Pseudoseizures

Overview of Pseudoseizures

Pseudosezures or psychogenic seizures are events simulating neurogenic seizures Opens in new window but without the accompanying abnormal neuronal activity. Differentiation from neurogenic seizures Opens in new window may be extremely difficult, even for experienced neurologists.

Neuorogenic Opens in new window and psychogenic seizures may coexist, making the diagnostic dilemma even more complex. Differentiation will often require video-EEG monitoring, but this facility is not available in the ED and other methods must be used. It is important to recognize pseudoseizures so as to prevent the possible iatrogenic consequences of unnecessary treatment, while at the same time not withholding treatment from patients with neurogenic seizures.

Pseudoseizures are more common in women, less common after 35 years of age, and rare in patients over 50. They may be associated with a conversion disorder, malingering, Munchausen syndrome or Munchausen syndrome by proxy. Patients with conversion disorder differ from malingerers by being unaware of the psychiatric cause of their actions.

Pseudoseizures typically last more than 5 minutes, compared to neurogenic seizures Opens in new window which usually terminate within 1–2 minutes. Multiple patterns of seizures tend to occur in individual patients, and post-ical periods are either very brief or absent. Patients with recall of events during what appears to be a generalized convulsive seizure are likely to have had a psychogenic seizure. Extremity movement out of phase from one side to the other and head turning from side to side typify pseudoseizures. Forward pelvic thrusting occurs in 44% of patients with pseudoseizures and is highly suggestive of the diagnosis.

Several maneuvers are useful in identifying pseudoseizures. Eye opening and arm drop tests are accompanied by avoidance, eyes turning away from the moving examiner, and termination of the event when the mouth and nostrils are occluded are characteristic. Simple verbal suggestion and reassurance are also frequently successful.

The most definitive means of differentiating pseudoseizures is by ictal EEG or video-EEG monitoring. Unfortunately, this is of little value in the ED. Blood gas determinations demonstrate a degree of acidaemia in neurogenic tonic-clonic seizures, but not in patients with pseudoseizures. Pulse oximetry will detect a fall in Sa0₂ during neurogenic but not pseudoseizures. Serum prolactin levels rise and peak 15–20 minutes after generalized tonic–clonic seizures, and then fall with a half-life of 22 minutes. The levels do not consistently rise with partal seizures, and remain normal with pseudoseizures.

Patients presenting with pseudoseizures are often treated with anticonvulsant medications, both acutely and for maintenance. Such patients usually demonstrate resistance to anticonvulsant medication, and many will therefore present with therapeutic or supratherapeutic levels. It is difficult to resist the temptation to immediately administer pharmacotherapy when confronted with a convulsing patient, but to do will result in patients with pseudoseizures receiving unnecessary and potentially harmful treatment.

Careful examination of eye movements, pupil reactions, asynchronous limb movements, rapid head turning from side to side, forward pelvic thrust movements, testing for avoidance maneuvers and monitoring pulse oximetry may enable the diagnosis to be made and drug therapy avoided. In doubtful cases, blood gas determinations are helpful and serum prolactin levels can be collected for later analysis. Doubtful cases should be discussed with a neurology service and arrangements made for emergency EEG.

Once the diagnosis is confirmed it must be presented in an open and non-threatening manner. Patients often have underlying personal and/or family problems that will need to be addressed. Psychotherapy is effective, but seizures often relapse at times of stress.

Alcohol-related Seizures

Seizures represent 0.7% of ED visits, and alcohol contributes to approximately 50% of these. The majority of alcohol-related seizures occur as part of the alcohol withdrawal syndrome.

Although the precise pathophysiology of alcohol-related seizures has not been elucidated, it is clear that alcohol is a direct CNS toxin with direct epileptogenic effects. Acute toxicity and withdrawal are both associated with an increased incidence of seizures. Alcohol intoxication and chronic alcohol abuse are also associated with increased incidences of intercurrent disease such as trauma, coagulopathy, falls, assaults and other drug intoxication, all of which further increase the likelihood of seizures. The management of seizures presumed to be alcohol related must include a search for associated disease and other causes.

Benzodiazepines are the principal anticonvulsant agent for acute seizures. These agents are also valuable in the treatment of withdrawal. Phenytoin is ineffective in the control of acute seizures or as a preventative.

Drug-related Seizures

Seizure activity in the setting of acute drug overdose is an ominous sign associated with greatly increased mortality and morbidity. The most commonly reported are in association with cyclic antidepressants (CA), antihistamines, theophylline, isoniazid, and drugs of addiction such as cocaine and amphetamines. The diagnosis and management of these toxic syndromes are discussed in the webpage on toxicology Opens in new window.

Some medications are also associated with lowering seizure threshold in susceptible individuals. Tramadol in particular has been increasingly prescribed for analgesia in recent times and associated with new-onset seizures at normal therapeutic doses. A complete medication history is therefore essential.

Similarly, motor activity Opens in new window that is coordinated and not bilateral, such as side-to-side head movements, pelvic thrusting, directed violence and movement that changes in response to external cues, are less likely to be true seizures. Conditions such as syncope Opens in new window may be accompanied by myoclonic activity and are important to distinguish from true seizures. Migraine, transient ischaemic attacks, hyperventilation episodes and vertigo are all important conditions to consider in the differential diagnosis. Pseudoseizures is discussed here Opens in new window.

The history, examination and investigation process is aimed at identifying associated conditions and treatable causes of seizures. The aetiology of seizures can be classified into five groups on the basis:

1. Acute symptomatic — Occuring during an acute illness with a known central nervous system insult.
2. Remote symptomatic — Occuring without provocation in a patient with a prior central nervous system insult known to be associated with an increased risk of seizures, e.g. encephalopathy, meningitis, head trauma or stroke.
3. Progressive encephalopathy — Occuring in association with a progressive neurological disease, e.g., neuro-degenerative diseases, neurocutaneous syndromes and malignancies not in remission.
4. Febrile — Patients whose sole provocation is fever. This is almost exclusively confined to children, and as such is beyond the scope of this entry.
5. Idiopathic — Patients who present de novo, or during the course of their illness, in the absence of an acute precipitating central nervous system insult. This is probably the most common group; however, this classification is by exclusion of the other causes.

A careful history is needed to decide whether this is part of an ongoing process or an isolated event. Patients may not recall previous events, may not recognize their significance, or may even avoid reporting previous episodes for fear of being labeled ‘epileptic’, with the associated consequences. Particular attention should be paid to any history of unexplained injuries, especially when they occur during blackouts or during sleep. Any history of childhood seizures, isolated myoclonic jerks and a positive family history increases the likelihood of epilepsy.

A complete physical and neurological examination is mandatory. Evidence of alcohol and drug ingestion and head trauma is particularly important. A comprehensive medication history may include agents known to reduce the seizure threshold in susceptible individuals, e.g. tramadol, selective serotonin reuptake inhibitors. A careful mental state examination in seemingly alert patients may reveal evidence of a resolving post-ictal state or of underlying encephalopathy. All patients not fully alert should not be assumed to simply be in a post-ictal state until other causes are excluded. Of particular importance is any evidence of underlying illness, such as fever, nuchal rigidity (meningitis) or cardiac murmurs (endocarditis). Needle tracks, evidence of chronic liver disease, dysmorphic features and marks such as café-au-lait spots (neurofibromatosis) are important aetiological clues. Complications such as tongue biting, broken teeth and peripheral injuries are not uncommon in generalized seizures. Stress fractures can occur, particularly in the elderly, and posterior dislocation of the shoulder is an uncommon but significant and easily overlooked finding.

The investigations necessary following an uncomplicated seizure are minimal. Although it is common practice to order a variety of tests, such as electrolytes, blood sugar level and full blood count, these are rarely of benefit in the fully recovered patient. Elevated neutrophil counts in blood and CSF may be seen as a result of a generalized seizure in the absence of an infectious disorder. Although electrolyte abnormalities may cause seizures they are unlikely to be the cause if the patient has recovered.

A serum prolactin level at 20 and 60 minutes post seizure may be helpful if the diagnosis is in doubt. Patients with an abnormal physical or neurological examination should be managed according to clinical findings and the results of laboratory and radiological investigations. Finding suggestive of meningitis, encephalitis or subarachnoid haemorrhage are indications for cranial CT scan and lumbar puncture.

There are no clear guidelines to the routine need for or urgency of neuroimaging following a single uncomplicated seizure. Patients with focal neurological signs, those who do not recover to a normal examination, and those with a history of head trauma or intracranial pathology should all undergo cranial CT as soon as possible. The dilemma arises in patients with complete recovery and no focal signs. The incidence of abnormalities on CT in this group of patients is less than 1%. The decision as to whether and when to scan patients in this group will be determines largely by local factors. Generally, a contrast CT (more sensitive for subtle lesions) is performed on an outpatient basis prior to review. MRI is more sensitive than CT for infarcts, tumors, inflammatory lesions and vascular lesions, but cost and availability limit its use as a primary investigative modality.

Electroencephalography (EEG) at the time of a seizure will make a definitive diagnosis. It is not usually performed in the acute setting except when non-convulsive activity is suspected. Typically, an EEG is obtained electively on an outpatient basis, when it may still indicate an underlying focus of activity and may be able to detect specific conditions.

Once a diagnosis of first seizure is made and intercurrent conditions are excluded or treated, the patient may be discharged home. In most cases no treatment is needed. It must be stressed to the patient that a diagnosis of epilepsy has not been made but is being considered. When the suspicion is reasonable the patient should be given the same precautionary advice as epileptic patients with regard to driving and other activities that may place them or others at risk.

The planning of investigation and follow-up for patients suspected of having a first seizure is best done in conjunction with a neurology service. Planning and consultation will ensure that appropriate investigations are completed in a timely fashion. Generallty, an inter-ictal EEG and contrast CT are completed prior to review.