What is self-induced amnesia

It doesn't always have to be epilepsy

Not everything that looks like epilepsy at first glance is also one. The following article discusses common clinical pictures that can be associated with seizures and possible differential diagnostic problems.

Seizure disorders are a domain of modern neurology. In addition to the knowledge of the differential diagnoses shown, video recording of seizure-like disorders by relatives, friends or helpers is of enormous importance nowadays. A seizure illness without a more precise diagnostic assessment is simply to be discontinued with medication in order to use the success of the treatment as diagnostic evidence for a diagnosis. In the following, common disorders that must be taken into account in the differential diagnosis are listed.

Narcoleptic Syndrome

A diagnosis of narcolepsy should be considered when adults, mostly between the ages of 20 and 40, report pronounced fatigue that is difficult to overcome and occurs several times a day [15]. Epileptic seizures can be confused with short loss of tone triggered by affects such as joy (laughing at a joke), sadness, excitement or sex, which can also lead to falls [16]. In addition, so-called sleep paralysis can occur. These are conditions in which those affected wake up, cannot move and only overcome the muscle atony again after a while or through addressing or touching them.


Somnambulism, pavor nocturnus and drowsiness are so-called NREM parasomnias and are characterized by dissociated awakening from NREM sleep. These parasomnias (see Table 1) have a high prevalence (up to 15%) and occur mainly in children [1], usually in the first third of sleep. They last 1 - 20 minutes, rarely up to 45 minutes, and begin with a screaming scream that wakes the parents or loved ones. During the stereotypical seizure sequences, one sees pronounced, mostly untargeted motor activity, which can be accompanied by fear, confusion and behavior that is not appropriate to the situation. Vegetative signs are common, amnesia for the period of the parasomnia is mandatory. Parasomnias usually appear in the 12th year of life. Symptoms can persist into adulthood in 1–2% [3].


Among the non-epileptic organic seizures, vasovagal (neurocardiogenic) syncope are the most common [11]. They can also take place with motor, in particular with tonic and convulsive expressions, but are always much shorter than large epileptic seizures. The complexion of the affected patients is pale with syncope, but red to bluish with large seizures [17] (see Table 2). The rapid reorientation of the patient after the syncope is typical of neurocardiogenic syncope. The anamnesis (long standing in overheated places) and the symptoms before the syncope with vegetative symptoms (weakness, turning black in front of the eyes while consciousness is still preserved) are typical [14]. In contrast to an epileptic seizure, a tongue bite is absent (which, however, only occurs in less than 50% of Grand Mal seizures).

Laboratory values ​​are mostly normal postictal, i. H. no increase in CK is found, however, prolactin is said to be increased in 20-30% after syncope [19]. Anamnesis and external anamnesis usually allow the diagnosis, especially if the duration of the syncope is considered. Syncope is usually shorter than 30 seconds [22]. Epileptic seizures, on the other hand, which can be mistaken for syncope, last 1½ to 3 minutes [14].

The tilt table examination, which is sensitive but not very specific and can lead to false positive results, is now a well-established diagnostic tool for diagnosing neurocardiogenic syncope. With exact exploration of prodromes and a precise description of the seizure, this method is very effective for recording syncope, especially if those affected recognize the prodromi as habitual on the tilting table [4].


Atypical variants of migraines can be mistaken for epilepsy. Migraine accompagnée, in particular, is difficult to diagnose if patients do not have a headache during the attack or if they only get it after the focal neurological disorders have subsided [12]. The migraine accompagnée can lead to very different neurological deficits, the duration of the symptoms, their sometimes paradoxical lateralization in migraines and the headache, which is usually questionable, are indicative for the diagnosis. The rare basilar migraine is one of the most important differential diagnoses for epileptic seizures. The aura includes visual illusions, dysarthria, dizziness, tinnitus, paroxysmal hearing loss, double vision, brief tetraparesis, bilateral paresthesia and ataxia. This is often followed by a fall with a brief loss of consciousness [23]. The symptoms, which usually last several minutes to hours, and the sometimes prompt response of the symptoms to sumatriptan are useful for differentiating basilar migraine from epileptic seizures [24].

Transient global amnesia

This disorder is characterized by symptoms lasting minutes to hours (on average 6 - 8 hours), which usually affect people in the second half of life (peak age: 6th decade of life). In these episodes, which are often triggered by physical or emotional stress, the patients sometimes behave as if they were in a psychomotor seizure; they are clear in consciousness, but appear disoriented, perplexed, anxious and repeat the same questions repeatedly [5].

In contrast to epileptic seizures, this disorder rarely recurs (in 10% of those affected). The main symptom is amnesia, a short-term memory disorder that makes it impossible for patients to remember even simple things for a short time. During amnesia, the EEG shows a subtle reduction in basic activity. The amnesia resolves within 24 hours [10]. The cause is unknown, a volatile hypoperfusion of the mesiotemporal structures has been discussed for a long time, an association with migraines has been proven by case control studies [7].


Tic disorders can present rare but important differential diagnostic problems, which are divided into simple motor and vocal tics and complex motor and vocal tics [2]. In particular, simple motor tics can be confused with partial seizures, and complex motor actions can resemble the automatisms in psychomotor seizures. Those affected are able to suppress the tics in the short term. Prodromi are common and sometimes offer patients a chance to hide socially undesirable tics by withdrawing. Vocal tics help to differentiate, especially in Tourette's syndrome. The awareness of tics is always maintained, the occurrence several times a day and the change in the localization of the motor tics usually help to differentiate them from epileptic seizures [6].

If an attack is accompanied by a fall, the causes mentioned in the overview should be included in the differential diagnosis.

Dissociative seizures

Dissociative seizures are seizures that may resemble epileptic seizures, but which can be used as an expression e.g. B. an unresolved conflict are a symptom of a mental disorder [21]. The term “dissociative” refers to the fact that behaviors can be split off from the fantasies on which they are based as well as from conscious experience. Expressions such as hysterical or pseudoepileptic attacks are no longer used because of their judgmental character [24].

There are many options for help in the differential diagnosis between epileptic and dissociative seizures, but no absolutely certain evidence [8]. Even the seizure with surface electrodes recorded with EEG recording only clarifies the diagnosis when there is evidence of epileptic activity; its absence does not mean anything [13]. Essential for the assumption of epileptic seizures is the stereotype of the seizures, the short duration (usually <2 min), the indication of a specific aura, the occurrence during sleep (not only as anamnestic information), the specifically changed ictal EEG and the lateral (as opposed to the apical) tongue bite. CK and prolactin increases may also be absent after epileptic seizures (especially after frontal seizures) [8].

In the case of dissociative seizures, the seizure symptoms fluctuate, the duration varies, usually the seizures last longer than 3 minutes and often take place in front of an audience. Good external medical history is essential for making a diagnosis [20]. For outpatient confirmation of the diagnosis, however, the use of mobile video cameras is urgently recommended in order to be able to confirm or confirm the diagnosis [24]. It should be noted, however, that 25% of patients with dissociative seizures also have epilepsy. It is rare to see patients after epilepsy surgery who are free from seizures postoperatively with regard to epileptic seizures, but then have dissociative seizures [18].

In addition, the usually very pronounced concern of relatives and loved ones when observing a dissociative seizure can be helpful. Vegetative signs (even wide, non-responsive pupils are rarely seen in dissociative seizures), salivation, automatisms, or injuries are not good separation criteria [13]. Correct diagnostic classification of these types of seizures is very important. Nevertheless, the diagnosis of a dissociative seizure should not lead to the doctor feeling “duped” and giving the patient the feeling that he has deliberately deceived him. Dissociative seizures are not simulated disorders [21].

Criteria for assuming a psychogenic movement disorder are [according to 9] the abrupt onset, inconsistent movement patterns, strange, inconsistent movements and postures. Additional abnormal movements such as rhythmic shaking, bizarre gait, deliberate slowness in the execution of requested movements, sudden gibberish speaking, bizarre movements induced by fright are also frequently observed.

Other symptoms include psychogenic tremor when prompted to perform rapid movements, demonstration of exhaustion and fatigue, spontaneous remissions (symptoms disappear when distracted), paroxysmal appearance and dystonia that begins in a fixed position. According to the same authors [9], medical indications for a psychogenic movement disorder are non-objectifiable weakness and paresis, non-objectifiable sensitivity disorders, multiple somatized complaints, self-induced injuries, psychiatric disorder (s), employment in the health care system, secondary gain from illness and ongoing or intended litigation.

1. Avidan AY, Kaplish N (2010) The parasomnias: epidemiology, clinical features, and diagnostic approach. Clin Chest Med. Jun; 31 (2): 353-70
2. AWMF guidelines tics. www.awmf.org from 03/15/11
3. AWMF guidelines for parasomnias www.awmf.org from 15.3.11
4. AWMF guidelines on syncope. www.awmf.org from 03/15/11
5. Bartsch T, Deuschl G (2010) Transient global amnesia: functional anatomy and clinical implications. Lancet Neurol. Feb; 9 (2): 205-14.
6. Conrad B, Ceballos-Baumann AO (2005) Movement disorders in neurology. Thieme Verlag Stuttgart, New York
7. Crompton DE, Berkovic SF (2009) The borderland of epilepsy: clinical and molecular features of phenomena that mimic epileptic seizures. Lancet Neurol. Apr; 8 (4): 370-81. Review
8. Devinsky O, Gazzola D, Lafrance WC Jr (2011) Differentiating between nonepileptic and epileptic seizures. Nat Rev Neurol. Mar 8. [Epub ahead of print]
9. Fahn S (1994) Psychogenic movement disoders. In: Movement Disorders 3, eds: Marsden CD, Fahn S. Butterworth, Heinemann Oxford, 359-372
10. Gallassi R (2006) Epileptic amnesic syndrome: an update and further considerations. Epilepsia. 47 Suppl 2: 103-5.
11. Grubb BP (2005) Clinical practice. Neurocardiogenic syncope. N Engl J Med. Mar 10; 352 (10): 1004-10
12. Kossoff EH, Andermann F (2010) Migraine and epilepsy. Semin Pediatr Neurol. Jun; 17 (2): 117-22
13. Kuyk J, Leijten F, Meinardi H, Spinhoven, Van Dyk R (1997) The diagnosis of psychogenic non-epilptic seizures: a review. Seizure 6/4 243-253
14. Lempert Th (1997) Syncope. Neurologist 68: 620-624
15. Mayer G (2000) Narcolepsy. Blackwell Wissenschafts-Verlag GmbH, Berlin; Vienna
16. Meier-Ewert KH (1989) Daytime sleepiness. In: Practical Neurology. Edition Medicine, VCH Verlagsgesellschaft, Weinheim
17. Mumenthaler M (1984) Syncope and falls. Thieme Verlag, Stuttgart, New York
18. Ney GC, Barr WB, Napolitano C, Decker R, Schaul N (1998) New-onset psychogenic seizures after surgery for epilepsy. Arch Neurol 55/5: 726-730
19. Oribe E, Amini R, Nissenbaum E, Boal B (1996) Serum prolactin concentrations are elevated after syncope. Neurology Jul; 47 (1): 60-2.
20. Reuber M (2008) Psychogenic nonepileptic seizures: answers and questions. Epilepsy Behav. May; 12 (4): 622-35
21. Reuber M (2009) The etiology of psychogenic non-epileptic seizures: toward a biopsychosocial model. Neurol Clin. Nov; 27 (4): 909-24
22. Roth B (1962) Narcolepsy and Hypersomnia. VEB Verlag, Berlin
23. Sances G, Guaschino E, Perucca P, Allena M, Ghiotto N, Manni R (2009) Migralepsy: a call for a revision of the definition. Epilepsia. Nov; 50 (11): 2487-96
24. Wolf P, Mayer Th (2003) Epilepsy practice book. Kohlhammer Verlag, Stuttgart

The author is a member of the advisory boards of UCB Pharma GmbH, Eisai GmbH, Pfizer AG and has received fees for lectures from these companies such as Desitin Arzneimittel GmbH, Novartis Pharma GmbH and GSK.

Specialist in neurology and psychiatry, with a focus on epileptology
Saxon Epilepsy Center Radeberg