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Cyclic vomiting syndrome

Cyclic Vomiting Syndrome (CVS) is a digestive disorder whose symptoms are recurring attacks of nausea, vomiting and abdominal pain for both children & adults. It has been recognized only since around 1995. This disease affects millions of people worldwide.

The cause of CVS has not been determined yet, although there are some professionals who are able to detect and cure CVS.

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Autism: a medical primer
From American Family Physician, 11/1/02 by Christopher D. Prater

Recognition of the disorder called autism may have its origin in Itard's 1801 description of the "wild boy of Aveyron," a violent child with no language skills who related to other people as if they were objects. It was not until 1943 that Kanner identified a complex set of characteristics (e.g., aberrations in social development, verbal and nonverbal communication, symbolic thinking) for a syndrome he labeled "autism."

Although Kanner theorized that a single, biologically based defect was responsible for the development of autistic disorders, treatment in the 1950s and 1960s was dominated by the psychodynamic theory of the etiology of autism that charged that pathologic parenting was responsible for the withdrawal of children from their environment. Following the 1970s discovery of neuroreceptors, endogenous neurohormones, and the stereospecific binding sites of neuropeptides to neurons, clinicians have discounted the psychodynamic theory of autism and repostulated Kanner's original supposition that biologically based deficits are responsible for the etiology of autism.


Autistic disorder is a pervasive developmental disorder defined behaviorally as a syndrome consisting of abnormal development of social skills (withdrawal, lack of interest in peers), limitations in the use of interactive language (speech as well as nonverbal communication), and sensorimotor deficits (inconsistent responses to environmental stimuli). (1,2) In this article, the more generic terms autism and autistic refer to the broad spectrum of pervasive developmental disorders that exhibit autistic features as their primary presenting behaviors. The term autistic disorder is used to describe the specific developmental disorder that occurs at the more severely affected end of this spectrum (Table 1). (1)

The development of impairments in autistic persons is varied (Table 2 (1)) and characteristically uneven, resulting in good skills in some areas and poor skills in others. Echolalia, the involuntary repetition of a word or a sentence just spoken by another person, is a common feature of language impairment that, when present, may cause language skills to appear better than they really are. There may also be deficiencies in symbolic thinking, stereotypic behaviors (e.g., repetitive nonproductive movements of hands and fingers, rocking, meaningless vocalizations), self-stimulation, self-injury behaviors, and seizures. Mental retardation is not a diagnostic criterion, but it is frequently present in the moderate to severe range.


In general, pervasive developmental disorders are estimated to occur at a rate of 63 per 10,000 persons. (3) While the reported incidence of autistic disorder ranges from about five per 10,000 (4) to 20 per 10,000 persons, (5) a recent meta-analysis reports the median rate for 11 surveys conducted since 1989 to be seven per 10,000 persons. (6) Male-to-female ratios vary with IQ scores from 2:1 in severely handicapped persons to 4:1 in moderately handicapped persons. (7) [Evidence level B, non-randomized studies] The occurrence rate in siblings is suspected to be from 3 to 7 percent, representing a 50- to 100-fold increase in risk. (8)


No single cause has been identified for the development of autism. Genetic origins are suggested by studies of twins and a higher incidence of recurrence among siblings. (9) In addition, an increased frequency of occurrence is noted in patients with genetic conditions such as fragile X syndrome and tuberous sclerosis. (10) Some reports have suggested a possible association with Down syndrome. (11)

In addition to the implication of neurotransmitters, such as serotonin, in the development and expression of autism, (12) many other disorders may result in brain dysfunction. Possible contributing factors in the development of autism include infections, errors in metabolism, immunology, lead poisoning, and fetal alcohol syndrome. (13)

Concerns have been raised in recent years that immunizations, particularly measles, mumps, and rubella (MMR) vaccine, may precipitate autism. In addition to reports from several parents who first detected autism in their children following an MMR vaccination at 12 to 15 months of age, an anecdotal study (14) reported similar suspicions on the part of physicians who provided care for 12 autistic patients. Subsequent studies in the United Kingdom (15,16) [reference 16, Evidence level B: epidemiologic study] and the United States (17) [Evidence level B: epidemiologic study] have failed to show an association between any vaccine and the development of autism. Information about ongoing studies being conducted by the Centers for Disease Control and Prevention and the National Institutes of Health (NIH) is available at their Web sites (Table 3).

Recognition and Screening

Indications for formal developmental evaluation include no babbling, pointing, or other gestures by 12 months of age, no single words by 16 months of age, no two-word spontaneous phrases by 24 months of age, and loss of previously learned language or social skills at any age. (18) Parental concerns about delayed speech and language development, typically noticed at about 18 months of age, should always be taken seriously.

Including developmental surveillance as a routine part of the well-child examination can enhance recognition of developmental disorders. While the Denver screening tools (19) have historically been used in primary care settings for routine developmental surveillance, they lack the sensitivity and specificity necessary for use as screening tools for developmental disorders. (20) More specific and sensitive screening surveillance tools, such as the Parents' Evaluation of Developmental Status (PEDS), (21) are available for assessing these conditions. Screening tools that are specific for autism include the Checklist for Autism in Toddlers (CHAT) (22) (Table 4 (23)) and the Pervasive Developmental Disorders Screening Test-Stage I (PDDST). (24) For a comprehensive review of available screening tools, the authors recommend an article by Filipek and colleagues. (18)

When an autistic disorder is suspected, referral should be made for further developmental evaluation and cognitive testing. Although there is currently no cure for autism, early diagnosis and initiation of structured multidisciplinary intervention can significantly enhance functioning in later life. (23) Experienced clinicians can reliably diagnose autism in children younger than three years and, frequently, as young as two years. Presently no biologic markers are available to identify patients with autistic disorders. Useful resources for identifying clinicians with expertise in the diagnosis of autism include the University Affiliated Program system and the National Institute of Child Health and Human Development (Table 3).

Once an autistic disorder is suspected, certain medical evaluations should be performed. A family history of limited cognitive abilities or the presence of dysmorphic features may suggest the need for genetic evaluation. Wood's light examination of the skin should be performed to help identify the depigmented macules of tuberous sclerosis. Lead screening and metabolic testing should be considered if there is a history of lethargy, cyclic vomiting, early seizures, dysmorphic features, or mental retardation. Electrophysiologic testing such as electroencephalography and central nervous system imaging studies are warranted to evaluate neurologic features that cannot be explained by the diagnosis of autism alone. (18) Because deafness or profound hearing loss can cause symptoms mimicking autism, a formal hearing evaluation should be given if the diagnosis of autism is being considered.

Autistic disorders should be distinguished from other psychiatric and pervasive developmental disorders. Table 5 (1) lists a differential diagnosis for several similar disorders.

Clinical Course

The typical presenting symptoms of autistic disorder are delayed speech or challenging behavior before three years of age. (7) Although parents frequently see these signs and suspect that something is wrong with their child by 18 months of age, a diagnosis of autism is frequently delayed by two to three years because of reluctance on the part of clinicians and families to incorrectly label a child as autistic. (25) Seventy-five percent of autistic persons have some level of mental retardation. (1) Developmental gains in childhood and adolescence are common, but some persons have behavioral regression during adolescence.

Low IQ scores and failure to develop communicative language by five years of age correlate positively with a poor prognosis for response to treatment. (1) About one third of autistic persons can achieve some degree of independent living, (1) although fewer than 5 percent go on to become self-sufficient adults. (13) Development of stereotypic behavior, self-injury behavior, and selective attention toward distracting stimuli (e.g., a ticking clock) markedly interfere with structured learning and working environments. (13)

Many autistic persons develop seizures in their first year of life in the form of infantile spasms, a particularly severe form of seizure that is difficult to treat. There is also a significant incidence of first occurrence of seizures during adolescence, (26) and as many as 35 percent may develop seizures by adulthood. (18) Comorbid anxiety is common, (27) as are depression and obsessional behavior. (28)

Management of Autism and Comorbid Conditions

The general goals of treatment for autistic patients are to improve language and social skills, decrease problem behaviors, support parents and families in their adjustment to and education of autistic children, and foster independence. Because autistic children who begin treatment at a young age have significantly better outcomes, (24) early intervention is critical. Public Law 99-457 and the Individuals with Disabilities Education Act (29) mandate referral to the special services departments of local preschool or school systems.

Because no treatment protocol meets the needs of every autistic child, it is helpful to get suggestions from a variety of sources. Organizations available to help families and educators are listed in Table 3.


Primary care physicians are commonly asked to address the stereotypic or disruptive behaviors of autistic patients. While numerous medications have been used to treat autistic symptoms, no single medication has been shown to be universally effective. Historically, psychotropic medications have been reserved for use in situations where all attempts at behavior management have failed, and the patients are considered to be harmful to themselves or others.

While use of behavior modification programs is often the primary method of managing challenging behaviors in autistic children, supportive medication use has been found to help reduce behavior problems. Obtaining a correct diagnosis is important before initiating any pharmacologic intervention. For example, attention deficit with or without hyperactivity can coexist with autism and may possibly be managed with the use of methylphenidate (Ritalin) (30) [Evidence level C: consensus opinion] or clonidine (Catapres). (31) [Evidence level C: consensus opinion] It can be difficult to distinguish between the behaviors associated with autism; attention-deficit/hyperactivity disorder; and mania, and an appropriate treatment for one disorder may be ineffective or exacerbate the symptoms of another.

When behavior management programs or the use of supportive medications are unsuccessful in correcting potentially dangerous behavior, the use of sedating medications may be necessary for brief periods while less invasive interventions are attempted. Sedative-hypnotics and neuroleptics such as buspirone (BuSpar), in a dosage of 5 to 20 mg two to three times a day (32) [Evidence level C: consensus opinion], or risperidone (Risperdal), in a dosage of 0.5 to 2 mg twice a day (33) are commonly used for this purpose. Benzodiazepines should be used with caution because they can cause disinhibition, resulting in more excitable behavior. (32)

Objective data collection and outcome monitoring are important because of the variable nature of individual responses to medication. Information should be collected by persons who have regular contact with the patient--family members, support personnel in day care and residential programs, case managers, and physicians. Given the multiple developmental, behavior, and medical problems associated with autism, coordination of services by a multidisciplinary team is highly recommended. (34) [Evidence level C: consensus opinion]


A number of methods for teaching communication and socialization skills have been developed over the years. One recent example is augmented communication, a method whereby nonverbal persons are assisted in communication by means of a letter board or a computer keyboard. When a facilitator helps the person choose letters, words, etc., the process is referred to as facilitated communication. While augmented communication devices have markedly improved communication potential in some patients, numerous controlled studies have failed to show that facilitated communication is reliably useful. (13)

Another treatment currently being advocated is auditory integration training (AIT), whereby persons with autism typically spend 10 hours during a two-week period listening to music that has been computer-modified to remove sensitive frequencies and reduce predictable patterns. AIT is said to improve auditory processing capabilities by correcting distortions in hearing and by conditioning patients to focus their attention more appropriately. Unfortunately, this technique also has little supporting scientific documentation. (35)

Another popular behavior-based intervention is the Lovaas program, (36) sometimes referred to as DTT because of its use of positive reinforcement through a series of intensive discrete trial training sessions. While initial reports suggested a 47 percent recovery rate from autism when preschoolers were treated, (36) subsequent studies have been unable to document long-term gains. (37) Studies using similar behavior interventions, however, have been able to document short-term improvements. (37) Verification of long-term success becomes important in view of the cost of such intensive treatment programs, which typically require extensive one-on-one training with autistic children for 40 hours a week for a minimum of two years--a cost of approximately $40,000 a year. (38) Controversies about fiscal responsibility are ongoing because some parents feel local school systems should make this level of care available for their children. (38)

Other interventional strategies include deep pressure therapy, nutritional supplements, and specialty diets. (39-42) [reference 40, Evidence level A: randomized controlled trial (RCT); reference 42, Evidence level C: consensus opinion] Anecdotal reports of success with alternative or complementary interventions are common, but efficacy in most cases remains clinically unproven. Generally speaking, most successful programs have several common components: (1) recognition of the importance of early identification and intervention; (2) use of behavior-oriented strategies (Table 6 (13)); (3) development of social communication; and (4) active involvement of parents and families.

Recently, there has been discussion about a possible role of the gastric hormone secretin as a pharmacologic intervention in the treatment of autism. This information was based on one study of three autistic persons. (43) Unfortunately, a subsequent study involving 56 autistic persons failed to support the initial findings. (44) [Evidence level B: lower quality RCT] At present, most investigators do not see a role for secretin in the treatment of autism, an opinion supported by ongoing research at the NIH.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.


(1.) American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: American Psychiatric Association, 1994:65-78.

(2.) World Health Organization. ICD-10: international statistical classification of diseases and related health problems. Geneva: World Health Organization, 1992.

(3.) Chakrabarti S, Fombonne E. Pervasive developmental disorders in preschool children. JAMA 2001;285:3093-9.

(4.) Fombonne E, Du Mazaubrun C, Cans C, Grandjean H. Autism and associated medical disorders in a French epidemiological survey. J Am Acad Child Adolesc Psychiatry 1997;36:1561-9.

(5.) Bryson SE. Epidemiology of autism. J Autism Dev Disord 1996;26:165-7.

(6.) Fombonne E. The epidemiology of autism: a review. Psychol Med 1999;29:769-86.

(7.) Bryson SE. Epidemiology of autism: Overview and issues outstanding. In: Cohen DJ, Volkmar FR, eds. Handbook of autism and pervasive developmental disorders. 2d ed. New York: Wiley, 1997:41-6.

(8.) Rutter M, Bailey A, Simonoff E, Pickles A. Genetic influences and autism. In: Cohen DJ, Volkmar FR, eds. Handbook of autism and pervasive developmental disorders. 2d ed. New York: Wiley, 1997: 370-87.

(9.) Szatmari P, Jones MB, Zwaigenbaum L, MacLean JE. Genetics of autism: overview and new directions. J Autism Dev Disord 1998;28:351-68.

(10.) Baker P, Piven J, Sato Y. Autism and tuberous sclerosis complex: prevalence and clinical features. J Autism Dev Disord 1998;28:279-85.

(11.) Howlin P, Wing L, Gould J. The recognition of autism in children with Down syndrome--implications for intervention and some speculations about pathology. Dev Med Child Neurol 1995;37:406-14.

(12.) Anderson GM, Hoshino Y. Neurochemical studies of autism. In: Cohen DJ, Volkmar FR, eds. Handbook of autism and pervasive developmental disorders. 2d ed. New York: Wiley, 1997:325-43.

(13.) Farber JM. Autism and other communication disorders. In: Capute AJ, Accardo PJ, eds. Developmental disabilities in infancy and childhood. 2d ed. Baltimore, Md.: Brookes, 1996:347-64.

(14.) Wakefield AJ, Murch SH, Anthony A, Linnell J, Casson DM, Malik M, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998; 351:637-41.

(15.) Miller D, Wadsworth J, Diamond J, Ross E. Measles vaccination and neurological events. Lancet 1997; 349:730-1.

(16.) Taylor B, Miller E, Farrington CP, Petropoulos MC, Favot-Mayaud I, Li J, et al. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 1999;353:2026-9.

(17.) DeStefano F, Chen RT. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. J Pediatr 2000; 136:125-6.

(18.) Filipek PA, Accardo PJ, Baranek GT, Cook EH Jr, Dawson G, Gordon B, et al. The screening and diagnosis of autistic spectrum disorders. J Autism Dev Disord 1999;29:439-84.

(19.) Frankenburg WK, Dodds J, Archer P, Shapiro H, Bresnick B. The Denver II: a major revision and restandardization of the Denver Developmental Screening Test. Pediatrics 1992;89:91-7.

(20.) Sciarillo WG, Brown MM, Robinson NM, Bennett FC, Sells CJ. Effectiveness of the Denver Developmental Screening Test with biologically vulnerable infants. J Dev Behav Pediatr 1986;7:77-83.

(21.) Glascoe FP. Collaborating with parents: using parents' evaluation of developmental status to detect and address developmental and behavioral problems. Nashville: Ellsworth & Vandermeer, 1998.

(22.) Baron-Cohen S, Allen J, Gillberg C. Can autism be detected at 18 months? The needle, the haystack, and the CHAT. Br J Psychiatry 1992;161:839-43.

(23.) Baird G, Charman T, Cox A, Baron-Cohen S, Swettenham J, Wheelwright S, et al. Current topic: screening and surveillance for autism and pervasive developmental disorders. Arch Dis Child 2001; 84:468-75.

(24.) Siegel B. Early screening and diagnosis in autism spectrum disorders: the pervasive developmental disorders screening test (PDDST). NIH State of the Science in Autism: Screening and Diagnosis Working Conference, Bethesda, Md., June 15-17, 1998.

(25.) Filipek PA, Accardo PJ, Ashwal S, Baranek GT, Cook EH Jr, Dawson G, et al. Practice parameter: screening and diagnosis of autism: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society. Neurology 2000;55:468-79.

(26.) Gillberg C, Steffenburg S. Outcome and prognostic factors in infantile autism and similar conditions: a population-based study of 46 cases followed through puberty. J Autism Dev Disord 1987;17: 273-87.

(27.) Muris P, Steerneman P, Merckelbach H, Holdrinet I, Meesters C. Comorbid anxiety symptoms in children with pervasive developmental disorders. J Anxiety Disord 1998;12:387-93.

(28.) Kobayashi R, Murata T. Behavioral characteristics of 187 young adults with autism. Psychiatry Clin Neurosci 1998;52:383-90.

(29.) Individuals with Disabilities Education Act-IDEA '97. Public Law 1997;105-17.

(30.) Arnold LE, Gadow K, Pearson D, Varley C. Stimulants. In: Reiss S, Aman MG, eds. Psychotropic medications and developmental disabilities: the international consensus handbook. Columbus, Ohio: Ohio State University Nisonger Center, 1998: 229-43.

(31.) Hagerman R, Bregman J, Tirosh E. Clonidine. In: Reiss S, Aman MG, eds. Psychotropic medications and developmental disabilities: the international consensus handbook. Columbus, Ohio: Ohio State University Nisonger Center, 1998:259-69.

(32.) Werry JS. Anxiolytics and sedatives. In: Reiss S, Aman MG, eds. Psychotropic medications and developmental disabilities: the international consensus handbook. Columbus, Ohio: Ohio State University Nisonger Center, 1998:201-14.

(33.) Demb HB, Espiritu C. The use of risperidone with children and adolescents with developmental disabilities: effects on some common challenging behaviors. Ment Health Aspects Dev Disabil 1999; 2:73-82.

(34.) Volkmar F, Cook EH Jr, Pomeroy J, Realmuto G, Tanguay P. Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders. J Am Acad Child Adolesc Psychiatry 1999;38(12 suppl):32S-54S.

(35.) Rimland B, Edelson SM. Auditory integration training in autism: a pilot study. Autism Research Institute 1992;112:1-7.

(36.) Lovaas OI, Smith T. A comprehensive behavioral theory of autistic children: paradigm for research and treatment. J Behav Ther Exp Psychiatry 1989; 20:17-29.

(37.) Sheinkopf SJ, Siegel B. Home-based behavioral treatment of young children with autism. J Autism Dev Disord 1998;28:15-23.

(38.) Mauk JE, Reber M, Batshaw ML. Autism and other pervasive developmental disorders. In: Batshaw ML, ed. Children with disabilities. 4th ed. Baltimore, Md.: Brookes, 1997:425-47.

(39.) Grandin T. Thinking in pictures: and other reports from my life with autism. New York: Vintage Books, 1996:62-81.

(40.) Rimland B, Callaway E, Dreyfus P. The effect of high doses of vitamin [B.sub.6] on autistic children: a double-blind crossover study. Am J Psychiatry 1978; 135: 472-5.

(41.) Rimland B. Megavitamin [B.sub.6] and magnesium in the treatment of autistic children and adults. In: Schopler E, Mesibov GB, eds. Neurobiological issues in autism. New York: Plenum, 1987:389-405.

(42.) Singh NN, Ellis CR, Mulick JA, Poling A. Vitamin, mineral and dietary treatments. In: Reiss S, Aman MG, eds. Psychotropic medications and developmental disabilities: the international consensus handbook. Columbus, Ohio: Ohio State University Nisonger Center, 1997:311-20.

(43.) Horvath K, Stefanatos G, Sokolski KN, Wachtel R, Nabors L, Tildon JT. Improved social and language skills after secretin administration in patients with autistic spectrum disorders. J Assoc Acad Minor Phys 1998;9:9-15.

(44.) Chez MG, Buchanan CP, Bagan BT, Hammer MS, McCarthy KS, Ovrutskaya I, et al. Secretin and autism: a two-part clinical investigation. J Autism Dev Disord 2000;30:87-94.

CHRISTOPHER D. PRATER, M.D., is assistant clinical professor in the Department of Family Medicine at the University of Tennessee College of Medicine, Chattanooga Unit. He also serves as medical director for the Orange Grove Center, a treatment facility in Chattanooga for developmentally delayed children and adults. Dr. Prater received his medical degree from the University of Tennessee College of Medicine, Memphis, and completed a family practice residency at the University of Tennessee in Knoxville.

ROBERT G. ZYLSTRA, ED.D., L.C.S.W., is assistant professor and director of behavioral science in the Department of Family Medicine at the University of Tennessee College of Medicine, Chattanooga Unit. Dr. Zylstra earned a master's degree in social work at the University of Michigan, Ann Arbor, and a doctorate in education at the University of Memphis.

Address correspondence to Robert G. Zylstra, Ed.D., L.C.S.W., Department of Family Medicine, Chattanooga Unit, University of Tennessee College of Medicine, 1100 E. Third St., Chattanooga, TN 37403 (e-mail: Reprints are not available from the authors.

COPYRIGHT 2002 American Academy of Family Physicians
COPYRIGHT 2002 Gale Group

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