Version May 2024
INTRODUCTION — Depersonalization/derealization disorder (DDD) is characterized by persistent or recurrent depersonalization and/or derealization that cause clinically significant distress or impairment. Reality testing remains intact, and the disturbance is not attributable to another medical condition or the physiologic effects of a substance or medication [1]. Depersonalization and/or derealization can be precipitated by acute or chronic traumatic experiences.
DDD has a prevalence of approximately 1 to 2 percent and is associated with significant morbidity, yet often goes undetected or misdiagnosed, leading to delays in treatment. DDD has high rates of comorbidity with depression and anxiety disorders, as well as avoidant and borderline personality disorders [1].
This topic discusses our overview of treatment for individuals with DDD. The epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis of DDD are discussed separately. Treatment with psychotherapy, including its administration, is discussed elsewhere. (See "Depersonalization/derealization disorder: Epidemiology, clinical features, assessment, and diagnosis" and "Depersonalization/derealization disorder: Psychotherapy".)
DEFINITIONS
Depersonalization — Depersonalization is a persistent or recurrent feeling of detachment or estrangement from oneself. An individual experiencing depersonalization may report feeling like an automaton, as if in a dream, or as if watching themself in a movie. Individuals with depersonalization may report the sense of being an outside observer of their mental processes or their body, or at its extreme, lacking a sense of self. Another common feature is hypoemotionality (emotional numbing or blunting), specifically detachment from feelings that an individual knows they have. Often a feeling of loss of control over their thoughts, perceptions, or actions are reported.
Derealization — Derealization is a subjective sense of detachment or unreality regarding the world around (eg, individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, seen through a glass, bubble, or veil, or visually distorted).
GENERAL PRINCIPLES OF TREATMENT — For all individuals, we incorporate the following elements of psychoeducation and supportive psychotherapy throughout treatment [2]:
Education and reassurance — We make sure to name the condition and provide information about the nature and course of the disorder. Many patients with depersonalization/derealization disorder (DDD) have struggled for years with misdiagnosis or inaccurate labelling of their symptoms. Educating the patient may be reassuring and give them a sense of hope. Specifically, we reassure the patient that:
●The condition will not evolve into a psychotic disorder [2].
●There is no evidence linking the disorder to permanent brain damage.
●Many patients improve or remit over time, with treatment or spontaneously. Precise data on prognosis are not available [3].
●Though not well studied, the heritability of DDD appears to be limited [3].
Discourage substance use — We advise patients with depersonalization triggered by illicit drug use to stop the use or risk intensification of symptoms. We explain to these patients that it is likely that they have an underlying disposition to depersonalize that may have been triggered by illicit substances or psychosocial stressors. Most patients with symptom onset triggered by substance misuse or substance use disorder become “drug phobic” after onset and stop using the substance; however, a small minority continue to use substances.
Emphasize neuropsychologic nature of symptoms — We emphasize that although the symptoms feel physical, the disorder is neuropsychologic. This understanding can provide the patient with a sense of control over the symptoms that may otherwise be perceived as physically imposed rather than mentally maintained. However, evidence suggests that specific brain regions are involved in the experience of dissociation underscoring opportunities for treatment of DDD [4-6].
INITIAL TREATMENT
CBT combined with exploratory psychotherapy as first-line treatment — For most patients, our preferred first-line treatment of depersonalization/derealization disorder (DDD) is with a combination of cognitive-behavioral therapy (CBT) to contain and alleviate acute symptoms, along with exploratory psychotherapy to address associated acute stressors.
As patients learn to use cognitive-behavioral techniques to lessen the intensity of their symptoms and the ruminations, checking, and avoidance associated with them, they are able to free up mental space to begin understanding and contextualizing their depersonalized experience and to create a meaningful narrative. For example, a patient may come to realize that a recent relationship loss or life transition was more traumatic than they were aware of, because it fundamentally shook up their sense of self or identity, or because it triggered unprocessed memories of a remote trauma from their past.
The focus of CBT for DDD is on normalizing the symptoms and their interpretation; blocking of ruminative thoughts surrounding the condition; diminishing checking behaviors; and grounding exercises that promote feeling “present.” Obsessional elaborations, phobic avoidance and checking behaviors are quite common in DDD, especially earlier in its course. For example, patients may keep looking in the mirror to see if their face looks more or less real; they are taught to instead to make a cognitive correction ("my face is real regardless of how it will look in the mirror”) and to resist mirror checking. One example of a grounding exercise engages multiple sensory modalities is the 5-4-3-2-1: the patient mindfully engages with the realness of five things they can see, four things they can touch, three things they can hear, two things they can smell, and one thing they can taste.
The efficacy for CBT in the treatment of DDD is based on clinical experience and a single uncontrolled prospective trial [7]. In the trial, from among 21 participants with DDD treated with CBT, 29 percent of them no longer met criteria for DDD at the end of therapy. CBT has not been compared with medications in randomized trials. However, in our clinical experience psychotherapy with all applicable modalities reduces the depersonalization and derealization associated with DDD, while medication has only been found to be effective for select target symptoms [8].
There are no clinical trials for other psychotherapy modalities, but clinical experience suggests that they can be quite effective.
Treatment of DDD with psychotherapy, including its administration, is discussed elsewhere. (See "Depersonalization/derealization disorder: Psychotherapy".)
Alternative first-line treatment for specific populations
Affect intolerance, alexithymia, identity confusion, trauma, and attachment disturbances — For individuals with symptoms of affect intolerance, alexithymia, unstable sense of identity, or with early trauma-related attachment disturbances, and in cases where the individual can critically examine their thoughts and feelings, we recommend beginning with psychodynamic psychotherapy. However, CBT may be more effective in individuals who engage in ruminations, checking or avoidance behaviors.
●Affect intolerance (eg, sensitivity to and intolerance of unpleasant emotional states).
●Alexithymia (eg, difficulty verbalizing or identifying internal emotional states). Individuals who have difficulty knowing their emotional states consequently have difficulty with the emotional processing of both recent stressors and more remote experiences that are contributing to their depersonalized state of mind.
●Identity confusion (eg, unstable or poorly consolidated sense of identity). This is particularly common with young adults first presenting with DDD in the context of major life and role transitions.
●Childhood maltreatment, especially emotional maltreatment (eg, constant criticism, threats, or rejection).
●Attachment disturbances. Alongside trauma, insecure attachment, and in particular fearful attachment, is common in DDD [9].
Treatment of DDD with psychodynamic psychotherapy and other psychotherapies are reviewed in greater detail separately. (See "Depersonalization/derealization disorder: Psychotherapy", section on 'Psychotherapies'.)
Co-occurring depression or anxiety — For individuals with DDD with co-occurring depression or anxiety, we suggest first-line treatment combining appropriate psychotherapy with either a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). (See 'Initial treatment' above.)
●Choosing and titrating serotonin reuptake inhibitors – We individualize the choice of serotonin reuptake inhibitors (eg, SSRI or SNRI) based on side effect profiles of medications, drug-drug interactions, patient treatment history, and patient preference. Antidepressant medications including starting dose, daily dose and half -life are presented on the associated table (table 1).
Time to onset of clinically meaningful effect varies by patient but can be four to six weeks or longer. Therapeutic doses of SSRI and SNRIs in the treatment of comorbid DDD and anxiety or depression are the same as for the treatment noncomorbid anxiety or depression. As examples:
•For treatment of DDD with concurrent depression, when using sertraline, we recommend beginning at 25 to 50 mg per day and titrating up by 50 mg each week until clinical effect is seen, side effects limit further titration or maximum dose of 200 mg per day is reached.
•For treatment of DDD with comorbid anxiety we begin at a slightly lower dose to avoid initial insomnia or worsening anxiety. When using sertraline we would begin at 12.5 to 25 mg per day and titrate as above.
Further discussion of the treatment of depression or anxiety with serotonin reuptake inhibitors including initial dose, titration, and side effects can be found in other topics. (See "Generalized anxiety disorder in adults: Management", section on 'Initial Pharmacotherapy' and "Unipolar major depression in adults: Choosing initial treatment", section on 'Choosing a treatment regimen'.)
●Efficacy of serotonin reuptake inhibitors for DDD – While limited data exists to support the use of serotonin reuptake inhibitors in the treatment of DDD, their use in the treatment of anxiety and depression are supported by randomized trials [10-15]. In our clinical experience, symptoms of DDD will often lessen as the co-occurring disorder is treated, especially in the acute phase of the illness. If left untreated, these symptoms may fuel an intensification of symptoms of DDD [3].
Limited data available on the treatment of DDD with SSRIs do not suggest clear improvement in symptoms. In the only randomized trial comparing an SSRI with placebo for DDD, 50 subjects with DDD without a diagnosis of current comorbid mood or anxiety disorder, were assigned to 10 weeks of treatment with fluoxetine (10 mg to 60 mg) versus placebo [16]. At treatment end, both fluoxetine and placebo led to similar modest improvements on clinician rated (Depersonalization Severity Scale) and self-report scales (Dissociative Experience Scale). However, clinical global improvement was greater in the fluoxetine than in the placebo group, and participants subjectively attributed this improvement to being less distraught by their DDD symptoms. Furthermore, in a retrospective report of patients with DDD who were consecutively recruited to research studies, among 60 individuals treated with SSRIs, 62 percent reported being the same or worse (as measured by the Dissociative Experience Scale) while among 9 subjects treated with SNRIs, 100 percent reported being the same or worse [3].
Although head to head comparisons between psychotherapy alone and combined psychotherapy with medication have not been made, it could be reasonably argued that for any patient with DDD and comorbid depression or anxiety, medication is better started sooner rather than later.
For individuals with severe, disabling anxiety who do not have a history of a substance use disorder, we occasionally add a benzodiazepine to the serotonin reuptake inhibitor and continue it for four to six weeks (ie, until the antidepressant has had time to take effect). For example, in an individual with intense and disabling anxiety who has started on a serotonin reuptake inhibitor, we would start clonazepam at a dose of 0.5 mg once and titrate slowly to two to three times daily over one week. Maximum daily dose is 4 mg/day. We continue the benzodiazepine for about four to six weeks and then taper over several weeks. While there are not controlled trials of benzodiazepines in the treatment of DDD, in the retrospective report above [3], 35 patients with DDD were treated with benzodiazepines, and 49 percent reported no change or worsening of their symptoms, while 51 percent reported slight to definite improvement on the Dissociative Experience Scale. (See "Generalized anxiety disorder in adults: Management", section on 'Adjunctive therapy for early side effects' and "Generalized anxiety disorder in adults: Management", section on 'Benzodiazepines'.)
SUBSEQUENT TREATMENT — Our subsequent treatment of individuals is discussed below. We monitor patients for treatment response at each visit. We recommend measuring improvement by patient reports of fewer dissociative symptoms and a greater sense of resilience to triggers and adversities than prior to treatment. It is helpful to use clinical rating scales to confirm the diagnosis and monitor for symptomatic improvement in cases where change is unclear. (See "Depersonalization/derealization disorder: Epidemiology, clinical features, assessment, and diagnosis", section on 'Rating scales'.)
Robust response — Data are inadequate to guide the duration of treatment for depersonalization/derealization disorder (DDD). Our preference, based on clinical experience, are as follows:
●Robust response to medication alone – We continue medication for a minimum of one year. At that time, we discuss the risks and benefits of continuing medication versus stopping medication. In individuals with a severe disorder (ie, prominent psychosocial disability, difficulty stabilizing symptoms, suicidal thoughts), we often continue medication for a longer period of time (up to 24 months or indefinitely). If tapering medication is chosen, we typically taper over one to three months and closely follow the patient for symptom relapse.
●Robust response to psychotherapy alone – We continue treatment for at least six months to one year after satisfactory improvement, to ensure that the gains hold up under the challenges of daily life. We encourage those with recurrent symptoms to reconnect for further booster sessions.
●Robust response to combined treatment – We typically taper the medication first (after 8 to 12 months or more) while continuing to monitor symptoms and provide psychotherapy. If stability is maintained without medication, we typically decrease the frequency of psychotherapy over one to two months.
Inadequate response — No treatment has consistently been found to be effective for DDD. Our preference is based on clinical experience and patient preference.
Noncomorbid DDD — For individuals with noncomorbid DDD (ie, no comorbid depression, anxiety, obsessional or compulsive behaviors), who have not responded to a trial of either cognitive-behavioral therapy (CBT) or psychodynamic psychotherapy our preference for subsequent treatment is with lamotrigine.
Comorbid DDD — For individuals with comorbid DDD who have not responded to combined treatment with psychotherapy (either CBT or psychodynamic psychotherapy) with a selective serotonin reuptake inhibitor (SSRI), our preference is augmentation of the SSRI with the antiseizure medication, lamotrigine [17-19].
●Lamotrigine – We typically start lamotrigine 25 mg per day for the first two weeks of treatment, then increased to 50 mg daily in divided doses for weeks 3 and 4. The dose is titrated to 100 mg daily on week 5 then 200 mg daily on week 6, each in divided doses. A common maintenance dose is 200 mg daily, but total daily doses up to 400 mg have been used. Lamotrigine has a boxed warning due to the possibility of serious rash including Stevens-Johnson syndrome. Starting dose and titration rates dose and rates must be adjusted in individuals taking medications that interact with lamotrigine metabolism. (See "Antiseizure medications: Mechanism of action, pharmacology, and adverse effects", section on 'Lamotrigine'.)
In three clinical trials the mood stabilizing anticonvulsant medication, lamotrigine, has shown conflicting results in the treatment of DDD [17-19].
For example, in a randomized trial including 74 individuals with DDD (but without other psychiatric comorbidity,) were assigned to treatment with 12 weeks of lamotrigine up to 300 mg versus placebo [19]. At treatment end, the percentage of subjects in the lamotrigine group who responded (defined as a 50 percent reduction on the Cambridge Depersonalization Scale) was greater than that in the placebo group (72 versus 16 percent, respectively). A concern about this study was the description of enrolled patients as “without psychiatric comorbidity,” which is unusual given the high rates of comorbidity in this population. However, in two other trials, interpretation is limited due to small sample size and conflicting results [17,18]. (See "Depersonalization/derealization disorder: Epidemiology, clinical features, assessment, and diagnosis", section on 'Comorbid conditions'.)
TREATMENT RESISTANCE — For continued or persistent inadequate response despite treatment with the above, other options include longer-term psychotherapy, hypnosis, or other medication strategies. In the absence of data comparing the efficacy of these interventions, the selection among them is made on the basis of patient preference and treatment availability.
●Longer-term psychotherapy – In individuals with depersonalization/derealization disorder (DDD) who experience an inadequate response to initial treatment, we encourage longer-term psychotherapy to better contain persisting symptoms and maximize functioning. Longer-term psychotherapy is typically given weekly for from two to five years. In our experience, some individuals, particularly those who are experiencing some benefit to the psychotherapy may actively seek out longer term psychotherapy. Additionally, after experiencing some benefit to the psychotherapy, those that may be less open to prolonged psychotherapy may be agreeable. We typically suggest longer-term psychotherapy including a combination of cognitive-behavioral therapy (CBT) and psychodynamic or supportive psychotherapy addressing underlying conflicts and traumas. (See "Depersonalization/derealization disorder: Psychotherapy", section on 'Cognitive-behavioral therapy' and "Depersonalization/derealization disorder: Psychotherapy", section on 'Psychodynamic therapy' and "Depersonalization/derealization disorder: Psychotherapy", section on 'Supportive psychotherapy'.)
●Hypnosis – In our experience, hypnosis can be a useful tool for treating patients with DDD who have not adequately responded to CBT. Hypnosis, a state of focused concentration may be useful in helping patients reconceptualize and control their symptoms of depersonalization or derealization [20-22].
There are no clinical trials testing the efficacy of hypnosis in patients with DDD. Treatment of DDD with hypnosis is reviewed in greater detail separately. (See "Depersonalization/derealization disorder: Psychotherapy", section on 'Hypnosis'.)
●Medication strategies – For individuals with an inadequate response to management with psychotherapy and medication management to this point, our preference is treatment with clomipramine. In cases where clomipramine is not preferred, naltrexone is a reasonable alternative. In our clinical experience, either clomipramine or naltrexone may be beneficial for symptoms of hypoemotionality or emotional numbing (which may be present either as a symptom of the disorder or a side effect to treatment with a selective serotonin reuptake inhibitor [SSRI]). Neither has been studied in randomized trials for DDD.
•Clomipramine – Due to drug interactions, our preference is to decrease SSRI medication while titrating clomipramine (cross taper). When using clomipramine, we typically begin at 25 mg each evening and titrate every three to four days in 25 to 50 mg increments to 100 mg per day depending on clinical response and tolerability. We typically monitor at 100 mg for up to one week and then continue titration by 50 mg to maximum dose of 250 mg/day given in a single dose at night. Further discussion of the use of clomipramine including dose, titration, cross taper, and medication interactions can be found elsewhere. (See "Tricyclic and tetracyclic drugs: Pharmacology, administration, and side effects", section on 'Clomipramine' and "Switching antidepressant medications in adults", section on 'SSRI to tricyclic'.)
In our clinical experience, clomipramine has similar efficacy to other serotonin reuptake inhibitors in treating DDD, though for some may be less well tolerated. Conversely, some DDD patients who are highly sensitive to the numbing adverse effects of serotonin reuptake inhibitors may do better with clomipramine. Evidence of efficacy was supported by a clinical trial [23].
•Naltrexone – In individuals with inadequate response to treatment with clomipramine, or when clomipramine is to be avoided, we prefer naltrexone as our next choice. We begin naltrexone at 50 mg per day and increase by 50 mg every one to two weeks, as tolerated, until an adequate response is seen or maximum dose of 100 mg per day is reached. We check liver functions (aspartate aminotransferase test alanine aminotransferase test), and total bilirubin at baseline, 8 to 12 weeks after beginning the medication, then quarterly thereafter. We don’t initiate treatment if values are two times the upper limit of normal. Common side effects include nausea, headache, and dizziness (which typically subside with continued use).
Naltrexone has not been studied in randomized clinical trials for DDD. A small uncontrolled trial including 14 patients with DDD, reported an average 30 percent improvement with four patients reporting marked improvement on validated scales [8]. In our clinical experience, the use of naltrexone in DDD is limited by poor tolerability and higher doses and often does not result in a marked amelioration of symptoms. However, some patients with chronic and severe dissociation report improvement when taking naltrexone, and relative relapse if they stop.
OTHER TREATMENTS WITH MINIMAL SUPPORT — We suggest one or more of the following treatments only in cases where there has been no response to the above treatments. Minimal data supports the use of these interventions in the treatment of depersonalization/derealization disorder (DDD). Our choice is based on treatment availability, patient preference and prior treatment history.
●Supportive psychotherapy – Some individuals with chronic DDD may benefit from long term supportive psychotherapy.
Although supportive psychotherapy has not been tested in the treatment of DDD, in our clinical experience it can be helpful in maintaining or improving occupational and social functioning, and in lessening the severe distress often associated with the disorder. It appears to do this by cultivating an attitude of acceptance within the context of striving for change. Participation in supportive psychotherapy by family members and significant others (who may have a limited understanding of DDD or may misunderstand the disorder) can at times be very helpful. Further discussion of supportive psychotherapy in the treatment of DDD can be found elsewhere. (See "Depersonalization/derealization disorder: Psychotherapy", section on 'Supportive psychotherapy'.)
●Stimulants or related medication – We occasionally use stimulants or related medications (eg, methylphenidate, atomoxetine, modafinil, donepezil) in individuals refractory to all treatments. This is particularly true in individuals with cognitive complaints, such as attention or memory, associated with DDD. Stimulants can be used for augmentation if there has been partial response to other medications, or switched if there has been no notable response. There are no randomized trials supporting their use and case reports have not consistently supported their use. However, based on our clinical experience, a small number of selected individuals with very prominent cognitive complaints treated with these medications may feel more grounded [3].
●Antipsychotic medications – We prefer to use antipsychotic medications as augmentation or monotherapy in patients with DDD accompanied by overvalued ideas, or psychosis. Though, by definition, reality testing is intact in DDD, individuals may either have distinct psychotic conditions, or may have developed highly overvalued ideas, bordering on psychosis (similar to those seen in obsessive-compulsive disorder). However, there are no controlled trials investigating their use in DDD [2]. In our clinical experience, patients often report feeling more dissociated or “cloudy” with more sedating agents. Our preference is to use aripiprazole or risperidone, as these are less sedating and can reduce symptoms of anxiety, depression, and overvalued ideas.
●Transcranial magnetic stimulation (TMS) – Given the cost and time commitment of TMS treatment (which is not US Food and Drug Administration [FDA]-approved for DDD), alongside the absence of controlled and replication trials for this modality, we recommend that it be used after psychotherapy and medication trials have been exhausted. Small open trials of TMS in patients with DDD have shown promising results [24,25]. As examples:
•TMS provided daily for three weeks (five sessions/week) was associated with decreased DDD symptoms in 6 of 12 patients studied. Five of the six patients received three additional weeks of treatment, experiencing a 68 percent reduction in DDD symptoms from baseline; TMS targeted the right inferior parietal lobule [24].
•In a smaller open trial [25], seven patients with medication-resistant DDD were treated with up to 20 sessions of right-sided TMS to the ventrolateral prefrontal cortex for 10 weeks, with an average 44 percent reduction in symptoms.
Patients with other comorbid mental disorders that clearly respond to TMS, such as depression and obsessive-compulsive disorder, are candidates for a TMS trial.
Treatment of other disorders (eg, unipolar major depression, obsessive-compulsive disorder, functional neurologic symptom disorder and somatic symptom disorder) using TMS are discussed elsewhere. (See "Unipolar depression in adults: Overview of neuromodulation procedures", section on 'Repetitive transcranial magnetic stimulation' and "Deep brain stimulation for treatment of obsessive-compulsive disorder", section on 'Alternative interventions' and "Functional neurological symptom disorder (conversion disorder) in adults: Treatment", section on 'Repetitive TMS'.)
●Other interventions – There are no controlled trial of electroconvulsive therapy for the treatment of DDD. Retrospective reports have shown no benefit, or worsening symptoms [2]. Stellate ganglion blockade, vagus nerve stimulation, and deep brain stimulation have not been studied.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dissociative disorders".)
SUMMARY AND RECOMMENDATIONS
●Definitions – Depersonalization is a persistent or recurrent feeling of detachment or estrangement from oneself.
Derealization is a subjective sense of detachment or unreality regarding the world around them (eg, individuals or objects are experienced as unreal, dreamlike or visually distorted). (See 'Definitions' above.)
●Cognitive-behavioral therapy (CBT) with exploratory psychotherapy as first-line treatment – For most patients with depersonalization/derealization disorder (DDD), we suggest first-line treatment with a combination of CBT to contain and alleviate acute symptoms, along with exploratory psychotherapy to address associated acute stressors, rather than other forms of psychotherapy (Grade 2C).
●Alternative psychotherapeutic approaches targeting affect intolerance, alexithymia, identity confusion, acute stressors, trauma and attachment issues – For individuals with DDD who are not overwhelmed by acute symptoms, who can critically examine their thoughts/feelings, and in whom the fluctuation of symptoms is linked to difficulties in emotional processing, or of traumatic origin, we suggest psychodynamic psychotherapy rather than CBT (Grade 2C). (See 'Affect intolerance, alexithymia, identity confusion, trauma, and attachment disturbances' above.)
●Combined modality for co-occurring depression or anxiety – For patients with DDD with co-occurring depression, anxiety disorder, or severe obsessional or compulsive symptoms, we suggest first-line treatment with the chosen psychotherapy plus a serotonin reuptake inhibitor (ie, a selective serotonin reuptake inhibitor [SSRI] or serotonin-norepinephrine reuptake inhibitor [SNRI]) rather than psychotherapy alone (Grade 2C). (See 'Co-occurring depression or anxiety' above.)
●Subsequent treatment
•Robust response – We continue medication for a minimum of 8 to 12 months or longer in those with severe disorder. (See 'Robust response' above.)
We continue psychotherapy for a minimum of 6 months. We encourage booster sessions for symptom recurrence.
•Inadequate response – For individuals with noncomorbid DDD, who have not responded to a trial of either CBT or psychodynamic psychotherapy we suggest treatment with lamotrigine (Grade 2C). (See 'Noncomorbid DDD' above.)
For individuals with comorbid DDD who have had inadequate response to both psychotherapy and an SSRI, our preference is augmentation with lamotrigine (Grade 2C). (See 'Comorbid DDD' above.)
●Treatment resistance – For continued or persistent inadequate response despite treatment with the above, other options include longer-term psychotherapy, hypnosis, or other medication strategies such as clomipramine or naltrexone. If these are ineffective, we occasionally use supportive psychotherapy, or pharmacologic management with a stimulant or second-generation antipsychotic. Transcranial magnetic stimulation is used only after inadequate response to the above treatments. As there is limited data in support of these treatments, and no data comparing efficacy, the selection among them is made on clinician experience, patient preference, and availability of treatment. (See 'Treatment resistance' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
