The Extreme Nocturnal Manifestation of Trauma: Trauma Associated Sleep Disorder

Article

Patients consistent with TSD

Demographic

PSG findings

Self-reported DNB

Nightmare content

Mysliwiec et al. [13]

4 (N = 4)

Male soldiers (ages 22–34)

Patient 1: defensive limb movements and repeated vocalizations, “oh f***, leave me alone!”

Sleep stage: REM

All patients: RWA, phasic bursts

Patient 1: screaming and combative movements

Patient 2: thrashing movements; episode of choking wife

Patient 3: somnambulism, combative movements

Patient 4: “screaming, crying, throwing pillows, and cursing” and witnessed punching/kicking wall with vocalization of “I am going to kill you”

Patient 1: assailants pursued and threatened him

Patient 2: combat-related experiences

Patient 3: flashbacks to combat environment

Patient 4: related to personal relationship

Hefez [10]

2 (N = 11)

Male maritime disaster survivors (ages 20 and 25)

Patient 1: violent body movement and vocalizations; 2 reports of falling out of bed

Sleep stage: REM

Patient 2: REM-related motor activity and vocalizations

Sleep stage: REM

None reported

Patient 1: reliving sea disaster

Patient 2: nightmares related to disaster

Schlosberg and Benjamin [19]

3 (N = 3)

Male soldiers (ages 25–35)

Patient 1: “awoke particularly violently, jumping out of bed screaming and hallucinating”

Sleep stage: N2

All patients: numerous body movements with RWA

None reported

All patients reported recurrent nightmares; descriptions not provided

Van der Kolk et al. [8]

2 (N = 15)

Male Vietnam veterans (ages not reported)

Patient 1: removed electrodes and walked around the room; later reporting thinking he was in an ambush

Sleep stage: REM

Patient 2: body movements and thrashing

Sleep stage: REM

Reported body movements accompanying nightmares with occasional physical attacks on bed partners

Patient 1: thought he was in an ambush

Patient 2: memory of being in gunfight; coming upon mutilated bodies

Abbreviations: DNB disruptive nocturnal behaviors, PSG polysomnogram, RWA REM without atonia, TSD trauma associated sleep disorder

Besides the patient’s symptomatology and PSG, there is a clinical instrument which evaluates posttraumatic sleep disturbances. The Pittsburgh Sleep Quality Index Addendum (PSQI-A) assesses the DNB that occur in trauma survivors with and without PTSD [6]. This instrument was initially developed to evaluate DNB in patients with PTSD but is now recognized as a better measure of trauma-related sleep disturbances as opposed to PTSD [15]. One study assessed 375 combat veterans using the PSQI-A and reported 59.1% had a score of >4, consistent with PTSD [16]. Nightmares were one of the most frequent symptoms, and participants reported abnormal movements during sleep, potentially suggestive of TSD. More recently, Thordardottir et al. evaluated the sleep of avalanche survivors 16 years after the inciting trauma using the PSQI-A [2]. They reported that compared to matched controls, survivors who were children at the time of the trauma had increased DNB, whereas adult survivors had TRN. Based on the previous cases consistent with TSD, the reports using the PSQI-A, and our clinical experience, the following features of TSD are outlined below.

Clinical Features of TSD

There are distinct clinical characteristics that define TSD and differentiate it from existing sleep disorders. See Table 18.2 for the proposed diagnostic criteria for TSD:

1.

Onset/precipitating factors : Every previously described case that is consistent with TSD developed following a traumatic experience [8, 17, 18]. In most cases, combat was the inciting event [8, 13, 19], though maritime disasters have also been described [10] and exposure to natural disasters [2] or other traumatic experiences are a potential trigger. These experiences typically occurred under extreme duress and more than likely lasted for a prolonged period of time, suggesting that the traumatic experience must be extremely stressful to induce TSD. Sleep deprivation or disruption also appears to contribute to the onset of TSD [19]. Military personnel serving in combat are exposed to disrupted, insufficient sleep or total sleep deprivation [20], and sailors likely experience similar conditions. Notably, sleep after trauma exposure appears to decrease the intensity and frequency of traumatic memories [21]. After the inciting trauma, symptoms including nightmares and DNB typically develop relatively acutely, within weeks to months [10, 13, 19]. In some cases, nightmares of the traumatic experience may precede DNB, or repeated exposure to trauma is required to unmask DNB [13].
2.

Patient demographics : In the majority of cases consistent with TSD, patients were young adult males [8, 10, 13, 17, 19]. This is likely due to increased combat exposure in males and under-recognition of TSD. To date, we have diagnosed TSD in two females, both of whom had substantial combat exposure. In the study by Thordardottir et al. [2], children ages 2–12 who had trauma exposure during their developmental years had more severe nocturnal symptoms (i.e., DNB) than adults. This finding suggests that the development of TSD in the pediatric population may not necessarily require concomitant sleep disturbance as this cohort likely had normal sleep prior to their traumatic exposure. Though further research is required, it is conceivable that TSD could develop at any age in individuals with trauma exposure and concurrent sleep disruption.
3.

Nightmares : Patients with TSD suffer from nightmares that are related to their traumatic experience. Nightmare content varies depending on the nature of the trauma [22], but may include elements of death or dying, combat, and imminent threat to the patient’s safety. Associated symptoms of anxiety, fear, or emotions felt at the time of the trauma may accompany the nightmare. Nightmares in TSD appear to occur primarily in REM sleep [3, 8, 10], but nightmares in NREM sleep [19, 23] have also been reported. The occurrence of nightmares in NREM sleep may account for the fact that some patients lack specific dream recall [24–26]. In those cases, the patient may vocalize or act out the dream, as reported by the bed partner, which results in the patient seeking clinical care.
4.

Disruptive nocturnal behaviors: Perhaps the most distinctive characteristic of TSD is the DNB that can accompany TRN. These symptoms , often reported by the bed partner, range from gross body movements to vocalizations. Some patients have limb movements or thrash and toss about [8, 17], whereas others report more purposeful movements consistent with dream enactment behavior (DEB) including combative behaviors such as striking or choking a bed partner [13]. A smaller number of patients experience vocalizations ranging from grunts and groans to yelling out expletives and frank screaming [8, 13, 19]. In documented cases, vocalizations are often related to the content of the nightmare and may occur repeatedly. Unfortunately, the patient’s nightmares and DNB that are reported to frequently occur in the habitual sleeping environment are difficult to characterize due to rare capture on PSG. One potential explanation for this phenomenon is that the monitored environment and presence of another person in the vicinity of the patient afford a feeling of safety which may reduce the probability of having a nightmare [27]. In the few cases that have documented DNB in the sleep lab, movements were typically purposeful and ranged from defensive posturing to escaping from the room [8, 10, 13, 19].
5.

Autonomic hyperarousal : Symptoms consistent with sympathetic nervous system activation including tachycardia, tachypnea, and night sweats are common in patients with TSD. Similar findings have been reported acutely and chronically in combat veterans with and without PTSD [17, 19]. Stress and sleep disruption are closely associated with physiologic hyperarousal in humans [28]. The hyperarousal physiology likely results from specific trauma exposure, such as that experienced during combat [29]. In TSD, the hyperarousal is likely a reflection of increased autonomic and limbic activity with dysfunctional processing of memories and emotions similar to PTSD [30], though occurring exclusively during sleep. Relative tachycardia during REM sleep, which is associated with phasic RWA, is the most common finding of autonomic hyperactivity on PSG.
6.

REM sleep without atonia : Patients with TSD have increased phasic EMG activity during REM sleep on PSG. Using the Sleep Innsbruck Barcelona criteria for “any” mentalis EMG activity [31], the amount of RWA may vary. It is suspected that the RWA coincides with the occurrence of nightmares with or without associated DNB. For this reason, the RWA may appear intermittently in REM with phasic bursts, and the overall “any” EMG activity may not be pathologically increased [13]. Figure 18.1 demonstrates a characteristic finding of RWA and DNB in a previously unreported patient with TSD.

Fig. 18.1

Epoch of REM sleep depicting characteristic findings of TSD. A 60-s epoch of REM sleep in a 31-year-old male with posttraumatic stress disorder who presented with nightmares and disruptive nocturnal behaviors. These symptoms developed after deployment to Iraq. His nightmares occurred >3 times per week and entailed reenactments of combat. The nightmares were accompanied with thrashing and falling out of bed. His episodes of thrashing included slapping, kicking, and rolling into his spouse. The epoch demonstrates REM without atonia (RWA) with increased electromyogram (EMG) tone in the submental and left lower extremity corresponding with a thrashing body movement. A 15-beat increase in heart rate was associated with this event (onset at *). His PSG was otherwise normal except for multiple similar occurrences of RWA
7.

Associated illnesses and comorbid sleep disorders : Posttraumatic stress disorder appears to frequently co-occur with TSD. Though trauma incites both disorders, they are distinct and can be mutually exclusive; only one of four patients with TSD had PTSD in our initial report [13]. Sleep disorders, including insomnia and obstructive sleep apnea (OSA), are also commonly comorbid with TSD. Multiple authors have reported insomnia in up to 74% of combat veterans with nightmares and symptoms of PTSD [19, 32]. Additionally, approximately half of patients with TSD have OSA, with the majority having mild sleep-disordered breathing. A similar association of OSA with PTSD has been posited, noting that in a review of sleep studies in PTSD patients, over half met clinical criteria for sleep-disordered breathing [33].
8.

Therapy: Potential therapies for TSD should target the core symptoms of the parasomnia . Enhanced sympathetic activity may be counteracted using prazosin, an alpha-1 adrenergic receptor antagonist that is active in the central nervous system (CNS). This medication has been effective in reducing nightmares in veterans with PTSD [34] and the nightmares and DNB of patients suffering from TSD [13]. Imagery rehearsal therapy may also have a therapeutic role in TSD given its efficacy in treating nightmares [35], but this remains to be determined. Clonazepam, a medication effective in controlling movements in RBD [18, 36], does not appear to be effective in counteracting the DNB of TRN in combat veterans [37]. Counseling regarding a safe sleep environment is essential for both the patient and his/her bed partner. Further research is required to determine additional treatment options, but a multidisciplinary approach including pharmacotherapy and behavioral therapy will likely be required to address the spectrum of TSD symptomatology.
9.

Clinical course : The nightmares and DNB of TSD appear to be most severe early in the disease course . In close proximity to the trauma (i.e., weeks to months), symptoms may occur nightly and sometimes more than once per night [13]. While nightmares and DNB persist over time, their frequency and severity tends to diminish. In a study of 59 elderly men with and without PTSD who had combat experiences 28–50 years prior to their evaluation, sleep was similar between the groups with the exception of increased REM sleep and decreased arousals in those with PTSD [38]. Notably, recrudescence of nightmare symptomatology can result from increased stress [39]. The clinical course of TSD likely follows a similar pattern, though longitudinal studies are required to determine the chronic nature of this disease.

Table 18.2

Proposed diagnostic criteria for TSD

1. Onset after combat or other traumatic experiences (often in the setting of sleep deprivation/disruption)

2. A history of altered dream mentation that is related to prior traumatic experience

3. Self- or witnessed reports of disruptive nocturnal behaviors to include at least one of the following:

(a) Abnormal vocalizations

(i) Screaming or yelling

(b) Abnormal motor behaviors in sleep

(i) Tossing, turning, or thrashing

(ii) Combative behaviors such as striking bed partner

4. Symptoms of autonomic hyperarousal or PSG monitoring demonstrates one of the following:

(a) Tachycardia

(b) Tachypnea

(d) If documented on PSG, these findings are not due to sleep-disordered breathing

5. PSG may demonstrate:

(a) REM sleep without atonia (variable amounts of RWA)

(b) Dream enactment behavior in REM sleep

6. Absence of EEG epileptiform activity on PSG

Adapted from Mysliwiec et al. [13]; with permission

Differentiating TSD from Established Parasomnias and Other Sleep Disorders

TSD has characteristics that overlap with other sleep disorders including the established REM parasomnias, RBD, and nightmare disorder. However, TSD has features that distinguish it from these diagnoses, and TSD fulfills the necessary criteria of a parasomnia with abnormal dreams, sleep-related movements and behaviors, and autonomic nervous system activity that are not better explained by another disorder [12]. Comparing and contrasting TSD with RBD and nightmare disorder bolsters its recognition as a distinct parasomnia (see Table 18.3).

Table 18.3

Characteristics of TSD compared to other parasomnias

Characteristics	TSD	RBD	Nightmare disorder
Onset/precipitating factors	Following traumatic experience Associated sleep deprivation or disturbance Rapid onset (weeks to months)	No specific precipitating factors Insidious onset	May be reactive to life stressors, but generally ubiquitous in general population Variable onset
Patient demographic (typical)	Young adults	Older males	May be seen in any age or gender
Nightmares	Related to prior trauma	Defense of sleeper against attack	Content may be stereotyped, but often random
Disruptive nocturnal behaviors	Gross body movements, defensive posturing Vocalizations Recorded in REM and NREM Rarely recorded in sleep lab	Dream enactment with combative, injurious behaviors Exclusive to REM Frequently recorded in sleep lab	Absent
Autonomic hyperarousal	Profound and concordant with dream content	Uncommon	Minor, even in highly disturbing dreams
REM sleep without atonia	Present, but “any” EMG index often normal	Present and “any” EMG activity index >18.2%	Absent
Associated illnesses	Posttraumatic stress disorder	Alpha synucleinopathies (Parkinson’s disease, Lewy body dementia, multiple system atrophy) Narcolepsy	Anxiety PTSD Personality disorders
Comorbid sleep disorders	Insomnia and OSA frequent	Periodic limb movements	Insomnia
Therapy	Prazosin	Clonazepam Melatonin	Prazosin Imagery rehearsal therapy Lucid dreaming
Clinical course	Frequency and severity of symptoms diminish over time	Dependent upon underlying etiology, but typically slowly progressive	Frequency and severity of nightmares diminish over time

Abbreviations: EMG electromyogram, OSA obstructive sleep apnea, PTSD posttraumatic stress disorder, RBD REM sleep behavior disorder, TSD trauma associated sleep disorder

REM Sleep Behavior Disorder

Vivid dreams with DNB, nightmares, and DEB that may be injurious are the presenting symptoms for RBD, and similar symptoms are present in patients with TSD [18, 36]. However, the relatively acute onset of DNB and nightmares in close temporal proximity to trauma is not consistent with the presentation of RBD [19]. There are reports of stressful situations such as being the victim of robbery or fraud, receiving a cancer diagnosis, or having a surgical procedure, which have been associated with the onset of idiopathic RBD (IRBD). Yet, these patients had clinical features which were otherwise consistent with IRBD [40]. RBD is associated with α-synucleinopathies, whereas TSD appears to have an association with PTSD [13, 41, 42]. Clinically, despite the report of frequent DNB by patients with TSD, it is rarely captured on PSG [6, 24, 43]. In contrast, DEB is frequently documented in RBD with two studies reporting a single PSG with video monitoring confirms the diagnosis of RBD in >80% of patients [40, 44]. Another distinguishing characteristic of TSD is the increased sympathetic output reported, most notably tachycardia [13, 19]. Conversely, even with vigorous DNB, there is a relative absence of autonomic activity in patients with RBD [36, 45]. In RBD, sleep quality is usually undisturbed, with 70% of patients reporting good sleep quality [40]. Disturbed sleep is present in all patients with TSD, with most patients meeting diagnostic criteria for insomnia. Regarding treatment, clonazepam, the drug of choice for RBD, does not have any efficacy in treating either the nightmares or DNB associated with TSD. In our experience, prazosin results in clinical improvement in >50% of patients with TSD.

The possibility that RBD could be precipitated by trauma was first posited by Husain et al. [46]. In their study of male veterans with ages ranging from 46 to 78 years, of 22 patients with PTSD, 15 also had RBD. The nightmare content of all 22 patients was trauma related. Notably, none of the patients with RBD had either Parkinson’s disease or dementia with Lewy bodies. Dallam et al. conducted a retrospective review of elderly military veterans [47] and found 16 of 197 (8%) patients, all of whom had PTSD and dementia, reported war-related nocturnal vocalizations. Seven of their patients reported combative nocturnal behaviors. Another study assessed 12 patients with PTSD, 10 of whom had DEB [48]. In this study, phasic RWA on PSG was reported in 80%. The absence of a clinical course describing the onset of symptoms after trauma in these studies leaves open the question as to whether these patients initially had unrecognized TSD, although it appears more likely that the patients in these reports developed RBD with some incorporation of PTSD symptoms later in life.

Medication-associated RWA and cases of secondary RBD are reported with the use of antidepressants, specifically serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRI), and tricyclic antidepressants (TCA) [49, 50]. As with classic RBD, one study postulated that antidepressants may expose an impending neurodegenerative disorder [51]. Yet, there is a different hypothesis which is supported by more robust research suggesting that psychiatric disease itself may increase the risk of RBD independent of antidepressant usage [50]. Additionally, a recent study reported that while RWA was significantly increased in patients taking SSRI or SNRI, patients on these medications were not at increased risk for RBD [52]. In our initial report of TSD, two patients were taking SSRIs. Notably, in both cases, the patients reported DNB and nightmares prior to initiating therapy. In another study, which assessed combat veterans with an average age of 30 years, Wallace et al. reported four patients with RWA, DEB, and sleep-related injury. All of these patients were taking SSRIs and were classified as having secondary RBD [9]. Given their young age and symptom onset after combat exposure, it is possible these patients had TSD. Ultimately, the use of antidepressants, which is frequent in trauma survivors, could confound or potentially exacerbate the underlying diagnosis of TSD.

Nightmare Disorder

Nightmare disorder is a REM-related parasomnia characterized by recurrent disturbing dreams that generally involve a threat to an individual’s safety and often result in awakening with the ability to recall the nightmare’s contents. Nightmares may be reactive to life stressors but are rather ubiquitous in the general population, affecting males and females of any age [12]. TSD is primarily distinguishable from nightmare disorder by the symptoms of excessive nocturnal movements and DNB, which do not occur with this established parasomnia. In nightmare disorder, autonomic hyperarousal is nearly always absent or at most minor, even in highly disturbing dreams [12]. This contrasts sharply with the profound sympathetic output experienced by TSD patients. Further, although nightmares in TSD are hypothesized to occur primarily in REM sleep [24], they have been reported in NREM [23]. An additional aspect is that TSD patients may not recall their nightmares; this finding has also been reported in PTSD patients with TRN [53]. However, as nightmares are a core symptom of TSD, a better understanding of this component of TSD is required.

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