I was called to place a labor epidural in a 17 year old G1P0 hispanic female. The health questionairre filled out by the patient was not available. Upon entering the room, I encountered the patient in significant pain. I briefly went through her past medical history which was only significant for PIH, with a blood pressure of 185/100 mmHg. Other laboratory values were within normal limits. she was on no medication at home, but was receiving magnesium via infusion for seizure prophylaxis. She was an other wise healthy female, and I proceeded to place a lumbar epidural (L 4-5). Although the patient was in a great deal of pain and very upset, she was able to cooperate long enough for smooth placement of the catheter. After encountering loss of resistance to air at 5.5 cm of depth, I attached a 10 mL syringe of 0.25% bupivacaine (6 mL). After negative aspiration, I slowly injected this volume into the epidural space and then immediately inserted the catheter 3 cm into the epidural space. I then immediately proceeded to inject 3 mL of 1.5% lidocaine with 1:200k epinephrine. HR was monitored and remained stable at 110 bpm. Within 30 to 45 seconds of injection, the patient began to slouch, then slowly slump to her side, and then loose all tone and crumpled to the bed. VS remained stable with a saturation of 98%, BP 180/90 and HR 110s. The patient was limp and non responsive. I noticed that her eyes were shut and I tried to open them to evaluate her pupils. I encountered resistance and was unable to effectively open her eyes. Shortly thereafter she began to thrash her head back and forth, hyperventilate and cry hysterically. I asked her to squeeze my hand, and felt no response. 100% oxygen was administered and preparations were made to intubate. The patient's VS remained unchanged except for HR which was now at 140 bpm. At this point the paitient began jerking and shaking both her arms and legs in a very random and non purposeful fashion while continuing to cry hysterically, hyperventilate and shake her head back and forth. Within about 90 seconds or so the thrashing ceased and the patient began to relax and became responsive. After a few moments she was breathing calmly responding to commands and able to answer further questions about her medical history. She asserted that 4 years ago she had had several similar episodes which had resulted in an extensive workup including EEG, MRI and hospitalization none of which revealed an etiology. The patient also asserted that she was aware during this brief episode but was unable to communicate in any way her fear. In other words she described a "locked-in" like episode.
Given this scenario, is it safe to proceed with dosing the labor epidural catheter in place, or should it be replaced?
The obvious differential as to what happened include:
- Intravenous injection of lidocaine with test dose resulting in fainting and then atypical seizure activity.
- Subdural injection of lidocaine via the catheter.
- Subarachnoid location of catheter and intrathecal test dose injection resulting in syncope and then weakness of the respiratory muscles and muscles of the upper extremities.
- Coincidental epileptic seizure of brief duration.
- Psychogenic non-epileptic seizure (PNES) also known as pseudoseizure
- Cataplexy as part of narcolepsy.
- Eclamptic seizure
Subarachnoid injection of lidocaine resulting in total spinal or high spinal was quickly ruled out when the patient begain moving her arms and legs during the "seizure" like activity. Furthermore, the time course in which the patient returned to full strength was far to rapid to account for a subarachnoid injection of lidocaine.
Cataplexy was considered less likely given the massive thrashing and crying that accompanied the episode. Although the patient did mention that in her previous episodes she had experienced "sleep paralysis". This is a symptom associated with narcolepsy and cataplexy patients.
Subdural injection was easily ruled out for the same reasons as that of sub arachnoid injection.
Coincidental epileptic seizure was considered extremely unlikely and previous medical work up was negative for epilepsy.
This left intravenous catheter placement with lidocaine injection resulting in the bizarre constellation of symptoms witnessed vs. psychogenic non-epileptic seizure (pseudoseizure) vs. eclamptic seizure.
Given the robust reaction the patient had upon injecting lidocaine via the catheter, I was a little concerned that the catheter was intravenous. But there was no obvious increase in heart rate within 30 seconds of the injection. The intravascular total dose of 45mg is unlikely to result in seizure activity. Although Morishima and Santos showed that pregnant ewes were more susceptible to LA cardiac toxicity, these studies were with bupivacaine[4,5]. Santos demonstrated as well that this is a result of decreased protein binding in pregnant ewes compared to non pregnant ewes resulting in more free bupivacaine in pregnancy. However, this did not occur with mepivacaine. Lidocaine has also been shown to be no more toxic to pregnant ewes compared to non pregnant ewes. In conclusion, given the small dose given and lack of cardiovascular response to epinephrine, an intravascular catheter was a very unlikely cause of the observed behavior. While some anesthesiologists would recommend replacing the epidural as the safest approach when in doubt, I would purpose, that in this case it could actually carry greater risk.
Psycogenic non epileptic seizure (PNES) is very difficult to distinguish from epileptic type seizures. In fact, these events often lead to expensive work ups, hospitalization and the initiation of antiepileptic drugs (AED). Obviously, since AEDs provide no benefit for those suffering from PNES, but often result in sigificant side effects (~25% of patients), it is ideal to avoid AED if possible. Unfortunately, reviews indicate that 80% of patients suffering PNES end up on AEDs at one point or another increasing costs and risks to the patient. The reason that so many patients with PNES end up being treated for seizures is that indeed they are extremely difficult to differentiate unless captured with video and EEG simulatneously. This requires expensive in-patient observation for several days in a highly specialized unit. Post ictal EEG is not very specific, sensitive or easily available on a L&D unit. Although Prolactin levels often increase (must draw within 20 to 30 minutes) to greater than 500 IU/mL after a generalized tonic clonic seizure (>90% of patients), easy clinical access to this laboratory test is lacking. Furthermore, prolactin levels only rise this high in 60% of patients after complex partial seizure, and there may be no rise at all of after simple partial seizure. Therefore, even if I had the presence of mind to order the test and had a laboratory that would run it in a clinically relevant time frame, it is unlikely to be very helpful.
Therefore, it requires an intimate understanding of the clinical differences observed plus a detailed history to make a confident diagnosis. There are risk factors for the development of PNES which include:
- being female (3:1)
- personality disorders often coincide as well as other psychiatric disorders.
- history of abuse (physical or sexual).
Features that are more likely associated with a true epileptic seizure include:
- severe injury (espeically burns)
- tongue biting (sides of tongue).
- stereotyped (with aura) i.e. similar presentation each time with little variation.
- duration of from 1 to 3 minutes.
Features that are associated with PNES:
- occurs exclusively when patient is emotionally stressed.
- gradual onset w/ buildup and controlled falls
- motor events with tremor, show variability, wax and wane, alternate or are out of phase between limbs
- "apparent" unconsciousness unmasked when eyes closed and resistant to opening.
- closed eyes, normal color (not cyanotic), and normal or panting breathing are common.
- biting of the lip or tip of tongue.
A recent study found that a very specific and sensitive test is to look at the eyes during the event, if closed, especially if resistant to forced opening, it is likely to represent a PNES. The mouth is also more often clenched tightly shut with PNES and open with ES.
After talking to the patient, and verifying that she was again at baseline, I proceeded to dose the epidural catheter in situ with lidocaine. I gave two more cc's of 1.5% lidocaine with epinephrine 1:200K and carefully watched the heart rate and observed the patient. This was uneventful and after several more cc's of lidocaine, she was pain free.
I made the diagnosis of psychogenic non epileptic seizure based on the following criteria:
Teenage pregnancy is higher risk group for sexual abuse.
Her history and work up revealing no evidence of epilepsy in the past.
The atypical thrashing, espcially head moving back and forth with hyperventilation and more or less coordinated arm and leg movements (although not purposeful).
lack of cyanosis, and importantly, at least according to one study, eyes closed with forceful resistance to my attempts to open the eyes.
I suspect that the stress of labor compounded by the additional stress of placing an epidural catheter was enough to push her over the edge and resulted in a recurrence of her psychogenic non epileptic seizure. Since PNES is triggered primarily by stressful events, replacing the epidural catheter in this patient puts her at risk. Another 'pseudoseizure' may have been enough to scare the obstetrician into performing a Cesarean Section which is not indicated.
In this case, the patient was pain free when I left the room, but still emotional and suffering from uncontrollable "shivering" despite not feeling at all cold. I was called again 45 minutes later when she once again became hysterical. This time, it was clearly a psycogenic event, the patient never lost consciousness, but was thrashing her head back and forth, hyperventilating, and crying hysterically. This lasted just 1 or 2 minutes and then resolved. The patient experienced a pain free delivery of a healthy baby girl 1 hour and 30 minutes later. The catheter was removed and the patient appeared to be perfectly calm and tranquil, a 180 degree change from her previous state of near hysterics.
 Benbadis SR. How many patients with pseudoseizures receive antiepileptic drugs prior to diagnosis? Eur Neurol 1999;41:114-5.
 Shukla G, Bhatia M, Vivekanandhan S, Gupta N, Tripathi M, Srivastava A, et al . Serum prolactin levels for differentiation of nonepileptic versus true seizures: Limited utility. Epilepsy Behav 2004;5:517-21.
 DeToledo JC, Ramsay RE. Patterns of involvement of facial muscles during epileptic and nonepileptic events: review of 654 events. Neurology. 1996 sep;47(3): 621-5.
 Morishima HO, Pedersen H, Finster M, et al. Bupivacaine toxicity in pregnant and non-pregnant ewes. Anesthesiology 1985; 63: 134-139
 Santos AC, Pedersen H, Harmon TW, et al. Does pregnancy alter the systemic toxicity of local anesthetics? Anesthesiology 1989; 70:991-995
 Morishima HO, Finster M, Arthur GR, Covino BG. Pregnancy does not alter lidocaine toxicity. Am J Obstet Gynecol. 1990;162:120-4.