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For tobram ycin buy discount naprosyn 250mg arthritis in knee in dogs, no difference in renal accu- 5 10 m ulation could be found discount 500mg naprosyn post viral arthritis pain, indicating the linear cortical uptake of 0 0 this particular am inoglycoside buy 250mg naprosyn visa arthritis pain relief options. These data naprosyn 500mg on-line arthritis in neck bone spurs, which supported 0 4 8 12 16 20 24 0 4 8 12 16 20 24 decreased nephrotoxic potential of single-dose regim ens, coincided Time, hrs with new insights in the antibacterial action of am inoglycosides A (concentration-dependent killing of gram -negative bacteria and prolonged postantibiotic effect). Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. Several risk factors have been identified and classified as patient related, Patient-Related Factors Aminoglycoside-Related Factors Other Drugs am inoglycoside related, or related to con- current adm inistration of certain drugs. Older age* Recent aminoglycoside therapy Amphotericin B The usual recom m ended am inoglycoside Preexisting renal disease Cephalosporins dose m ay be excessive for older patients Female gender Larger doses* Cisplatin because of decreased renal function and Magnesium, potassium, or Treatment for 3 days or more* Clindamycin decreased regenerative capacity of a dam - calcium deficiency* aged kidney. Preexisting renal disease Intravascular volume depletion* Cyclosporine clearly can expose patients to inadvertent Hypotension* Dose regimen* Foscarnet overdosing if careful dose adjustm ent is Hepatorenal syndrome Furosemide not perform ed. H ypom agnesem ia, Sepsis syndrome Piperacillin hypokalem ia, and calcium deficiency m ay Radiocontrast agents be predisposing risk factors for conse- Thyroid hormone quences of am inoglycoside-induced dam - age. Liver disease is an im portant clinical risk factor for am inoglycoside * Similar to experimental data. Acute or chronic endotoxem ia am plifies the nephrotoxic potential of the am inoglycosides. FIGURE 11-9 PREVENTION OF AM INOGLYCOSIDE Prevention of am inoglycoside nephrotoxicity. Coadm inistration NEPHROTOXICITY of other potentially nephrotoxic drugs enhances or accelerates the nephrotoxicity of am inoglycosides. Com prehension of the phar- m acokinetics and renal cell biologic effects of am inoglycosides, Identify risk factor allows identification of am inoglycoside-related nephrotoxicity risk Patient related factors and m akes possible secondary prevention of this im portant clinical nephrotoxicity. Drug related Other drugs Give single daily dose of gentamicin, netilmicin, or amikacin Reduce the treatment course as much as possible Avoid giving nephrotoxic drugs concurrently Make interval between aminoglycoside courses as long as possible Calculate glomerular filtration rate out of serum creatinine concentration 11. The drug acts as a counterfeit phospholipid, with the C15 hydroxyl, C16 carboxyl, and C19 m ycosam ine groups situated at the m em brane-water interface, and the C1 to C14 and C20 to C33 chains aligned in parallel within the m em brane. The heptaene chain seeks a hydrophobic environm ent, and the hydroxyl groups seek a hydrophilic environm ent. Thus, a cylindrical pore is form ed, Cholesterol the inner wall of which consists of the hydroxyl-substituted carbon chains of the Am B m olecules and the outer wall of which is form ed by the heptaene chains of the m olecules and by sterol nuclei. C20-C33 heptaene segment Amphotericin B Pore C O N H Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. N ephrotoxicity of Am B is a m ajor problem associated with clin- ical use of this im portant drug. Disturbances in both glom erular and tubule function are well described. The nephrotoxic effect of Age Am B is initially a distal tubule phenom enon, characterized by a loss Concurrent use of diuretics of urine concentration, distal renal tubule acidosis, and wasting of potassium and m agnesium , but it also causes renal vasoconstriction Abnormal baseline renal function leading to renal ischem ia. Initially, the drug binds to m em brane Larger daily doses sterols in the renal vasculature and epithelial cells, altering its m em - Hypokalemia brane perm eability. Am B-induced vasoconstriction and ischem ia to Hypomagnesemia very vulnerable sections of the nephron, such as m edullary thick Other nephrotoxic drugs (aminoglycosides, cyclosporine) ascending lim b, enhance the cell death produced by direct toxic action of Am B on those cells. This explains the salutary effect on Am B nephrotoxicity of salt loading, furosem ide, theophylline, or calcium channel blockers, all of which im prove renal blood flow or inhibit transport in the m edullary thick ascending lim b. FIGURE 11-12 Indication for amphotericin B therapy Proposed approach for m anagem ent of Clinical evaluation: Correction: am photericin B (Am B) therapy. Correct salt depletion form ulations of am photericin have been yes Avoid diuretics developed either by incorporating am pho- Liberalize dietary sodium tericin into liposom es or by form ing com - W ill salt loading exacerbate underlying disease? In early studies, Seek alternatives nephrotoxicity was reduced, allowing an Does patient require concommitant antibiotics? Few studies have established a therapeutic index Is potassium (K) or magnesium (M g) depleted? To date, the only clinically Begin amphotericin B with sodium supplement, 150 mEq/d Begin amphotericin B therapy proven intervention that reduces the inci- dence and severity of nephrotoxicity is salt supplem entation, which should probably be Routine M onitoring: given prophylactically to all patients who Clinical evaluation (cardiovascular/respiratory status; body weight; fluid intake and excretion) can tolerate it. Laboratory tests (renal function; serum electrolyte levels; 24 -hours urinary electrolyte excretion); with perm ission. Is serum creatinine >3 mg/dL or is renal deterioration rapid? Interrupt amphotericin B therapy, yes resume on improvement Is K level ,3. Use oral or intravenous yes supplementation No Continue amphotericin B therapy and routine monitoring Close follow-up of serum electrolytes 11. The diagnosis of cyclosporine-induced acute renal dysfunction is not difficult when the patient has no other reason for reduced renal function (eg, psoriasis, rheum atoid arthritis). In renal trans- plant recipients, however, the situation is com pletely different. In this clinical setting, the clinician m ust differentiate between cyclo- sporine injury and acute rejection. The incidence of this acute cyclosporine renal injury can be enhanced by extended graft preser- vation, preexisting histologic lesions, donor hypotension, or preop- erative com plications. The gold standard for this im portant dis- tinction rem ains renal biopsy. In addition, cyclosporine has been associated with hem olytic-ure- m ic syndrom e with throm bocytopenia, red blood cell fragm enta- tion, and intravascular (intraglom erular) coagulation. Again, this drug-related intravascular coagulation has to be differentiated from that of acute rejection. The absence of clinical signs and of rejec- FIGURE 11-13 (see Color Plate) tion-related interstitial edem a and cellular infiltrates can be helpful. Intravascular coagulation in a cyclosporine-treated renal transplant Vanrenterghem and coworkers found a high incidence of recipient. Recent of the afferent arteriole entering the glom erulus. W hen severe studies have shown that im paired fibrinolysis, due m ainly to enough, this can decrease glom erular filtration rate. Although the excess plasm inogen activator inhibitor (PAI-1), m ay also contribute precise pathogenesis of the renal hem odynam ic effects of to this im balance in coagulation and anticoagulation during cyclosporine are unclear, endothelin, inhibition of nitric oxide, cyclosporine treatm ent. Lithium-Induced Acute Renal Failure FIGURE 11-14 SIGNS AND SYM PTOM S OF Sym ptom s and signs of toxic effects of lithium. Lithium can cause TOXIC EFFECTS OF LITHIUM acute functional and histologic (usually reversible) renal injury. W ithin 24 hours of adm inistration of lithium to hum ans or ani- m als, sodium diuresis occurs and im pairm ent in the renal concen- Toxic Effect Plasma Lithium Level Signs and Symptoms trating capacity becom es apparent. The defective concentrating capacity is caused by vasopressin-resistant (exogenous and endoge- Mild 1–1. The clinical picture features nonspecific signs of progression to coma), delirium, degenerative changes and necrosis of tubule cells. The m ost ataxia, generalized fasciculations, distinctive and specific acute lesions lie at the level of the distal extrapyramidal symptoms, tubule. They consist of swelling and vacuolization of the cyto- convulsions, impaired renal plasm of the distal nephron cells plus periodic acid-Schiff–positive function granular m aterial in the cytoplasm (shown to be glycogen). Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11.

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Furthermore discount 250mg naprosyn overnight delivery arthritis l5, recent regulatory and mar- toms with normalization of function) to define a clinical ket forces have encouraged studies in depressed children order naprosyn 250mg otc rheumatoid arthritis emedicine, 'success generic 500mg naprosyn with amex joint arthritis medication for dogs,' contrary to clinical practice recommendations adolescents generic naprosyn 500 mg free shipping arthritis pain uk, and geriatric patients. The National Institute of Mental Health (NIMH) has Routine clinical diagnoses often sharply disagree with recently begun to address some of the knowledge gaps noted those established by structured interviews (51) (Kashner et in the preceding by emphasizing effectiveness trials of anti- al. In addition, global judg- depressant treatments in children/adolescents, adults, and ments of the severity of illness, even if codified by the Clini- geriatric patients. The emphasis (50) was based on the reali- cal Global Impression-Improvement Scale (CGI-I) (52), zation that efficacy trials for regulatory approval are only may relate only modestly to symptom severity ascertained by the first step in defining a treatment. That is, they establish itemized clinician ratings, such as the Montgomery-Asberg˚ the safety and efficacy of an agent in carefully conducted, Depression Rating Scale (MADRS) (53) or the Hamilton highly internally valid designs. Generalizability of tolerabil- Rating Scale for Depression (HRS-D) (54,55) or the Inven- ity and efficacy findings requires different study designs. These When to use one as opposed to another agent (alone or in differences in clinical procedures used in efficacy RCTs and combination) requires still different study designs. For example, there is a reasonably strong basis DEPRESSION to believe that medications differ in their spectrum of ac- tions (1). That is, some patients/depressions respond to one Clinicians routinely confront a host of practical questions agent, whereas others respond to a different agent (58,59), that are not addressed in efficacy RCTs designed for regula- especially if the medications differ regarding presumed tory approval. These questions include the following: mechanisms of action. What is the 'next best' treatment following either an 'fit' into a multistep treatment plan is often left to tenuous unsatisfactory clinical response or intolerance to the inferences based on presumed mechanisms of action, to 'ex- first agent? What is a sufficient trial duration beyond which re- How to treat depressions that respond minimally or partially sponse is not likely (minimal duration)? What is a sufficient trial duration for those benefiting Perhaps pharmaceutical companies are reluctant to from the treatment beyond which further treatment search for specific indicators of when an agent is preferred (unchanged) is unlikely to produce any more sympto- or to study agents used as second or third steps in treatment- matic or functional improvement (maximal duration)? When is it best to augment the first agent with a second tors. Without specific indications of when to use an agent, treatment? When is it best to switch from the first agent a 'broad' spectrum of action can be claimed. Do antidepressants differ in their ability to produce largely avoided by the pharmaceutical industry, perhaps in response or remission, and if so, for which depression fear of finding that their agent will not fare as well as a is each better? Do different medications differ in the time to onset of economic forces within the industry provide a strong impe- clinical benefit or time to remission? What treatments are recommended if there is a return vital—information (e. Selecting the Initial Treatment In spite of these knowledge gaps, the industry has devel- oped a large number of newer antidepressants that are sim- All antidepressant medications have established efficacy in pler to take, better tolerated, and safer in overdose. Some even have placebo-con- 1084 Neuropsychopharmacology: The Fifth Generation of Progress trolled evidence supporting efficacy in dysthymic disorder drug–drug interactions, or likelihood of remission play a (sertraline) (15) or other 'nonmajor' disorders, such as pre- major role in selecting the first agent. However, when to How to Select the 'Next Best' Treatment select one over another agent is not well defined. Clinicians following an Unsatisfactory Response (or use 'rules of thumb' to make these judgments, but such Intolerance) to the First Agent reasonable guesses are rarely supported by prospective RCT evidence. A major clinical problem is selecting the 'next' agent if For example, more recently, efficacy for some antidepres- the first is ineffective, only partially effective, or not well sants has been established for other psychiatric conditions tolerated. When TCAs fail, the MAOIs have roughly a 50% commonly found in the presence of major depressive disor- response rate based on both open and randomized trials der, including: (a) venlafaxine for generalized anxiety disor- (58,59). Based on open trials (70), paroxetine (71,72), and sertraline (73) for panic disor- (80–83), a second SSRI is associated with a 40% to 60% der. It is logical to argue that if a clinical depression is response rate following failure with the first SSRI, although accompanied by a concurrent additional psychiatric disor- not all studies agree (84,85). Open trials (following initial der for which an antidepressant has established efficacy, SSRI failure) also support switching 'out of class' to venla- then that agent is preferred (because it should be effective faxine (86,87), bupropion (88,89), nefazodone (90,91), for both disorders) (34–37). However, this logical inference mirtazapine (92,93), or reboxetine (94). However, no ran- has not been evaluated prospectively in double-blind com- domized, comparative studies of a second SSRI (as com- parative trials. Thus, both within and out Another clue used to select among antidepressants is of class switches following initial SSRI failure can be recom- cross-sectional symptom features. As noted, depressions mended, but the strength of the evidence is weak (95). For line for those who tolerated but who did not respond to example, a common belief is that selective serotonin reup- imipramine. This large, double-blind, definitive study, pro- take inhibitors (SSRIs) should be more effective than selec- vides substantial evidence for an 'out-of-class' switch as a tive noradrenergic reuptake inhibitors (SNRIs) for major second step following unsatisfactory response to an SSRI or depression with marked anxiety. It also reveals that an SSRI (in this case sertraline) is has not withstood empirical study. Bupropion was as effec- effective even if a TCA (imipramine) is not—a finding that tive as sertraline in outpatients with major depressive disor- does not agree with the suggestion of greater efficacy of der, whether pretreatment anxiety was high or low (74). However, whether a within SSRI class Similarly, higher levels of pretreatment insomnia are not switch (e. Reboxetine, an SNRI, is effective in both panic disor- der (76) and depression (77,78). When to Augment or Switch Although family history of response to a MAOI or TCA Inadequate benefit to an initial treatment comes in degrees should point the clinician to choose between these two that range from literally no benefit whatsoever, to a clinically classes (79), studies of family history and patient responses significant response but without full remission (i. In such cases, clinicians and patients In sum, only psychotic or atypical symptom features have must choose between switching (i. Concurrent and starting a second treatment) and augmenting (adding comorbid conditions logically recommend an initial agent, a second treatment to the first). This decision, in part, rests but this recommendation has not been evaluated prospec- on patient and clinician preference, desirability of simple tively. It would appear that other parameters such as safety (i. However, some reports indicate that of no or only one prior unsuccessful treatment attempt, various agents, such as mirtazapine (107–109) or venlafax- monotherapy (i. For more resistant depressions, even a modest bene- to more selective agents. Whether they differ from other fit to the first treatment may recommend augmentation. More recently, open trials or small case series sug- gest a benefit of adding bupropion to an SSRI (98), venla- What Is a Sufficient Trial Duration faxine (99), mirtazapine, or nefazodone. Furthermore, whether augmentation is as effective 0 to 6 weeks (33). Thus, although response is unlikely to for patients who have a minimal response, as opposed to at begin after 8 weeks of medication treatment, remission may least a partial response, or a response with residual symp- not occur until 12 weeks (or even longer) with treatment toms with newer agents is not known. Indeed, in a recent study of outpa- tients with chronic major depressive disorder, 40% of acute What Is an Adequate Trial Duration to phase responders who had residual symptoms (i.

An MRI study of the basal CONCLUSION ganglia in autism buy naprosyn 250 mg mastercard arthritis essential oil. Numerous complementary strategies are currently being Acta Psychiatr Scand 1999;99:399–406 order naprosyn 500 mg amex arthritis in back and feet. The UCLA- studies have identified a number of suggestive loci naprosyn 500mg low price arthritis zinc, most University of Utah epidemiologic survey of autism: recurrence notably distal 7q cheap 500 mg naprosyn visa arthritis treatment by acupuncture. Interest in this region is supported by risk estimates and genetic counseling. Am J Psychiatry 1989; findings from language-disorder families and from a small 146:1032–1036. Genetics of au- number of 7q chromosomal anomalies in individuals with tism: overview and new directions. Chromosomal anomalies also implicate 15q11-q13 28:351–368. Autism as a strongly genetic of the region have not been as impressive. These findings disorder: evidence from a British twin study. Twin and adoption studies in child and adolescent harboring genes in autism. As sample sizes continue to grow psychiatric disorders. How commonly are known medical methods improve, and as complementary strategies such as conditions associated with autism? J Autism Dev Disord 1998; the use of the BAP emerge, it seems plausible that in the 28:273–278. Autism and tuberous sclerosis complex: near future more disease loci will be uncovered and specific prevalence and clinical features. J Autism Dev Disord 1998;28: autism disease genes may be identified. Prenatal and perinatal factors in the etiology of autism. Obstetric compli- is caused by mutations in X-linked MECP2, encoding methyl- cations in autism: consequences or causes of the condition? J of whole blood serotonin and plasma norepinephrine within Autism Child Schizophr 1977;7:69–81. Serotonin relation- approaches and findings for autism. J Child Psychol Psychiatry ships of autistic probands and their first-degree relatives. Chromosome abnormalities in infan- Chapter 41: The Molecular and Cellular Genetics of Autism 561 tile autism and other childhood psychoses: a population study 53. Support for linkage based study and a literature survey. J Child Psychol Psychiatry of autism and specific language impairment to 7q3 from two 1999;40:335–345. J Psychia- the Prader-Willi/Angelman syndrome region: clinical implica- try Neurosci 1999;24:159–165. Intrachromosomal of recurrence risks for complex phenotypes with selection and triplication of 15q11-q13. Brief report: duplication of Am J Hum Genet 1995;57:717–276. A full genome screen for autism with evidence for Med Child Neurol 1994;36:736–742. A case of autism associated with partial Genetic Study of Autism Consortium. Am J netic and molecular analysis of inv dup(15)chromosomes ob- Med Genet 1999;88:609–615. Autistic disorder and additional inv dup(15)(pter- International Sibpair Study. Autism associated nonparametric linkage analysis: a unified multipoint approach. J Am Acad Child Adolesc Psychiatry Am J Hum Genet 1996;58:1347–1363. Inherited interstitial fraction values in human genetics. Ann Hum Genet 1963;27: duplications of proximal 15q: genotype-phenotype correlations. Three patients with val mapping and exclusion for complex genetic traits: sampling autistic disorder and isodicentric 15 chromosomes: implications considerations. Asymptotic properties of affected-sib-pair linkage mosomes. Search for autism susceptibility loci: Genome screen children and young adults with isodicentric chromosome 15. Genetic stud- retardation and atypical bipolar disorder in a 33-year-old female ies of autistic disorder and chromosome 7. Imprinting in Prader- (5-HTT)gene variants associated with autism? Cytogenetic and molecular HTT)and gamma-aminobutyric acid receptor subunit beta3 studies in the Prader-Willi and Angelman syndromes: an over- (GABRB3)gene polymorphisms are not associated with autism view. Small nuclear ribonucleo- Study of Autism Consortium. Am J Med Genet 1999;88: protein polypeptide N (SNRPN), an expressed gene in the 492–496. Regulation of gene expression by natural autistic individuals. An imprinted anti- ties with the hnRNP-A2 promoter region. Hum Mol Genet sense RNA overlaps UBE3A and a second maternally expressed 1997;6:2051–2060. Masquerading repeats: paralogous pitfalls of the ated with autism in three females. NF1 microdele- syndrome of an imprinted X-linked locus affecting cognitive tion breakpoints are clustered at flanking repetitive sequences. Molecular mechanism for deletions of the short arm of the X chromosome. The ancestral gene for of-origin effect of the X chromosome. Am J Med Genet 2000; transcribed, low-copy repeats in the Prader-Willi/Angelman re- 96:312–316. Autism and the X which is deficient in mice with neuromuscular and spermiogenic chromosome.

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Psychiatry Res 1999; compulsive disorders practical management cheap naprosyn 500mg fast delivery arthritis bike classic, third ed cheap 500mg naprosyn fast delivery rheumatoid arthritis differential diagnosis. A two- to seven- ogy of behavioral inhibition in children discount 250mg naprosyn otc arthritis in dogs labradors. Child Dev 1987;58: year follow-up study of 54 obsessive-compulsive children and 459 discount 250mg naprosyn free shipping arthritis fingers pregnant. In: Jenike MA, Baer L, Minichiello WE, 85 patients with obsessive-compulsive disorder. Obsessive-compulsive disorders practical management, third 1994;151:441–442. Childhood movement disorders and for patients with obsessive-compulsive disorder. Pediatric autoimmune during the long-term course of unipolar major depressive disor- neuropsychiatric disorders associated with streptococcal infec- der. Clinical findings of significance to of obsessive-compulsive disorder. Am J Psychiatry 1995;152: neuropharmacologic trials in OCD. Arch Gen Psychiatry 2000;57: York: Guilford Press, 1993. Haloperidol compulsive disorder in behavioral treatment studies: a quantita- addition in fluvoxamine-refractory obsessive-compulsive disor- tive review. Behav Res Ther 1996;34:47–51 (revised May 21, der: a double-blind placebo-controlled study in patients with 1997). Concomitant obses- from a multicenter trial of clomipramine. J Clin Psychiatry 1994; sive-compulsive disorder and schizotypal personality disorder. Effect of axis II diagnoses in obsessive-compulsive disorder. J Anxiety Disord 1988;2: on treatment outcome with clomipramine in 54 patients with 229–317. Behav Res exposure for obsessive-compulsive rituals. Six-year follow- pulsive beliefs and treatment outcome. Psychol Med 1988;18: up after exposure and clomipramine therapy for obsessive-com- 697–702. The treatment of severe, chronic, resistant 102–108. The epidemiology and clinical features try 2001;42:494–497. The clinical significance of obsessions in schizophrenia. The prognostic significance of nervous system dysfunction in obsessive compulsive disorder. Computerized tomography and neuropsychologi- cal test measures in adolescents with obsessive-compulsive disor- 87. Obsessive-compulsive disorder in children and adolescents. Obsessive compulsive disorder—five clinical ques- ington, DC: American Psychiatric Association, 1988:107–118. Factor analysis of symptom subtypes of obsessive-com- Psychiatry 1988;49:27–28. Neuroimaging in OCD: disorder in bipolar and unipolar disorders. The genetics of obsessive-compulsive disorder and 92. Psychiatr Clin North Am 1992; depression Acta Psychiatr Scand 1975;52:336–373. Obsessive com- rosis: record, follow-up, and family studies. Inpatient record pulsive disorder with and without a chronic tic disorder. Agoraphobia and panic 1608 Neuropsychopharmacology: The Fifth Generation of Progress disorder: development, diagnostic stability ad course of illness. Phenomenology of inten- Arch Gen Psychiatry 1986; 43:1029–1036. New York: Guilford Press, disorder among patients with anorexia nervosa and bulimia ner- 1988, 319–355. Anorexia nervosa 6 years anxiety disorder in patients with adult anxiety disorders. KENNEDY Multiple converging lines of evidence suggest that neurobi- At the same time, there has been considerable research ology plays a significant role in the etiology of obsessive- that has documented the familial nature of OCD (7). During the past decade, there family data, when taken together with twin studies, suggest has been considerable progress in the identification of neu- that genetic factors are important in the manifestation of roanatomic substrates involved in the expression of OCD. Segregation, linkage, and association studies The brain areas most frequently identified by in vivo neu- have begun and the results are similar to those observed for roimaging studies as potentially involved in the manifesta- other major psychiatric disorders: The mode of transmission tion of OCD are the orbitofrontal cortex (OFC), the ante- within families is complex and the precise genetic mecha- rior cingulate area (ACA), and the head of the caudate nism is not known. Furthermore, pharmacologic and neurobiologi- In this chapter the main pathophysiologic findings for cal studies have implicated several central neurotransmitter OCD are reviewed as well as the evidence that genetic fac- systems in the pathophysiology of OCD and related condi- tors are of etiologic importance. The strongest pharmacologic evidence concerns the studies examining candidate genes proposed as the result of serotonergic system and the well-established efficacy of po- several lines of investigation that implicate both the seroto- tent serotonin reuptake inhibitors in the treatment of OCD nergic and dopaminergic neurotransmitter systems are sum- (2,3); however, other systems have also been implicated. The most widely accepted alternative neurochemical theory Historically, the serotonin (5-HT) hypothesis has its basis for OCD suggests that the dopamine (DA) neurotransmis- in the pharmacology of OCD. In the late 1960s it was sion system also may be important in the pathophysiology observed that clomipramine, the only tricyclic antidepres- of some cases of OCD (3–6). Specifically, the DA hypothe- sant with potent 5-HT reuptake blocking properties, had sis has been proposed for those cases of OCD that appear antiobsessional activity (8,9). Subsequently, several studies to be related to Gilles de la Tourette syndrome (GTS) or have shown that clomipramine and several other selective other tics disorders, and/or those that occur with schizotypal serotonin reuptake inhibitors (SSRIs) are effective antiob- personality disorder and/or poor insight. In fact, results were taken as evidence that etiologic hypothesis for OCD involving an autoimmune serotonin plays a fundamental role in the pathogenesis of mechanism, particularly relevant for early-onset cases. These observations have led to the examina- tion of the serotonin system and its function in OCD pa- tients. Peripheral markers for the 5-HT system and a num- ber of parameters of the 5-HT function have been David L. Pauls: Child Study Center, Yale University School of Medicine, investigated.

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