Obsessive-compulsive disorder (OCD) has a lifetime prevalence of about 2% of the population and causes substantial impairment for many individuals.1 OCD is characterized by intrusive thoughts, images, or urges (obsessions), which are usually coupled with repetitive behaviors (compulsions) that the person feels driven to perform. These symptoms often begin in childhood and have a chronic course, which can become debilitating. Fortunately, empirically supported treatments exist for OCD, including pharmacotherapy and cognitive-behavior therapy (CBT). This article presents an introduction to one form of CBT that has accumulated the most empirical support for the treatment of OCD: exposure and response prevention (EX/RP). The fundamental processes involved in EX/RP are behavioral in nature.2 However, cognitive therapy for OCD has also been described and tested. Several clinical trials have compared CBT consisting of EX/RP to cognitive therapy, and suggested that the two treatments have similar effectiveness.3,4 However, a recent re-analysis of one of these trials suggested that EX/RP was associated with significantly better outcomes than cognitive therapy alone.5 In addition, EX/RP has been tested more extensively in the literature and is currently the recommended first-line psychotherapy for OCD.6,7 Therefore, the present article focuses on research evidence for CBT that includes EX/RP.
We begin by describing the development of EX/RP and offering a practical overview of how this treatment is typically conducted. Next, we review the research for the efficacy of EX/RP, both as a monotherapy and in combination with pharmacotherapy. We conclude with a discussion of the potential mechanisms of action for EX/RP and future directions in EX/RP research.
Development of Exposure and Response Prevention
Prior to the 1960s, OCD was considered an intractable condition, as both psychodynamic therapy and medications proved to be largely ineffective. A breakthrough occurred in the middle of the decade with the development of behaviorally oriented treatments that included prolonged exposure to anxiety-provoking stimuli coupled with strict prevention of rituals (ie, EX/RP). Meyer8 is often credited with the first trial of EX/RP for OCD, in which patients hospitalized for OCD spent 2 hours per day deliberately confronting situations and stimuli that they usually avoided, while simultaneously refraining from their rituals. The treatment was highly successful in 10 of 15 cases, and the remainder experienced at least partial improvement. Moreover, at the 5-year follow-up period, only two of these patients experienced relapse.9
Subsequently, EX/RP was expanded and refined by others.2,10,11 One important addition to the treatment was the development of imaginal exposures. Whereas in vivo exposures involve confronting real-world cues that trigger obsessions (ie, objects, situations, words or images), imaginal exposures involve asking patients to imagine in detail the disastrous consequences they fear will materialize if they do not complete their rituals (eg, their house burning down, becoming infected with HIV). Contemporary EX/RP involves a combination of both in vivo and imaginal exposures.12
A course of EX/RP typically begins with a careful assessment of the OCD symptoms to identify specific obsessional triggers and highlight the functional connection between obsessions and compulsions, which relieve the distress associated with obsessions. The therapist provides psychoeducation about OCD and the rationale for using exposures to decrease obsessional distress. The patient and therapist collaboratively build an exposure hierarchy and agree on a treatment plan. Exposure sessions involve therapist-directed repeated and prolonged confrontations with situations that provoke obsessional distress. Exposure exercises are tailored to the specific fears of the patient. For example, a patient with contamination concerns might be asked to touch door handles in a public restroom, whereas a patient with obsessions about being responsible for something terrible happening might be asked to leave his house without checking that the stove is off. Likewise, a patient with religious obsessions might be asked to purposefully confront blasphemous thoughts in an imaginal exposure.
Refraining from compulsions (response prevention) is a central component of treatment, as this allows patients to learn that anxiety and distress are tolerable and will decrease with time. During processing, the patient and therapist discuss the patient’s experience during exposures, highlighting important lessons and pointing out ways in which the patient’s expectations have been disconfirmed (ie, feared consequences do not occur).
A typical course of EX/RP includes two introductory treatment planning sessions followed by 15 exposure sessions, although longer treatment trials are sometimes necessary.12 Once sufficient progress has been made, sessions focus on relapse prevention planning. EX/RP is often delivered in an intensive fashion, with twice weekly or even daily sessions. In addition to within-session exposures, patients are also assigned self-directed exposures as homework between sessions. Thus, EX/RP requires both the patient and therapist to dedicate a substantial amount of time and effort to the treatment. However, as reviewed below, this commitment typically yields significant improvements in OCD symptoms.
Efficacy of Exposure and Response Prevention
In randomized controlled trials (RCTs), EX/RP has been shown to be superior to several other treatments, including both other psychotherapies and medication. For example, RCTs have shown EX/RP to be more effective than both progressive muscle relaxation13 and anxiety management training.14 Nakatani et al.15 compared EX/RP to a psychologic placebo condition (autogenic training) and fluvoxamine and found that EX/RP was superior to both. In another RCT, Foa et al.16 found that EX/RP with or without clomipramine (CMI) was superior at reducing OCD symptoms compared to CMI alone and to pill placebo. Meta-analyses of EX/RP treatment trials have found large pre- and posttreatment effect sizes, ranging from 1.12 to 1.39.17,18 A recent meta-analysis19 of RCTs comparing EX/RP to medications found that EX/RP proved more effective than serotonin reuptake inhibitors (SRIs), although this difference was reduced when comparing EX/RP only to selective SRIs (SSRIs).
EX/RP is also effective when combined with pharmacotherapy. SRIs (clomipramine and the SSRIs) are the only US Food and Drug Administration-approved first-line medications for OCD. However, SRIs typically lead to only a partial response.20 Several RCTs have supported the use of EX/RP as an SRI augmentation strategy in such instances. Tenneij et al.21 found that adding EX/RP to pharmacotherapy (with paroxetine or venlafaxine) led to superior outcomes as compared to continuing pharmacotherapy alone in patients with mild OCD symptoms. In a subsequent study, Simpson et al.22 randomized OCD patients with clinically significant symptoms despite at least 12 weeks of an SRI to receive either EX/RP or stress management (control condition). Both treatments were delivered over 8 weeks via seventeen 90-minute sessions. Patients receiving EX/RP had significantly lower symptoms at the end of treatment, and these effects were maintained for most patients over a 6-month follow-up period.23 Finally, Simpson et al.24 compared augmenting SRIs with EX/RP, low-dose risperidone (mean dose = 1.9 mg/day), and pill placebo. Patients who received EX/RP had superior outcomes to both pill groups, and risperidone was not any better than placebo. Current practice guidelines recommend EX/RP as the first option for SRI augmentation.7
Predicting Exposure and Response Prevention Outcome
Although the evidence supporting EX/RP is substantial, not all patients benefit. Across multiple studies, about 25% to 30% of patients who begin EX/RP discontinue treatment prematurely; of those who complete treatment, up to 24% do not respond.20 Substantial effort has been made to identify predictors of improvement with EX/RP to identify patients at risk for poor outcome. Not surprisingly, the degree to which patients adhere to EX/RP procedures appears to be the most robust predictor of treatment outcome.25 In line with the separation of hoarding from OCD to form a distinct diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition,26 prominent hoarding symptoms have been associated with poorer response to EX/RP than other OCD symptoms.27
Other predictors of poor EX/RP outcomes have included higher initial OCD symptom severity and severe comorbid depression.27 However, a recent meta-analysis found no relationship between either pretreatment OCD severity or depression severity and EX/RP treatment effect size.17 One possibility is that these individual risk factors might affect outcome by reducing patients’ adherence to treatment procedures.25 In general, the effect sizes for individual predictors tend to be relatively small, which may explain the inconsistency between studies in terms of which variables emerge as significant predictors.17 However, when combined together in aggregate, predictor variables account for a substantial proportion of the variability in EX/RP outcomes, suggesting that evaluating a combination of risk factors may identify individuals at risk for poor outcomes.28
Enhancing Exposure and Response Prevention Outcome
Given the established efficacy of EX/RP, recent research has focused on ways to modify EX/RP to enhance its potency. Because noncompliance with treatment procedures is the strongest predictor of poor EX/RP outcome, clinical researchers have attempted to improve treatment adherence and engagement. For example, EX/RP has been modified to incorporate elements of motivational interviewing (MI), a patient-centered approach designed to resolve ambivalence and enhance treatment willingness. In an open pilot trial, the addition of MI to EX/RP appeared to enhance treatment participation in five OCD patients,29 although a subsequent randomized trial of EX/RP plus MI did not find this combined treatment to be more effective at reducing OCD symptoms than EX/RP alone.30 Therefore, MI techniques may not be required for every patient, but could be flexibly deployed in cases where resistance arises.
Recent research has also attempted to improve EX/RP outcomes by incorporating medications that facilitate extinction learning, an important factor in EX/RP (discussed below). D-cycloserine (DCS) is a partial agonist at the N-methyl-D-aspartate receptor that has been shown to increase extinction learning in animal research, and has since been used as a way to augment exposure therapy for anxiety.31 Three small randomized trials examined the ability of DCS to enhance EX/RP for OCD.32–34 The results of these trials have been mixed, indicating that adding DCS to EX/RP may not provide extra benefit compared to EX/RP alone. However, DCS appears to reduce the number of sessions needed to see a treatment response,35 suggesting that DCS augmentation may quicken improvement in EX/RP. This combination might shorten treatment time, leading to faster relief for patients and making treatment more efficient.
Increasing Access to Exposure and Response Prevention
A notable limitation of EX/RP is that well-trained EX/RP therapists are not available in all communities. To increase dissemination and access to EX/RP, several studies have incorporated technology. For example, Andersson et al.36 developed an online treatment platform that incorporates EX/RP and involves only minimal therapist contact (via phone and email). In an RCT that enrolled 101 OCD patients, this online EX/RP treatment proved more effective than an online supportive therapy, and led to clinically meaningful improvements in 60% of patients.37 Treatment programs such as this have great promise to increase EX/RP availability in a cost-effective manner in the future.
Exposure and Response Prevention Mechanism of Action
There are several theories for how EX/RP works, and these theories have influenced how EX/RP is delivered in clinical practice. Early behaviorist views held that exposure therapy reduces anxiety by dissociating pathologic stimulus-response associations for conditioned fears; the focus then was on breaking these stimulus-response associations. However, OCD does not necessarily involve learned fear.38
Foa and Kozak39 proposed that exposures activate pathologic fear structures (sets of information about feared stimuli stored in memory), and then can modify these fear structures (eg, when the feared event does not occur). In the original formulation of this emotional processing theory (EPT), initial fear activation and subsequent habituation were key elements of effective EX/RP. However, how much fear decreases from the beginning to the end of exposures is not predictive of overall outcomes.40 A modification to EPT41 proposed that exposures instead create new, nonpathologic fear structures, rather than modifying existing ones. In clinical practice, EPT emphasizes activating the patient’s anxiety response and then incorporating incompatible information (eg, disconfirmation of the feared outcomes and fear habituation), and practicing exposures in various contexts to increase the likelihood that the nonpathologic fear structure will be activated instead of the original one.42
Another theory highlights inhibitory learning as a mechanism for exposure therapy.43,44 According to this perspective, exposures allow the patient to form new memories that include safety-based information about the originally feared stimuli. These new nonfear associations then inhibit the original fear memory. Rather than emphasizing fear reduction during exposure exercises, the inhibitory learning approach stresses tolerating fear while maximizing inhibitory associations and also suggests practicing exposures in a range of situations to facilitate future memory retrieval of the inhibitory associations.40
From a cognitive perspective, EX/RP works by correcting dysfunctional beliefs that underlie OCD symptoms. According to this view, changing these beliefs is the active ingredient in treatment. In clinical practice, the cognitive perspective then frames exposures as experiments to test underlying beliefs, and uses them as one way to restructure distorted thinking. A recent analysis, however, suggests that change in beliefs may follow, rather than precede, reductions in OCD symptoms.5
There are also neurobiologic models for how EX/RP may work. For example, a recent OCD model conceptualizes compulsions as manifestations of excessive habit formation, and suggests that EX/RP may work by breaking habits through response prevention.45
Relatively little empirical research has directly tested these proposed mechanisms of EX/RP, which may not be mutually exclusive. In addition, although imaging studies have found brain changes following EX/RP (including changes in brain metabolism, neurochemistry, and function46), it is not yet clear how these brain changes are linked to specific neural processes that then lead to reductions in OCD symptoms.
Conclusions and Future Directions
EX/RP is an effective treatment to reduce OCD symptoms, both as a monotherapy and in combination with medication. Consistent research suggests that with skilled therapists and ideal conditions, more than 75% of patients respond to EX/RP, and up 40% achieve minimal symptoms. What is less clear is why some patients achieve excellent outcomes, and others do not. The field has a pressing need to be able to identify who will be helped by EX/RP and who may need an alternative treatment. In addition, although the efficacy of EX/RP has been established for some time, the exact mechanism through which EX/RP works remains to be discovered.
- Ruscio AM, Stein DJ, Chiu WT, Kessler RC. The epidemiology of obsessive-compulsive disorder in the National Comorbidity Survey Replication. Mol Psychiatry. 2010;15(1):53–63. doi:10.1038/mp.2008.94 [CrossRef]
- Foa EB. Cognitive behavioral therapy of obsessive-compulsive disorder. Dialogues Clin Neurosci. 2010;12(2):199–207.
- van Balkom AJ, de Haan E, van Oppen P, Spinhoven P, Hoogduin KA, van Dyck R. Cognitive and behavioral therapies alone versus in combination with fluvoxamine in the treatment of obsessive compulsive disorder. J Nerv Ment Dis. 1998;186(8):492–499. doi:10.1097/00005053-199808000-00007 [CrossRef]
- Whittal ML, Robichaud M, Thordarson DS, McLean PD. Group and individual treatment of obsessive-compulsive disorder using cognitive therapy and exposure plus response prevention: a 2-year follow-up of two randomized trials. J Consult Clin Psychol. 2008;76(6):1003–1014. doi:10.1037/a0013076 [CrossRef]
- Olatunji BO, Rosenfield D, Tart CD, Cottraux J, Powers MB, Smits JA. Behavioral versus cognitive treatment of obsessive-compulsive disorder: an examination of outcome and mediators of change. J Consult Clin Psychol. 2013;81(3):415–428. doi:10.1037/a0031865 [CrossRef]
- Koran LM, Hanna GL, Hollander E, Nestadt G, Simpson HBAmerican Psychiatric Association. Practice guideline for the treatment of patients with obsessive-compulsive disorder. Am J Psychiatry. 2007;164(7 Suppl):5–53.
- Koran LM, Simpson HB. Guideline Watch (March 2013): Practice Guideline for the Treatment of Patients With Obsessive-Compulsive Disorder. APA Pract. Guidel. 2013;1–22.
- Meyer V. Modification of expectations in cases with obsessional rituals. Behav Res Ther. 1966;4(4):273–280. doi:10.1016/0005-7967(66)90023-4 [CrossRef]
- Meyer V, Levy R, Schnurer A. The behavioural treatment of obsessive-compulsive disorders. In: Beech HR, ed. Obsessional States. London, UK: Methuen; 1974:233–258.
- Rachman S, Hodgson R, Marks IM. The treatment of chronic obsessive-compulsive neurosis. Behav Res Ther. 1971;9(3):237–247. doi:10.1016/0005-7967(71)90009-X [CrossRef]
- Marks IM, Hodgson R, Rachman S. Treatment of chronic obsessive-compulsive neurosis by in-vivo exposure: a two-year follow-up and issues in treatment. Br J Psychiatry. 1975;127(4):349–364. doi:10.1192/bjp.127.4.349 [CrossRef]
- Foa EB, Yadin E, Lichner TK. Exposure and Response (Ritual) Prevention for Obsessive-Compulsive Disorder. New York, NY: Oxford University Press; 2012. doi:10.1093/med:psych/9780195335286.001.0001 [CrossRef]
- Fals-Stewart W, Marks AP, Schafer J. A comparison of behavioral group therapy and individual behavior therapy in treating obsessive-compulsive disorder. J Nerv Ment Dis. 1993;181(3):189–193. doi:10.1097/00005053-199303000-00007 [CrossRef]
- Lindsay M, Crino R, Andrews G. Controlled trial of exposure and response prevention in obsessive-compulsive disorder. Br J Psychiatry. 1997;171(2):135–139. doi:10.1192/bjp.171.2.135 [CrossRef]
- Nakatani E, Nakagawa A, Nakao T, et al. A randomized controlled trial of Japanese patients with obsessive-compulsive disorder--effectiveness of behavior therapy and fluvoxamine. Psychother Psychosom. 2005;74(5):269–276. doi:10.1159/000086317 [CrossRef]
- Foa EB, Liebowitz MR, Kozak MJ, et al. Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry. 2005;162(1):151–161. doi:10.1176/appi.ajp.162.1.151 [CrossRef]
- Olatunji BO, Davis ML, Powers MB, Smits JA. Cognitive-behavioral therapy for obsessive-compulsive disorder: a meta-analysis of treatment outcome and moderators. J Psychiatr Res. 2013;47(1):33–41. doi:10.1016/j.jpsychires.2012.08.020 [CrossRef]
- Rosa-Alcázar AI, Sánchez-Meca J, Gómez-Conesa A, Marín-Martínez F. Psychological treatment of obsessive–compulsive disorder: a meta-analysis. Clin Psychol Rev. 2008;28(8):1310–1325. doi:10.1016/j.cpr.2008.07.001 [CrossRef]
- Romanelli RJ, Wu FM, Gamba R, Mojtabai R, Segal JB. Behavioral therapy and serotonin reuptake inhibitor pharmacotherapy in the treatment of obsessive-compulsive disorder: a systematic review and meta-analysis of head-to-head randomized controlled trials. Depress Anxiety. 2014;31(8):641–652. doi:10.1002/da.22232 [CrossRef]
- Simpson HB, Huppert JD, Petkova E, Foa EB, Liebowitz MR. Response versus remission in obsessive-compulsive disorder. J Clin Psychiatry. 2006;67(2):269–276. doi:10.4088/JCP.v67n0214 [CrossRef]
- Tenneij NH, van Megen HJ, Denys DA, Westenberg HG. Behavior therapy augments response of patients with obsessive-compulsive disorder responding to drug treatment. J Clin Psychiatry. 2005;66(9):1169–1175. doi:10.4088/JCP.v66n0913 [CrossRef]
- Simpson HB, Foa EB, Liebowitz MR, et al. A randomized, controlled trial of cognitive-behavioral therapy for augmenting pharmacotherapy in obsessive-compulsive disorder. Am J Psychiatry. 2008;165:621–630. doi:10.1176/appi.ajp.2007.07091440 [CrossRef]
- Foa EB, Simpson HB, Liebowitz MR, et al. Six-month follow-up of a randomized controlled trial augmenting serotonin reuptake inhibitor treatment with exposure and ritual prevention for obsessive-compulsive disorder. J Clin Psychiatry. 2013;74(5):464–469. doi:10.4088/JCP.12m08017 [CrossRef]
- Simpson HB, Foa EB, Liebowitz MR, et al. Cognitive-behavioral therapy vs risperidone for augmenting serotonin reuptake inhibitors in obsessive-compulsive disorder: a randomized controlled trial. JAMA Psychiatry. 2013;70(11):1190–1199. doi:10.1001/jamapsychiatry.2013.1932 [CrossRef]
- Simpson HB, Maher MJ, Wang Y, Bao Y, Foa EB, Franklin M. Patient adherence predicts outcome from cognitive behavioral therapy in obsessive-compulsive disorder. J Consult Clin Psychol. 2011;79(2):247–252. doi:10.1037/a0022659 [CrossRef]
- Mataix-Cols D, Frost RO, Pertusa A, et al. Hoarding disorder: a new diagnosis for DSM-V?Depress Anxiety. 2010;27(6):556–572. doi:10.1002/da.20693 [CrossRef]
- Keeley ML, Storch EA, Merlo LJ, Geffken GR. Clinical predictors of response to cognitive-behavioral therapy for obsessive-compulsive disorder. Clin Psychol Rev. 2008;28(1):118–130. doi:10.1016/j.cpr.2007.04.003 [CrossRef]
- Maher MJ, Huppert JD, Chen H, et al. Moderators and predictors of response to cognitive-behavioral therapy augmentation of pharmacotherapy in obsessive–compulsive disorder. Psychol Med. 2010;40(12):2013–2023. doi:10.1017/S0033291710000620 [CrossRef]
- Simpson HB, Zuckoff A, Page JR, Franklin ME, Foa EB. Adding motivational interviewing to exposure and ritual prevention for obsessive-compulsive disorder: an open pilot trial. Cogn Behav Ther. 2008;37(1):38–49. doi:10.1080/16506070701743252 [CrossRef]
- Simpson HB, Zuckoff AM, Maher MJ, et al. Challenges using motivational interviewing as an adjunct to exposure therapy for obsessive-compulsive disorder. Behav Res Ther. 2010;48(10):941–948. doi:10.1016/j.brat.2010.05.026 [CrossRef]
- Hofmann SG, Pollack MH, Otto MW. Augmentation treatment of psychotherapy for anxiety disorders with D-cycloserine. CNS Drug Rev. 2006;12(3–4):208–217. doi:10.1111/j.1527-3458.2006.00208.x [CrossRef]
- Kushner MG, Kim SW, Donahue C, et al. D-cycloserine augmented exposure therapy for obsessive-compulsive disorder. Biol Psychiatry. 2007;62(8):835–838. doi:10.1016/j.biopsych.2006.12.020 [CrossRef]
- Storch EA, Merlo LJ, Bengtson M, et al. D-cycloserine does not enhance exposure-response prevention therapy in obsessive-compulsive disorder. Int Clin Psychopharmacol. 2007;22(4):230–237. doi:10.1097/YIC.0b013e32819f8480 [CrossRef]
- Wilhelm S, Buhlmann U, Tolin D, et al. Augmentation of behavior therapy with D-cycloserine for obsessive-compulsive disorder. Am J Psychiatry. 2008;165(3):335–341. doi:10.1176/appi.ajp.2007.07050776 [CrossRef]
- Chasson GS, Buhlmann U, Tolin DF, et al. Need for speed: evaluating slopes of OCD recovery in behavior therapy enhanced with D-cycloserine. Behav Res Ther. 2010;48(7):675–679. doi:10.1016/j.brat.2010.03.007 [CrossRef]
- Andersson E, Ljótsson B, Hedman E, et al. Internet-based cognitive behavior therapy for obsessive compulsive disorder: a pilot study. BMC Psychiatry. 2011;11:125. doi:10.1186/1471-244X-11-125 [CrossRef]
- Andersson E, Enander J, Andrén P, et al. Internet-based cognitive behaviour therapy for obsessive-compulsive disorder: a randomized controlled trial. Psychol Med. 2012;42(10):2193–2203. doi:10.1017/S0033291712000244 [CrossRef]
- Rachman S. The passing of the two-stage theory of fear and avoidance: fresh possibilities. Behav Res Ther. 1976;14(2):125–131. doi:10.1016/0005-7967(76)90066-8 [CrossRef]
- Foa EB, Kozak MJ. Emotional processing of fear: exposure to corrective information. Psychol Bull. 1986;99(1):20–35. doi:10.1037/0033-2909.99.1.20 [CrossRef]
- Abramowitz JS. The practice of exposure therapy: relevance of cognitive-behavioral theory and extinction theory. Behav Ther. 2013;44(4):548–558. doi:10.1016/j.beth.2013.03.003 [CrossRef]
- Foa EB, McNally RJ. Mechanisms of change in exposure therapy. In: Rapee RM, ed. Current Controversies in the Anxiety Disorders. New York, NY: Guilford Press; 1996:329–343.
- Foa EB, Huppert JD, Cahill SP. Update on emotional processing theory. In: Rothbaum BO. The Nature and Treatment of Pathological Anxiety. New York, NY: Guilford Press; 2006:2–24.
- Craske MG, Kircanski K, Zelikowsky M, Mystkowski J, Chowdhury N, Baker A. Optimizing inhibitory learning during exposure therapy. Behav Res Ther. 2008;46(1):5–27. doi:10.1016/j.brat.2007.10.003 [CrossRef]
- Craske MG, Liao B, Brown L, Vervliet B. Role of inhibition in exposure therapy. J Exp Psychopathol. 2012;3(3):322–345. doi:10.5127/jep.026511 [CrossRef]
- Gillan CM, Robbins TW. Goal-directed learning and obsessive-compulsive disorder. Philos Trans R Soc Lond B Biol Sci. 2014;369(1655). doi:10.1098/rstb.2013.0475 [CrossRef]
- Barsaglini A, Sartori G, Benetti S, Pettersson-Yeo W, Mechelli A. The effects of psychotherapy on brain function: a systematic and critical review. Prog Neurobiol. 2014;114:1–14. doi:10.1016/j.pneurobio.2013.10.006 [CrossRef]