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.

Post-traumatic Seizures

Post-traumatic epilepsy develops in 10–15% of serious head injury survivors. More than half will have their first seizure within 1 year. Significant risk factors are central parietal injury, dural penetration, hemiplegia, missile wounds and intracerebral haematomas. Early treatment with phenytoin for severe head injuries reduces the incidence of seizures in the first week only.

Seizures developing after significant head trauma have a higher incidence of intracranial pathology. Contrast CT is the initial investigation of choice. MRI will demonstrate more abnormalities but has not been shown to affect outcome. Long-term treatment with anticonvulsants should be planned in conjunction with a neurosurgical service.

Future Directions

Non-invasive portable modalities allowing definitive precise diagnosis of seizures in the emergency department (ED) will reduce the need for subsequent investigations in the majority of patients who do not have true epilepsy, and permit early focused therapy. Advances in pharmacotherapy and neurosurgical techniques will improve seizure control with minimal side effects, allowing patients to more effectively resume normal activities.