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REVIEW ARTICLE
Year : 2006  |  Volume : 9  |  Issue : 2  |  Page : 60-71
 

The diagnosis and management of pseudoseizures or psychogenic non-epileptic events


Department of Clinical Neurophysiology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK

Correspondence Address:
Aline J.C Russell
Department of Clinical Neurophysiology, Institute of Neurological Sciences, Southern General Hospital, 1345 Govan Road, Glasgow, UK G51 4TF

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.25978

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  Abstract 

Pseudoseizures or psychogenic non-epileptic seizures (PNES) are often misdiagnosed as epilepsy. This review discusses what is known about PNES, the importance of differentiating PNES from epileptic seizures (ES), avoiding iatrogenic harm and of identifying and managing the underling psychological stressors to optimise outcome. Clinical suspicion and careful history taking with witness accounts is mandatory. Supportive investigations including video-EEG (VEEG) and the utility of VEEG and provocation are discussed. Resources to diagnose and manage PNES are an issue for most countries and clinical expertise may also be lacking. VEEG is an expensive diagnostic tool and there is variable collaboration between neurology and psychiatry which will influence how patients are managed. Confounding this, is the lack of evidence for best practice in managing PNES. The prognosis for the majority of patients with PNES appears to be poor, despite a wider recognition of the problem. Well conducted studies are needed to test the different treatment options.


Keywords: Pseudoseizures, conversion reaction, hysteria, non epileptic events, pyschogenic attacks


How to cite this article:
Russell AJ. The diagnosis and management of pseudoseizures or psychogenic non-epileptic events. Ann Indian Acad Neurol 2006;9:60-71

How to cite this URL:
Russell AJ. The diagnosis and management of pseudoseizures or psychogenic non-epileptic events. Ann Indian Acad Neurol [serial online] 2006 [cited 2017 Mar 25];9:60-71. Available from: http://www.annalsofian.org/text.asp?2006/9/2/60/25978



  Introduction Top


Misdiagnosis in epilepsy is well recognised in patients newly presenting with seizures, as well as in those with recurrent seizures unresponsive to antiepileptic drugs (AEDs).[1],[2] While newly presenting seizures are most commonly confused with syncope, a significant proportion of patients with a long history of drug resistant epilepsy do not have epilepsy, but are experiencing non-epileptic attacks of psychological origin which have been mistakenly identified and treated as epilepsy.[3]

The purpose of this review is to examine what is known about psychogenic non-epileptic seizures (PNES), the potential causes of diagnostic confusion, how these events can be accurately diagnosed and current best practice in management.

Defining the problem

Non-epileptic seizures of psychogenic origin are episodes of altered behaviour which include motor activity and altered sensation and/or perception which may appear similar to those experienced and seen in epileptic seizures. The origin of this behaviour is however a psychological or emotional response and not due to the consequence of abnormal electrical discharges in the brain.[4],[5],[6] Rarely, such behaviour is the consequence of deliberate mimicry or malingering.[7]

Naming the problem

These psychologically mediated events are referred to in the literature by a variety of names [Table - 1]. Pseudoseizure is still the most recognised term, but may be considered derogatory, implying that the events are somehow fake and not to be taken seriously. Scull highlighted the difficulties and concluded that non-epileptic seizures (NES) was perhaps the least judgemental and would be more acceptable to patients as it describes the problem without implying causation.[8] Stone et al found that the terms 'stress related' or 'functional seizures' were more acceptable to a group of Scottish general neurology out-patients.[9]

It is important that terminology is an accurate reflection of the medical disorder, but it should also be acceptable to patients in terms of diagnosis, treatment and prognosis. From the medical perspective, referring to these episodic attacks as non epileptic events, may lead to confusion with other pathological or physiological events, which can also be confused with epilepsy [Table - 2]. Avoiding the use of the word 'seizure' when talking to patients, may help avoid confusion with seizures of epileptic origin. The terminology needs to be clear also, in order to inform and to share research with colleagues. Psychogenic non-epileptic seizures (PNES) or NES are the main terms now in common use. In order to be consistent with the current literature, psychogenic nonepileptic seizures (PNES) will be used in this review.


  Pathophysiology and Differential Diagnosis Top


It is important to recognise that PNES comprises a heterogeneous disorder, although the underlying mechanisms are considered to be consistent with conversion or dissociative disorders in response to a variety of psychosocial stressors.[10],[11],[12],[13],[14]

It is also important to distinguish PNES from other psychiatric disorders such as panic disorder, impulse control, post-traumatic stress disorder, psychosis and factitious disorder. Psychiatric co-morbidity is common.[15] Patients may be significantly depressed or anxious. In Moore's study of 187 patients with PNES, an absence of relevant psychological factors was found in only 5% of patients and from the patient's descriptions of their attacks, it appeared that many symptoms were related to anxiety.[16] A prospective population- based Dutch study compared 138 patients with epilepsy or other non-epileptic organic events, against 40 patients with PNES. The latter reported more psychopathological complaints, more dissociative symptoms and more state and trait anxiety.[17] There is also an excess of patients with dependent or borderline personality disorder who have poor coping strategies.[18] There may also be an excess of patients with mild learning disability.[5],[19] Non-epileptic seizures however, should not be confused with stereotypic behaviour seen in more severely learning disabled patients.

To confuse the issue further, between 5 and 50% of patients with PNES also have epilepsy, depending on the population studied.[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31] For example, Martin et al examined consecutive patients undergoing in-patient video-EEG (VEEG) monitoring and found that around 5 of the 514 patients with PNES had both PNES and epilepsy.[30] In Sigurdardottir's population based study however, half the patients also had epilepsy.[31] Co-existing PNES and epileptic seizures (ES) may considerably delay the diagnosis of PNES by up to 16 years for PNES and ES.[32],[33]

The extent of the problem

Non-epileptic events have been recognised since ancient times, the term hysteria coming from the Greek word for uterus.[34] Modern studies still continue to show an excess of female patients in their study populations.[31] Sigurdardottir's population- based VEEG study from Iceland found an incidence of 1.4 in 100,000, equal to almost 4% of that reported for epilepsy.[31] This study may be an underestimate as it relied on video EEG before diagnosis. Szaflarski's retrospective video-EEG study suggests a higher incidence.[35] Benbardis estimates a prevalence of 2-33 per 100,000, making PNES a significant neurological condition.[36] The prevalence of co-existing epilepsy and non-epileptic seizures also depends on the population studied and as already noted, ranges between 5-50%.[28],[30] The clinical features however of ES and PNES occurring in the same patient are usually different.[37],[38] PNES is most common in young and middle aged women, but also occur in the very young and the very old.[38],[39],[40],[41]

Kellinghaus showed that non-epileptic seizures were a frequent problem in elderly patients referred to a comprehensive epilepsy centre. In contrast to a younger control group however, events with a physiological or organic basis were almost as common as PNES. Although most of the patients did not have any evidence for epilepsy and more than two thirds of these patients were taking AEDs. Around 25% adults are male. A female predominance however is not found in children or in the elderly.[38],[39]

Although most of the research into PNES comes from Europe and North America; PNES are reported from around the world, including India and are therefore not a phenomenon exclusive to westernised societies. The underlying psychopathology however may show cultural differences and this may influence management.[42],[43],[44],[45],[46]

The problem with misdiagnosis

The consequences of misdiagnosis are significant. Anticonvulsants or anti-epileptic drugs (AEDs) will not stop non-epileptic attacks. Up to 80% of patients with PNES will be taking AEDs at the time of diagnosis.[47],[48]

AEDs have many adverse effects including teratogenesis.[49],[50],[51],[52],[53],[54],[55] There are also concerns regarding AEDs and neurodevelopmental outcome in exposed offspring.[56],[57] The consequences of inappropriate treatment are not confined to the adverse effects of individual AEDs. Combination use is common. In the more prosperous countries, there is a tendency to use combinations of the newer and more expensive anticonvulsants. Oto et al found in their cohort of PNES withdrawing from AEDs, that at the time of referral, patients were taking a median of two AEDs and 28% reported side effects.[48]

As up to a third of patients with PNES may present in non-epileptic status, so called pseudo-status; there are significant dangers of inappropriate intervention including cardio-respiratory arrest from over-medication, invasive procedures such as central line insertion or intubation and all other complications of ITU care.[58],[59] The risk of iatrogenic harm is therefore high.[60],[61] PNES complicating other medical scenarios can also be problematic.[62],[63],[64],[65] As well as to direct medical harm from inappropriate treatment, these patients also carry a significant psychiatric morbidity from suicide or attempted suicide.[66]

A diagnosis of epilepsy whether correct or otherwise, is stigmatising in most cultures and may result in loss or downgrading of employment, disruption of family relationships and over-dependence. There are also significant economic costs.[67],[68] Where non-epileptic seizures are misdiagnosed, ongoing disordered functioning is reinforced, establishing illness behaviour and the underlying psychological factors are not addressed. This also contributes to health and economic costs.[69] The correct diagnosis may be considerably delayed. Reuber et al report a mean delay of 7.2 years. Younger age, interictal epileptiform potentials in the EEG and anticonvulsant treatment were associated with longer delays. de Timary found similar delays between the first event and diagnosis for PNES alone, but delays of over 16 years for patients with PNES and ES.[32],[33]

Why are PNES so commonly misdiagnosed as ES?

PNES can be intensely emotional events distressing to a witness. During a PNES, there may be a great deal of vigorous motor activity with a risk of injury. The patient may also display clear emotional distress, including crying. Family and caretakers are distraught and there is pressure on attending medical personnel to do something. It requires a confident clinician to stand back and let a major motor non-epileptic event settle without intervention.[70] A less confident clinician may feel more comfortable medicalising the situation, by not 'seeing' what is actually happening. It is tempting in this situation to follow the usual protocols for treating prolonged or recurrent epileptic seizures. The recurrent Accident and Emergency or clinic case note entry "known epileptic", is also a dangerous scenario. AED prescription for conditions other than epilepsy may also be misinterpreted by the attending physician faced with an unresponsive and 'convulsing' patient.[71] Over-reaction and over-investigation intensifies any underlying patient and carer anxiety and will only exacerbate the situation if it does not harm the patient physically as well.

A common presenting scenario is a complex faint with some over-reaction by the patient, inducing considerable over-reaction from surrounding observers, including friends and family. This highly charged emotional atmosphere with the presence of ambulance sirens and flashing lights and immediate first aid which may include an ECG, oxygen, IV infusion and parenteral drugs such as diazepam, can induce further panic as well as disinhibition in the patient. This may be followed by the experience of an Accident and Emergency room environment and perhaps transfer to the intensive care unit. Medical tests such as a lumbar puncture and 'brain' tests, e.g., brain imaging and EEG, heighten alarm and anxiety. Any test thought to show an abnormality, however minor, will be registered by the patient and their caretakers. Inappropriate non-specifically 'abnormal' tests may make it more difficult later, to accept a diagnosis of a functional or psychological type rather than an organic disorder and adversely affect prognosis. An inaccurate diagnosis of epilepsy delivered with variable confidence by an inexpert clinician, along with a prescription of AEDs, sometimes as a 'trial of treatment' or 'just in case', completes the scene.

Diagnosis

The correct diagnosis of PNES requires careful detailed history, taking with appropriate and adequate witness accounts. If PNES are suspected, then recording an event with time- locked VEEG and confirming that this event, was typical with the patient and witness is the most reliable investigation. This needs to be performed by a clinician experienced in the procedure and who is familiar with all the potential pitfalls. Arriving at the correct diagnosis may be very straight forward, as with epilepsy, but in some patients this process can be very protracted, especially where accounts are vague, witnesses unforthcoming, unreliable or unavailable e.g., crucial witnesses to early episodes. Similarly, events may prove difficult to record and coexisting or previous epilepsy may confound. It cannot be overstressed that the clinician undertaking this must have adequate training and expertise in the diagnosis of paroxysmal disorders, especially epilepsy.


  Clinical Characteristics of Non-Epileptic Seizures Top


Careful history-taking requires awareness of the clinical characteristics associated with PNES, which may aid diagnosis. The first detailed descriptions of PNES as a specific disorder were made in the late 19th century, as proposed by Gowers in 1881, along with the classic demonstrations of Charcot.[72],[73],[74]

Typically, patients with PNES are young to middle aged, female, with a history of psychosocial and psychiatric problems. However, this stereotype can be very misleading. As already noted, PNES have been reported in children as young as 4 and in adults well into old age and approximately 25% patients with PNES are male.[38],[39],[40],[41]

Patients with epilepsy however, can also have considerable psychosocial difficulties and have a higher prevalence of psychiatric problems too.

However, a history of medically unexplained symptoms such as fibromyalgia, chronic pain, chronic fatigue and a history of childhood traumatic experiences, with an absence of risk factors for epilepsy should increase suspicion of PNES.[18],[21],[24],[75],[76],[77],[78],[79] Studies of personality profiles distinguishing patients from the general population and from patients with epilepsy, are not particularly helpful.[18],[80]

It is important to remember that PNES are mistaken for epilepsy, because the activity seen during both superficially share many similar characteristics. PNES follow two main patterns of activity. Approximately two thirds of PNES involve excess motor activity, sometimes referred to as convulsive or positive motor attacks and one third show a paucity of movement often after an initial seemingly controlled fall, sometimes referred to as negative motor or atonic attacks. One of my colleagues refers to the latter as 'fall down, lie still attacks'.[81] Patients may exhibit one or both types separately or as one attack. 20% of patients report more than one type of attack.[13],[24],[82] Events may occur consecutively. Onsets are not always gradual with a long prodrome, but may be quite abrupt in onset as with epilepsy, with apparent unresponsiveness or partial responsiveness. They may occur from apparent sleep.[83],[84] Onsets may appear 'focal' e.g., with initial lateralised tremor. Patients can injure themselves, bite their tongues and be incontinent. Peguero et al compared 73 patients with PNES diagnosed by VEEG, with 30 patients with refractory epilepsy. In a telephone survey 40% of patients with PNES reported injuries, 44% showed tongue biting, 44% had urinary incontinence and 32% had attempted suicide. Injuries of all types were more commonly reported by patients with epilepsy, with burn injuries exclusively reported by the epilepsy group.[66] Following a PNES, they may appear confused, complain of headache and exhaustion and have a need to sleep. Events may be very similar and appear stereotyped. Our own review of 59 consecutive VEEG patients with convulsive PNES showed that 89% of the 46 patients with more than one event recorded, had stereotyped events showing a very similar pattern of activity. 20% had onsets which were consistently lateralised and 41% looked as if they were asleep at onset, but were actually electrographically awake.[85]

Studies of the clinical profile of those individuals with both epileptic and PNES suggest that different types of event are usually clinically distinct.[37] Early age of onset, interictal epileptiform EEG abnormalities and risk factors for epilepsy should always raise suspicion of co-existent epilepsy, even if several PNES have been recorded.[32],[86]

So it is easy to understand that PNES can be confused with epilepsy. Tables of clinical features distinguishing epileptic from nonepileptic seizures may be misleading, because so many important features are common to both disorders.[5],[75],[87]

Which clinical features are more suggestive of PNES?

Events which occur in situations unusual for spontaneous ES, e.g., events occurring exclusively when upset or triggered some minutes after exposure to flashing lights. Prodromal symptoms lasting hours or even days, a protracted onset with a gradual build up of movements and controlled falls with minimal injury are unlikely to be epilepsy. Motor events where 'convulsive' movements resemble tremor, show variability, wax and wane, alternate or are out of phase between limbs, show features which are inconsistent with and last far longer than the motor activity expected in association with an epileptic discharge and its propagation. Apparent 'unresponsiveness' can be unmasked by demonstrating resistance to eye opening or if open, diversion of gaze away.[88] If the patient's arm is held over the face, it will fall to the side. Directed aggression or rage attacks are highly unlikely to be epileptic and need to be distinguished from post ictal confusion. Typical injuries include 'carpet burns' resulting from prolonged repeated rubbing movements and biting the tip of tongue. Closed eyes, normal colour, pallor or appearing flushed but never cyanosed with normal or panting breathing, are common observations. PNES can also often be provoked and controlled by suggestion.

Which clinical features are more suggestive of ES?

These include: onset in early childhood especially if unremitting, abrupt onset of stereotyped complex but sometimes bizarre motor activity lasting < 1-3 minutes and cyanosis. Burns are specific to ES and severe lateral tongue and mouth laceration is highly specific to generalized tonic-clonic seizures. Brief stereotyped indescribable auras which are always the same, are typically epilepsy. When recorded with EEG, only ES occur in sleep.[27],[89],[90],[91]


  Misdiagnosis of Epileptic Seizures as PNES Top


Perhaps because there is more awareness of PNES, Parra et al have reported an increase in misdiagnosis of epilepsy as non-epileptic seizures.[92] Surface EEG changes may be obscured by movement and muscle artefact in seizures of abrupt onset, with the marked and often bizarre motor activity associated particularly with frontal seizures.[27] Not all epileptic seizures will show surface EEG change when recorded, particularly when consciousness is preserved.[93],[94],[95] Epileptic seizures may also induce anxiety and evolve in to an event exhibiting behaviour which is non-epileptic.[96],[97] There are also rare examples of bilateral motor ES with retained consciousness.[98],[99]

How are non-epileptic seizures best diagnosed and investigated?

As with epilepsy, non-epileptic seizures are essentially a clinical diagnosis. It requires a clinician who is confident with epilepsy diagnosis and who is prepared to take and re-take a history, interview and re-interview all the appropriate witnesses, being mindful that there may be unobtainable witnesses (ex-partners, deceased parents) in order to establish a strong suspicion of either exclusively non-epileptic seizures or a mixed disorder of non-epileptic and epileptic events. When taking a history, neurologically contradictory features should be sought. Witnesses may demonstrate, for example, tremor rather than clonic movements. History taking may reveal significant psychological stresses and a history of psychiatric disorder, although it is important to remember that patients with epilepsy and other types of non-epileptic events may be anxious, depressed and may have been subject to significant traumatic life events.

There have been various attempts to try and produce a clinical profile for patients experiencing non-epileptic attacks, as opposed to epileptic seizures as already discussed.[5],[20],[21],[37],[100] Certain features are useful, but none are absolute.[4] However, such lists are not mutually exclusive, as noted above. PNES may be stereotyped, result in significant injury, there may be tongue biting, incontinence and colour and respiratory changes. Episodes occurring from sleep are reported (apparent sleep when actually recorded with EEG) and patients with PNES may also have risk factors for epilepsy.[101]

For some patients, it may be possible to reach a confident diagnosis with the help of a home video. For most patients however, it is useful to confirm the diagnosis by recording a typical witness- confirmed event in its entirety. This is best done with video co-registered with EEG and ECG. It is important to record all types of events if multiple types are reported. Showing recorded events to the appropriate witnesses may also prompt memory of other more distant past events which may have been epileptic. As one would expect, most patients with both ES and PNES will present initially with epilepsy.

When recording non-epileptic events, it is important that the reporting physician and technologists are as familiar and expert in the clinical aspects of epilepsy and non-epileptic attacks, as with the pitfalls of surface EEG recording, including the appearance of artefacts and normal variants.[102]

Co-registered VEEG is an expensive resource in terms of equipment, expert personnel and use of hospital facilities, especially if this requires to be done as an in-patient.

How useful is a simple video recording?

Home video is very useful, although such equipment may not be standard in every home, but a camcorder can be borrowed.[103],[104],[105] Cameras on mobile phones are increasingly used. However, beginnings of events are often missed and this can be a diagnostic problem.

How useful is EEG?

Interictal EEG

Inter-ictal EEG is of limited usefulness because of its low sensitivity and specificity. A normal EEG does not exclude epilepsy and epileptiform activity on an EEG does not confirm epilepsy. Epileptiform and other EEG abnormalities are reported in patients who do not have epilepsy.[32],[106],[107],[108],[109],[110] However, where unequivocal epileptiform activity is seen on EEG in a patient with unequivocal PNES, the probability of a mixed disorder with ES will be increased. Often the epilepsy is not concurrent, but there may be a past history of epilepsy, now well controlled with AEDs. Interictal epileptiform abnormalities flag up the need for caution when withdrawing AED treatment.

Ictal EEG

Ictal EEG also has some limitations, especially where there is no video. Epileptic seizures, where there is a change in experience or sensation with retained awareness, may be particularly difficult as there may be nothing to see on video and no surface EEG change.[93],[94],[96] Abrupt onset frontal seizures and other epileptic seizures with a great deal of motor activity may also be obscured by muscle artefacts.[27]

Epileptic attacks need to be occurring very frequently, to be captured during a standard out-patient video EEG recording. This has led to the development of long term epilepsy monitoring with ambulatory and video-EEG, using cable or wireless telemetry.[111] While ambulatory EEG-monitoring can be carried out in an out-patient or home setting, there are difficulties in co-registering behaviour with the EEG even with video, unless the two are time- locked.[112] Video co-registered with EEG is the most reliable method of recording ES and other events of diagnostic uncertainty, if occurring at least weekly, preferably daily. This has led to the development of in patient epilepsy monitoring units. This is a costly exercise in terms of equipment, training and employment of expert medical, nursing and technical staff and of only limited availability in many countries.

There is a frequent observation in these units however, that non-epileptic seizures occur early on during the recording period and these patients may require shorter recording time.[113],[114] Where there is a mixed disorder however, one may need to record for significantly longer with drug reduction to record epileptic seizures.[21]


  Provocation of Seizures Top


Provocation techniques increase the chance of recording events. ES can be provoked by reducing AEDs, by hyperventilation (childhood absence seizures), photic stimulation (photosensitive epilepsy) and by sleep deprivation. When trying to provoke an ES, the patient should be fully informed about possible risk and their consent must be obtained.

Patients with PNES are suggestible and not infrequently have events in medical settings, such as clinics and during tests. When admitted for in-patient diagnostic VEEG, they frequently have PNES within the first 24-48 hours. Parra found that 96% had had their diagnostic PNES events spontaneously, within 48 hours of in-patient monitoring.[113] However, PNES can be recorded in ambulatory care settings with significant success. In McGonigal's study, 66% of patients randomised to simple suggestion and an expectation that an event would occur during a standard out-patient EEG had a diagnostic PNES.[115] Benbadis reported a higher yield of 84% in their own small study.[116] Suggestion as a technique, appears to be acceptable to patients and does not appear to be harmful.[26],[117]

The yield from simple suggestive techniques may be improved further using other techniques, which include hypnosis, IV injections of saline, placing and removing patches on the forehead or neck, the use of tuning forks, head up-tilting or even Woods light. [118],[119],[120],[121],[122],[123],[124],[125],[126] Slater et al found that using procedures such as intravenous infusion of saline up to 90% of patients will have a diagnostic PNES.[122]

Although the yield may be higher with suggestion combined with other methods of provocation, there is considerable debate as to whether such practice is ethical. Concern has been expressed about the risk to the relationship between the clinician and the patient, which might be detrimental to successful management and outcome. Patients may experience atypical symptoms, including patients who have epilepsy. They may become very angry and upset, when confronted by the deception. There is also a lack of long term follow up data.[127],[128] Others stress the importance of making the correct diagnosis to avoid iatrogenic harm from continuing misdiagnosis and the opportunity to give appropriate treatment earlier, which may improve prognosis. There are also economic reasons, reducing the need for expensive monitoring.[5],[133],[134]

Devinsky, Benbadis and McGonigal prefer the simple expectant and transparent approach which is our current practise in Glasgow.[119],[129],[130] Our experience of long term follow-up is encouraging.[131] Patients give their informed consent, and understand we feel it is essential to record an event and we expect one to occur during the procedure. We always ask a reliable witness to be in attendance and to confirm if an event is recorded, whether it is typical, comment on severity and on features recorded and not recorded. Most importantly, witnesses will guide whether the recorded attack is representative and whether they have ever seen anything different. If there is no witness, then, with the patient's consent, the video is stored on CD or videotape and shown to a suitable witness at a later date. Prior to the recording, it is helpful to go through the history in detail, particularly the patient's experience of an attack and what is normally seen by the witness. This may also have an additional suggestive effect. As the recording proceeds, any clinical change is noted. The witness attending is often the first to notice subtle early changes. The patient is asked for comments on what they are experiencing and the witness is also encouraged to comment. Responsiveness can be checked. The circumstances in which attacks usually occur can be helpful. We may also make use of patient- specific triggers.

Over the last 5 years, 449 patients suspected of having PNES in the West of Scotland have had events using this simple technique, which takes approximately 1 hour. 51% had events and 40% were diagnostic PNES. The yield in patients having very frequent events was higher at 70%. In 8%, the habitual event was epileptic, demonstrating that even expert clinicians can get it wrong. Of those who had no event or atypical episodes, attempts to record one with prolonged periods of EEG monitoring was unrewarding in 43%. Uluc at al noted a tendency to have events off camera during VEEG.[132]

Although our yield of diagnostic events might be higher using additional provocation techniques; we consider our approach to be intrinsically honest and which will not potentially impair the relationship between clinician and patient or be detrimental to successful management and outcome.[133]

The disadvantages of a short out-patient induction include the short sampling time for interictal EEG, and concurrent ES. Raymond et al recommend recording at least five PNES to reduce the chance of missing ES.[86]

However, very few of our patients with suspected PNES only and diagnostic attacks recorded by out-patient VEEG, have later also produced ES on slow reduction of AEDs.[48]

It may therefore be unnecessary to use in-patient VEEG for the initial diagnostic recording of habitual PNES in the majority of cases. Ambulatory or out-patient techniques are now standard practice in some centres using provocation techniques.

Other investigations

Prolactin, creatine kinase, serum neuron-specific enolase

Prolactin levels are often raised, following a generalised convulsive epileptic seizure. Serum prolactin rises to concentrations greater than 500 IU/ml in over 90% of patients after a tonic-clonic seizure and 60% of patients after a complex partial seizure. However, prolactin concentrations may be normal after prolonged status epilepticus and show no rise after simple partial seizures. Prolactin levels may also be raised following PNES and syncope. Sampling needs to undertaken between 20-30 minutes after the event and compared with a baseline level sample. Sensitivity and specificity is therefore too low for this to be a reliable test.[134],[135],[136] Creatine kinase may be raised after any activity and is not useful and all three assays are of such limited discriminative power, that none can be considered helpful in differentiating PNES from ES.[136]

ECG

Always consider performing an ECG in patients with paroxysmal episodes with syncopal features.

Management of PNES

The management of PNES remains a controversial subject due to the lack of good evidence for effective treatment and how it should be provided.[137],[138],[139]

PNES are heterogeneous in aetiology and prognosis is also variable. Delayed diagnosis may contribute to a poorer prognosis.[33] Uncertainty regarding concomitant epilepsy confounds the problem. Most major research groups however would agree that management involves a number of important steps. First the diagnosis needs to be delivered in a non-judgemental sympathetic manner by someone with expertise in the disorder, who can explain the diagnosis and provide treatment options, as well as deal with the consequences of presenting the correct diagnosis. The explanation should include why the diagnosis is not epilepsy and patients may need to be reassured that they are not 'crazy' or malingering. Treatment should include removal of inappropriate AEDs if there is no concurrent epilepsy, treating any underlying psychiatric disorder and offering and providing appropriate psychological support. Long term follow up may also be necessary.[75],[101],[139],[140]

Delivering the diagnosis

This is best undertaken by the clinician who plans to coordinate treatment and the follow up. In Glasgow, Oto et al usually discuss the likely diagnosis of PNES with the patient before any diagnostic tests. A definite diagnosis is delivered once a diagnostic attack has been recorded. The diagnosis is given in a clear, but understanding and sympathetic manner. Empathy with the patient is important. Some patients do become very angry and upset, especially if there has been diagnostic delay for a considerable time, which may run in to decades. It is stressed that the diagnosis of PNES is a positive step, allowing for more appropriate treatment. Patients are strongly reassured that their attacks are an expression of genuine distress and that they are not 'making it up'.[48] Mellers, Devinsky and Shen adopt a similar approach.[75],[141] Once the initial impact of the diagnosis has been registered, the treatment strategy is then discussed.[48]

Withdrawing AEDs

Approximately 80% of patients with PNES have been treated with AEDs before the correct diagnosis is made.[47] Oto et al recommend withdrawing AED treatment as the next stage using the same protocols for withdrawing AEDs, in patients with epilepsy.[48]

Leaving the patient on a small dose of AED 'just in case', is unhelpful. It gives a confused message to the patient, carers and other health practitioners. During AED withdrawal, if new events appear, further diagnostic testing can be carried out. Infrequently the new events are epileptic, the epilepsy having been in remission and 'forgotten' or not recognised by patient or witnesses. Where a past history of epilepsy is suspected, AED withdrawal may be undertaken in an in-patient setting e.g., in a residential epilepsy assessment centre with VEEG monitoring faculties.

Treatment

Treatment includes psychotherapy and use of adjunctive medications to treat coexisting anxiety or depression. Psychiatric and neuropsychological assessment is best undertaken by those with special expertise in PNES. Oto et al offer, after a detailed psychological assessment, a course of cognitive behavioural therapy (CBT).[142] However, there is currently a lack of evidence as to which types of psychological intervention are most effective or whether certain patients will respond better to particular types of intervention.[137] LaFrance and Barry recently published a helpful review of published studies on treatment and the various treatment models currently under study.[143] Underlying aetiological factors may determine the best treatment model for that individual, but the heterogeneity of the condition hinders the design of good clinical studies of treatment. Selective serotonin reuptake inhibitors (SSRIs) may be helpful. Patients with significant psychiatric co-morbidity such as anxiety or depression should be offered appropriate treatment and psychiatric referral as appropriate. Issues such as previous abuse and traumatic experiences will need to be explored.[78],[79],[142],[144]

Prognosis

Reuber et al found that after a mean follow up period of three years, 71% of patients continued to have PNES and more than half remained dependent on social security. Four years after diagnosis, 41% continued treatment with AEDs. Lempert's experience over a decade earlier is similar.[5],[24],[145] Reuber et al also provide an overview of other studies.[145] Prognosis is poorer if the diagnosis is delayed, there are motor attacks, if there is psychiatric co-morbidity, personality disorder, lower IQ and poorer socioeconomic status.[5],[75],[77],[145]

PNES in children

It should be noted that there is a far wider differential diagnosis in children, compared to adults.[146] Boys are as commonly affected than girls. PNES have been described in children as young as 4. Only fairly short periods of VEEG may be necessary to record diagnostic events.[147],[148],[149] The prognosis also appears better with upto 81% event- free 3 years after VEEG diagnosis.[150],[151],[152]


  Conclusion Top


Patients with PNES are commonly misdiagnosed as having epilepsy. There may be considerable delay before correct diagnosis and as a consequence, patients are exposed to inappropriate AED treatment and are at risk of iatrogenic harm from inappropriate interventions for uncontrolled 'seizures'. Any patient with frequent pharmacoresistent seizures should have the diagnosis of epilepsy reviewed by someone with an expertise in epilepsy.[153] Although there is consensus that the diagnosis is best confirmed by VEEG, prolonged in-patient monitoring may be unnecessary. There is no good evidence-based data as to which psychological interventions are the most effective for managing PNES and improving outcome, but gradual withdrawal of AEDs has been recently shown to be achievable and safe, where there is no evidence of concurrent epilepsy.


  Acknowledgment Top


I would like to thank all my colleagues from the West of Scotland Epilepsy Service for their support; and in particular, Arup Mallik, Sandra Lauder, Maria Oto and Norman Peden for their helpful comments.

 
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   Abstract
   Introduction
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   Introduction
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