Articles On ADD
Articles On ADD
Articles On ADD
ABSTRACT
OBJECTIVE Toreviewtheetiology,diagnosis,andmanagementofattentiondeficitdisorder(ADD)in
adults.
CONCLUSION Attentiondeficitdisorderinadultsrepresentsasubstantialburdenofillness.Itcanbe
diagnosedandtreatedsuccessfully. RSUM
This article has been peer reviewed. Cet article a fait lobjet dune rvision par des pairs. Can Fam Physician 2006;52:961-964.
Vol 52: august aot 2006 CanadianFamilyPhysicianLeMdecindefamillecanadien
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tisimportantforfamilyphysicianstobefamiliarwith attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD). These fairly common conditionshaveaprevalenceof6%to9%inchildrenand 3% to 6% in adults. We once thought that children with ADHDwouldoutgrowtheconditionatpuberty.Wenow know,thankstolong-termfollow-upstudies,thatabout 40%to70%ofchildrenwithADHDwillcontinuetohave residual symptoms throughout adolescence and adulthood.1-3Inadulthood,theconditionisusuallyreferredto asattentiondeficitdisorder(ADD)ratherthanADHD.
Sources of information
PsycINFO,PubMed,andPsychiatry24x7.comweresearched. TwoworksofDrEdwardHallowellandDrJohnRatey,4,5who havewrittenextensivelyonADDinadults,werereviewed. I also drew on my own clinical experience, more than 20 yearsassessingandtreatingadultswithADD.
Case
MsA.,a43-year-oldmarriedwomanwholiveswithher husband and their 3 children, works as a chemist in a research laboratory. She came to her family physician concernedthatshemighthaveADD.Her10-year-oldson had been recently diagnosed with ADHD, and she had noticed similar characteristics in herself. After her son wasdiagnosed,shereadextensivelyonthesubjectand filled out a questionnaire on the Internet. She reported that she has always had trouble concentrating and that she is disorganized, impulsive, and forgetful. She frequently loses or misplaces objects. She has problems managinghertime,especiallyasregardspunctualityand procrastination.Shehasmissedoutonopportunitiesfor promotionatwork,andshefeelslikeanunderachiever. Although her husband is supportive and helps with the housework, she feels overwhelmed by her household chores.Shecallsherhomeadisasterarea.
diagnosis
In 1994, the Diagnostic and Statistical Manual of Mental Disorders,4thedition(DSM-IV),11subdividedADHDinto subtypes:predominantlyinattentivetype;predominantly hyperactive-impulsive type; and combined type. The DSM-IV lists the following diagnostic criteria for ADHD. Patientscouldhavethefirstset,thesecondset,orboth setsofcriteria. Sixormoresymptomsofinattention,includinghaving ashortattentionspan;makingcarelessmistakes;not seemingtolisten;notfollowingthrough;notfinishing projects; being disorganized, impulsive, and forgetful; orfrequentlylosingormisplacingobjects. Six or more symptoms of hyperactivity-impulsivity, includingbeingfidgety,notbeingabletositstill,havinginnerfeelingsofrestlessness,beingalwaysonthe go,talkingtoomuch,beingimpatient,blurtingthings out,orofteninterrupting. Symptoms must be present before age 7; interfere with abilitytofunctioninoccupational,academic,orsocialsettings;persistformorethan6months;manifestinmultiple settings;andnotbeaccountedforbyotherdisorders.
Biologic cause?
Many authors have written about the biologic basis of ADD. Family studies, twin studies, and adoption studies all support a genetic risk of ADD, which is now considered to be one of the most heritable psychiatric disorders.4-8 Environmental factors, such as maternal smoking and drinking during pregnancy, also have a role. Zametkin et al9 postulated that the neurobiologic deficit in ADD was due to frontal cortex hypometabolism. Positron emission tomographic scans of adults with ADD who were diagnosed in childhood showed reduced cerebral glucose metabolism, both global and regional. The largest reductions were in the premotor cortexandthesuperiorprefrontalcortex,areasinvolved incontrollingattentionandmotoractivity. MuchresearchonADDhasfocusedondopaminergic pathways.Thefrontallobes,whicharerichindopamine receptors, have been shown to be smaller in patients withADD.Bushetal10concludedthatthefrontal-striatal circuitryisprobablydysfunctionalinpatientswithADD. Thiscircuitryincludesthecaudate,putamen,anddorsal anteriorcingulate.Theanteriorcingulatefailstoactivate Dr Matas practises psychiatry in Winnipeg, Man.
History of Add
Books about ADD have become bestsellers in recent years, yet ADD is not a new condition. In 1930, it was called minimal brain damage. It was postulated that the condition was caused by birth trauma or low birth weight. In 1960, the name was changed to minimal brain dysfunction. In 1968, it was called hyper-kinetic reactionofchildhood.In1980,thenamewaschanged once again to ADD with or without hyperactivity. In 1987, the label ADHD was introduced. The name keeps changing, but the condition remains the same. Just as ADD is not a new disorder, use of stimulants to treat it is also not new. Amphetamines were first used to treat theconditionin1937.Methylphenidatehasbeenonthe marketsince1955.
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Screening
Attention deficit hyperactivity disorder is a clinical diagnosis, based on presenting symptoms, personal history, andfamilyhistory.Whileratingscales,collateralhistory, report cards, and psychological testing can prove helpful, they are not always available. Two brief screening questionnairesthatcanbefilledoutinadoctorswaiting roomaretheWenderUtahRatingScale,13whichisused tomakearetroactivechildhooddiagnosisofADHD,and theADHDchecklist.14
Comorbid disorders
Biedermanetal15havewrittenextensivelyoncomorbidity in adults with ADD; 75% of patients with ADD also haveatleast1comorbiddisorder.InchildrenwithADD, weoftenseemooddisorders(majordepression,bipolar disorder); tic disorders (including Tourette syndrome); anxiety disorders (social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder);conductdisorders;andlearningdisabilities.In adults,themostcommoncomorbiddisordersaremood disorders, anxiety disorders, substance use disorders, andantisocialpersonalitydisorders.
Management
If patients have more than one comorbid condition, it is besttotreattheconditioncausingthegreatestimpairment first.PatientswithmajordepressionandADDmightrequire both selective serotonin reputake inhibitors for the depression and a stimulant for the ADD. Spencer et al16 wrote a comprehensive review of treating comorbid ADD. Agents that elevate intrasynaptic norepinephrine or dopamine appear to be helpful.17,18 Stimulants, tricyclic antidepressants,andbupropionblockreuptakeofnorepinephrineand dopamine. Stimulants are the first-line treatment for ADD. Morethan250controlledstudieshaveshowntheeffectiveness of stimulants in treating the core symptoms of ADD. About80%ofpatientswithADDwillrespondtostimulants. Methylphenidate (MPH) is usually the first drug prescribed, becauseithaslesspotentialforabusethanamphetamines. If MPH is ineffective, patients might respond to dextroamphetamine. When patients are switched from MPH to dextroamphetamine,theirdoseishalved.
Drug-drug interactions with stimulants are rare; monoamine oxidase inhibitors (MAOIs) are the only absolute contraindication. The most common side effects of stimulants are insomnia, nervousness, diminished appetite, weight loss, and dysphoria. Nausea, stomachache, and headache are usually mild and transitory.Sideeffectsaredose-relatedandcanbelessened or eliminated by lowering the dose. Stimulants should not be prescribed for patients with a recent history of substance abuse. Patients older than 40 should have a baseline electrocardiogram before stimulants are prescribed; heart rate and blood pressure should be monitored.TherecommendedstartingdoseforMPHis10mg twicedaily(8:00 amandnoon).Doseisincreasedin10mg increments at weekly intervals until patients have side effects or better control of symptoms. A typical doseofMPHis10to20mg3timesdaily,althoughsome patientsrequireamuchhigherdoseandothersrequire amuchlowerdose.AsingledoseofMPHlasts4hours, withpeakeffectsin2hours.Longer-actingMPH(RitalinSR)lasts6to8hours.Thereislessreboundanxietywith thelonger-actingformula. New medications include the long-acting preparations MPH HCl (eg, Concerta) and mixed amphetamine salts(AdderallXR).Adderallwastakenoffthemarketby HealthCanada,butwasrecentlyallowedbackon.19 Atomoxetine(Strattera)isthefirstnonstimulantmedicationapprovedfortreatingADHD.Itisnotacontrolledsubstance.Itisaselectivenorepinephrinereuptakeinhibitor20 thatisassociatedwithanincreaseindopamineactivityin the frontal cortex. It takes 1 to 4 weeks to see improvement.Therecommendedstartingdoseis40mgoncedaily. The most common side effects are nausea, dry mouth, sedation or insomnia, appetite suppression, urinary hesitancy, and erectile dysfunction. In some instances, atomoxetine could be a first choice if a patient has a history of drug abuse or a tic disorder. Contraindications include angle-closureglaucomaoruseofMAOIs. Bupropion has been shown to be a safe and effective treatmentforADHD.21-23Itcanbeconsideredafirstchoice ifapatientisasmokerorhasotheraddictions,becauseit has anticraving properties. Side effects are insomnia, agitation,andseizures.Itshouldnotbeprescribedifpatients have a history of seizure disorders or eating disorders. Tricyclics are effective, but they are not as effective as stimulants,andtheirusefulnessislimitedbysideeffects.24 Medication alone might prove insufficient. Patients with ADD might also require counseling, group therapy, family therapy, coaching, tutoring, structure, physical exercise, proper rest, and adequate nutrition. These patientsoftenbenefitfromattendingpeersupportgroups. Theymightalsorequirepsychotherapytohelpthemdeal withunresolvedtraumasorself-esteemissues.
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inattentivetype.Shewastreatedwith10mgofMPH twice daily, which was increased to 10 mg 3 times daily (8:00 am, noon, and 4:00 pm). She and her husbandagreedtoseekcouplescounseling,andshealso chosetoattendasupportgroupforadults.Shereportedthatshewasthinkingmoreclearlyandcouldhave a conversation without interrupting other speakers. Hermindwasnolongerracing,shewassleepingbetter, and she was able to focus clearly. Concentration and memory were improved. She was making an effort to keep to a schedule, which included eating regularmealsandgettingsufficientsleepandphysical exercise. She reported feeling much more in control and more satisfied with her life. Her self-confidence improved,andsheappliedforapromotionatwork.
Conclusion
Attention deficit disorder is frequently unrecognized in adults.Itisworthidentifyingduetothesubstantialburdenofillnessitrepresentsandthepotentialforimprovementwithtreatment. Competing interests None declared Correspondenceto: Dr Manuel Matas, 1200233 Kennedy St, Winnipeg, MB R3C 3J5; e-mail [email protected] References
Attention deficit disorder (ADD) in adults has only recently been acknowledged as a legitimate diagnosis. It has a strong hereditary component. Attention deficit hyperactivity disorder (ADHD) in children is much more common in boys, due to the hyperactivity component. Girls often have the inattentive type of ADHD. In adulthood, the prevalence of ADD among women is almost as high as it is among men. A diagnosis of ADD is made from a clinical history of symptoms and personal and family history. Use of symptom-rating scales can help confirm the diagnosis. Management includes treating comorbid conditions, such as depression. Use of stimulants (methylphenidate and dextroamphetamine are the most common) is well supported in the literature, and other adjunct treatments, such as counseling, tutoring, and attending to diet and exercise, are recommended.
poinTS dE REpRE dU RdACTEUR
1.WenderP.Attention deficit hyperactivity disorder in adults.NewYork,NY:Oxford UniversityPress;1995. 2.BiedermanJ,MickE,FaraoneSV.Age-dependentdeclineofsymptomsofattention deficithyperactivitydisorder:impactofremissiondefinitionandsymptomtype.Am J Psychiatry2000;157(5):816-8. 3.WeissG,HechtmanLT.Hyperactive children grown up.2nded.NewYork,NY:Guilford Press;1993. 4.HallowellEM,RateyJJ.Driven to distraction.NewYork,NY:Simon&Schuster;1994. 5.HallowellEM,RateyJJ.Delivered from distraction.NewYork,NY:BallantineBooks;2005. 6.FaraoneS,BiedermanJ,LehmanBK,KeenanK,NormanD,SeidmanLJ,etal. Evidenceforindependentfamilialtransmissionofattentiondeficithyperactivitydisorderandlearningdisabilities:resultsfromafamilygeneticstudy.Am J Psychiatry 1993;150(6):891-5. 7.CantwellDP.Geneticfactorsinthehyperkineticsyndrome.J Am Acad Child Psychiatry 1976;15:214-23. 8.WelnerZ,WelnerA,StewartM,PalkesH,WishE.Acontrolledstudyofsiblingsof hyperactivechildren.J Nerv Ment Dis1977;165(2):110-7. 9.ZametkinAJ,NordahlTE,GrossM,KingAC,SempleWE,RunseyJ,etal.Cerebral glucosemetabolisminadultswithhyperactivityofchildhoodonset.N Engl J Med 1990;323:1361-6. 10.BushG,FrazierJA,RauchSL,SeidmanLJ,WhalenPJ,JenikeMA,etal.Anteriorcingulatecortexdysfunctioninattentiondeficit/hyperactivitydisorderrevealedbyfMRI andtheCountingStroop.Biol Psychiatry1999;45(12):1542-52. 11.AmericanPsychiatricAssociation.Diagnostic and statistical manual of mental disorders.4thed.Washington,DC:AmericanPsychiatricAssociation;1994. 12.SoldenS.Women with attention deficit disorder.GrassValley,Calif:UnderwoodBooks;1995. 13.WardMF,WenderPH,ReimherrFW.TheWenderUtahRatingScale:anaidinthe retrospectivediagnosisofattentiondeficithyperactivitydisorder.Am J Psychiatry 1993;150(6):885-90. 14.BarkleyRA.Attention deficit hyperactivity disorder: a handbook for diagnosis and treatment.NewYork,NY:GuilfordPress;1990. 15.BiedermanJ,FaraoneSV,SpencerT,WilensT,NormanD,LapeyKA,etal.Patternsof psychiatriccomorbidity,cognitionandpsychosocialfunctioninginadultswithattentiondeficithyperactivitydisorder.Am J Psychiatry1993;150(12):1792-8. 16.SpencerT,BiedermanJ,FaraoneS,MickE,CoffeyB,GellerD,etal. Pharmacotherapyofattentiondeficithyperactivitydisorderacrossthelifecycle.J Am Acad Child Adolesc Psychiatry1996;35:409-32. 17.ShaywitzBA,CohenDJ,BowersMDJr.CSFmonoaminemetabolisminchildrenwith minimalbraindysfunction:evidenceofalterationofbraindopamine.Apreliminary report.J Pediatr1977;90:67-71. 18.ShettyT,ChaseTN.Centralmonoaminesandhyperactivityofchildhood.Neurology 1976;26:1000-2. 19.HealthCanada.HealthCanadaallowsAdderallXRbackontheCanadianmarket [newsreleaseontheInternet].Ottawa,Ont:HealthCanada;2005.Availablefrom:
Ce nest que rcemment que le trouble dficitaire de lattention (TDA) chez ladulte a t reconnu comme diagnostic vritable. Il a une forte composante hrditaire. Chez lenfant, le trouble dficitaire de lattention avec hyperactivit (TDAH) est beaucoup plus frquent chez les garons, cause de la composante dhyperactivit. Les filles ont souvent un TDAH de type inattentif. Chez ladulte, la prvalence du TDA est presque aussi leve chez la femme que chez lhomme. Le diagnostic du TDA est bas sur les symptmes et sur les antcdents personnels et familiaux. Une chelle dvaluation des symptmes peut faciliter le diagnostic. Le traitement comprend celui de la co-morbidit, comme la dpression. Lutilisation de stimulants (les plus frquents tant mthylphnidate et dextroamphtamine) est bien appuye par la littrature; on recommande aussi certains traitements dappoint, tels que le counseling, le tutorage et certaines prcautions concernant lalimentation et lexercice.
http://www.hc-sc.gc.ca/ahc-asc/media/nr-cp/2005/2005_92_e.html.Accessed 2006July4. 20.MichelsonD,AllenAJ,BusnerJ,CasatC,DunnD,KratochvilC,etal.Once-dailyatomoxetinetreatmentforchildrenandadolescentswithattentiondeficithyperactivity disorder:arandomized,placebo-controlledstudy.Am J Psychiatry2002;159(11):1896901. 21.CasatCD,PleasantsDZ,SchroederDH,ParlerDW.Adouble-blindtrialofbupropion inchildrenwithattentiondeficitdisorder.Psychopharmacol Bull1987;23(1):120-2. 22.SimeonJG,FergusonHB,VanWyckFleetJ.Bupropioneffectsinattentiondeficitand conductdisorders.Can J Psychiatry1986;31(6):581-5. 23.BarrickmanLL,PerryPJ,AllenAJ,KupermanS,ArndtSV,HerrmannKJ,etal. Bupropionversusmethylphenidateinthetreatmentofattentiondeficithyperactivity disorder.J Am Acad Child Adolesc Psychiatry1995;34:649-57. 24.GarfinkelBD,WenderPH,SlomanL,ONeillI.Tricyclicantidepressantandmethylphenidatetreatmentofattentiondeficitdisorderinchildren.J Am Acad ChildPsychiatry 1983;22:343-8.
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