consultation with a sympathetic gastroenterologist without drug therapy may decrease the frequency of episodes up to 70% (Li, Int Semin Pediatr Gastroenterol Nutr, 2000).

Prognosis

• Most published series indicate that cyclic vomiting syndrome (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. The fact that some children with CVS progress to abdominal migraines and then to migraine headaches implies that a sequential progression of age-dependent manifestations of migraines may exist.
• A survey by Abu-Arafeh and colleagues (1995) revealed the mean ages of children with CVS, abdominal migraines, and migraine headaches to be 5.3, 10.3, and 11.5 years, respectively. This supports the developmental progression from vomiting to abdominal pain to headache.
• In unpublished data, Li and Hayes found that nearly one third of patients develop migraines after resolution of CVS and predict that nearly 75% develop migraines by age 18 years (Li and Hayes, 1999).

MULTIMEDIA

Section 9 of 10  

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• References

Media file 1:  Cyclic versus chronic temporal patterns of recurrent vomiting. The number of emeses is plotted over a 2-month period. The chronic pattern, represented by a thin dashed line, has low grade on nearly a daily basis (eg, gastroesophageal reflux). The cyclic pattern, represented by a heavy solid line, involves high-intensity episodes intermittently once every several weeks (eg, cyclic vomiting syndrome).
	View Full Size Image
Media type:  Graph

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
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• References

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Article Last Updated: Sep 12, 2006