Elsevier

Sleep Medicine Reviews

Volume 18, Issue 6, December 2014, Pages 489-493
Sleep Medicine Reviews

Clinical review
Exploding head syndrome

https://doi.org/10.1016/j.smrv.2014.03.001Get rights and content

Summary

Exploding head syndrome is characterized by the perception of abrupt, loud noises when going to sleep or waking up. They are usually painless, but associated with fear and distress. In spite of the fact that its characteristic symptomatology was first described approximately 150 y ago, exploding head syndrome has received relatively little empirical and clinical attention. Therefore, a comprehensive review of the scientific literature using Medline, PsycINFO, Google Scholar, and PubMed was undertaken. After first discussing the history, prevalence, and associated features, the available polysomnography data and five main etiological theories for exploding head syndrome are summarized. None of these theories has yet reached dominance in the field. Next, the various methods used to assess and treat exploding head syndrome are discussed, as well as the limited outcome data. Finally, recommendations for future measure construction, treatment options, and differential diagnosis are provided.

Introduction

Exploding head syndrome (EHS) is the provocative phrase used to describe perceptions of loud noises when going to sleep or awakening [1], [2]. These noises have a sudden onset, are typically of brief duration, and are quite jarring for the sufferer. Though not often associated with pain, EHS episodes result in a great deal of fear, confusion, and distress. It is usually a benign and infrequent experience, but can manifest in more chronic forms and engender clinical consequences.

In spite of its frightening nature and memorable name, relatively little is known about EHS. Many sleep medicine texts either omit it altogether or only make brief mention of its core features. Perhaps not surprisingly, EHS is infrequently assessed in both practice and research and, as will be argued below, this lack of attention may result in misdiagnosis, unnecessary testing, and continued feelings of embarrassment for patients. Therefore, an up-to-date and comprehensive review of the existing theoretical and empirical literature on EHS was undertaken.

Section snippets

Review method

The literature search began on October 31st, 2013 with key word searches of “exploding head,” “exploding head syndrome,” “sensory sleep starts,” and “snapping of the brain” using PubMed (88 results), PsycINFO (11 results), Google Scholar (626 results), and Medline (23 results). Reference lists of identified articles and chapters were searched for additional sources. Publications were selected on the basis of whether or not they reported empirical findings, provided background information, or

A brief history of exploding head syndrome

The term exploding head syndrome was first coined by J.M.S. Pearce [3]. However, descriptions of this phenomenon are much older. Credit for the first clinical description of EHS is often given to Robert Armstrong-Jones, who described the phenomenon in detail and named it a “snapping of the brain” [4]. He identified this phenomenon in several patients suffering from early melancholia, neurasthenia, and psychasthenia, and further reported that the beginning of their illnesses could be traced to

Classification

EHS formally entered psychiatric and medical nosology in the International Classification of Sleep Disorders – 2nd Edition (ICSD-2) [1]. Currently, EHS can be classified in the International Statistical Classification of Diseases and Related Health Problems – 10th Edition Revised (ICD-10) [6], or the Diagnostic and Statistical Manual of Mental Disorders – 5th Edition (DSM-5) [7] as either an “other specified sleep–wake disorder” (codes: 780.59 or G47.8) or “unspecified sleep–wake disorder”

Symptomatology

Vivid descriptions of EHS can be found in any number of published case studies [3]. The three main diagnostic criteria per ICSD-3 [2] are listed in Table 1. It is worth noting that, in many instances, complaints of pain during EHS are actually misperceptions of shock and fear. However, mild pain is occasionally reported. Regarding the specific auditory content of episodes, examples can be found in Table 2. Their perceived location appears to vary, with some patients hearing explosions in both

Frequency and course

Both the frequency and the course of EHS appear to be fairly variable. Patients range from having one episode in a lifetime to upwards of seven episodes per night [10]. The course of EHS can be constant or irregular, and may go into a full or partial remission only to be followed by a seemingly unexpected recrudescence of attacks ∗[11], [13].

The prevalence of EHS

Accurate prevalence rates for EHS are not currently available due to a predominance of case studies in the literature. It has been claimed that EHS is rare [9] but the limited data imply that this pronouncement may be premature. In the one study identified that allowed for rough prevalence estimates [14], 13.8% of psychiatric patients, 10.0% of patients with a sleep disorder, and 10.7% of healthy controls screened positive for EHS symptoms on a self-report measure (total N = 180). A smaller (N

Risk factors

Perhaps not surprisingly, descriptions and hypotheses about the risk factors for EHS can be found in the very earliest descriptions of the phenomenon. From Mitchell's first case studies [5] to more recent empirical work ∗[10], ∗[11] psychological factors such as stress, emotional tension, and malaise have been thought to make EHS more likely to occur. However, this appears to be based upon informal patient interviews as opposed to a more structured assessment of stress and psychopathology.

Clinical consequences of EHS

Along with discussions of risk factors, preliminary explorations into the consequences and clinical sequelae of EHS have begun. Fear, shock, and surprise are often experienced in the wake of episodes. Reports of tachycardia and palpitations are also common [10]. Some patients take these various symptoms further and, much like individuals with panic disorder, catastrophically misinterpret EHS experiences as evidence that they are suffering from a more serious condition (e.g., subarachnoid

Polysomnographic findings

Several polysomnographic studies of EHS have taken place, and the preliminary findings are revealing. Specifically, in spite of the fact that EHS is sometimes confused with nocturnal epilepsy (with some patients presenting for assessment/treatment on antiepileptic drug regimens [23]), all electroencephalogram (EEG) recordings to date are inconsistent with epileptiform activity. However, it should be noted that a lack of cortical EEG epileptiform activity does not necessarily eliminate a

Etiology

There have been five main theories proposed for the etiology of EHS. First, a variety of ear dysfunctions have been put forward. These include sudden perturbations of middle ear components or the Eustachian tube [4], [9], labyrinthine membrane ruptures, (esp. of the round window [29]), and perilymph fistulas [29]. Second, brief temporal lobe complex partial seizures have been discussed as well [9]. Third, EHS has been discussed in terms of being a side-effect of rapid withdrawal from either

Assessment

Formal assessment of EHS at the present time is quite limited. Only three measures were identified. The first, the Duke Structured Clinical Interview for Sleep Disorders [31], contains three prompts (see Table 3). As it is limited to the minimal ICSD-2 [1] diagnostic criteria, its utility in assessing associated features and the overall severity of EHS episodes is fairly limited. However, the wordings are clear and easy to utilize in any number of clinical settings. The Munich Parasomnia

Differential diagnosis

Given that EHS 1) is so infrequently assessed, 2) is rarely a patient's primary presenting problem, and yet 3) can result in a great deal of patient distress, misdiagnosis can easily occur. Along with the above-mentioned possibilities for misdiagnosis (e.g., as nocturnal epilepsy), EHS must also be differentiated from various headache syndromes (e.g., hypnic headaches, thunderclap headaches, migraine cluster headaches [30]). In determining EHS versus headache, clinicians should inquire into the

Treatment

No open or controlled clinical trials for EHS have yet been conducted, but several case studies of effective treatments have been documented. For example, three patients with EHS benefitted from the tricyclic antidepressant clomipramine (50 mg/d taken at night) [11]. Calcium channel blockers may also be useful. Specifically, flunarizine (10 mg/d) [18] and slow-release nifedipine (90 mg/d) [8] were both effective in a total of three cases, with the latter drug resulting in a complete remission

Conclusions

The existing literature on EHS was reviewed. Unlike many other syndromes, a great deal of basic information does not exist. For instance, accurate prevalence rates are not yet available, but the limited data indicate that EHS may be more common than initially thought. The frequency of attacks also appears to be quite variable.

The range and degree of clinically-significant distress/interference caused by EHS is also unknown. In most cases it does indeed appear to be a benign and relatively

Acknowledgments

The author would like to thank Stephany Fulda for graciously providing unpublished gender data from her 2008 article and the anonymous reviewers for their helpful suggestions. There are no conflicts of interest to declare.

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