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Explaining dissociative seizures: a neuropsychological perspective
  1. Claire Rockliffe-Fidler1,
  2. Mark Willis2
  1. 1 Department of Clinical Psychology, North Monmouthshire CMHT, Maindiff Court Hospital, Abergavenny, UK
  2. 2 Department of Neurology, University Hospital of Wales, Cardiff, UK
  1. Correspondence to Dr Claire Rockliffe-Fidler, Department of Clinical Psychology, North Monmouthshire CMHT, Maindiff Court Hospital, Abergavenny NP7 8NF, UK; Claire.Rockliffe-Fidler2{at}


Dissociative seizures are common in routine neurological practice and cause considerable morbidity. However, explaining such episodes to patients is rarely straightforward. Taking a neuropsychological perspective, we present a strategy for communicating this diagnosis to both patients and families.

  • dissociative seizures
  • non-epileptic seizures
  • neuropsychology
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Dissociative seizures, or psychogenic non-epileptic seizures, are ‘involuntary experiential and behavioural responses to internal or external triggers that superficially resemble epileptic seizures but which are not associated with the abnormal electrical activity associated with epileptic seizures’.1 Dissociative seizures are common in neurological practice with a prevalence of up to 33/100 000.2 Despite this, neurologists often experience difficulty in explaining this diagnosis to patients and families.3

Patients within our neuropsychology service will have all first seen a neurologist. They are initially invited to attend a group session with other patients and carers, where we aim to deliver baseline information to as many patients as possible, within our limited resources. Ideally, patients are then followed up individually in neuropsychology to meet specific needs.

Here we present an approach to communicating the diagnosis of dissociative seizures—informed by the methods used in our group and individual sessions—aiming to help neurologists to explain the diagnosis and to communicate treatment strategies. We have not attempted to describe features that distinguish dissociative seizures from epileptic seizures and other causes of transient loss of consciousness.

Step 1: getting the vocabulary right

One of the first stumbling blocks is in the nomenclature that we offer to patients, which has generated much debate.4 The name for the events can describe either what they are not (non-epileptic attacks) or can imply to the patient and others that the events are faked (pseudoseizures). The ICD-115 lists such attacks as ‘Dissociative neurological symptom disorder, with non-epileptic seizures’. It is fully understandable that colleagues might talk about ‘real seizures’ since they work in an environment where the term 'seizure' seems to relate to the confirmed presence of epileptic neurological activity, rather than to the observable manifestation of such activity. However, using the term ‘seizure’ in this way can leave even the most compassionate epilepsy specialists being unintentionally misinterpreted as implying that patients’ experiences are ‘not real’.

We therefore recommend using the term ‘dissociative seizures’ because it comes closer to describing what they are, and furthermore holds more face validity as to why we might be recommending psychological assessment.

Step 2: video demonstration

It is useful to offer a rationale for the biological response (what is going on) before addressing the reason as to why these attacks are happening. As part of the initial explanation, we first explain to patients that seizures may have a range of potential causes, including fever, drugs, alcohol and epilepsy. We then describe another ‘cause’ of seizure-type symptoms and introduce the term 'autonomic self-defence strategy'.6 Schauer and Elbert6 discuss the full repertoire of this autonomic defence strategy, which includes ‘fight’/‘flight’—with which most of us are familiar—and the less well known ‘freeze’, ‘fright’ (tonic immobility), and ‘flag’, ‘faint’ (shut down) responses. Freeze/fright and flag/faint are understood to be at play during a dissociative seizure, with the latent energy of unspent ‘fight/flight’ being released during the muscular shaking for those patients who experience these symptoms.7 Physiological data demonstrating an increased parasympathetic response during a dissociative episode on a generalised background of increased sympathetic activity would support this and suggest that dissociation occurs as a reprieve to a constant state of hypervigilance.8

These ideas are very effectively illustrated in a YouTube video clip of a baboon saving an impala from a leopard attack (figure 1),9 which we recommend watching together with the patient in clinic. A word of caution, however, that some patients might consider the video to be upsetting, particularly if there is a history of personal trauma.

Figure 1

Still image from YouTube video clip—‘Baboons save impala from leopard and hyena’.9

The video begins with an impala whose fight/flight response was insufficient, lying in the jaws of a leopard and having apparently been killed. Some baboons then disturb the leopard, which leaves the lifeless impala behind. However, after several seconds, the impala shows signs of life; it begins to breathe deeply and eventually sits up on its forelegs. Following this, it shakes in a manner reminiscent of ‘seizures’ that patients experience. The impala then stands up and runs away. An explanation of this phenomenon is that the impala’s sympathetically driven flight response was overridden by parasympathetic ‘shut down’ in the face of escape being impossible. In this state, the impala could be understood to have dissociated (separated/disconnected from) observable pain reflexes and struggle, all of which have a theoretical survival imperative.10 On recovering, the impala shakes off the latent energy from unsuccessful fight/flight hormones.7

Anecdotally, many patients welcome the explanation of this representation of similar events in the natural world, although is not evidence based. They may feel a sense of relief that their experiences are ‘real’, and it can also be reassuring for family members who can accept that such experiences are possible, and that they do not necessarily represent some unidentified neurological pathology. Additionally, this video appears to confirm that there is some level of awareness during the ‘shut down’ period—the impala must have had some awareness that it was safe in order to begin to recover—which reinforces the importance of a calm response by family/carers when patients experience dissociative seizures.

Step 3: how dissociative seizures occur

Integrative cognitive model

Following the understanding that a dissociative seizure is a real event, we offer further explanation of how these attacks occur. Brown and Reuber11 have hypothesised an integrative cognitive model (figure 2), a theory suggesting that the clinical manifestations of dissociative seizures result from the automatic execution of a learnt mental representation of seizures, which they refer to as the 'seizure scaffold'. They postulate that this occurs on the backcloth of high-level disinhibitory functioning due to, among others, chronic stress.1 The seizure scaffold is said to consist of a sequence of perceptions and motor activities formed by experiences, such as inherent reflexes, physical symptoms and also personal knowledge of seizures. This can then be triggered by different internal or external stimuli, such as elevated autonomic arousal, or be triggered by neutral thoughts or perceptions. As well as physical stress, Reuber and Brown also suggest that the seizure scaffold can be activated in the context of illness or medication.1

Figure 2

Integrative cognitive model. Adapted from Reuber and Brown.11

Although the level of sympathetic background activity is increased before an attack, and parasympathetic activity is increased during an attack,8 the integrative cognitive model also postulates that symptoms of either hyper-arousal (sympathetic), hypo-arousal (parasympathetic) or even neutrality may act as triggers.11 Thus threatening thoughts or a threatening environment may provoke hyper-arousal, although some patients report that symptoms begin when they start to relax.11 We explain this model of dissociative seizures to patients, and so offer a biological rationale for their symptoms.

Window of tolerance

We next use Siegal’s ‘window of tolerance’12 (figure 3) to help patients to understand the difference between these hyper-arousal and hypo-arousal states. This model describes the ‘window’ between hyper-arousal (sympathetic dominance) and hypo-arousal (parasympathetic dominance). Within the window of optimal arousal for normal functioning we can regulate our emotions, focus and switch our attention at will and solve problems. However, this window narrows if our resilience is depleted, lowering our threshold for hyper-arousal or hypo-arousal. This is often true for people with dissociative seizures—their resilience may be severely depleted for several reasons—giving chronic hyper-arousal (especially those with traumatic histories) and triggers that are particular to a patient’s situation. This model helps patients to understand the difference between hyper-arousal and hypo-arousal and also helps the therapist to determine whether patients should increase or decrease arousal in order to return to the window of optimal arousal.

Figure 3

The window of tolerance. Adapted from Siegal.12

Step 4: why dissociative seizures occur

Although the above video and explanation can help patients to understand the what/how, the next inevitable question is why this is happening in their circumstances. It is important to re-emphasise to patients and their families that they are not ‘faking’ or 'making them up' and that their symptoms have a biological rationale. Some patients have a readily identified obvious prior traumatic event or current external pressure13 but others are unable to recall a metaphorical leopard in their lives.14 Using Reuber and Brown’s integrative cognitive model, the therapist can explain that although prior traumatic experiences may confer vulnerability to dissociative seizures, attacks can also occur without them being present.11

Step 5: prevention strategies

Focusing the patient on symptoms of hyper-arousal and hypo-arousal can lead to effective strategies to combat the onset of an attack. For example, if a patient is hyper-aroused (ie, thoughts racing, palpitations, trembling, feeling hot) we recommend that they slow down their breathing, focus on breathing out, rest and use calming strategies. These may include focusing on a picture or token that has positive associations, using calming smells, identifying effective distraction techniques such as counting down from 200 in 7 s, or using grounding techniques such as naming five things they can see, four things they can hear, three things they can touch, two they can smell and one thing they can taste. Alternatively, if patients are experiencing symptoms of hypo-arousal (ie, heaviness, feeling as if their energy is draining from them, coldness, speech slowing/slurring) then they need to activate themselves by increasing tension. This could involve tensing muscles and squeezing their arms across their chest, taking in deeper breaths, splashing cold water on their face or across the back of the neck, throwing a soft ball to and for, or using smelling salts. Interestingly, a lack of a willed action is sometimes a conscious decision whereby patients choose to submit to an attack in order to avoid the symptoms of autonomic arousal.15

As well as these techniques, we also encourage patients to address any modifiable external issues such as chronic insufficient sleep, pain, excessive caffeine intake or inadequate nutrition, which could potentially activate their 'seizure scaffold'.

Step 6: sources of further information

Following this detailed discussion, we recommend to patients further sources of relevant information to help them consolidate what has been covered and to manage specific symptoms. These may include mindfulness courses, or pain and stress management groups; there are many such courses available in primary care, mental or public health services, either free to access or requiring general practitioner referral. We also signpost patients to useful resources, including apps such as ‘Headspace’ and ‘CBT-i coach’, and websites such as and

Unfortunately, resource constraints in our own practice mean that we can provide only limited specialist psychological follow-up for people with dissociative seizures. In better resourced centres, we would recommend supporting patients to individualise their approach and aiding family/carers in their response to dissociative seizures. Patients with more complex and severe difficulties may need referral to specialist psychological services, for example, community mental health team, pain management clinic and trauma services.


Dissociative seizures are relatively common in neurological practice. Although explaining these attacks is often difficult, we have used methods employed during group and individual neuropsychology sessions to set out a framework for patient management. Introducing the what/how leads to discussion of the why, and subsequent prevention strategies. Developing proactive skills, for example, learning to notice and to manage arousal at either end of the spectrum, along with lifestyle changes if appropriate, may be enough to break the dissociative seizures cycle. For many patients, however, dissociative seizures occur in the context of complex physiological difficulties and/or family dynamics, which are best addressed within a multidisciplinary team approach, although this may not always be feasible in a resource-limited setting. The outcome of large randomised control trials investigating the effectiveness of cognitive behavioural therapy in people with dissociative seizures will be of particular future interest.16 Given the encouraging results of previous pilot trials,17 18 cognitive behavioural therapy might offer a much-needed, viable treatment for people with this condition.

Key points

  • We recommend using the term ‘dissociative seizures’ to describe the episodes.

  • We encourage shared viewing and discussion of the impala video to explain such events.

  • We discuss Reuber and Brown's integrative cognitive model to explain how these events occur.

  • We discuss symptoms of hyper-arousal (sympathetic) and hypo-arousal (parasympathetic) to help patients to develop effective prevention strategies.

  • We await evidence from randomised controlled trials of cognitive behavioural therapy in patients with dissociative seizures, which may reshape their clinical management.


We thank Janice Sharp, Medical Illustrator at the University Hospital of Wales, Cardiff for figure 2 and 3.


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  • Contributors Both authors wrote and edited the manuscript.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned. Externally peer reviewed by Jon Stone, Edinburgh, UK.

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