Found this article on Facebook in a PNES group, figured I should share it here, since it applies.
Psychogenic Non-Epileptic Attacks (PNEA)
If you’ve been around the Emergency Department for a while, then you’re likely to have seen your fair share of pseudoseizures. This infamous condition can be frustrating for a busy ED doc (this post from GomerBlog captures the feeling for many). Additionally, it can be challenging at times to tell a pseudoseizure from an epileptic seizure. All in all, they are a bit of a strange entity – Neurological? Psychological?… Faking?
Most of us have much to learn about pseudoseizures. Even the name is wrong: what used to be called pseudoseizures was re-defined as PNES (psychogenic non-epileptic seizures) at the turn of the century, and even this has now changed to PNEA (psychogenic non-epileptic attacks).
I offer the following two papers to help us understand PNEA. The first is a recent opinion piece, co-authored by a neurologist and a psychiatrist. The second is a systematic review and meta-analysis looking at which clinical signs can distinguish PNEA from epileptic seizures.
Paper 1 – overview of PNEA
This is a succinct and sensible presentation of what PNEA is and what it is not. In summary…
Defining and diagnosing
- PNEA is a type of ‘conversion disorder’, listed in DSM-5 under somatic symptom disorders – i.e. it is a psychiatric rather than medical diagnosis
- It is often the result of past trauma, psychological or physical
- It is not the same as malingering or drug-seeking (although these can co-exist)
- The symptoms of PNEA are not consciously produced by the patient (i.e. they are not ‘faking it’)
- The standard criteria for diagnosis require the capture of an episode on video EEG, demonstrating normal brain activity before, during and after the event, with clinical features consistent with PNEA as determined by an experienced epileptologist
- The treatment of choice is cognitive behavioral therapy (CBT) or another type of psychotherapy. Treatment options do not generally include anticonvulsants or benzodiazepines
- It is common for patients suffering from PNEA to be disparaged or ignored in the ED. We should bear in mind that they can usually hear everything we say during an episode. The following are real quotes from the recollections of patients: “Get up… Stop faking… You are wasting my time… Why do I have to put up with patients like you?… Everyone has left, so the drama can stop now… Pull yourself together and go home…” 
- There are reports of physical abuse by clinicians, in an effort to “snap [them] out of it” or assess the GCS. Patients have reported being slapped, having to inhale noxious chemicals, having multiple needle-pricks and even IO injections… Don’t do this. 
- The most appropriate ED management of PNEA is primarily reassurance. You can tell patients that they’re in a safe place, that you’re going to take care of them, that you’re not going to do anything painful or distressing.
- It’s worth remembering that even tonic-clonic seizures don’t need to be terminated urgently within the first 2 minutes, so you have some time to observe and make a decision about what you’re looking at.
Paper 2 – how can you be sure it’s PNEA?
Avbersek A, Sisodiya S. Does the primary literature provide support for clinical signs used to distinguish psychogenic nonepileptic seizures from epileptic seizures? J Neurol Neurosurg Psychiatry. 2010;81:719-725
This is a systematic review of studies investigating the semiology (signs) of PNEA, especially papers comparing epileptic seizures (ES) to PNEA. They considered a specific sign to be “well supported by the primary literature” if there were at least two controlled studies demonstrating its usefulness and if the data from other studies were not contradictory. Only those studies using video-EEG as a reference standard were included.
Signs that favour PNEA
- Long duration: it is rare for ES to last longer than 2 minutes, whereas PNEA can last anywhere from 1 to 150 minutes
- Fluctuating course: brief pauses in rhythmic movement are strongly suggestive of PNEA
- Asynchronous movements: tonic clonic seizures tend to produce bilateral, synchronous movements
- Pelvic thrusting: this sign was never observed in ES, but found in up to 30% of cases of PNEA
- Side-to-side head or body movement: generally not found in ES, but present in 25% of PNEA
- Closed eyes during episode: this happened 3% of ES and 96% of PNEA
- Ictal crying (i.e. during the episode): present in no ES but 14% of PNEA
- Memory recall: present in 6% of ES and 85% of PNEA
Signs that favour epileptic seizure
- Occurrance during sleep: 30-60% of ES occur during sleep, but PNEA never does (note that the ‘diagnosis’ of sleep may require an EEG, which limits the usefulness of this sign in the ED)
- Postictal confusion: present in up to 100% of ES, but only 16% of PNEA
- Postictal stertorous breathing: present in up to 91% of ES and no episodes of PNEA
- Serum lactate: if drawn within 2 hours of the episode, a level >2.45mmol/L suggests ES rather than PNEA (sensitivity and specificity 64% and 85% respectively). A level drawn within 1 hour increases the sensitivity and specificity considerably.[6,7]
- Serum prolactin: a level more than double the baseline suggests ES rather than PNEA, but this must be drawn 10-20 minutes after the episode
Signs with inconclusive evidence
- Tongue biting: can be found in both entities (no significant difference found)
- Urinary incontinence: present in around 20% of ES and 10% of PNEA, but this difference was not statistically significant
The bottom line
Patients with PNEA are not consciously in control of their ‘seizure’. Therefore they should not be subjected to painful stimuli to ‘test’ them. An episode of PNEA is not associated with the same risks as an epileptic seizure. Therefore we should not give benzodiazepines to terminate it.
“This is something I think we all need to think about – and move away from the idea that “they’re putting it on”. These patients are often frequent attenders who ultimately need proper care plans.”
(Dr Dwynwen Roberts, ED consultant)
More FOAMed on this…
1.Tolchin B, Martino S, Hirsch LJ. Treatment of Patients With Psychogenic Nonepileptic Attacks. JAMA [Internet] 2019;1967. Available from: http://dx.doi.org/10.1001/jama.2019.3520
2.American Psychiatric Association . Diagnostic and statistical manual of mental disorders. 5th ed. Washington D.C.; 2013.
3.LaFrance WC Jr, Baker GA, Duncan R, Goldstein LH, Reuber M. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: A staged approach. Epilepsia [Internet] 2013;2005–18. Available from: http://dx.doi.org/10.1111/epi.12356
4.Robson C, Lian OS. “Blaming, shaming, humiliation”: Stigmatising medical interactions among people with non-epileptic seizures. Wellcome Open Res [Internet] 2017;55. Available from: http://dx.doi.org/10.12688/wellcomeopenres.12133.2
5.Avbersek A, Sisodiya S. Does the primary literature provide support for clinical signs used to distinguish psychogenic nonepileptic seizures from epileptic seizures? Journal of Neurology, Neurosurgery & Psychiatry [Internet] 2010;719–25. Available from: http://dx.doi.org/10.1136/jnnp.2009.197996
6.Matz O, Heckelmann J, Zechbauer S, Litmathe J, Brokmann JC, Willmes K, et al. Early postictal serum lactate concentrations are superior to serum creatine kinase concentrations in distinguishing generalized tonic–clonic seizures from syncopes. Intern Emerg Med [Internet] 2017;749–55. Available from: http://dx.doi.org/10.1007/s11739-017-1745-2
7.Doğan EA, Ünal A, Ünal A, Erdoğan Ç. Clinical utility of serum lactate levels for differential diagnosis of generalized tonic–clonic seizures from psychogenic nonepileptic seizures and syncope. Epilepsy & Behavior [Internet] 2017;13–7. Available from: http://dx.doi.org/10.1016/j.yebeh.2017.07.003
8.Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology [Internet] 2005;668–75. Available from: http://dx.doi.org/10.1212/01.wnl.0000178391.96957.d0