DIAGNOSTIC DILEMMA

PSEUDOSEIZURES
P.C GILWAZ
Consultant Neurologist
Elite Mission Hospital, Trichur.
  In has been estimated that upto 20% of patients in a common epilepsy clinic may not have epilepsy at all, emphasizing the diagnostic  pitfalls in the assessment of cases with seizure disorders.
  The tern pseudoseizure itself is problematic. The oxford English Dictionary gives the definition of "Pseudo" as false, counterfeit, or spurious. Thus the term pseudoseizure is misleading, in that, the seizures being discussed are none of these. They are real, in so far as they are experienced by patients and observed by bystanders and physicians alike. Several alternative terms such as Hysterical Pseudoseizure s, pseudoepileptic seizures, Hystero-epilepsy and psychogenic seizures, are all indiquate and a preferred term for what is being discussed here would be Non-epileptic seizures. this acknowledages that these phenomena are different from those of epilepsy, but the patient nevertheless has had s sudden paroxysmal experience that may be interpreted as being epileptic like. There are a number of non epileptic conditions that lead to such attacks. however the core of diagnostic pitfalls usually relates to the diagnosis of psychopathology, which will form the main area of discussion here.
INCIDENCE
  Pseudoseizures are common in neurologic setting s. Among patients with conversion symptoms "seizures" are particularly prominent. Approximately 25% of males and 41% of females with conversion phenoment present with "fits".
  It must be emphasized at this point that patients with epilepsy may also have Pseudoseizures and here it will be difficult to separate the true from the Pseudoseizure. Pseudoseizures may occur at any time during the life epileptic, but it is at the tail end of the true seizures when the physician considers drug withdrawal that the patient is loath to give up his "Sickness tole " and Pseudoseizures manifest.
DIAGNOSIS
  Textbooks from the time Gowers have given advice as to how to distinguish between epileptic and non-epileptic seizures and it is reasonable to state that with the exception of EEG and neurohormonal data, the stated critieria have changed little over the last 100 years. The table given below will probably be of some use in this regard.

FEATURES HELPFUL IN DIFFERENTIATING CONVULSIVE PSYCHOGENIC FROM CONVULSIVE EPILEPTIC SEIZURES

EPILEPTIC SEIZURE

 

     PSYCHOGENIC SEIZURE
Precipitant Usually none Often an emotional precipitant /or provoked by suggestion
Circumstances:      
In Sleep Common Rare
When alone Common Less common
Prodroma Rare Common
Onset Usually abrupt. May have a short aura May be gradual with increasing emotional sumptoms
Cry at onset Common Unusual
Vocalisation During automatism only Common during seizure
Motor activity Stereotyped usually both tonic and clonic phase. Clonic Movements slow as seizure continues Variable. Often tonic or clonic only. Clonic Components vary in amplitude and frequency during the attack. Pelvic thrusting. Pseudo-clonic mivements.
Injury Common Rare
Incontinance Common Unusual
Tongue biting Common Rare
Consciousness Usually totally lost in convulsive seizures Variable. often possible to communicate during an attack
Restaint No effect May resist, sometimes terminates an attack
Duration Usually short May be prolonged
Termination of attack Usually shotr (but with automatism sometimes longer) Confusion, drowsiness or sleep common May be gradual, often with emotional display, confusion, drowsiness or sleep (unusual)
  As is the rule in medicine, the essential part of the investigation is the history. It always helps, if the physician understands the patient in whom the symptoms are observed without being unduly biased by well meaning relatives who want to push him into a diagnosis. Information regarding the setting in which they occur, the timing of the event and the precipitating factors are very important.
  It is a truism that seizures occuring many times a day in the presence of a normal interictal EEG are most likely non-epileptic; so also screaming, or displays of emotional behaviour, especially if target oriented are likely to lead to a similar conclusion. Provocation of seizures by suggestion, or for a doctor's benefit are also common features.
  On the other hand, the presence of Paroxysmal abnormalities on EEG does not neceesarily mean a diagnosis of epilepsy and it must be remembered that paroxysmal discharges such as generalised Spike and wave complexes are found approximately in 3% of healthy people
  Henry and Woodruff described a physical sign that provides a positive basis for the diagnosis of pseudoseizures during an attack, based on variation of ocular deviation with the patient's posture. In non-neurologic state of coma or seizures, when the patient is lying on the ground and is turned from side to side, the eyes are always deviated to the ground, thus changing their position with posture. In the case of epileptic seizures, any deviation of eyes tends to be constant and not related to body position.
  Fenton lists the folowing features for the diagnosis of pseudo-seizures:
  Variability in seizure pattern with bizzare features not consistent with a seizure discharge speading within the brain, Inconsistent and changing seizure description, evidence of responsiveness to envionmental stimuly (Retention of corneal reflexes), resistance to eye opening, head retractions on supraorbital pressure, change of position to avoid discomfort, verbal expression of obscenities, compative, behaviour, emotional display etc.
  It must be noted that tongue biting, and incontinence though rate, do occur in non-epileptic seizures.
  Self injury is not uncommon but usually involve the same sites, suggesting the reopening of old wounds.
  A word of caution perhaps will be in order at this point. All of us with experience in this field have seen the most unusual manifestations of epileptic seizures, which without the benifit of much detailed investigation could have been dumped into the already bulging bag of Pseudoseizures.
NEUROHORMONAL CHANGES IN SEISURES
  Medical basal hypothalmic stimulation has been shown to increase prolactin levels. It was proposed therefor the abnormal electrical activity in epilepsy which passed through the mid-brain should raise prolactin concentrations.
  studies by trimble and others in patients with generalised epilepsy, control group with ECT ane full neuro-mascular relaxation, and a group of patients with hysteria, showed significant elevation of serum prolactin within 15-20 minutes to  values of more than 1000iu inepileptic patients in the presence of normal base line values, while in the hystreic group the level did not rise about 500iu/ml 
  FSH changes littil in male patients, but significantly elevated following generalised seizures in the 20 minute sample in female patients.
  Estimation of prolactin, LH and FSH at I mt, 20mts and 60 mts. showed that prolactin levels were elevated in 1 mt. and 20mt sample (? relased before clinical seizure) and returned to normal in 60 mts. Sample while LH was still rised at that time.
  Following complex partial seizure rise in prolactin at 1 & 20 mts. Was noted, LH was elevated at 20mts. sample in female patients. The magnitude of rise is lessthan for generatised tonic clonic seizures.
  Canges after simple partial seizures were minimal and insignificant Indian. 
MANAGEMENT OF PSEUDOSEIZURES
 It is first of all, assential to accept the fact that there are patients who are going to continue to have symptoms despite the most intensive treatment. This is the case with pseudoseizures, as it is with  epileptic seizures, and while it does not mean that the patient should be abandoned and discharged from the clinic, it emphasizes a different therapuetic relationship that emerges between the treating physician and the patient. the treatment of nonepileptic seizures is, to some extent, related to whether or not the patient has associated epileptic seizures. Thus, in nnonepileptic patients, it is obvious that they do not require anticonvulsant medication, and one of the first assentials in treatment is to slowly remove them from the prescription if they are on such agents. Often, this is best done in a hospital setting, and indeed, the acceptance by the patient that he should be admitted to a psychiatric unit, rather than requiring further attendance at a neurologic clinic, is in many cases an important step towards attaining a positive therapeutic result.
  If there is underlying psychopathology which has already been diagnosed and does not require further investigation, this, of course would be treated in its own right. Depressive illness generally requires psychotherapy and psychotropic medication, as does anxiety. Usually some initial explorations may unravel complex issues that have led to the oresentation of non-epileptic seizures and, in the absence florid psychopathology, particularly in a younger age group, this may be all that is required to bring about relief of the clinicall problem. Nonetheless, such patients often require more prolonged support, in which case this can be continued on an outpatient basis. It is important that the patient is not dismissed as somebody who is "Putting it on" and is not made to feel that he or she is mailingering. Some patients are extremely reluctant to give up their epileptic label, not the least because their lifestyle has been altered so radically by this diagnosis that the change would require another radical shift in the whole of their life pattern. Clearly, in these cases, therapy is long-term and, of necessity, includes involving other members of the patient's family and social support system.
  In some cases, when the attacks are clearly precipitated by anxiety, some form of anxiety relief or behavior therapy may be instituted. Behavior modification or both are useful in individual patients.
  Medications, in addition to antidepressant medications, which are sometimes helpful, include benzodiazepine derivatives. In particular, such drugs as lorazepam and clobazam and monoamina oxidase inhibitors (MAOLs) have a clear place in some patients such as those with a phobic anxiety depersonalization syndrome.
  If the patient has epilepsy, similar techniques of management are used, although withdrawal if anticonvulsant drugs is not indicated. nevertheless, patients on polytherapy may benefit from a judicious alteration in their regimen. In addition, if psychopathology, particularly effective disturbance, is intermingled with epilepsy and may be related to the onset of nonepileptic seizures, an attempt to achiev monotherapy, preferably with a drug such as carbamazepine, can be rewarding; this regimen may ameliorate symptoms of both enxiety and depression.
CONCLUSION
  The diagnosis and management of pseudoseizures is difficult and time consuming. It requires careful and involved history taking, if possible with a video recording or direct observation of the seizure. EEG and neurohormonal studies are helpful. In the management, one should realize that one is in a borderland between neurology and psychiatry and as always in such situations, it is wise to tread softly as one goes along.