Curr Treat Options Neurol (2014) 16:312 DOI 10.1007/s11940-014-0312-7

Headache (JR Couch, Section Editor)

Treatment of PTSD and Chronic Daily Headache Todd A. Smitherman, PhD* Anna Katherine Black, BS Christal N. Davis Address *Department of Psychology, University of Mississippi, Oxford, MS 38677, USA Email: [email protected]

* Springer Science+Business Media New York 2014

This article is part of the Topical Collection on Headache Keywords Posttraumatic stress disorder I Chronic daily headache I Chronic headache I Migraine I Tension-type headache

Opinion statement Posttraumatic stress disorder (PTSD) is often comorbid with chronic migraine (CM) and chronic tension-type headache (CTTH). Trauma-focused cognitive behavioral psychotherapies, selective serotonin reuptake inhibitors (SSRIs), and venlafaxine have demonstrated efficacy in the treatment of PTSD. Amitriptyline, topiramate, sodium valproate, and botulinum toxin A are efficacious for treatment of chronic daily headache (CDH). Treatment studies on individuals with CDH and comorbid PTSD, however, are limited. As such, multiple therapeutic agents or modes of interventions typically are necessary, such that comprehensive treatment simultaneously utilizes approaches with established efficacy for each individual condition.

Introduction Chronic daily headache “Chronic daily headache” (CDH) is an umbrella term referring to any headache disorder that occurs on 15 or more days per month. The prevalence of CDH among adults is 3–5 % [1–3]. Most individuals with CDH present with chronic migraine (CM) or chronic tension-type headache (CTTH), primary headache disorders each affecting 1–2 % of the population [4–7]. These disorders are disproportionately common among individuals seeking treatment, particularly those presenting to specialty clinics.

In addition to the disability and treatment challenges that these conditions portend, a growing body of literature underscores the high prevalence of comorbid psychiatric disorders among individuals with CDH [8]. Large population studies indicate that individuals with CM are almost twice as likely to report significant depression or anxiety as those with episodic migraine (EM) [9, 10]. Moreover, existing data suggest the presence of a dose–response relationship between psychiatric symptomatology and risk of progression from episodic to chronic migraine (i.e., “headache

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chronification”), in that more severe psychiatric sympt o m a t o l o g y i s a s s o c i a t e d w i t h g r e a t e r r i s k of chronification [11]. Comorbid depression and anxiety disorders also function as temporal risk factors that typically precede overuse of acute headache medications [12], which over time can lead to chronification in the form of medication overuse headache (MOH), a common secondary form of CDH.

Trauma, PTSD, and CDH Although most research on CDH and psychiatric comorbidities has focused on major depression and anxiety disorders, recent interest has emerged in trauma and posttraumatic stress disorder (PTSD), both of which are more common among migraineurs than those without headache [13, 14]. The criteria required for diagnosis of PTSD include exposure to a traumatic event/stressor and subsequent development of each of the following symptoms that last at least 1 month: 1) intrusion (e.g., recollections such as nightmares or flashbacks, prolonged distress, or physiologic reactivity to trauma reminders), 2) avoidance (of trauma-related thoughts, feelings, or environmental stimuli), 3) negative changes in cognition and mood (e.g., anhedonia, self-blame, negative emotions), and 4) alterations in arousal/reactivity (e.g., irritability, hypervigilance, sleep disturbance, or problems in concentration) [15]. Several studies have found an association between headache and childhood experience of abuse/maltreatment [14, 16–19], and a growing body of evidence attests to an association between military service and headache [20], particularly CDH subsequent to concussion (i.e., posttraumatic headache, PTHA) [21–24]. Exposure to at least one traumatic event, however, is nearly ubiquitous among adults [25], which calls into question the validity of this criterion as

a risk factor for recurrent headache. PTSD, alternatively, requires exposure to a traumatic event and subsequent persistent behavioral, cognitive, and affective symptoms. Significant PTSD symptomatology is present in 30–43 % of treatment-seeking CM patients [26, 27], and 19 % of CDH sufferers in the general population meet the structured interview criteria for PTSD, reflecting a minimum threefold increased odds of PTSD compared to those without headache [13]. With regard to the primary headache disorders, a pattern that has emerged across several studies suggests that headache is more strongly associated with PTSD than with trauma exposure per se, implying that PTSD may mediate the relationship between trauma and headache. For instance, Smitherman and Kolivas [28] found that PTSD was strongly associated with migraine whereas trauma exposure alone was not. Similarly, a recent study among veterans found that use of prescription headache medication (a proxy for headache diagnosis) was more robustly associated with PTSD than with lifetime traumatic events [29]. Further supporting the differential utility of PTSD symptomatology is the observed higher prevalence of PTSD among individuals with CM vs. EM [26, 27] despite the similar prevalence and frequency of traumatic events experienced by both CM and EM patients [13, 26, 27]. As PTSD interacts with depression and compounds headache-related disability [26], treating patients with PTSD and CDH presents particular challenges, and there are few treatment studies pertaining to this comorbid presentation. This paper provides an overview of evidence-based pharm a c o l og i c a n d b eh a v i or a l i nt er v e nt i o ns f o r treating PTSD, CDH, and their comorbid presentation in adults, as informed by systematic reviews, controlled trials, and practice guidelines.

Treatment of PTSD Psychotherapies with Class I Evidence Trauma-focused cognitive behavioral psychotherapies that promote desensitization to trauma-related memories, thoughts, and feelings are well-established by numerous agency guidelines and reviews as firstline treatment options for PTSD [30–35]. Cognitive behavioral therapies (CBT) for PTSD aim to reduce symptomatology via desensitization or habituation to trauma-related triggers/memories and include,

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to varying degrees: psychoeducation about the disorder, therapeutic exposure to avoided trauma-related memories and other stimuli, attempts to challenge or modify maladaptive thought processes (i.e., cognitive restructuring), and promotion of adaptive coping (e.g., skills-based training, anxiety management) [30, 33]. Clinical psychologists or other mental health providers with advanced training in empirically supported psychological interventions typically administer these treatments.

Prolonged exposure (PE) Prolonged exposure (PE) conceptualizes repeated efforts to avoid trauma reminders as the mechanism that perpetuates anxiety over time. As such, the cornerstone of PE is gradual and repeated therapeutic exposure to the patient’s memory of the trauma(s) (i.e., imaginal exposure). During imaginal exposure, patients are instructed to close their eyes and imagine the traumatic event while retelling it aloud and in great detail, as if it were happening at that moment. Patients are encouraged to verbalize any thoughts or emotional reactions that occurred during the trauma and to provide a variety of sensory descriptors. Imaginal exposure is often repeated several times in a single session, typically over a span of 30 to 60 minutes. The exposure sessions are audio-recorded so that patients can listen to them daily in order to promote further habituation to the feared memories. When it is feasible, imaginal exposure is supplemented with in vivo exposure to real-life environmental cues that trigger trauma-related memories and anxiety (e.g., exposure to automobiles following a traumatic car accident) to further reduce maladaptive avoidance behaviors. Fear hierarchies are often used to structure the content and pacing of exposure sessions, in which patients rank-order traumatic events or feared stimuli, evaluate their predictions and safety pertaining to each, and then conduct repeated exposure to each stimulus until it no longer produces significant anxiety.

Cognitive processing therapy (CPT) In contrast to the primary emphasis on exposure in PE, the major emphasis in CPT is on cognitive restructuring that involves formally identifying, evaluating, and modifying maladaptive thought processes stemming from a traumatic event. Patients are taught to self-monitor and identify maladaptive thinking, evaluate the evidence for and against these thoughts, and to then rationally challenge and modify these maladaptive thoughts. “Behavioral experiments” are employed in many cases, in which the patient is instructed to directly test both the validity (truth/accuracy) and utility (usefulness) of a given belief, particularly those beliefs that cannot be easily modified in-session. Safety, trust, power and control, self-esteem, and intimacy are the major themes addressed in CPT. In addition to the primary emphasis on cognition, CPT includes a written exposure component in which patients construct a detailed narrative about their trauma and reread the narrative throughout treatment.

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Eye movement desensitization and reprocessing (EMDR) Many practice guidelines also recommend eye movement desensitization and reprocessing (EMDR) as efficacious for PTSD. EMDR includes eight treatment phases, incorporating elements of imaginal exposure, coping skills training, and cognitive restructuring. During imaginal exposure, the patient engages in horizontal saccadic eye movements for 20–30 seconds. After each set of eye movements, the patient discusses the thoughts and emotions experienced during the procedure. This process is repeated, with a specific focus on persisting memories. (Presumably, the bilateral stimulation from the directed eye movements facilitates the orientation of attention and memory retrieval in a way that currently lacks a cogent neurobiological explanation.) EMDR is not without controversy, as the mechanisms underlying its established efficacy are unclear, with multiple early reviews concluding that the eye movements are superfluous [36– 38].

Overview of psychotherapies &

&

& &

Standard procedure: PE, CPT, and EMDR are short-term approaches that generally involve 8 to 12 sessions lasting 60 to 120 minutes. Sessions are longer (90–120 minutes) during imaginal exposure. Sessions occur once or twice a week and work best if administered consecutively. Patients are often assigned “homework” between sessions to practice specific interventions and to promote generalization of skills and treatment gains. Contraindications: Trauma survivors who are adamantly opposed to behavioral treatment or who are reluctant to confront traumatic memories or triggers are unlikely to benefit from CBT. Exposure therapy may not be as effective for individuals whose primary emotional response is anger or guilt, as opposed to anxiety [39]. Complications: Patients often report a temporary increase in anxiety when beginning exposure therapy. Special points: Several agencies (American Psychiatric Association, Australian National Health and Medical Research Council, National Institute for Health and Clinical Excellence, U.S. Veterans Affairs/ Department of Defense) recommend these interventions over pharmacotherapy. Treatment gains are likely maintained longer than with pharmacotherapy.

Pharmacologic treatment Pharmacologic treatment for PTSD is typically used in conjunction with psychotherapy, although support has increased in recent years for the use of pharmacotherapy as a first-line treatment for PTSD based on results from numerous randomized controlled trials (RCTs) [34, 40].

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SSRIs (paroxetine/sertraline/fluoxetine) and SNRIs (venlafaxine) (Class I Evidence) SSRIs are the most studied and well-established pharmacologic treatments for PTSD, with paroxetine and sertraline the only drugs approved by the Food and Drug Administration (FDA) to treat PTSD. These two agents, as well as a third SSRI, fluoxetine, have shown efficacy in reducing PTSD symptom clusters in multiple RCTs across various trauma types [41, 42, 43•, 44]. Several large RCTs have concluded that the SNRI venlafaxine is equally efficacious[33, 34, 42, 45]. Other SNRIs lack research support and are therefore not recommended. Paroxetine, sertraline, fluoxetine, and venlafaxine are considered first-line treatments, and may also be effective in treating comorbid depression [33, 34].

& & &

&

Standard dosage: Varies by drug (see Table 1). Treatment should continue for at least 6–12 months. Contraindications: Uncontrolled hypertension. Main side effects: Nausea, loss of appetite, agitation, insomnia, gastrointestinal symptoms, fatigue, headache, sexual dysfunction. Venlafaxine can cause seizures at high doses, in patients with a history of seizures, or among those with a low seizure threshold. Special points: May be particularly useful when PTSD is comorbid with depression. Venlafaxine must be carefully tapered during discontinuation to reduce rebound symptoms.

Table 1. First-line treatments for posttraumatic stress disorder (PTSD) and chronic daily headache PTSD Class I Medications (Efficacious)

Chronic Daily Headache (CM/CTTH) Usual Therapeutic Dose/Day

Antidepressants • Fluoxetine (SSRI) • Paroxetine (SSRI) • Sertraline (SSRI) • Venlafaxine (SNRI)

20–60 mg 20–60 mg 50–200 mg 150–375 mg

Class I Psychotherapies (Efficacious) Prolonged exposure Cognitive processing therapy

– –

Eye movement desensitization and reprocessing

–

Class I Medications Usual Therapeutic (Efficacious) Dose/Day Tricyclic Antidepressants (Primarily CTTH) • Amitriptyline 50–200 mg Anticonvulsants (CM) • Topiramate 25–200 mg • Valproate 250–1500 mg Botulinum toxin A 155–195 units IM (CM only) Class I Behavioral Therapies (Efficacious) Relaxation training – Thermal biofeedback + – relaxation EMG biofeedback – Cognitive behavioral therapy

–

Class I: Evidence provided by one or more well-designed randomized controlled clinical trials, including meta-analyses of such trials IM = intramuscularly

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MAOIs (phenelzine) and TCAs (amitriptyline/imipramine) Findings on the efficacy of MAOIs and TCAs in treating PTSD have been inconsistent [34], and neither class is recommended as a first-line treatment. Although some small studies of these two drug classes have shown promise, side effects and required dietary restrictions limit their use [41]. MAOIs appear to be more effective than TCAs in reducing re-experiencing symptoms and in global improvement, but TCAs tend to have comparatively fewer side effects [33].

Anticonvulsants With the exception of topiramate, anticonvulsants have not shown efficacy for the treatment of PTSD. Contrary to current practice guidelines [33], two recent meta-analyses concluded that topiramate had demonstrated some efficacy in treating PTSD [43•, 46], but the drug is typically not recommended as first-line treatment due to the comparatively stronger evidence base of the SSRIs and venlafaxine, as well as their more favorable side effect profiles. Topiramate may be particularly useful for patients who have not responded to other first-line treatments, but larger studies are needed [47].

Benzodiazepines Benzodiazepines are contraindicated for PTSD monotherapy as they do not reduce the core symptoms of PTSD, have high abuse potential, and may exacerbate comorbid depression [33, 34, 42]. They are also contraindicated when used in combination with psychotherapy because their effects can interfere with the fear extinction process integral to exposure therapy [48].

Treatment of CDH (CM and CTTH) General principles of treating CDH include establishing the correct CDH diagnosis through the use of a thorough headache history and prospective headache diary, identifying secondary causes of CDH (e.g., medication overuse, head injury), and initiating preventive treatment (pharmacologic and/or behavioral), while cautioning the patient against frequent use of acute agents. In cases of MOH, supervised withdrawal (or, at a minimum, tapering) from the offending acute medication and initiation of a suitable preventive medication is usually required [49, 50]. Treatment for PTHA is based upon the primary headache disorder that it phenotypically resembles, most commonly migraine [24, 51, 52]. This article focuses on treatment of the primary headache disorders of CM and CTTH.

Diet and lifestyle The central nervous system of patients with CDH is hypersensitive to both internal and external stimuli, and as such, is reactive to deviations from routine. The following lifestyle recommendations provide benefits

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for some patients when used in combination with medication or behavioral treatments:

& & & & & &

Maintain regular patterns of eating (i.e., avoid fasting or skipping meals). Keep consistent bedtime/rise time each day. Initiate and maintain a program of regular exercise if possible. Identify common triggers of headache attacks; work to eliminate those that are modifiable and manage those that are not (e.g., reduce stress). Incorporate a regular practice of stress management (e.g., relaxation, yoga). Avoid smoking.

Preventive pharmacologic treatment The preventive pharmacotherapies most effective in treating CDH are those typically used for migraine prevention: amitriptyline, topiramate, and valproate [53••, 54••]. In clinical trials, these pharmacotherapies generally yield clinically significant reductions in headache frequency (≥50 % reduction) for 50–55 % of patients. With each preventive agent, the dosage is gradually titrated upward until an adequate therapeutic response is achieved or adverse events preclude further increase. Acute agents such as the triptans or long-acting NSAIDs may be used in conjunction with preventive pharmacotherapy, but the patient should be cautioned about the consequences of acute medication overuse.

Amitriptyline (Class I evidence, particularly for CTTH) [55–57] & & & &

Standard dosage: See Table 1 (titrated up from 25 mg). Contraindications: Cardiac disease. Use cautiously in older adults. Main side effects: Dizziness, constipation, drowsiness, dry mouth, weight gain, irritability, depression. Can cause seizures in patients with low seizure threshold. Special points: Monitor amitriptyline and nortriptyline blood levels in patients taking ≥200 mg amitriptyline per day. Nortriptyline has lower rates of anticholinergic effects.

Anticonvulsants: topiramate for CM (Class I evidence) [58–62] & & & &

Standard dosage: See Table 1. Contraindications: History of kidney stones, pregnancy or planned pregnancy, hepatic dysfunction. Main side effects: Cognitive impairment (concentration, word-finding), sleepiness, paresthesia, weight loss, kidney stones. Special points: Consider monitoring of hepatic and renal function. Anticonvulsants worsen depression in some patients.

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Anticonvulsants: valproate for CM (Class I evidence) [58, 63, 64] & & & &

Standard dosage: See Table 1. Contraindications: Pregnancy or planned pregnancy, hepatic dysfunction. Main side effects: Cognitive impairment, weight gain, nausea, vomiting, gastrointestinal upset, hair loss. Special points: Consider monitoring of hepatic and renal function. Anticonvulsants worsen depression in some patients. Far more trials have evaluated topiramate than valproate.

Venlafaxine (Class I Evidence) One double-blind RCT has evaluated venlafaxine extended-release among adults with high-frequency TTH (mean headache days per month=14), in which venlafaxine 150 mg/day was superior in reducing headache frequency compared to placebo [65].

Botulinum toxin A (Class I Evidence) Botulinum is a naturally occurring neurotoxin that inhibits acetylcholine release at the neuromuscular junction in a dose-dependent fashion. Although early studies were limited by small samples and inconsistent findings, positive results from two double-blind placebo-controlled RCTs [66, 67] prompted the FDA in 2010 to approve botulinum injection for the prevention of CM. A recent meta-analysis of these and other studies concluded that botulinum was effective in reducing headache frequency among individuals with CDH (broadly) and CM, but not in those with CTTH [68]. The clinical benefit of the reduction in headache frequency for CDH and CM was modest, however, equating to a reduction of two fewer days per month versus placebo.

& & & &

Standard procedure: 155–195 units injected intramuscularly (fixed-site/fixeddose and follow-the-pain approaches; see Blumenfeld [69]). Contraindications: Neuromuscular junction diseases, drugs affecting neuromuscular transmission (e.g., aminoglycosides) Side Effects: Blepharoptosis, muscle weakness, neck pain or stiffness, paresthesia. Special points: Typically requires insurance pre-authorization to verify medical necessity, as well as re-administration every 3–4 months. Costprohibitive for some patients.

Behavioral therapies Behavioral therapies for CDH focus on preventing headache attacks and reducing headache-related disability during and between attacks. Behavioral interventions target common precipitants of headache and physiological arousal that may perpetuate sensitization of the central nervous system over time. The well-established behavioral headache therapies in-

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clude “stress management,” relaxation, and biofeedback (either thermal [hand warming] or electromyographic [EMG]); often two or all three of these components are delivered in combination. Stress management principally involves teaching patients to recognize common stressors associated with headache and to develop adaptive means of coping with them. Some variations of stress management are commonly termed “cognitive behavioral therapy” when including more formal emphasis on altering headache-related cognitions. Progressive muscle relaxation and biofeedback are targeted at lowering sympathetic activation and fostering patient self-efficacy in managing their headache condition. Numerous empirical reviews support the efficacy of behavioral interventions for migraine and TTH [70–75], and many of the reviewed studies included patients with CDH. Importantly, randomized controlled trials indicate that adding behavioral interventions to preventive pharmacotherapy improves outcomes (beyond either treatment alone) for both adults with CTTH [57] and adolescents with CM [76•].

Relaxation, biofeedback, and stress management (Class I evidence) &

& &

Standard procedure: 3–5 biweekly or monthly sessions in medical settings (with periodic phone check-ins); 8–12 weekly sessions in mental health settings. Patients are typically instructed to practice learned skills daily to promote generalization of treatment gains. Contraindications: Psychosis or profound cognitive deficits. Special points: Minimal-contact behavioral interventions are costcompetitive with inexpensive migraine prophylactics and are less costly over time than continuous pharmacotherapy [77].

Emerging treatments One small trial among individuals with CDH (CM or CTTH) has shown promise for acceptance and commitment therapy (ACT) in reducing headache-related disability and affective symptoms compared with treatment-as-usual [78].

Treatment of comorbid PTSD and CDH (CM and CTTH) Diet and lifestyle &

See recommendations under “Chronic Daily Headache.”

Pharmacologic treatment and botulinum toxin As is evident in comparisons of first-line interventions for PTSD and CDH (see Table 1), medications with the strongest efficacy for treating PTSD are not efficacious in treating CDH, and medications efficacious in treating CDH do not

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Curr Treat Options Neurol (2014) 16:312 have strong efficacy in PTSD treatment. The SSRIs, while agents of choice for PTSD, are not effective for migraine prophylaxis [79, 80], and the anticonvulsants currently used for CDH do not have consistent empirical support as primary agents for treating PTSD. The dosage of amitriptyline required to treat PTSD typically exceeds the required dosage for reducing headache, and adverse events often prompt discontinuation at these higher doses. Venlafaxine is the one drug that has shown both efficacy in treating PTSD and promise for CDH treatment, but further studies are needed on its efficacy in CDH. In consideration of these issues and the absence of pharmacologic studies on this dual presentation, treating the patient with comorbid PTSD and CDH often requires the use of separate agents or treatment methods, each targeted to the index condition and with attention toward potential drug-drug interactions. Treatment of PTSD should incorporate either an SSRI/venlafaxine or one of the trauma-focused psychotherapies, and a CDH preventive agent may be used in combination so long as potential interactions, toxicity, and adverse events are closely monitored, particularly in older adults. For instance, anticonvulsants should not be first-line agents for CDH in depressed patients, and serotonin syndrome can occur with coadministration of amitriptyline with an SSRI. Pharmacologic agents that cause sedation, cognitive impairment, or sleep disturbance should be avoided in patients undergoing one of the trauma-focused cognitive behavioral therapies, as these side effects can interfere with the process of fear extinction.

Behavioral therapies Given the strong evidence base for trauma-focused psychotherapies for PTSD, these nonpharmacologic interventions for PTSD may be supplemented with amitriptyline or an established anticonvulsant for CDH. Alternatively, pharmacologic intervention for PTSD can be combined with behavioral interventions for CDH. Trauma-focused CBT for PTSD (PE, CPT) shares much in common with empirically-supported behavioral interventions for CDH, such as self-monitoring behaviors of interest, efforts to eliminate maladaptive avoidance behaviors, training in stress management and coping skills, and action plans/skills practice that foster patient self-efficacy in managing their condition [81]. However, as with pharmacotherapy, formalized protocols integrating behavioral treatments for CDH and PTSD are lacking, as are studies on the efficacy of various interventions for the patient with both PTSD and CDH. Until such studies are available, treatment should be guided by use of the most efficacious approach for each condition.

Compliance with Ethics Guidelines Conflict of Interest Todd A. Smitherman has received research support from Merck. Anna Katherine Black and Christal N. Davis declare no conflict of interest. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors.

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