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Obsessive-compulsive disorder (OCD) is classified as an anxiety disorder. It has a lifetime prevalence rate of between 2.0% and 2.5% in the general population (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). Typically, OCD is a chronic condition with an early onset where 33-50% of sufferers exhibit symptoms before the age of 18 (Pigott,Dubbert,L'Heureux,Canter & Murphy,1996). While symptoms are seldom present throughout the day, less than 10% of patients experience more than 1 month without OCD symptomatology (Pigott,Dubbert,L'Heureux,Canter & Murphy,1996). In addition, individuals with a primary diagnosis of OCD often suffer from comorbid conditions. It is estimated that at least 50% of patients have another Axis I disorder and 40% have at least one Axis II personality disorder (Pigott,Dubbert,L'Heureux, Canter & Murphy,1996). Major depressive disorder and other anxiety disorders are the most frequently diagnosed comorbid conditions (Pigott,Dubbert,L'Heureux, Canter & Murphy,1996). OCD patients are classified into 3 groups:

  1. individuals with obsessions and compulsions,
  2. individuals with obsessions only, and
  3. individuals with compulsive rituals only.

A diagnosis of OCD is recommended if a patient can be assigned to one of these groups and if the "symptoms are time-consuming or significantly interfere with the person's functioning" (Andrews,Crino,Hunt,Lampe & Page,1994,263).

Obsessions are present in the form of "ideas, thoughts, images and impulses" (Andrews,Crino,Hunt,Lampe & Page,1994,263) which are perceived as unwanted and nonsensical. It is common for obsessive-compulsives to experience more than one form of obsession and most sufferers will attempt to resist these thoughts and push them from their mind. The most frequent primary obsessions are:

In the majority of OCD cases, compulsions are also present. These consist of "repetitive or stereotyped behaviours" (Andrews,Crino,Hunt,Lampe & Page,1994,263) and are executed in response to obsessions because of a belief that these actions can prevent disastrous consequences, or to alleviate anxiety or tension which follows from the obsessive thought. Compulsions generally fall into one of several categories. The most common is washing/cleaning behaviour which is typically prompted by a fear of contamination and can involve complex decontamination rituals, as well as extensive avoidance of feared contaminants (Andrews,Crino,Hunt,Lampe & Page,1994). Another frequently observed compulsion is checking, through which sufferers will engage in repeated checking to prevent a feared event or disaster (Andrews,Crino,Hunt,Lampe & Page,1994). Other common compulsions are repeating behaviours, ordering and obsessional slowness (Andrews,Crino,Hunt,Lampe & Page,1994).

The precise cause of OCD is still unknown. Different psychological perspectives have proposd theories which attempt to explain how OCD might develop. Psychoanalytic theory views obsessive ideation to be the consequence of repression (Emmelkamp,1982). As the defense mechanism fails, repressed material is remembered, but it is altered before reaching consciousness and emerges in the form of obsessive thoughts. Psychoanalytic theory also suggests that OCD is related to the "anal character type" (Emmelkamp,1982,182) which is defined by obstinacy, parsimony and orderliness; however, there is insufficient scientific evidence to support this view (Emmelkamp,1982).

From a behavioural perspective, Mowrer's two-stage theory of fear acquisition (Emmelkamp,1982) suggests that classical conditioning plays an important role in the formation of obsessions and compulsions; however, this explanation is doubtful for 3 reasons.

  1. The classical conditioning of fear occurs after a traumatic incident, yet most OCD patients report that they cannot relate such an experience to the onset of OCD symptoms,
  2. If there was a trauma, it usually occurs at a time much earlier than the onset of OCD, which is not consistent with the operation of classical conditioning (Emmelkamp,1982),
  3. Several obsessions can be present within one individual and the obsessions can change without the occurence of new traumas.

From the cognitive perspective, theorists suggest that obsessive-compulsives suffer from impaired information-processing. The impairment is present in rigidly defined categories and boundaries which are maladaptive and result in an over-structuring of input (Emmelkamp,1982); but there is no evidence to show that this is the cause, rather than a consequence of OCD symptoms. Another cognitive theory suggests that OCD "fear structures" (Kozak,Foa & McCarthy,1988,91) are especially heterogeneous and numerous stimuli can become associated with threat or danger. Passive avoidance of such a large number of stimulus associations would be extremely difficult and, therefore, compulsions become necessary for the individual to feel safe. Although cognitive theories do provide insight into the expression of OCD, they fail to clarify how and why OCD and this cognitive impairment arises.

Investigations of the physiological basis of OCD have taken diverse forms. Several areas where recent research has focused are:

  • drug therapy studies which provide evidence of neurotransmitter dysregulation,
  • psychosurgical procedures which reduce obsessive-compulsive symptoms,
  • the influence of genetics in the tiology of OCD,
  • various motor system disorders which also manifest obsessive-compulsive behaviours,
  • and the presence of neurological abnormalities in patients with OCD.

    Drug Therapy Studies
    The most effective treatments for OCD are behavioural therapy and pharmacotherapy. Behaviour therapy consists of exposure and response prevention (ERP); exposure addressed the fears and response prevention confronts ritualized compulsions. The presence of depression, overvalued ideation, schizotypal personality and checking rituals have all been found to predict a poor response to ERP (Stanley & Turner,1995). For some of these individuals the conjuctive use of medication may improve the response to treatment. Overall, after drop-out and refusal rates are considered, approximately 36% of patients will show at least 70% reduction in symptoms, 27% will show a reduction of 31% to 69%, and 7% fail to benefit from ERP (Stanley & Turner,1995).

    The predictors of drug therapy outcome are similar to those for behaviour therapy. The pretreatment severity of OCD can affect some drugs' effectiveness in reducing symptoms, although this appears to be less of an influence with clomipramine (CMI) (Stanley & Turner,1995). The presence of major depression had been thought to predict a poor response and some researchers believed that the primary effects of drug treatment were due to the alleviation of depressed mood. However, some tricyclic antidepressants (TCAs) have been shown to possess an anti-obsessive effect in OC subjects who are not clinically depressed (Stanley & Turner,1995). Finally, drug therapy may be adversely affected by the presence of personality disorders, especially schizotypal personality. Patients with comorbid OCD and schizotypal type personality may have a better response when OCD drug treatment is augmented with a neuroleptic drug (Stanley & Turner,1995).

    Pharmacological treatment has been shown to be effective with the administration of TCAs, but the class of selective serotonin reuptake inhibitors (SSRIs) are the most beneficial. TCAs were developed from a larger family of tricyclic drugs, phenothiazines, which are used to treat psychotic states. TCAs have a 3-ring chemical structure, but differ from phenothiazines in that the center ring's sulphur atom is replaced by an ethylene bridge, which changes the drug's attraction to particular receptor sites (Thase & Shipley,1988). The more recently developed TCAs have undergone further modifications to the center ring, the side chain or to both segments (Thase & Shipley,1988).

    Many antidepressants are not effective agents for the treatment of OCD. For example, some TCAs, such as, noritriptyline and desipramine, which are more potent inhibitors of norepinephrine reuptake (Thase & Shipley,1988), have shown no anti-obsessive properties when compared with placebo or clomipramine (CMI), a TCA which selectively inhibits serotonin reuptake (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). The agents with demonstrated effectiveness in the treatment of OCD, in controlled studies, are the SSRI class of TCAs. CMI is the TCA which has received the most attention from researchers. CMI has been found to be superior to placebo and other more selective SSRIs (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). The CMI Collaborative Study Group findings show that compared with a placebo control group, CMI results in a significant reduction in symptoms (mean reduction=40%) (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). It is estimated that approximately 50-60% of OCD sufferers will respond to CMI treatment with at least a 35% reduction in symptoms (Stanley & Turner,1995). CMI's primary effect is on the inhibition of serotonin reuptake, but its metabolite, desmethylclomipramine has an inhibitory effect on norepinephrine reuptake. CMI also effects adrenergic, dopaminergic and histamine receptors (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). In the past it was proposed that CMI was useful in the treatment of OCD because it adjusted abnormalities in serotonergic mechanisms. To test this hypothesis researchers began studies with TCAs that were more selective and potent in their inhibition of serotonin reuptake. SSRIs such as fluoxetine, fluvoxamine, sertraline and paroxetine have all be shown to be effective in OCD treatment, but in comparative studies they are generally less effective than CMI (Piggot, Dubbert, L'Heureux, Canter & Murphy,1996). An analysis of the effect sizes of these drugs has been carried out to determine which are the most effective for treating OCD. The data suggests that CMI, the least potent and selective in its inhibition of serotonin reuptake, is relatively more effective in its ability to reduce obsessive-compulsive symptoms than the other SSRIs (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). At the present time however, there is uncertainty as to whether the presence of other factors may be confounding the results on these drug trials. Consequently, future comparative studies should consider the following influences:

    1. clinical severity of the condition,
    2. percentage of treatment resistant patients,
    3. differences in placebo response rates,and
    4. the presence of comorbid conditions (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996).

    The data from these drug trials does suggest that an abnormality in serotonergic mechanisms is an important element in the pathology of OCD, but none of the SSRIs have been able to completely eliminate obsessive-compulsive symptoms. Accordingly, researchers have also focused on methods to increase the availability of serotonin. The addition of adjuvant medications to SSRI drug therapy is a technique designed to acheive this goal, although it has delivered mixed results. One study assessed the efficacy of adding buspirone to fluvoxamine-refractory drug therapy (McDougle et al,1993). Buspirone is a 5-HT1A (serotonin) partial agonist, as it affects only a particular binding site. The results showed that the addition of buspirone to fluvoxamine treatment, compared with the addition of a placebo, did not result in a statistically significant difference in symptom reduction (McDougle et al,1993). The authors note that previous research has found that when a selective 5-HT1A receptor ligand, ipsapirone, was administered to OCD patients and a control group, the neuroendocrine and behavioural responses were not significantly different. These findings suggest that an abnormal 5-HT1A receptor is probably not a significant factor in OCD (McDougle et al,1993).

    Other medications have also been used to augment SSRI treatment. The addition of lithium carbonate to SSRI therapy obtained contradictory results in different studies and is believed to improve the condition of patients by alleviating depression, not obsessive-compulsive symptoms (Pigott, Dubbert, L'Heureux, Canter & Murphy,1994). In an uncontrolled trial, tryptophan, the precursor of serotonin, was added to SSRI therapy and an improvement in symptoms was noted (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). The addition of fenfluramine (Prozac), an amphetamine agonist which presynaptically releases serotonin and which possesses some reuptake inhibiting effects, also led to a further reduction in OCD symptoms, but again the trials were not controlled (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). In a double-blind/placebo control group study, clonazepam, a benzodiazepine with known anxiolytic effect, was added to fluoxetine or CMI. It was found that augmentation of either drug with clonazepam resulted in additional reductions in OCD symptoms (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). Finally, the addition of neuroleptics, such as, haloperidol, also resulted in an improvement and was found to be especially beneficial in subjects with comorbid tics or Tourette's syndrome (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). The result of SSRI augmentation with various drugs is beneficial in some situations, but the effects are generally not robust and controlled trials are required before the contradictory evidence can be resolved. At this time researchers do suggest that serotonin dysregulation is a prominent factor in OCD; however, "facilitation of 5-HT function, by a drug ... may not be a sufficient condition for efficacy in the treatment of OCD" (McDougle et al,1993).

    A longitudinal study has shown that after 2 years of drug therapy, subjects still exhibited a 42% improvement in symptoms from baseline measures (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996). Unfortunately, medication discontinuation studies report that most subjects experience a rapid relapse after stopping treatment. In one study, 89% of subjects showed a "substantial and progressive recurrence of syptoms" (Stanley & Turner,1995) after approximately 4 weeks, when a placebo was substituted for CMI. Similarly, 89% relapsed when desipramine was substituted for CMI (Stanley & Turner,1995). Overall, the data suggests that patients can maintain the benefits of drug treatment only as long as the medication is continued and even long-term pharmacological treatment will not prevent the return of OCD symptoms when medication is stopped. There is recent evidence, however, to suggest that patients may be able to maintain an improved condition on a lower dosage after acute drug treatment (Pigott, Dubbert, L'Heureux, Canter & Murphy,1996).

    In sum, data from these studies suggests that serotonin dysregulation is evident in OCD; and yet, when the effect sizes of the various medications are compared, the most selective and potent SSRIs are not as effective as CMI, which implies that other neurological abnormalities are involved or that the genuine mechanism of action of the SSRIs for OCD is still not recognized. For example, the nature of the receptor site and the possibility of noradrenergic and dopaminergic receptor involvement in OCD are still uncertain (Stanley & Turner,1995). Moreover, alternative mechanisms of action for SSRIs have also been suggested. One study has shown that CMI produces a dramatic reduction in autonomic activity to disorder-specific and nonspecific stimuli (Stanley & Turner,1995). It is known that SSRIs affect areas of the frontal lobe, which in turn affect the autonomic division of the nervous system. As such, some researchers have speculated that SSRIs may result in a decreased metabolism in the frontal lobe which would eliminate excessive functioning in this region and consequently reduce OCD symptoms and anxiety (Stanley & Turner,1995).

    The involvement of the limbic system in the emotional response to stimuli has led researchers to focus surgical techniques for OCD on disconnecting the "orbital and medial frontal cortex from the limbic system" (Turner, Beidel & Nathan,1985,438). It is believed that OCD symptoms can be reduced by disconnecting a parietofrontal system, involving a circuit through which limbic input from the cingulate gyrus is transmitted to the inferior parietal lobe and is fed back to the cingulate (Turner, Beidel & Nathan,1985). Limbic leucotomies are reported to decrease neuroticism, depression, anxiety and obsessions, and result in decreased physiological arousal, without disturbing intellectual functioning (Turner, Beidel & Nathan,1985). In a controlled study, it was found that the severity of obsessions was reduced for the experimental group who received leucotomies, but not in the control group. However, after 5 years, the control group had also experienced an improvement in condition (Turner, Beidel & Nathan,1985). When OCD is severe and has not been responsive to other therapeutic procedures; cingulotomy, anterior capsulotomy or modified leucotomy have been used and have demonstrated beneficial results. However, it is recommended that psychosurgery be followed by behavioural and/or drug therapy, because it is not a cure for OCD; instead, it restores "the patient to a status that is more amenable to such techniques" (Andrews, Crino, Hunt, Lampe & Page,1994,273).

    Evidence for the genetic basis of OCD is derived from twin studies and evaluations of first-degree relatives. The twin studies have provided data which shows some degree of heritability, but early studies have severe methodological problems and later studies cannot dismiss the effects of social learning (Andrews, Crino, Hunt, Lampe & Page,1994). An investigation by Rasmussen and Taung revealed that 5% of parents of OCD patients met the diagnosis criteria for OCD and 11% exhibited OCD traits (Torgersen,1988). A recent study, by Black et al, reported that first degree relatives of OCD patients were "significantly more likely to develop anxiety disorders than relatives of the control group" (Andrews, Crino, Hunt, Lampe & Page,1994,267), but that the prevalence of actual OCD in either index or control groups was no larger than the estimated prevalence in the general population (Andrews, Crino, Hunt, Lampe & Page,1994). Overall, the evidence for the genetic transmission of OCD, from this type of study, is contradictory and inconclusive. Some of the discrepancy may be accounted for through differences in interview techniques or differences in proband selection, but further investigations with improved methodology are recommended.

    Other Disorders with Obsessive-Compulsive Symptoms
    Researchers have also directed attention to other disorders that exhibit OCD symptoms. Disorders that implicate basal ganglia dysfunction have been particularly important in this area. One study by Pauls, Towbin, Leckman, Zahner & Cohen (1986) reviewed the occurence of OCD among probands with Tourette's syndrome (TS). The authors proposed that there is a possible relationship between OCD and TS and that "OCD symptoms may represent a different expression of the same etiologic factors also responsible for the manifestation of TS and/or CMT (chronic multiple tics) (Pauls, Towbin, Leckman, Zahner & Cohen,1986,1180). The results show that 50% of probands met the criteria for a diagnosis of OCD and that these individuals were not significantly different from TS patients without OCD. The occurence of OCD in the families of both groups (TS with OCD and TS without OCD) was significantly higher than the control families. Finally, there was no significant difference in the risk of acquiring OCD, TS or CMT in the families of either experimental group. These results suggest that OCD, TS and tic disorders are caused by the same underlying factors, but that they are manifested differently depending on the individual patient (Pauls, Towbin, Leckman, Zahners & Cohen,1986).

    Another study of Tourette's and tic disorder in obsessive-compulsive children (Leonard et al,1992) revealed that the only difference between individuals with OCD and individuals with TS was an earlier age of onset for OCD. These groups could not be differentiated by the nature of their obsessions or compulsions and the clinical character of these disorders was essentially similar. The occurence of TS could only be predicted by early age of onset of OCD and male sex. Subjects with comorbid OCD and CMT were distinguished from subjects without comorbidity by an earlier age of onset of OCD, a higher basline anxiety rating and higher CSF 5-hydroindoleactic acid (5-HIAA) to homovanillic acid (HVA). The increased CSF 5-HIAA/HVA ratio is evidence supporting an abnormality in serotonin/dopamine ratio in OCD and TS (Leonard et al,1992). The results of this study also support the notion that OCD and TS are "alternative manifestations of the same underlying (genetic) illness (Leonard et al,1992).

    Another study investigated the occurrence of OC behaviour in Sydenham's chorea (Swedo et al,1989). This condition is a neurological disorder which is assumed to involve a basal ganglia dysfunction because of the characteristic involuntary movements of the arms and legs. Sydenham's chorea is often present in children with rheumatic fever; and therefore, this study compared OC symptoms in children who had suffered from Sydenham's chorea and children who had had rheumatic fever without chorea. It was found that subjects who previously had Sydenham's chorea scored higher on 2 different obsessionality scales than subjects who had experienced rheumatic fever. Due to the implication of basal ganglia dysfunction in Sydenham's this evidence supports other data relating OCD with a disease of the basal ganglia. The difference of the 2 groups of subjects is the presence of anticaudate and antithalamic nuclei antibodies with Sydenham's patients. The "autoantibody hypothesis" (Leonard et al,1989,248) was tested on a separate occasion, but no antibodies were found in patients with OCD; although, this result may be due to an extended interval between the incidence of the disease and the testing for antibodies.

    Finally, a unique study was undertaken when researchers were approached with an unusual animal disorder called canine acral lick dermatitis (ALD) (Rapoport, Ryland & Kriete,1992). ALD is a disorder in which the animal will lick its paws or flank to a point where ulcers and infection develop. Previous studies have shown that disorders involving repetitive excessive grooming actions, such as trichotillomania and onychophagia respond well to clomipramine (Rapoport, Ryland & Kriete,1992). From this evidence some researchers have hypothesized that OCD is similar to these disorders in that the "compulsive rituals involve phylogenetically old patterns of behavior" (Rapoport, Ryland & Kriete,1992,517). Consequently, the authors of this study proposed SSRI treatment and decided to evaluate the validity of ALD as an animal model for OCD. Clomipramine, fluoxetine and sertraline were compared with a placebo, a noradrenergic antidepressant and fenfluramine. The results were similar to most human drug trials. CMI and fluoxetine produced a 50% reduction in ALD symptoms and sertraline demonstrated a less robust effect. The authors are uncertain of the utility of ALD as an animal model for OCD. Face validity is present in that the behaviours manifested in both disorders are analogous. The similarity in SSRI efficacy also provides some predictive validity, but the construct validity for ALD is tentative because the underlying cause of both disorders is still undetermined.

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