Psychiatric Annals

CME Article 

Psychopharmacologic Treatments for Dissociative Identity Disorder

Richard J. Loewenstein, MD

Abstract

Dissociative identity disorder (DID) can be understood as an extreme variant of complex posttraumatic stress disorder (CPTSD), a construct that attempts to account for the myriad dimensions of disrupted function, beyond the core symptoms of PTSD, in survivors of repeated, sustained traumatic experiences that occur over long periods of time, multiple developmental periods, or both.1–3 These disruptions include difficulties with regulation of mood that are reflected in severe affective dysregulation; problems in regulation of state stability and consciousness; difficulties with sense of self and body image, with secondary problems in maintaining a stable sense of identity, eating disorders, lack of attention to medical needs, and somatization; alterations in the ability to form relationships with intense mistrust co-existing with vulnerability to victimization and exploitation; deformations in self-attribution and systems of meaning with the world seen as dangerous and traumatizing and the self as damaged, shameful, defective, and responsible for traumatization; and a significant propensity for self-destructiveness including suicide attempts, substance abuse, self-injury, and risk taking behaviors.

Studies comparing DID and PTSD subjects on neurobiological variables such as salivary cortisol, 24-hour urine catecholamines, low-dose dexamethasone suppression test, and hippocampal and amygdala volumes measured using magnetic resonance imaging show few differences between DID and PTSD patients.4 There are both clinical and neurobiological similarities between DID and complex PTSD.

Dissociative experience appears to be dependent on a broad range of alterations in neurochemical systems. Current neurobiological theories of dissociation suggest a possible role for glutamate in at least some dissociative symptoms. High-dose ketamine, an N-methyl D-aspartate (NMDA) receptor antagonist and glutamate agonist, produces dose-dependent increases in symptoms such as slowed perception of time, tunnel vision, derealization, and depersonalization, similar to that described by acute trauma victims, with “peritraumatic dissociation.”5–7 The neurotoxic effects of glutamate on brain cells is thought to account, in part, for the structural brain changes in the hippocampus found in MRI studies of DID and PTSD subjects and controls.8–10

In some studies, dissociation measures strongly correlated with volume loss in key brain regions implicated in PTSD.11 Challenge studies with marijuana, the serotonin agonist metachlorophenylpiperazine (mCPP), and the α-2 antagonist yohimbine suggest that both serotonin and noradrenergic systems may play roles at least in the generation of “positive” dissociative symptoms such as flashbacks and other intrusive PTSD symptoms.4,5 In studies of military subjects undergoing high-stress training, a strong negative relationship was found between levels of the anxiolytic peptide neuropeptide Y (NPY) and acute dissociative symptoms, primarily perceptual changes, depersonalization, and derealization.12,13

A broad range of altered psychophysiological responses to stress also appears to underlie dissociative experience. Functional magnetic resonance imaging (fMRI) studies have found neural network patterns that differentiate PTSD subjects with and without dissociation.14,15 A subgroup of these dissociative PTSD subjects showed decreased heart rate with a traumatic script, further supporting the idea of a different psychobiology to dissociative PTSD, possibly involving increased endorphinergic tone, vagal tone, or both.16

Preclinical studies using fMRI and postitron emission tomography (PET) scans have begun to suggest neural networks that may characterize dissociative amnesias, as well as the sequestration of affect and memory in DID alternate identities.16–18 Despite these findings, other core DID symptoms such as development of alternate identities, switching, passive-influence, pseudopsychotic dissociative hallucinosis, recurrent complex amnesias, and DID autohypnotic symptoms do not have a known neurobiology and may be caused by alterations in multiple neurobiological substrates and systems.19

Psychopharmacology for the patient with DID must be understood in the context of the total treatment of the patient (Chefetz, see page 657, and Welzant, see page 678). In DID treatment, psychopharmacologic interventions are primarily adjunctive and empirical in nature, as no double-blind, placebo-controlled studies…

Dissociative identity disorder (DID) can be understood as an extreme variant of complex posttraumatic stress disorder (CPTSD), a construct that attempts to account for the myriad dimensions of disrupted function, beyond the core symptoms of PTSD, in survivors of repeated, sustained traumatic experiences that occur over long periods of time, multiple developmental periods, or both.1–3 These disruptions include difficulties with regulation of mood that are reflected in severe affective dysregulation; problems in regulation of state stability and consciousness; difficulties with sense of self and body image, with secondary problems in maintaining a stable sense of identity, eating disorders, lack of attention to medical needs, and somatization; alterations in the ability to form relationships with intense mistrust co-existing with vulnerability to victimization and exploitation; deformations in self-attribution and systems of meaning with the world seen as dangerous and traumatizing and the self as damaged, shameful, defective, and responsible for traumatization; and a significant propensity for self-destructiveness including suicide attempts, substance abuse, self-injury, and risk taking behaviors.

Studies comparing DID and PTSD subjects on neurobiological variables such as salivary cortisol, 24-hour urine catecholamines, low-dose dexamethasone suppression test, and hippocampal and amygdala volumes measured using magnetic resonance imaging show few differences between DID and PTSD patients.4 There are both clinical and neurobiological similarities between DID and complex PTSD.

Neurobiology and Preclinical Psychopharmacology of the Dissociative Disorders

Dissociative experience appears to be dependent on a broad range of alterations in neurochemical systems. Current neurobiological theories of dissociation suggest a possible role for glutamate in at least some dissociative symptoms. High-dose ketamine, an N-methyl D-aspartate (NMDA) receptor antagonist and glutamate agonist, produces dose-dependent increases in symptoms such as slowed perception of time, tunnel vision, derealization, and depersonalization, similar to that described by acute trauma victims, with “peritraumatic dissociation.”5–7 The neurotoxic effects of glutamate on brain cells is thought to account, in part, for the structural brain changes in the hippocampus found in MRI studies of DID and PTSD subjects and controls.8–10

In some studies, dissociation measures strongly correlated with volume loss in key brain regions implicated in PTSD.11 Challenge studies with marijuana, the serotonin agonist metachlorophenylpiperazine (mCPP), and the α-2 antagonist yohimbine suggest that both serotonin and noradrenergic systems may play roles at least in the generation of “positive” dissociative symptoms such as flashbacks and other intrusive PTSD symptoms.4,5 In studies of military subjects undergoing high-stress training, a strong negative relationship was found between levels of the anxiolytic peptide neuropeptide Y (NPY) and acute dissociative symptoms, primarily perceptual changes, depersonalization, and derealization.12,13

A broad range of altered psychophysiological responses to stress also appears to underlie dissociative experience. Functional magnetic resonance imaging (fMRI) studies have found neural network patterns that differentiate PTSD subjects with and without dissociation.14,15 A subgroup of these dissociative PTSD subjects showed decreased heart rate with a traumatic script, further supporting the idea of a different psychobiology to dissociative PTSD, possibly involving increased endorphinergic tone, vagal tone, or both.16

Preclinical studies using fMRI and postitron emission tomography (PET) scans have begun to suggest neural networks that may characterize dissociative amnesias, as well as the sequestration of affect and memory in DID alternate identities.16–18 Despite these findings, other core DID symptoms such as development of alternate identities, switching, passive-influence, pseudopsychotic dissociative hallucinosis, recurrent complex amnesias, and DID autohypnotic symptoms do not have a known neurobiology and may be caused by alterations in multiple neurobiological substrates and systems.19

Psychopharmacology of DID

Psychopharmacology for the patient with DID must be understood in the context of the total treatment of the patient (Chefetz, see page 657, and Welzant, see page 678). In DID treatment, psychopharmacologic interventions are primarily adjunctive and empirical in nature, as no double-blind, placebo-controlled studies have been performed to study any psychopharmacologic agent or medication regimen for DID.20–22 Informed consent for psychopharmacologic interventions in DID should include this information.

Because the patient with DID can present with myriad symptoms, it is important for the psychiatrist to attempt to find legitimate psychopharmacologic targets. This task may be further complicated because the patient with DID may present with symptoms seemingly encapsulated within one or a few alternate identities, with other identities denying the symptom or endorsing different symptoms. Patients with DID also may produce remarkably realistic conversion symptoms mimicking a whole host of conditions. This can confound evaluation for medications or assessment of efficacy and side effects.

The psychiatrist should attempt to treat symptoms that are found across most or all alternate identities. Epidemiological studies have identified PTSD and depressive disorders as the most common outcomes of psychological trauma.23 Clinical studies have found that as many as 80% to 100% of patients with DID will meet diagnostic criteria for major depressive disorder, PTSD, or both during some point in the clinical course.24,25,26 Accordingly, these are usually the most salient symptoms that can be addressed with psychotropic medications in DID.

However, at least one study27 has found that a history of childhood maltreatment predicts a much less robust antidepressant response in depressed patients treated with medications and a more robust response to cognitive-behavior therapy. Thus, it is most helpful to conceptualize medication treatment for DID as a kind of “shock absorber” in which partial effects are the rule; the clinician attempts to find the best medication or combination of medications to address symptoms at a given time. Frequent symptom exacerbations will be common given the problematic life circumstances that many of these patients face and treatment that requires challenging dissociative defenses. Actual medication responses in patients with DID often result in the patient feeling mildly to moderately improved over time, with a sense of sustained symptom containment, ability to tolerate stress with overall less anxiety or depressive symptoms, and greater resiliency in the face of adverse life events.

Affective Symptoms

The majority of problems, symptoms, and difficulties in DID are most efficaciously addressed psychotherapeutically, hypnotherapeutically, or both, not with medications. Nonetheless, medications, if properly conceptualized and administered, may have a significant beneficial adjunctive role in DID treatment.

For example, affective instability and rapid mood shifts are very common in patients with DID, often occurring within minutes or hours, not days or weeks, as in even the most rapid bipolar mood swings. Most clinicians have been taught to conceptualize these symptoms as manifestations of an atypical bipolar process or mixed-state mood disorder. In fact, there is no evidence that bipolar disorder is any more common in patients with DID than in the general population.22 These mood shifts usually are best understood as manifestations of both posttraumatic affective dysregulation and core dissociative processes: shifting states, subtle switching, PTSD intrusions, and overlap and interference between DID alter self-states.

These symptoms are only infrequently responsive to mood stabilizing medications. However, in general, they are definitively responsive to psychotherapeutic interventions that target the coordination and cooperation of the DID alters.

Psychiatrists have been taught that refractory mood symptoms require a series of antidepressant trials, ultimately leading to electroconvulsive therapy (ECT) if the medication trials fail. In DID, apparent treatment-refractory depression and suicidality are most responsive to psychotherapeutic interventions that target posttraumatic reactivity and alter self-states that encapsulate depressive, demoralized, shame-filled, and suicidal cognitive sets. At the time of DID diagnosis, it is very common for patients to report years of minimal response to conventional psychopharmacologic interventions and ECT. In fact, treatment failure in multiple well-conducted psychopharmacologic trials should raise diagnostic suspicion that DID or another posttraumatic condition is present.

On the other hand, a small subgroup of patients with DID, in well-conducted trauma treatment, may manifest a “double depression” — a severe, protracted exacerbation of depression, with melancholic symptoms and signs, different in quality from the patient's chronically depressed baseline. These patients may respond to aggressive antidepressant management or ECT. Here, again, complete remission of the mood disorder rarely occurs; these treatments return the patient to his or her chronically dysphoric baseline, with relief of the melancholic symptoms.

Depression, childhood maltreatment, and PTSD each increase the risk of attempted suicide independently. Childhood maltreatment itself is a significant risk factor for parasuicidal behaviors. Accordingly, patients with DID are at risk for serious suicidal acts and frequent parasuicidal behavior. The primary interventions for these behaviors involve psychotherapeutic interventions (eg, CBT, dialectical behavior therapy, hypnotherapy, psychodynamic therapy) to target the self-destructive alternate identities and their disturbed cognitions.

However, a subgroup of patients with DID may respond to naltrexone with a reduction in parasuicidal and self-destructive behaviors, especially if these are accompanied by a subjective “high.” This patient group frequently describes several different kinds of compulsive self-destructive or self-stimulatory behavior, including compulsive self-injury, recurrent bulimia, compulsive exercising, and compulsive (often bizarre and self-injurious) masturbation. Successful responses to naltrexone may include reduction in subjective pressure to self-harm or actual loss of dissociative anesthesia for self-harm. Side effects are minimal in most patients.

Patients with DID often have noteworthy, if only partial, responses to anti-depressant medications, usually selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs). Rather than responding slowly, patients with DID often report early response to antidepressant medications, often within days, not weeks, if they are going to respond at all. Medication efficacy then continues as dose is adjusted.

Frequently, mood improves first in DID, not vegetative symptoms. Vegetative symptoms (eg, disrupted sleep, low energy, poor concentration) frequently remain relatively unaffected by antidepressant medications due to intercurrent PTSD. Patients with DID frequently report that antidepressant medications “burn out” or stop working after some months of efficacy, requiring a change to another antidepressant. Later, the patient may respond again to the medication that had previously ceased being efficacious.

Addition of a second antidepressant (eg, buproprion to an SSRI, or a TCA to an SSRI, such as fluoxitene plus desipramine, or sertraline plus imipramine), while carefully monitoring blood levels of the TCA, may increase efficacy of the antidepressant regimen or re-establish efficacy if the initial medication seems to be waning in potency. Lower doses of both SSRIs and TCAs, in combination, may be possible, with reduced side effect profiles.

Pseudopsychotic Symptoms in DID

The hallucinated voices, visual images of the DID alternate identities, and similar complex hallucinatory phenomena commonly found in DID are best conceptualized as building on the same substrates as those caused by self-hypnosis, flashbacks, or both. In patients with DID, these pseudopsychotic symptoms rarely are ameliorated by antipsychotic medications, even in high doses, although a few patients may report some attenuation of hallucinatory phenomena with antipsychotic medications. These types of symptoms are most responsive to psychotherapeutic and hypnotherapeutic interventions that target the DID alter system.

On the other hand, in many patients with DID and severe intrusive PTSD, anxiety, confusion, and cognitive dysfunction due to PTSD and switching, low doses of atypical neuroleptics may ameliorate these symptoms, not the perceptual alternations. Only one small controlled study in complex PTSD patients has been performed using risperidone, demonstrating efficacy for these indications.28 Some very chronically and persistently ill patients with DID and severe PTSD, cognitive slippage, thought disorder, mixed psychotic and dissociative symptoms, and poor reality testing may respond to a trial of clozaril.25 Similarly, a small subgroup of patients with DID with an intercurrent psychotic disorder may be able to distinguish between the “inside” voices of the alternate identities and the bizarre “outside” voices that are a manifestation of psychosis. These patients may note that the latter voices are medication responsive, while the former are not.

There are no systematic data leading the clinician to prefer one atypical agent to another, except patient response and side effect profiles. Only a few patients with DID respond to or better tolerate the older, typical neuroleptics.

Anxiety Management in DID

Patients with DID manifest extreme hyperarousal, panic, and anxiety states, usually best conceptualized as manifestations of PTSD. SSRIs, mood stabilizers, atypical antipsychotics, and benzodiazepines have efficacy in treating these symptoms in patients with DID. Despite standard problems with benzodiazepines, these medications often are experienced as the most efficacious for anxiety by patients with DID. This may have to do with preferential effects of benzodiazepines and related agents on the hyperactivation of the locus ceruleus in PTSD.9

Many patients with DID may require long-term treatment with benzodiazepines, particularly lorazepam or clonazepam, for management of anxiety states. Some patients may not respond unless given relatively high doses of benzodiazepines (eg, 3 to 6 mg daily of lorazepam or clonazepam). These patients frequently tolerate these dosages without drowsiness. In fact, these medications are not useful as hypnotics in some patients with DID due to lack of sleep induction. The severe PTSD hyperarousal in these patients, possibly combined with altered benzodiazepine receptor binding due to severe panic, may account for the relative baseline insensitivity to these medications in this population.29 Tolerance, physical dependence, and addiction must be carefully monitored in patients with DID using benzodiazepines, as many of these patients have a history of addictions and alcohol misuse, and a subgroup estimated at about 15% has a severe chronic addiction comorbidity.30

The surprisingly common obsessive-compulsive symptoms found in DID preferentially respond to antidepressants with anti-obsessive efficacy, such as fluvoxamine and clomipramine.31 The psychiatrist should inquire routinely about obsessive-compulsive symptoms in DID, PTSD, and CPTSD patients.

Pharmacologic Approaches to PTSD in DID

Well-conducted double-blind studies have shown the efficacy of paroxetine and sertraline for PTSD, particularly intrusive symptoms.32 However, these trials have excluded PTSD patients with multiple traumas and comorbidities, such as CPTSD and patients with DID. One small, uncontrolled study of CPTSD patients found improvement with fluoxetine for depressed mood, anxiety, and PTSD.28 In actual clinical practice, there is no reason to assume greater efficacy of one SSRI over another in treatment of PTSD in DID, other than when obsessive-compulsive symptoms are present.

Also, it may be difficult in many patients with DID to see where the PTSD ends and the major depressive disorder begins, as there is so much overlap of symptoms of these disorders in DID. Older studies of combat veterans with PTSD showed efficacy for tricyclic antidepressants and monoamine oxidase inhibitors for PTSD symptoms.32 These medications may still be useful for some patients with DID or CPTSD, if they can take them safely and tolerate the side effects.

A variety of uncontrolled studies have looked at mood stabilizers such as lithium and anticonvulsants for PTSD, primarily in male combat veterans. In these studies, some PTSD patients were thought to have shown improvement on these medications, particularly with carbamazepine, valproate, and lamotrigene. However, clinical experience with patients with DID or CPTSD suggests only a subgroup show diminution of PTSD symptoms with these agents. Lithium is rarely effective for this indication in this population. Patients with DID and a clear-cut intercurrent true bipolar disorder will show response of these symptoms to mood stabilizing medications. However, the dissociative and PTSD symptoms may be relatively unaffected.

A subgroup of patients with DID will respond to beta-blockers for severe hyperarousal symptoms, such as pronounced startle response. Long-acting forms of propranolol are used most frequently for this indication. Similarly, the α-agonist clonidine may be effective in a few patients with DID with PTSD characterized by severe hyperarousal symptoms.32 The most common side effects of these latter medications include hypotension and bradycardia. An increase in nightmares may occur in this population with these medications but also can occur with trazadone, clonazepam, and atypical neuroleptics, among others, sometimes requiring medication discontinuation.

Psychopharmacology for Sleep in DID

Most patients with DID report severe disorders of sleep initiation and maintenance. Sleep problems are complex in most of these patients and rarely respond to pharmacological interventions alone. Most patients with DID have a mixture of sleep disturbances related to depression, PTSD nightmares and sleep disruptions, phobias of sleep, beds, or nighttime related to reported nocturnal childhood maltreatment, or actions of nocturnal alternate personalities who report “staying awake” for various reasons. Some patients with DID report nocturnal wandering and fugues. Some awaken disoriented and may need several minutes to recall where they are.

A polysomnographic study of sleep in DID subjects demonstrated that subjects often awoke from sleep in dissociative states that were subjectively experienced as nightmares.33 The polysomnogram showed a waking electroencephalogram associated with dissociative fugue behaviors and confusion, not REM sleep.

Accordingly, psychotherapeutic interventions targeting the nocturnal PTSD triggers and alters is crucial in managing sleep problems in this population. Medications for sleep (Table, see page 670) are much more efficacious if combined with psychotherapeutic interventions. It is vital to educate the patient with DID about these issues to help prevent the fruitless pursuit of a magic pharmacologic elixir to cure sleep problems.

Common Medications for Sleep Disorders in DID

Table.

Common Medications for Sleep Disorders in DID

Medications for Acute Agitation in Hospitalized Patients with DID

In general, a combination of an intramuscular benzodiazapine (usually lorazepam at a dose of 1 to 2 mg) and an intramuscular typical neuroleptic (eg, haloperidol, fluphenazine, at a dose of 2.5 to 5.0 mg) may abort an episode of acute agitation related to events such as self-destructive behavior, catastrophic levels of panic, fear, or anger, or severe, unremitting flashbacks. Hypnotherapeutic and similar interventions also may be effective but often are available only in specialized trauma units. Sublingual olanzapine or intramuscular ziprasidone may be used as well for this indication. Ziprasidone can only be administered if an electrocardiogram has shown that the QTc interval is normal to minimize the possibility of lethal arrhythmias.

Droperidol also is useful for acute agitation in hospitalized patients with DID. However, it can only be given with cardiac monitoring due to a “black box” warning of fatal arrhythmias with its administration. Oral or sublingual benzodiazapines such as clonazepam and lorazepam and oral/sublingual neuroleptics (typical or atypical) also may be useful on an as-needed basis for acute anxiety or agitation in inpatient and outpatient patients with DID.

Psychological Aspects of Psychopharmacologic Interventions in DID

The psychiatrist who is not the primary therapist for the patient with DID should carefully define his or her role as a specialist in psychopharmacologic and medical management and should avoid acting as an additional intensive individual psychotherapist. It is important to maintain communication with the primary psychotherapist of the patient, at least by sharing voice mail, e-mail, or brief phone calls. The psychiatrist should communicate with and educate a nonmedical therapist about realistic expectations for medications and should receive information from the primary therapist about issues in therapy that may be exacerbating symptoms.

Some patients with DID may be medication phobic. However, many others may be susceptible to strong wishes for medications to solve all problems and to avoid dealing with issues in psychotherapy. Many of the latter patients may come to the psychiatrist on a number of medications from prior psychiatric treatment or many medications from other physicians. It may be challenging to attempt a more rational medication regimen because many patient with DID are strongly attached to their medications, especially those that target pain syndromes. Many of the latter actually are manifestations of somatoform PTSD symptoms.

It is essential to educate the patient about the “shock absorber” effects of medications and not promise a “cure” from psychopharmacologic agents. This allows the patient to provide a much more realistic evaluation of the efficacy of the medications. The entire alternate personality system may be engaged in evaluating the efficacy of medications. It is most helpful to ask the patient to assess whether, in the current life situation, given the current life stressors, the medications act as a container or buffer to current symptoms as they oscillate from day to day. A good outcome might be that the patient reports a less depressed mood, better resilience to stress, better control of intrusive PTSD symptoms, less confusion, or more ability to use psychotherapy effectively.

Patient consent to receive medications does not require consent by each alternate personality; general assent from the person is sufficient. However, it is helpful to ask if any alternate personality objects to trying the proposed medication regimen and to discuss the concerns or objections of these alter identities. A subgroup of patients with DID report being drugged or given alcohol in the course of childhood abuse and, accordingly, may have phobic reactions or feelings of loss of control when psychotropic medications are proposed. Others may report exploitation or abuse by physicians or prior psychiatrists in which drugs were used as part of the exploitation. Accordingly, this may contribute to the patient's fearfulness of medications or of the encounter with the psychiatrist.

It is vital to assess these issues, as medication-phobic alternate identities may sabotage the medication trial, either by not taking the medications as prescribed, by misusing medications, or by creating distressing subjective symptoms that may confound the efficacy of medications. It is sufficient to ask, without seeking details, if the patient recalls being given drugs or alcohol in the context of childhood or adult abuse. If so, it may be enough to ask the patient to work on separating the current situation form the harmful one from the past, to freely give current medications a chance to help.

Summary

Despite the partial and adjunctive effects of medications on DID psychopathology, the psychiatrist has a crucial role in DID treatment. If properly understood in the overall context of DID treatment, medications can make a real difference in helping the patient with DID ameliorate severe, disabling symptoms. Also, the psychiatrist can act as a liaison between the patient, the nonmedical therapist, and the patient's nonpsychiatric physicians in the overall rationalization of the patient's medication regimen, the differential diagnosis of medical and somatoform symptom, and the clarification of which symptoms are likely to respond to psychotherapy and which to psychopharmacologic interventions.

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  34. Raskind MA, Peskind ER, Kanter ED, et al. Reduction of nightmares and other PTSD symptoms in combat veterans by prazosin: a placebo-controlled study. Am J Psychiatry. 2003;160(2):371–373. doi:10.1176/appi.ajp.160.2.371 [CrossRef]12562588

Common Medications for Sleep Disorders in DID

DrugDose rangeBenefitsSide EffectsOther
Trazadone25 to 400 mgAdded SSRI effect; good safety; well tolerated.Morning sedation; dysphoria, low blood pressure; nightmares.Priapism risk may limit use in men.
BenzodiazepinesVarying doses depending on agent.Anti-anxiety effects.Does not sedate; tolerance, addiction, withdrawal; synergy with alcohol and central nervous system depressants; oversedation, ataxia, etc.Some patients use to “anesthetize” themselves (chemical dissociation) with multiple medications, including benzodiazepines, zolpidem, etc.
Zolpidem5 to 10 mg every night at bedtimeGenerally well tolerated.Hangover; ataxia, dizziness; amnesia; some patients may misuse.Same as benzodiazepines.
Neuroleptic (usually low dose; eg, quetiapine 25 to 50 mg every night at bedtime)Varying depending on agent, usually low dose of sedating atypical or typical neuroleptics.May help with intrusive PTSD, panic, thought confusion, etc. (see text).Weight gain; lactation; extrapyramidal symptoms; akathisia; postural hypotension.Patients phobic of medication for “schizophrenia/psychosis.””
Tricyclic antidepressants (usually low dose; eg, amitriptaline 10 to 50 mg every night at bedtime)10 to 100 mg every night at bedtimeAntidepressant; may augment SSRI efficacy; chronic pain.Anticholinergic side effects; postural hypotension; cardiac arrythmiasDose must be lowered if co-administered with SSRIs. Lethal overdose potential.
Anticholinergic agents (eg, diphenhydramine 25 to 100 mg every night at bedtime)Varying dose, depending on agentFew side effects; well tolerated.Anticholinergic effects; some patients have paradoxical activation.Overdose can give rise to severe anticholinergic toxicity.
Mirtazapine15 to 30 mg every night at bedtimePossible adjunctive anti-depressant effects.Sedation; weight gain; nightmares.
Prazosin341 to 10 mg per dayReduces PTSD nightmares in controlled study in combat veterans.Hypotension, dizziness.May be a helpful adjunct specifically for PTSD nightmares in DID.

Educational Objectives

  1. Describe current models of the neurobiology of dissociation and dissociative disorders.

  2. Explain the principles of psychopharmacologic management of dissociative identity disorder (DID).

  3. Discuss psychological management of psychopharmacology for DID.

Authors

Dr. Loewenstein is medical director, Trauma Disorders, Sheppard Pratt Health Systems, and clinical associate professor, University of Maryland School of Medicine, Department of Psychiatry and Behavioral Sciences, Baltimore, MD.

Address reprint requests to: Richard J. Loewenstein, MD, 6501 N. Charles St., Baltimore, MD 21204; or e-mail rloewenstein@sheppardpratt.org.

Dr. Loewenstein has no industry relationships to disclose.

10.3928/00485713-20050801-08

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