I’d like to use this month’s blog post to highlight a superb article that was published this year on psychogenic non-epileptic seizures in Clinical Psychology Review (issue 47). In my opinion, this publication is what all professionals who work with PNES should be aspiring to contribute to the field.
In past blog posts I have talked about professional publications that represent static and noise and contribute little to nothing to the advancement of the field of PNES. In sharp contrast, this article is the exact opposite; it is a treasure trove of sophisticated thought that has the potential to contribute significantly to our theoretical work as PNES researchers. I hope to do it justice in correctly summarizing it here.
Note: Usually my blog posts aim to be no longer than 500 words, but this one will necessarily be much longer in order to fit in all the comments I need/want to make about it. And some of my explanations about the article are my interpretations, not necessarily the authors’ explanations.
Patients with PNES are all very different in terms of histories, personality profiles, comorbidities, and therefore in how they will respond to treatment. Some explanatory models have been proposed by theorists before but these tended to explain only a portion of cases. For example, although a substantial number of adults with PNES have suffered trauma, not all have, so to explain the origin of PNES as trauma-based is insufficient.
Brown and Reuber tackle the complex phenomena of psychogenic seizures carefully examining existing models of PNES and integrating these into a novel explanatory framework that has the potential to apply to all PNES patients. The authors provide thorough and clear explanations of four previous models including: 1) PNES as the activation of dissociated materials, 2) PNES as hard-wired responses, such as “panic without panic”, 3) PNES as a physical manifestation of emotional distress, and 4) PNES as learned behaviors. An important difference is that their model focuses less on etiology and more on mechanism.
They use the Integrative Cognitive Model of medically unexplained symptoms as a foundation. They posit that “the central feature of all PNES is the automatic activation of a mental representation of seizures (the “seizure scaffold”).” This is triggered by cues (for example, trauma reminders or conditioned stimuli) that lead to a “threat perception” that leads to disturbances in arousal levels, which leads to predicting or anticipating that a seizure is about to occur and in the context of a high level inhibitory processing dysfunction, the seizure occurs. Chronic stress can play a big role in lowering inhibitory processing functions. After the seizure, there tends to be a reduction in arousal which explains why many patients with PNES describe being confused, tired and even sometimes oddly “relieved.” Seizure scaffold shaping elements include many of the explanatory factors that were included in previous models (e.g. hard-wired behavioral tendencies, seizure models, experiences misinterpreted as seizures in the past, prior physical injury, past traumatic events, etc.).
The Brown-Reuber Model stages are:
Stage 1: a sudden increase in sympathetic arousal associated with autonomic symptoms (e.g. changes in heart rate, breathing). These are not necessarily accompanied by perceived anxiety. As seizures repeat over time, conditioned stimuli will be able to bring on a seizure before the patient consciously experiences any arousal or threat. Inhibitory processing is compromised. Secondary attentional systems that manage processes such as problem solving, behavioral inhibition, planning, goal setting, and decision making are disabled.
Stage 2: The patient then “predicts” (consciously or not) that a seizure is coming and that leads to a mega-activation of the seizure scaffold. This triggers the second stage, in which the cognitive-behavioral component of the scaffold is executed, resulting in the onset of the actual seizure.
Stage 3: The sympathetic response is interrupted and the event is terminated with a reduction in arousal.
Since many patients with PNES have traumatic histories, the authors speculate that the changes in arousal that accompany trauma reminders may be relatively common for many who suffer PNES. For other patients who do not have trauma in their history, the changes in arousal may be due to different triggers including thoughts, feelings, or behaviors resulting in the patient feeling tension and anxiety.
As time passes, additional experiences (e.g. visits to the neurologist, unnecessarily prescribed anti-epileptic drugs, misleading information found on-line) multiply and reinforce the scaffolding.
As for treatment of PNES, the authors conclude that the focus according to this model is on identifying and addressing factors that are activating the seizure scaffold and diminishing attentional functioning. This model is also useful in explaining why traditional cognitive behavioral therapy, prolonged exposure therapy, mindfulness-based therapies, psychodynamic therapies, etc. might each have the potential to help patients with PNES.
The article is much more detailed than the summary I have written here and I encourage professionals working with PNES to get their hands on the whole article and read it carefully. https://www.ncbi.nlm.nih.gov/pubmed/27340856
As a purported PNES patient, I have a few problems with the article.
The first is the implication that patients who seek information about their PNES just reinforce their symptoms. I think this is an overgeneralization, as for many people, “information is power,” and information can help a person better cope with his or her diagnosis. Information seeking behavior should not be seen as universally pathological or predictive of further PNES in patients who inquire about their condition; rather I propose that it is part of coping with the condition. This is why there needs to be a higher quality (and perhaps quantity) of information about PNES available to patients and physicians alike.
The second is that there seems to be an emphasis on symptoms that can be shared by patients with true epileptic seizures, i.e. psychological stressors as triggers, and a sense of impending seizure including arousal of sympathetic phenomena. These symptoms are confusing to PNES patients, and emphasizing them in the ICM may contribute to further confusion about what are and are not epileptic phenomena.
Finally, the prediction of PNES based on a “sense of relief” following the seizure is not well-distinguished from the psychological sense of relief reported by some patients with epilepsy – a phenomenon relied upon by those who use electroconvulsive therapy as treatment for severe depression. If PNES patients are indeed more likely to suffer from depression and other psychological comorbidities, then it would seem the cycle would end shortly after the patient’s first seizure, rather than occur with heightened frequency (the latter being a predictor of PNES vs. epilepsy.)