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RESIDENTS CORNER
Year : 2013  |  Volume : 16  |  Issue : 3  |  Page : 447-449
 

A resident's (unique) position on non-epileptic seizures


Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA

Date of Submission10-Apr-2013
Date of Decision24-Apr-2013
Date of Acceptance12-May-2013
Date of Web Publication26-Aug-2013

Correspondence Address:
Vaishnav Krishnan
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.116938

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How to cite this article:
Krishnan V. A resident's (unique) position on non-epileptic seizures. Ann Indian Acad Neurol 2013;16:447-9

How to cite this URL:
Krishnan V. A resident's (unique) position on non-epileptic seizures. Ann Indian Acad Neurol [serial online] 2013 [cited 2019 Sep 15];16:447-9. Available from: http://www.annalsofian.org/text.asp?2013/16/3/447/116938


I was the night float resident. 40 min into my shift, I was paged to evaluate a patient seizing in room 1102. I quickly reviewed my patient hand-off sheet: "22yo right handed woman (RHW) h/o chronic lyme, anxiety disorder, multiple motor vehicle accidents? Bulimia." This was now her third spell of the day and her dilantin had been held for 24 h. 72 h of electroencephalogram (EEG) recording had captured numerous events that were all "without EEG correlate." A meeting with a social worker and psychiatry had been planned for the next day.

As I entered her room, I noticed a thin young woman lying supine with her eyes closed. There were numerous cut marks on her forearms and she had poor dentition with gingival bleeding. Her head and left arm shook rhythmically. Her mother watched over her anxiously and tried to dampen the shaking in her left arm. Her right leg also shook, at times in phase and at other times, out of phase with her head. The left leg and right arm lay motionless and limp. "O 2 sats 95%, heart rate 102," the nurse reported. Every 30 s, she made a loud gasping noise and held her breath. A bedside EEG displayed several lead tracings obscured by muscle artifact, but a 9 hz posterior dominant rhythm was evident. 4 min into the event, her movements dampened. All of a sudden, she developed left sided facial twitching movements with rhythmic toe flexion. 5 min later, we administered 1 mg of intravenous lorazepam. Her shaking soon stopped, she opened her eyes and appeared scared and worried.
"What happened to me?"
"You had a seizure," I replied. "We gave you some medicine to stop the seizure."
"How long did it last?"
"About 10 min." I could sense that this was not going to go very well.
"Why did you let me seize for so long?"

Gulp.

I quickly formulated an explanation about how we were trying to "collect data" about the "nature of these events," so that "we can know the best treatment for them." I regurgitated old talking points about how "this is a safe place to have a seizure" with "close monitoring." I tried to be scientific and logical, but compassionate and empathetic at the same time. She wasn't buying it.
"I want you to restart my dilantin."

She had made this request once before already and the team had agreed to not use antiepileptic medications at this time.
"Well, based on what we have seen so far, we don't think that dilantin is really an optimal medication for you. Additionally, it has a lot of side- effects including …"

She cut me off. "I need dilantin because it stops me from having these long seizures. Why can't you and your team understand that? I want to leave now."

The nurse and I worked to console her and she agreed to stay in the hospital for one more night. 30 min later, she started to seize again.

Psychogenic non-epileptic seizures (PNES) are remarkably common, estimated to affect between 12% and 20% of patients in epilepsy clinics. [1] Emergency room visits and hospital admissions for such seizures are associated with a magnanimous financial cost to our health care system. [2] The quality of care received by PNES patients is quite varied and overall outcomes are generally poor. [2] The International League Against Epilepsy recently commissioned a group of PNES researchers to provide a set of guidelines for the treatment of PNES. [3] Three main pillars of therapy have been proposed: (1) Adequate communication and education particularly at the time of initial diagnosis, (2) continued neurological follow-up to safely withdraw anticonvulsant medications and (3) combined management with psychiatry to address comorbid psychiatric diagnoses. [2],[4] A number of promising treatment modalities have emerged including cognitive behavioral therapy, [2] selective serotonin reuptake inhibitors [5] and electroconvulsive therapy. [6] There still remains a poor consensus among neurologists on how to treat prolonged non-epileptic seizures, [7] such as in the case described above. This is of grave significance, particularly since much of the morbidity associated with PNES comes from endotracheal intubation in emergency rooms for presumed status epilepticus, followed by intensive care unit admissions and associated iatrogenesis. [2]

In spite of the remarkably high prevalence and cost of this condition, we have a very rudimentary understanding of the pathogenesis of these events. Our best explanations are primarily psychological models, whereby psychogenic non-epileptic events are thought to represent a subconscious dissociative physical response to distressing internal emotional stimuli. [4] These hypotheses are based on the unique psychological and personality profiles of PNES patients when compared to patients with epilepsy as well as the comparatively higher incidence of prior physical and sexual trauma. [2] PNES has thus been grouped among other disorders of "conversion" (i.e., "psychogenic"), though it should be noted that there are currently no definitive research methodologies to unambiguously prove this point.

More neurobiologically oriented explanations of the pathophysiology of PNES are less well-developed. We know that PNES is associated with decreased serum levels of brain derived neurotrophic factor (BDNF) and increased diurnal cortisol levels, [8],[9] both serum biomarkers that have been previously correlated with stress and depression-related behavior. [10] To date, no genetic or post-mortem investigations have been conducted in patients with this disorder. Structural and functional neuroimaging studies are limited. One study identified cortical thinning in the right motor and premotor regions as well-bilateral cerebellar cortices and these features correlated with depressive symptoms. [11] While, older studies have also identified other subtle brain magnetic resonance imaging (MRI) changes in a proportion of patients with PNES, it remains clear that currently available structural MRI technologies are not likely to be sensitive enough to pick up the anatomical subtleties of a disorder like PNES. Encouragingly, functional MRI is beginning to be applied to patients with PNES. Preliminary studies have identified abnormally strong functional connectivity between the insula and frontal regions involved in the executive control of motor action, [12] including the supplementary motor area, which also appears to demonstrate heightened spontaneous neural activity in patients with PNES. [13] It is worth mentioning that similar results have been demonstrated using patients with motor conversion disorder, [14],[15] thought to be etiologically similar to PNES in many ways. A working model of PNES and other dissociative motor symptoms has been proposed, whereby strong emotional triggers can bypass the normal executive control of motor behavior through pathologically strengthened functional connections between emotional centers and motor regions. [16] Further studies are required to test this hypothesis.

Improving our knowledge of the neurobiology and treatment of PNES will be fundamental to altering some of the misconceptions held among our non-Neurologist colleagues. A recent survey of emergency room and primary care physicians showed that 45% of these practitioners felt comfortable diagnosing PNES based on clinical history alone and believed that provoking a similar event at the bedside "confirms the diagnosis of pseudoseizures." Interestingly, even though half of the respondents agreed with the statement "most pseudoseizures are voluntarily induced (patients are fakers)," 76% vowed to refer these patients to a Neurologist, over a psychiatrist or psychologist. [17] This is ironic, since most neurologists themselves tend to present the diagnosis of PNES and make psychiatric referrals; thus, ending their responsibility. [2] This reluctance to continue to treat patients may stem from a significant dissonance that exists between PNES patients and their neurologists on the degree to which they can exert "physical control" over these events and patients' insistence on "physical" treatments. [18]

There is a deep-rooted belief among many in our field that since these events are "non-epileptic," they are therefore "non-neurologic" or "non-organic," and thus, "not-my-problem-anymore." This view, that "he/she's just crazy/faking," develops early in residency education and is a sign of the lack of formal training for neurology residents in how to connect with and manage patients with PNES and conversion disorders. [19] It reflects a critical lesion in our longstanding approach to neurologic illness that is largely centered on "localization" and "deficits." After ruling out "organic" causes, we assume that non-epileptic events are not "organic," thereby completely ignoring the fact that our current diagnostic modalities are simply not sensitive enough to detect the subtle neurological derangements that lead to PNES. This represents a dangerous catch-22: the dismissal of these patients as lacking an "organic" neurologic illness has led to an overwhelmingly feeble research effort to identify the genuine neuropathology of the illness, thereby continuing the dominance of psychology-based etiological models.

PNES patients do not have a focal lesion, but rather dysfunction that is distributed across a wide array of limbic and cortical substrates modulated by several key endocrine signals (e.g., BDNF and cortisol). It is simply up to us to identify new ways to demonstrate and further characterize this dysfunction. In addition to expanding our knowledge of serum and genetic biomarkers for PNES, we need to continue to pursue real-time functional approaches to understanding abnormalities in emotional processing. Further insights may be gained from comparing individual differences between trauma-exposed individuals such as war veterans who either do and do not develop PNES. [20] Only after learning about the contribution of individual anatomic nodes involved in PNES, can we begin to explore more refined approaches to therapy, including modalities such as deep brain stimulation, which has offered hope for patients severely affected with a host of psychiatric disorders. [21] Finally, we must improve on the education and awareness of this condition among the lay public and our physician colleagues. [22]

As neurologists, we pride ourselves as being experts in functional neuroanatomy and have made significant strides in our understanding of several neurodegenerative and paroxysmal disorders. Neurologists remain at the forefront of diagnosing PNES - perhaps it's time we played a leading role in clarifying this disease's pathophysiology and refining treatment.

 
   References Top

1.Goldstein LH, Mellers JD. Recent developments in our understanding of the semiology and treatment of psychogenic nonepileptic seizures. Curr Neurol Neurosci Rep 2012;12:436-44.  Back to cited text no. 1
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2.Dickinson P, Looper KJ. Psychogenic nonepileptic seizures: A current overview. Epilepsia 2012;53:1679-89.  Back to cited text no. 2
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3.LaFrance WC Jr, Reuber M, Goldstein LH. Management of psychogenic nonepileptic seizures. Epilepsia 2013;54 Suppl 1:53-67.  Back to cited text no. 3
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4.Brown RJ, Syed TU, Benbadis S, LaFrance WC Jr, Reuber M. Psychogenic nonepileptic seizures. Epilepsy Behav 2011;22:85-93.  Back to cited text no. 4
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5.Bravo TP, Hoffman-Snyder CR, Wellik KE, Martin KA, Hoerth MT, Demaerschalk BM, et al. The effect of selective serotonin reuptake inhibitors on the frequency of psychogenic nonepileptic seizures: A critically appraised topic. Neurologist 2013;19:30-3.  Back to cited text no. 5
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6.Blumer D, Rice S, Adamolekun B. Electroconvulsive treatment for nonepileptic seizure disorders. Epilepsy Behav 2009;15:382-7.  Back to cited text no. 6
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7.Dworetzky BA, Bubrick EJ, Szaflarski JP, Nonepileptic Seizure Task Force. Nonepileptic psychogenic status: Markedly prolonged psychogenic nonepileptic seizures. Epilepsy Behav 2010;19:65-8.  Back to cited text no. 7
    
8.Bakvis P, Spinhoven P, Giltay EJ, Kuyk J, Edelbroek PM, Zitman FG, et al. Basal hypercortisolism and trauma in patients with psychogenic nonepileptic seizures. Epilepsia 2010;51:752-9.  Back to cited text no. 8
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9.LaFrance WC Jr, Leaver K, Stopa EG, Papandonatos GD, Blum AS. Decreased serum BDNF levels in patients with epileptic and psychogenic nonepileptic seizures. Neurology 2010;75:1285-91.  Back to cited text no. 9
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10.Krishnan V, Nestler EJ. Linking molecules to mood: New insight into the biology of depression. Am J Psychiatry 2010;167:1305-20.  Back to cited text no. 10
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11.Labate A, Cerasa A, Mula M, Mumoli L, Gioia MC, Aguglia U, et al. Neuroanatomic correlates of psychogenic nonepileptic seizures: A cortical thickness and VBM study. Epilepsia 2012;53:377-85.  Back to cited text no. 11
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12.van der Kruijs SJ, Bodde NM, Carrette E, Lazeron RH, Vonck KE, Boon PA, et al. Neurophysiological correlates of dissociative symptoms. J Neurol Neurosurg Psychiatry 2012.  Back to cited text no. 12
    
13.An D, Ring J, Chen S, Yan B, Liao W, Fang J, et al. FMRI study of psychogenic nonepileptic seizures using fALFF analysis. Abstract at Organization for Human Brain Mapping. Beijing, China; 2012.  Back to cited text no. 13
    
14.de Lange FP, Toni I, Roelofs K. Altered connectivity between prefrontal and sensorimotor cortex in conversion paralysis. Neuropsychologia 2010;48:1782-8.  Back to cited text no. 14
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15.Voon V, Brezing C, Gallea C, Ameli R, Roelofs K, LaFrance WC Jr, et al. Emotional stimuli and motor conversion disorder. Brain 2010; 133:1526-36.  Back to cited text no. 15
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16.van der Kruijs SJ, Bodde NM, Vaessen MJ, Lazeron RH, Vonck K, Boon P, et al. Functional connectivity of dissociation in patients with psychogenic non-epileptic seizures. J Neurol Neurosurg Psychiatry 2012;83:239-47.  Back to cited text no. 16
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18.Whitehead K, Kandler R, Reuber M. Patients' and neurologists' perception of epilepsy and psychogenic nonepileptic seizures. Epilepsia 2013;54:708-17.  Back to cited text no. 18
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19.A.A.N. American Academy of Neurology Core Curricula Resources Available from: http://www.aan.com/residents-and-fellows/fellowship-resources/core-curricula/ [last accessed on July 18, 2013]  Back to cited text no. 19
    
20.Salinsky M, Spencer D, Boudreau E, Ferguson F. Psychogenic nonepileptic seizures in US veterans. Neurology 2011;77:945-50.  Back to cited text no. 20
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21.Hamani C, Temel Y. Deep brain stimulation for psychiatric disease: Contributions and validity of animal models. Sci Transl Med 2012;4:142rv8.  Back to cited text no. 21
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22.England MJ, Liverman CT, Schultz AM, Strawbridge LM. Epilepsy Across the Spectrum: Promoting Health and Understanding. Institute of Medicine.2012.  Back to cited text no. 22
    




 

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