Interictal anticipatory anxiety: A key to formulation and treatment of psychopathology in epilepsy

To the Editor

Epilepsy can be conceptualised as a quintessential paradigm of unpredictable loss of control. Anxiety can commonly arise in anticipation of future seizures (Beyenburg et al., 2005). Although such anticipatory anxiety has been mentioned in the literature, its uniqueness to the setting of epilepsy and associated psychopathology has not been fully characterised.

The author proposes the term interictal anticipatory anxiety (IAA) to refer to this construct. The adjective interictal emphasises the persistence of this symptom between seizures such that it might result in more ongoing disability than the seizures themselves. Focusing on this entity can allow us to better understand the evolution of various anxiety disorders in the setting of epilepsy. It would also more specifically inform psychotherapeutic strategies such as graduated exposure therapy and mindfulness-based techniques.

Although IAA might not always be sufficiently severe to cause disability, if it progresses to become associated with disabling avoidance and panic attacks in response to triggers of varying specificity, or with generalisation to free-floating anxiety and nonspecific intolerance of uncertainty, this may lead to the development of seizure phobia (Newsom-Davis et al., 1998), social anxiety disorder, panic disorder or generalised anxiety disorder. Alternatively, IAA might form part of post-traumatic stress disorder if it is associated with re-experiencing phenomena involving traumatic ictal or peri-ictal experiences. IAA could also foster hypervigilance extending to non-epileptic sensory symptoms, out of worry that they might represent aura heralding an imminent seizure – a picture akin to illness anxiety disorder.

Even when IAA is below clinical thresholds, it could mobilise coping mechanisms which might themselves cause disability. Obsessive–compulsive disorder or an eating disorder could arise through attempts to reclaim a sense of control over one’s environment or one’s body, respectively. Self-medication, e.g., with alcohol or benzodiazepines, might result in a substance use disorder. The mobilisation of somatisation as a defence could result in the emergence of psychogenic non-epileptic seizures or other somatic symptom disorders.

IAA might also lead to a vicious cycle if higher levels of stress result in increased frequency of seizures, which could in turn increase IAA. Vulnerability to IAA is likely mediated by the interplay of psychological and biological factors. Seizure-related factors may include higher seizure frequency as well as history of seizures with impaired awareness, ictal fear, status epilepticus and peri-ictal physical injury – all of which might be associated with a greater sense of loss of control. Further research is warranted to explore IAA – which can help us better understand and treat unique aspects of psychopathology in epilepsy.