Pseudoseizures

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billypilgrim37

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For our consult folks,

How much of a C/L doc's caseload deals with non-epileptic events? I'm on my peds neuro rotation right now, and there's no shortage of girls with rigorous negative medical workups and non-epileptic spells. I tried to do some literature searches, and was sorta shocked just how little seems to be written about the subject relative to how common these events seem to be. I couldn't find a single DBT trial in a journal our library subscribed to, and I don't think that's because our library doesn't subscribe to a LOT of journals. The CBT trials seemed lacking as well. Maybe I'm thinking too much and not seeing these events as just a subset of conversion disorder, but they're ridiculously fascinating cases that seem to make everyone else shudder in dread while I'm still excited.

I'm guessing centers with healthy primary inpatient neurology teams see much more of this than folks out in the community trenches.

I guess I'm just always looking for a possible niche, and an excuse to do another fellowship. ;)

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This is in no way answers your question, but when I was rotating on peds neuro we saw something similar. This patient was a 15 year old girl with a Parkinsonian tremor in the right upper limb with no identifiable organic cause after an extensive work-up by our team and others. Our attending tried every trick in the book to see if she was faking this, but concluded that she was not consciously producing this tremor. We even tried a trial of L-DOPA (which had no effect) while we were waiting for the patient to get imaging studies. During one of the later visits (when a proper social history was finally taken), we discovered that this girl had experienced a traumatic event involving her ex-boyfriend and she has been mostly keeping to herself, avoiding social events. By the end of all this, our attending had a strong suspicion this was a conversion disorder and gently suggested the family see a psychiatrist.

I too find these cases to be so fascinating.....

For our consult folks,

How much of a C/L doc's caseload deals with non-epileptic events? I'm on my peds neuro rotation right now, and there's no shortage of girls with rigorous negative medical workups and non-epileptic spells. I tried to do some literature searches, and was sorta shocked just how little seems to be written about the subject relative to how common these events seem to be. I couldn't find a single DBT trial in a journal our library subscribed to, and I don't think that's because our library doesn't subscribe to a LOT of journals. The CBT trials seemed lacking as well. Maybe I'm thinking too much and not seeing these events as just a subset of conversion disorder, but they're ridiculously fascinating cases that seem to make everyone else shudder in dread while I'm still excited.

I'm guessing centers with healthy primary inpatient neurology teams see much more of this than folks out in the community trenches.

I guess I'm just always looking for a possible niche, and an excuse to do another fellowship. ;)
 
How much of a C/L doc's caseload deals with non-epileptic events?

I've seen a handful during 4 years of residency. Don't have an exact number but maybe around 5. 3 of them were during my neurology rotation.

A thing that happened at the hospital where I did residency was pseudoseizures went to the neurologist first-& this makes sense since the physical has to be ruled out before the psychiatric.

The neurologist often times after diagnosing a pseudoseizure often times did not refer the case to psychiatry. The neurologists did tell me they did get pseudoseizure cases more often than psychiatry.

Is it a subset of conversion disorder? No one really knows. We know that the person is not truly having a seizure, but is the person voluntarily faking it, or is it conversion? No one can tell because we can't tell if the patient is lying to us or not when we ask them.

A study that could investigate this is to do a lie detector test which from what I understand have 80-90% accuracy. Ask the patient if they were voluntarily faking a seizure. If there were enough subjects a useful range of which cases were probably conversion & which were not. This however has some controversy because lie detectors are not 100% accurate. (This however is BS in my opinion. Yes I know they're not 100% accurate, but several medical tests are not & we still use them in studies).

I also have had cases that IMHO I was convinced was not conversion, but the patient, of their own volition, faking a seizure. How do I know? Well one of my patients only had a seizure at convenient moments where it would get her what she wanted. She was addicted to ativan, and called it the "miracle drug I've been looking for all my life"-in regards to the euphoria it gave her. She learned that on the medical floor, anytime she faked a seizure she got it. Unfortunately she did have real seizure disorder so each time she faked one, it had to be treated as real because the hospital didn't have a video EEG.

But she started having seizures at key moments. E.g. she'd ask for ativan, we told her on the psyche floor we weren't giving it to her & then within 10 seconds seizure (or more likely pseudoseizure). We were though doing serum prolactin levels & they were all within normal range.

We transferred her to a long term care facility-which she did not want to go to, and during the ambulance ride--again had another (pseudo) seizure.
 
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Depends on where you work. For me, at a major neurology center, it's multiple times weekly. The group from Brown just presented some awesome results from a trial they did on CBT in NES - very hopeful looking. I don't think it's published yet, but the lead guy is W. Curt LaFrance.
In terms of work-up, the gold standard is vEEG that actually captures an episode, and even then you might be missing some subcortical activity. Depending on symptomatology, PET or SPECT might be indicated.
 
I have seen quite a few patients with pseudoseizures (in the UK, we call them "functional seizures", or "non-epileptic seizures" - goes over much better than "pseudoseizures" with both patients and their families).

I worked with a nationally recognized expert in psychosomatic illness, who has written several textbooks on conversion disorders, Munchausen and malingering. In his opinion, functional seizures most often (but not always) represent a subset of conversion disorder. Difficult to differentiate between conversion vs malingering, but if there is no clearly identified secondary gain and more or less clearly identified acute stressor, conversion is more likely.

There is very little literature on treating functional seizures. Approach we use is "explanation, managing expectations, follow up". Explain that it is not epilepsy, there is nothing physically wrong with their brain, and further invx and meds are likely to be harmful. Give the label - "functional disorder" - draw a parallel with something like IBS (which is much more common, much better recognised and does not have much stigma associated with it). Labels make these patients happy. Manage expectations - there is no cure, advise relaxation techniques, maybe a short course of benzos/antidepressants (if significant anxiety/mood component), best management is to avoid injuries during the fits (which they already do anyway) and carry on with normal life. Re-iterate: NORMAL life. Follow-up: offering follow-up means you are not getting rid of them, you recognise they have illness and are prepared to support them through the illness.

Just my 2 cents.
 
Use of the Personality Assessment Inventory as an efficacious

and cost-effective diagnostic tool for nonepileptic seizures

Mark T. Wagner
a,*, Joy H. Wymer a, Kris B. Topping b, Paul B. Pritchard b


a Division of Neuropsychology, Department of Neurology, Medical University of South Carolina, Charleston, SC 29425, USA

b Department of Neurology, Medical University of South Carolina, Charleston, SC 29425, USA

Received 14 March 2005; revised 23 May 2005; accepted 25 May 2005

Available online 25 July 2005


Abstract
Video electroencephalographic monitoring (VEEG) is considered the ‘‘gold standard'' for making the differential diagnosis between epileptic seizures (ES) and nonepileptic seizures (NES), but is a costly, time-consuming procedure and not readily available in all communities. Of the various diagnostic techniques and measures that have been used, the Personality Assessment Inventory (PAI) has shown promise as an effective psychological screening tool to aid in the differential diagnosis of ES/NES. Using VEEG results as the outcome measure, this study examined the diagnostic effectiveness of the PAI in a group of adults with treatment-refractory seizures. Results indicated that, on psychological screening, patients with NES endorse significantly greater functional consequences of their seizure-like episodes than participants with ES. A ‘‘NES Indicator'' score, calculated from the PAI Somatization subscales, provided a sensitivity of 84% and specificity of 73% for the diagnosis of NES versus ES. The PAI appears to be a useful screening tool prior to hospital admission for VEEG.


Discussion
On psychological screening, patients with NES endorsed functional impairment associated with neurological-like symptoms (i.e., conversion disorder), whereas patients with ES did not. Psychological markers of conversion-like symptomatology, depressive symptoms, social detachment, and lower irritability seem to be distinctive personality characteristics that may aid in distinguishing NES from ES patients. Further interpretation of personality findings indicated that both groups are quite concerned about their health. However, the nature of the concern differed significantly. The ES group was preoccupied with their health status and physical function. The NES group had the same concerns, but they rated their symptoms as having greater functional consequences. Using the difference between the Health Concerns and Conversion subscales of the Somatization scale of the PAI, the resulting NES Indicator provides a high level of accuracy and appears to be a useful screening tool for the diagnosis of NES versus ES. While neither group showed the broad spectrum of symptoms typical of clinical depression, the NES group complained of the physiological symptoms of depression, which included sleep disturbance, loss of appetite, weight loss, and decrease in level of sexual interest. The NES subjects also tended to have more uncertainty about major life issues and were more likely to describe themselves as being empty, bored, or unfulfilled. Based on our data demonstrating unique personality characteristics for each group, it is our opinion that the results of the PAI can help begin to build the foundations of the treatment reconceptualization that ultimately will be necessary for patients receiving a diagnosis of NES. At this time, although there are no empirically supported treatments for conversion disorder, the individual results from the PAI during the ES/NES diagnosis evaluation may help in the reconceptualization of a psychological rather than neurological model for aberrant behavior and could potentially serve as a starting point for the formulation of a psychological treatment. One potential limitation of this study is the homogeneity of study groups and resultant lack of generalizability to the general population. Future research should include a mixed ES/NES group. The excluded noncompliant patients also limit generalizability and should be more closely examined in the future. Low reading level and/or impaired intellectual functioning can be reduced as an exclusionary criterion in the future by using a PAI on audiotape. Larger sample sizes will increase the power of future replication studies. The diagnostic accuracy of the NES Indicator in this data set seems robust. The reliability of this finding will be evaluated as replication studies are conducted. Nonetheless, data suggest that the PAI may be able to play an important, cost-effective role in screening this patient population. A clinical interview and PAI generally cost under $300. A several-day, inpatient, 24-hour VEEG hospital admission can cost up to $15,000. Further, the availability of such monitoring units is limited given the prevalence of the disorder. This estimated cost does not include the cost of inappropriate antiepileptic drug treatment prior to the accurate diagnosis. Although VEEG is the current gold standard, further investigation of the PAI NES Indicator is warranted to determine its usefulness in differential diagnosis.
 
....But she started having seizures at key moments. E.g. she'd ask for ativan, we told her on the psyche floor we weren't giving it to her & then within 10 seconds seizure (or more likely pseudoseizure). We were though doing serum prolactin levels & they were all within normal range.

We transferred her to a long term care facility-which she did not want to go to, and during the ambulance ride--again had another (pseudo) seizure.

Famous (possibly apocryphal) story from my intern days.
Neuro team is consulting in VA ED on a stroke pt when a pt notorious for pseudoseizures (even has it on his official problem list) falls to floor in full-blown grand mal. They observe him, wait till it ends, and order Dilantin IV. Pt immediately starts seizing again, and between convulsions grunts out, "Won't....work....must....have....ati....van..." :rolleyes:
 
Pt immediately starts seizing again, and between convulsions grunts out, "Won't....work....must....have....ati....van.. ."

1 patient, as I was walking out of the ER (shift just ended) was waiting in the ER to be seen. He was told he would have to wait several hours. Right then & there, he fell as if he fainted. The ER staff picked him up, put him in an ER bed, bypassing the wait he would've had to have normally done & when the ER doctor showed up in just 1-5 minutes, he was all of a sudden awake & alert. The guy did not have any risk factors for syncope, and it was pretty much apparent he BS'd the entire thing to bypass the line.

Another patient was having seizure like activity. They hit him with a lot of ativan in the ER. He was brought up to the medical floor. EEG was negative. At that point I was no longer covering his case, but the IM residents who were I noticed in his room as I was walking by it (while on my IM rotation).

The guy was again having seizure like activity. The senior resident stated yelling at him-SIR!! SIR!!, I don't think you understand. We're going to have to insert a breathing tube into you if you don't stop this!, its very uncomfortable.!"

I didn't follow up with the case. Just wondering if that guy was conversion or malingering for ativan. I don't know if he got intubated, but if he did, man would that have been a rude awakening.
 
Famous (possibly apocryphal) story from my intern days.
Neuro team is consulting in VA ED on a stroke pt when a pt notorious for pseudoseizures (even has it on his official problem list) falls to floor in full-blown grand mal. They observe him, wait till it ends, and order Dilantin IV. Pt immediately starts seizing again, and between convulsions grunts out, "Won't....work....must....have....ati....van..." :rolleyes:

:laugh:
Seriously, we need a "roflmao" icon...
 
there is now a roflcopter icon.

Pseudoseizures and IBS are high on my list of disorders that I'm convinced are somatization/conversion responses to adjustment, mood, or anxiety difficulties.

Removing stigma is fine. Support is fine. But I think you always need to look for what they're somatizing about and deal with it, preferably through counseling, but antidepressants are good too.

I am far from an expert in this or any other aspect of psychiatry but NES is something I've seen a lot of for an MS4 (15+). The majority were going through obvious adjustment issues relating to an event that started 2-4 weeks before they started having episodes (my current attending who deals with this issue a lot insists that his patients call them 'spells' and not seizures). The others were long-time MDD/GAD/dysthymics who were becoming increasingly frustrated with the lack of symptomatic relief therein.

I have noticed that many of them do indeed suffer less attacks when they get their benzos, even the ones who don't come off to anyone (including attendings with 30+ year experience) as drug-seekers. It'd be interesting to figure out whether this relates to their anxiolytic effects, dependance, or anti-seizure effects.
 
But with IBS, how do you explain the diarrhea as somatization? I mean, it is hard to deny there is something going on on on a cellular receptor level in that case. Maybe you could say it is caused by STRESS, but a lot of things are worsened by stress and we don't just call it all somatization.

Do patients ever cross over, say, presenting with seizures for awhile, then IBS? Or do people typically stick to a "type?"
 
But with IBS, how do you explain the diarrhea as somatization? I mean, it is hard to deny there is something going on on on a cellular receptor level in that case. Maybe you could say it is caused by STRESS, but a lot of things are worsened by stress and we don't just call it all somatization.

Do patients ever cross over, say, presenting with seizures for awhile, then IBS? Or do people typically stick to a "type?"

The gut has more serotonin than the brain. Mood disturbance = serotonin disturbance in the brain. Not a big leap to say that in some serotonin could also be disturbed in the gut. Emotions manifesting physically is the basis of somatization.
 
I do remember reading that Irritable Bowel Syndrome has an association with personality disorders.

http://www.healthcentral.com/anxiety/news-152818-66.html

People who experience high levels of stress and anxiety appear to be more likely to develop irritable bowel syndrome (IBS) following a severe gastric infection, UK and New Zealand researchers report

A variety of studies have suggested that the cause of IBD has psychological and behavioral components, Dr. Rona Moss-Morris of the University of Southampton and Dr. Meagan J. Spence of the University of Auckland point out in the medical journal Gut.

Makes sense to me. I did a GI rotation in medschool. The GI docs were telling me that their patients with IBS seemed to be the ones that annoy them more often.
 
I do remember reading that Irritable Bowel Syndrome has an association with personality disorders.

http://www.healthcentral.com/anxiety/news-152818-66.html



Makes sense to me. I did a GI rotation in medschool. The GI docs were telling me that their patients with IBS seemed to be the ones that annoy them more often.

But then you get into chicken/egg arguments. You don't need to be Freud to believe that living with IBS could predispose to (at least) an obsessive personality style, or is it a pre-existing personality style that produces the stress that could cause IBS?
 
But then you get into chicken/egg arguments.

Of course.

I had a patient who has several cluster B traits & kept complaining to the IM doctor that she had bad constipation--to the point where she was actually "pulling stones" out of her rectum using her fingers. The IM doc on my psyche ward pretty much just blew her off.

I talked to the patient, most of her symptoms were consistent with Irritable Bowel Syndrome, and I figured-why not, order some metamucal. I did so specifically because I remembered an association between PD & IBS.

She said her GI symptoms went away and was happy with that metamucil. She had been going through that problem for several months on the unit-and she kept getting blown off by the IM doc.

From my own anectdotal experience, I've never seen too many psychiatrists (or other doctors) factor in IBS as an association with personality disorders. When those Cluster B patients complained, their psychiatrists who already had a lot of countertransference just blew off their somatic complaints. Only docs I've seen that actively tried to factor this in were GI docs.
 
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