NADD Bulletin Volume XI Number 4 Article 1

Complete listing

Obsessive-Compulsive Disorder: Diagnosis and Treatment

Jarrett Barnhill, MD

Over the past 20 years, obsessive-compulsive disorder has gone from a rarely diagnosed condition to one that occurs in between 1-2% of the population (8, 15, 19). If we expand the diagnostic criteria to include OC spectrum and subclinical forms of the disorders, the prevalence rates more than triples. Looked at from this angle, Obsessive-compulsive Spectrum Disorder (OCSD) occur in a substantial part of the population (6, 7).

Clinical studies suggest a considerable degree of overlap and comorbidity with other anxiety or mood disorders. Because of these comorbidities, we should anticipate that prevalence rates among women are far higher than males. But this is not the case (1, 5). One variable that affects prevalence and typology of OC behaviors is age of onset. The exception to equal gender distribution emerges when the age of onset is prior to age ten. In this age category, males with early onset OCD outnumber females, but the majority of these males may go on to develop tics disorders (5, 12, 14).

The gender dimorphism observed in clinic samples suggests that there is considerable clinical heterogeneity among individuals with OCD and OCSD (6. 7). This heterogeneity can present problems for clinicians and requires a careful investigation of many forms of repetitive behaviors, tic disorders, and neurocognitive disorders dominated by behavioral inflexibility and perseveration. The presence of other movement and brain disorders suggests that there is a common neurobiological substrate that underlies OC spectrum disorders (OCSD) (13, 15). 

Diagnosing OCSD in individuals with IDD requires an even greater attention to the details of differential diagnosis. The relationship between OCSD and the complex mosaic of stereotypies, mannerisms, self-stimulating behaviors, tic disorders and many challenging behaviors such as SIB or aggression is not easy (2,3,7, 17). This paper addresses the many steps needed to reliably diagnose OCSD in individuals with autistic spectrum and intellectual disabilities (2, 3, 17).

 

OCD versus OCDS

Obsessive-compulsive disorder (OCD) is an anxiety disorder characterized by recurring and intrusive thoughts (obsessions) and urges to undo or neutralize the antecedent thoughts (compulsions). Both symptoms are disturbing (alien to normal mental activity) and time-consuming. Attempts to ignore or not comply with obsession-driven compulsions generate anxiety that is relieved by performing the action. Insight into the odd nature of these symptoms is also a part of the diagnostic criteria for OCD, but may absent in nearly 50% of individuals seen in clinical settings (1, 6, 15). The majority of individuals with OCD respond to treatment with clomipramine, SSRIs, NSRIs, and cognitive behavioral/response prevention behavioral programs (1, 11). 

The presence of obsessions and the relatively limited repertoire of classic OCD symptoms (cleaning washing, checking etc) may be difficult to parse out of repetitive behaviors seen in individuals with severe IDD (8). These individuals are less likely to report obsessions, and or report distress from their repetitive behaviors. The level of distress may be disassociated from their repetitive behaviors in ways that diverge form classic OCD: overt distress triggers behavior; engaging in the RB reduces distress; there are few self-directed attempts to interrupt the behaviors; and preventing the behaviors may escalate distress and trigger aggressive responses or SIB (17,18).

It may be easier to diagnose OCD among individuals with mild IDD. This generality is not valid for individuals with long standing tic or autistic spectrum disorder. These two groups increase the likelihood of repetitive behaviors and require a more intensive level of analysis.

Among individuals with severe/profound IDD, the marked deficits in adaptive behaviors and the increased prevalence of co-existing neurological conditions increases the risk of other forms of RB. The boundary between obsession-driven OCD and these other sources of repetitive behaviors (RBs) is blurred by symptom modifications imposed by severe cognitive and neurological deficits (2, 3,18). There are also limits to eliciting subjective symptoms necessary for the diagnosis. 

In OCD obsessions (cognition) and a limited range of anxiety reducing behaviors (compulsion); discomfort and anxiety-provoking attempts at inhibition; contamination/hand washing; checking; obsessions are the most common presentations. Individuals with OCD and comorbid tic disorders seem to bridge the gap between movement disorders, OCD and OCSD. These individuals may have classic OCD symptoms (more common in females) but more often than not, differ in the following ways: arranging, need for symmetry, touching and more aggressive or sexual obsessions may appear. Greater problems with impulse control, less need to inhibit because of anxiety and “just right” cue to cease are more common in ticquers (1, 5, 12).

OCSD on the other hand, tend to cluster among individuals with impulse control difficulties. These individuals often do not report obsessions, but can describe intrusive images or communications that make it difficult to distinguish from  auditory or visual hallucinations in psychosis. The types of  RBs differ, most often presenting as hoarding, arranging-organizing, counting, aligning, touching, or requiring symmetry (6,7, 12).   Examples of OCSD (6, 7, 12) include: (a) Tic disorders, (b) Frontal lobe/basal ganglia injuries, (c) Schizophrenia- schizo-obsessional disorder

Body dysmorphic disorder/Restriction anorexia nervosa- body image disorders, (d) Impulse control disorders- sexual compulsions, gambling, trichotillomania, and addictions, and (e) Specific behavioral phenotypes such as Prader-Willi: compulsive eating and skin picking; compulsive SIB; stereotypic and ritualistic behaviors in patients with MR/DD, but classic OCD symptoms are less common.

 

Table 1. Differentiating behaviors

 

SubtypeOCDOCSD   

ObsessionsPresent, intrusive, troublesome, hard to  ignoreUsually absent, intrusive violent or sexual images, repeating experiences- a song gets stuck in the head   

compulsionsWashing, cleaning checking, repeating a fixed numberHoarding, touching arranging, counting, need for symmetry,

AnxietyHarm avoidance, other anxiety disorders, behaviors reduce anxietyImpulsive, less anxiety, motivation appears in terms of urges or feeling impelled to act   

Discomfort with symptomsAnxiety reduced by action, perceive symptom as a source of distress Urges reduce by anxiety, troubled by outcome of behavior   

Tic disordersFemales may have OCD instead of tic disorders, course of tic disorders- greater number of compulsionsCommon, boundary problem with complex sensory tics (16)- just right terminates behaviors, addiction behaviors, trichotillomania, SIB in some personality disorders, compulsive gambling etc (6, 7)  

Treatment responseSSRIs, CBT/RP effective in combination or individually (2, 3) Less effective, supplementation with second generation APDs, Clonazepam; behavioral disinhibition more common with SSRIs (6. 7)

 

 

IDD, OCSD, OCD: Where is the boundary?

This is the $64,000 question. The most obvious answer is “I don’t know but I’ll know it when I see it”. This question also divides us into philosophical camps. Are we “lumpers” who put most RBs under the umbrella category of OCD or are we “splitters” who spend a great deal of energy searching for endophenotypes? If we are lumpers the OCD is perfectly acceptable and we can se the diagnosis regardless of DSM-IV-TR inclusion or exclusion criteria. This approach makes diagnosis more pleasant but leads to a great deal of psychopharmacological shopping until we find something that works- empiricism at its best.

 

As a splitter, the author is constantly looking for more homogenous groups that give us more common ground in terms of symptom-clusters, comorbid or associated symptoms (company that the RBs keep), genetics, functional neuroanatomy, neurochemistry, longitudinal course, and differential treatment response. This approach takes enormous effort in terms of time for observation, examination, and dissection of target symptoms.

Each of the following is used inclusively and exclusively. At the end of this sequence the clinician has a good idea of the differences between various forms of RBs. For example:

Presence of autism and related spectrum disorders- RBs, behavioral and cognitive inflexibility, and reliance on ritualized approaches to daily living suggest that when present OCD should meet the full criteria ( 1).

Level of IDD- inverse relationship between level of IDD and rates of other RBS, SIB, and ease of diagnosing OCD (7, 18).

Presence of other neurological disorders- tics, severe brain disorders that make it less likely to observe obsessions, and classic OCD and more apt to find OCSD like symptoms (10).

Sensitivity to ecological/interpersonal distress; state of physiological arousal; response to efforts to interrupt the RBs (17, 18). 

Associated disruptive behaviors, including SIB (17, 18).

Presence of known genetic disorders or behavioral phenotypes associated with RBs- Lesch-Nyhan, Cornelia de Lange, Smith Magenis etc ( 17, 18).

Presence of or genetic risk for primary psychiatric disorders- schizophrenia, mood disorders, other anxiety disorders, substance dependency (6, 7).  

Past history of treatment interventions. The failures are as important as the successes in doing a pharmacological dissection of this group of behaviors (6, 7)   

Once these data are collected, then we can focus on which subtype of OCSD are present. One approach is to distinguish a syndrome (OCD) from challenging behavior (SIB, stereotypies)/or pattern of RB consistent with developmental age (17, 18). The evolution of repetitive behaviors during an individual’s lifetime is also of great interest. The emergence of repetitive behaviors that allow one to escape demands (neg. reinforcement) may have a more troublesome outcome than those that appear intrinsically reinforcing and appropriate to developmental age (18).

The ultimate goal of any diagnosis is specifying which treatments are effective and which should be avoided. Accurate diagnosis involves both subtyping- and addressing comorbid conditions- “company that it keeps”. Tic disorders and ASD present example of the need to match treatment to target behaviors and clinical condition. We also need to modify treatment when tics disorders, ADHD/impulse control disorder, or comorbid psychiatric disorders are present.

SSRIs are often quite effective for OCSDs but the need for high doses, duration of latency prior to treatment response, and the degree of symptomatic relief can vary considerably.  The presence of comorbid bipolar disorder or schizophrenia may require the addition of APDs or mood stabilizers prior to or during the early phases of pharmacotherapy (6, 7).

SSRIs are not always effective in individuals with OCSDs. Under many circumstances the individual may worsen either due to pharmacokinetic issues (metabolic rate for the drug), or intolerance due to provoking BPAD, behavioral disinhibition, or increases anxiety (akathisia). Differences between drugs are based on genetic factors within metabolic pathways; inhibition of selected CYP by other drugs, and side effect profile. Anxiety and high harm avoidance are the best predictors of response (12, 19).

 

Cognitive behavior/exposure-response prevention therapy can serve as either a primary treatment or adjunctive intervention. It may be less effective in individuals with severe/profound ID. In these settings, attention to environmental triggers (antecedents), level of arousal or affective state, and factors that sustain the behavior allow for more directed interventions. No one size fits all, so creativity may be important (6, 7, 8).

Adjunctive therapies include mood stabilizers, second and third generation antipsychotic drugs, clonazepam, GABA-agonists, and a range of new therapies are available or on the horizon. The critical issue is matching treatment to individual (11). 

References

 

1. Baer L.(1994) Factor analysis of symptom subtypes of obsessive-compulsive disorder and their relationship to personality and tic disorders. Journal of Clinical Psychiatry, 55(3sppl), 18-23.

 

 

 

2. Bodfish JW, Madison JT (1993), Diagnosis and fluoxetine treatment of compulsive behavior disorder of adults with mental retardation. American Journal of Mental Retardation , 98(3), 360-7.

 

3. Brasic JR, Barnett JY, Kaplan D, Sheitman BB, Aisemberg P, Lafargue RT, Kowalik S, Clark A (1994). Clomipramine ameliorates adventitious movements and compulsions in prepubertal boys with autistic disorder and severe mental retardation. Neurology, 44(7),1309-12.

 

 

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8. Hollander E, and Rosen J (1999). OC spectrum disorders: the impulsive and Schizo-obsessive clusters. CNS Spectrums, 6(5 Suppl),16-22.

 

9. Hollander E and Stein DJ (eds) Obsessive-Compulsive Disorders. Marcel Dekker, New York. 1997.

 

10. Iiada J, Sakiyama S, Iwasaka H, Hirao F, Hashino K, Kawabata Y, Ikawa G (1996).  The clinical features of Tourette’s disorder with obsessive-compulsive symptoms.  Journal of Psychiatry Clinical Neurosciences , 50(4),185-9.

 

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12. Robertson MM, Yakeley J. Gilles de la Tourette’s Syndrome and Obsessive-Compulsive Disorder. In Fogel BS, Schiffer RB and Rao SM (eds) Neuropsychiatry. Williams and Wilkins Baltimore. 1996;827-70

 

13. Saint-Cyr JA, Taylor, AE, Nicholson K (1995). Behavior and the basal ganglia. In: Werner WJ and Lang (Eds) Advances in Neurology New York, USA: Raven Press, (65), pp 1-28.

 

14. Santangelo SI, Pauls DL, Goldstein JM, Farone SV, Tsuang MT and Leckman JF (1994). Tourette’s syndrome: what are the influences of gender and comorbid obsessive-compulsive disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 33(6), 795-804.

 

15. Saxena S, Bota RG, and Brody AI (2001). Brain behavior relationships in obsessive-compulsive disorders. Seminars in Clinical Neuropsychiatry,; 6(2), 82-101.

 

16. Scahill LD, Leckman JF, Marck KL (1995). Sensory phenomena in Tourette’s syndrome. In: Werner WL and Lang AL (eds) Advances in Neurology, New York, USA: Raven Press, 65, pp 273-81.]

 

17 Schoeder SR, Oster-Granite ML, Berkson G, Bodfish JW, Breese GR, Cataldo MF, Cook EH, Crnic LS, DeLeon I, Fisher W, Harris JC, Horner RH, Iwata B, Jinnah HA, King BH, Lauder JM, Lewis MH, Newell K, Nyhan WL, Rojahn J, Sackett GP, Sandman C, Symmons F, Tessel RE, Thompson T, Wong DF (2001). Self-injurious behavior: gene-brain-behavior relationships. Mental Retardation and Developmental Disabilities Research,  7(1), 3-13.

 

18. Troster H (1994(. Prevalence and functions of stereotyped behaviors in nonhandicapped children in residential care. Journal of Abnormal Child Psychology, 22(1), 79-97.

 

19. Zohar J, Insel T, and Rasmussen S (eds) The Psychobiology of  Obsessive-Compulsive Disorder. Springer New York. 1991.