Can an EEG be wrong

Starting epilepsy or not?

When a patient comes to the doctor about a current seizure event, the first question that arises is whether it was an epileptic seizure at all, and if so, what type of seizure. Since epileptic seizures are symptomatic, the second step is to diagnose the epilepsy syndrome.

The epilepsy syndrome and not the type of seizure (or types of seizures) determines the further diagnostic and therapeutic approach and allows prognostic statements. Epileptic seizures and epilepsy (syndromes) are therefore classified separately [1, 2, 3]. According to the new classification of epilepsies [5], an epileptic seizure is sufficient to diagnose epilepsy if a recurrence probability of at least 60% can be assumed. This probability is achieved if, in addition to a confirmed seizure, there is a pathology in the EEG and / or a lesion in the MRI that explains the seizure [8]. But even the new definition cannot prevent many people with seizures from being diagnosed with epilepsy that is actually none:

  1. The first seizure was not epileptic, but syncopal, dissociative, or of a different origin (syncope, with a lifetime prevalence of 50%, is much more common than epileptic seizures!)
  2. The first attack was acutely symptomatic, e.g. B. with alcohol withdrawal or in a diabetic coma.
  3. The acute EEG did not show any pathology, but artifacts or normal variants that were considered to be suspicious of epilepsy.
  4. The MRI shows abnormalities that are either not pathological or were not the cause of the seizure and are not epileptogenic at all.

Epileptic seizure or not?

If an observed event cannot be assigned, it should not be dealt with without a more detailed analysis. The external description or a recording by smartphone are groundbreaking. An MRI or long-term EEG examination without a good hypothesis should be rejected, as should the implantation of an event recorder without a good idea of ​​what it was. The event recorder does not identify either the epileptic seizure or the syncope [17] that is induced by a drop in blood pressure. Premature epileptification of seizure events has significant socio-medical consequences (ban on driving a vehicle, occupational disability for a large number of occupations, long-term use of medication), so an unclear seizure-like event should always be presented to a seizure clinic and then, if it remains unclear, to the cardiologist [18]. Rules of thumb can help: As a rule, epilepsy begins before the age of 20 or after the age of 55, rarely in between. Epileptic seizures are short, rarely longer than 2 minutes, the post-phase can last several minutes. If the patient does not remember in the ambulance or hospital after a seizure, it is more likely to be an epileptic seizure; if he still knows how the first aider met him on site, it speaks more for syncope. It is not a malpractice to leave a 1st or 2nd epileptic seizure untreated, even if the occurrence of the next seizure can be delayed in this way [18]. Psychogenic seizures are also confused with epilepsy. However, seizures longer than 10 minutes are mostly psychogenic [11].

Diagnostic methods

The most important diagnostic tool for diagnosing epileptic seizures is personal and external medical history [9]. The laboratory is of little help, the postictal creatine kinase value is increased 1–3 days after a major epileptic seizure, but it does not always have to be. It is usually not increased after other attacks [18]. Prolactin values ​​are imprecise and often only increased after large and temporally generated seizures, but must always be determined in comparison to the morning baseline value and can be both false-positive (syncope!) And false-negative. The lateral bite of the tongue is very specific, but not very sensitive. The EEG on the day of the epileptic seizure is pathological in up to 50% of cases, later often only meaningful in long-term and sleep mode [18]. Imaging examinations of the head should always be provided with specific questions in order to obtain findings relevant to epilepsy. Otherwise unspecific findings arise that have little relation to epilepsy, or dysplasias, which are overlooked as typical lesions of epilepsy [16].

Seizure classification

In Table 1, typical symptoms are assigned to the different types of seizures; it is not crucial for the general practitioner to always assign the seizure to exactly one type, it is much more important to recognize auras and motor and non-motor seizures as epileptic seizures. The following is often helpful for this:

Seizure description and documentation:

Questioning the patient, relatives or other witnesses of the seizure from the beginning to the end of the seizure is elementary for the classification of the seizure [10]. You can orientate yourself on a list of points to note (see Table 2). The description of initial seizure symptoms by the patient often provides decisive localization clues to the first brain region affected by epileptic discharges. The patient should be given time to reformulate apparently indescribable phenomena and only ask again later in detail [19].

The video documentation of a seizure makes seizure classification much easier, especially in the case of inadequate seizure descriptions. Today this is often possible with a smartphone. In individual cases, the final classification is only possible under stationary conditions of video EEG monitoring.

It is often particularly difficult to assess the seizure semiology in childhood, since the shape of the seizures is often more polymorphic than in adults and can change depending on age. In very young children, it is difficult to assess reactivity in the event of an attack. Children are often unable to provide any information about a possible aura [12].

Seizure classification:

The new 2017 Classification of Epileptic Seizures by the International League Against Epilepsy [5] separates focal seizures, in which the first clinical or electroencephalographic features indicate a localized onset in a region of a hemisphere, from generalized seizures, in which the first clinical or electroencephalographic signs of seizure appear indicate an inclusion of both hemispheres at the beginning of the seizure [11] (Fig.1). This dichotomy "focal" versus "generalized" thus relates exclusively to the onset of the seizure. In principle, every focal seizure can generalize secondarily. Any clear focal neurological symptom at the onset of the seizure (e.g. aura with tingling paresthesia in one hand, rhythmic clones in one hand) enables a focal seizure to be diagnosed. Focal seizures are divided into motor and non-motor (see Fig. 1).

From seizure to syndrome diagnosis

Acute symptomatic seizures:

One speaks of epilepsy only when two seizures have occurred without a current symptomatic cause or one seizure with a high risk of recurrence for further seizures [5]. In contrast, acute-symptomatic seizures are mostly generalized tonic-clonic seizures (grand mal, GTKA) that only occur under certain circumstances that lower the seizure threshold [1]. Such circumstances are e.g. B. Hypoglycaemia, CNS infections, manipulation of the brain, circulatory disorders.

Epilepsy Syndromes:

In addition to the focal or generalized seizure semiology, the diagnosis of the epilepsy syndrome is made by the mode of occurrence of the seizures (e.g. attachment of the seizures to the sleep-wake cycle, random versus cluster-shaped occurrence), provocation factors of the seizures, the etiology, the neurological and psychological clinical findings, the interictal and - if available - ictal EEG findings and the results of the imaging. The epilepsy syndromes are classified according to whether they are focal, generalized or not clearly identifiable as focal or generalized. According to the latest epilepsy classification [13, 14], the etiologies are regarded as essential for the subdivision of epilepsy.

Generalized epilepsies:

The most common idiopathic generalized form of epilepsy is juvenile myoclonic epilepsy (JME). In addition to the typical types of seizures (absences, myoclonic seizures, generalized tonic-clonic seizures without a focal onset), they show a sensitivity to non-specific factors that promote seizures, such as shifts in the sleep-wake rhythm or excessive alcohol. In symptomatic generalized epilepsies, the brain is diffusely affected and the EEG changes encephalopathically. Generalized seizures in the context of such syndromes are also tonic seizures, nodding attacks and the atonic seizure.

Focal epilepsies:

For focal epilepsies, the seizure classification provides the first building block for determining the zone of origin of the seizure and thus for determining an anatomically defined epilepsy syndrome. It should be noted, however, that seizures can also begin in clinically silent areas. Furthermore, seizures that begin in the same location can spread in different ways. Patients often speak of absences when they mean seizures with impaired consciousness, or large seizures when the seizure lasts long or falls occur. Here you have to ask carefully what is meant by absence or a major attack. Typical focal seizures are complex sensations (so-called auras), (psycho) motor and hyperkinetic seizures as well as focal motor seizures. The GTKA can also be a focal seizure (detectable by clinical signs and the ictal EEG), even if the patient does not remember anything before the attack or if the attack occurs from sleep.


The general practitioner should use his or her own and third-party anamnesis (which can often be obtained over the phone) and the external findings to get an idea of ​​whether an epileptic seizure is present or whether it is B. could be a syncope. He should also ask himself whether the event is to be assessed as acutely symptomatic (seizure one week after a stroke); then you do not have to treat or only for a short time (3 months). If epilepsy is beginning (seizure 3 weeks after a stroke!), Then the syndrome classification and differential therapy is important, which is best carried out by a specialized neurologist. The new classification of seizures and syndromes helps to give an exact classification based on the etiology and the type of seizures. A therapy without a precise diagnosis, based on the motto "if it works, it will have been a seizure", is clearly to be rejected. In case of doubt, the general practitioner should leave the diagnosis open and seek a second opinion from an epilepsy specialist. This relieves him particularly with regard to the socio-medical consequences of the diagnosis of epilepsy. Low-threshold help is available from the epilepsy advice centers (;,id,38.html).

1. Beghi Ettore et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia, 51 (4): 671-675, 2010
2. Berg A et al. Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005-2009, Epilepsia, 51 (4): 676-685, 2010
3. Commission on Classification and Terminology of the International League against Epilepsy (1981). Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia 22: 489-501.
4. Commission on Classification and Terminology of the International League Against Epilepsy (1989). Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 30: 389-399.
5. Fisher et al. A practical clinical definition of epilepsy Epilepsia, 2014 Apr; 55 (4): 475-82
6. Fisher R on behalf of the ILAE Commission for Classification and Terminology Instruction manual for the ILAE 2017 operational classification of seizure types Epilepsia, 58 (4): 531-542, 2017
7. Fisher R. on behalf of the ILAE Commission for Classification and Terminology Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology Epilepsia, 58 (4): 522-530, 2017
8. Hauser W.A. et al. Risk of Recurrent Seizures after Two Unprovoked Seizures N Engl J Med 1998; 338: 429-434
9. Janz D: The epilepsies. Special pathology and therapy. Thieme, Stuttgart 1969 (2nd unchanged edition 1998).
10. Mayer T et al (1997). Seizure documentation. Instructions for observing, describing and documenting epileptic seizures, Bethelverlag, Bielefeld
11. Noachtar S et al: The semiological classification of epileptic seizures. Nervenarzt 1998, 69, 2, 117-126
12. Roger J et al. (2008): Epileptic syndromes in infancy, childhood and adolescence (5th edition) John Libbey, London, Paris Rome
13. Scheffer I et al. on behalf of the ILAE Commission for Classification and Terminology Classification of the epilepsies: New concepts for discussion and debate — Special report of the ILAE Classification Task Force of the Commission for Classification and Terminology1 Epilepsia Open, 1 (1): 37-44, 2016
14. Scheffer IE et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology Epilepsia, 58 (4): 512-521, 2017
15. Scheffer IE: Autosomal dominant nocturnal frontal lobe epilepsy. In: Berkovic SF, Genton P, Hirsch E, Picard F (eds): Genetics of Focal Epilepsies. J. Libbey, London 1999, 81-84.
16. von Oertzen J et al. Standard magnetic resonance imaging is inadequate for patients with refractory focal epilepsy. J Neurol Neurosurg Psychiatry 2002; 73: 643-647
17. Soteriades ES et al. Incidence and Prognosis of Syncope N Engl J Med 2002; 347: 878-885
18. Wolf P, Mayer T. Praxisbuch Epilepsien, Schattauer Verlag 2003
19. Wolf P: Behavioral therapy for the treatment of epileptic seizures. TW Neurologie Psychiatrie 6 (1992), 712-717.

Kleinwachau epilepsy center

Conflicts of Interest: The author is a member of the advisory boards of UCB, Bial, Eisai, GW pharmaceuticals and most recently received lecture fees from UCB, Eisai, Bial and Desitin.

You can find more articles on similar topics here: