As distinct from unprovoked seizures, epileptic seizures that occur in close temporal relation to acute systemic or structural brain damage are considered acute symptomatic. In this regard, the International League Against Epilepsy (ILAE) has defined operationally specific constellations. The time latency after onset of the causative disorder within which a seizure is considered acute symptomatic depends on the etiology (Table 1; [1]). Acute symptomatic seizures account for up to 40% of all first-time epileptic seizures. They are often short-term sequelae of acute structural brain lesions [2]; however, this constellation is not considered in the current guidelines on the appraisal of driving eligibility of the German Federal Highway Research Institute (Bundesamt für Straßenwesen, BASt; [4]).

Table 1 Examples for the operational definition of acute symptomatic seizures of various etiology according to ILAE [1]
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Case report

A 62-year-old, previously neurologically healthy male professional driver suffered a bilateral tonic–clonic seizure for the first time and without any precursors shortly after getting out of his truck following a long drive. The findings of the neurological examination at the hospital providing initial care were unremarkable. Immediate cranial computed tomography (cCT) and cranial magnetic resonance imaging (cMRI) performed a few hours later revealed a left frontal intraparenchymal hemorrhage adjacent to the cortex (Fig. 1). The patient was taking phenprocoumon (Marcumar®; MEDA Pharma GmbH & Co. KG, Bad Homburg, Germany) for atrial fibrillation; the international normalized ratio (INR) at the emergency department was 4.3 (target range: 2–3). The area of bleeding was resected 3 weeks later at another hospital since an underlying cavernoma was suspected. However, histopathological workup revealed unremarkable findings.

Fig. 1
figure 1

Native cranial computed tomography (a) and cranial magnetic resonance imaging (b native T1; c FLAIR) on the day of the seizure with evidence of intracerebral hemorrhage. Fluid–fluid level is typical of coagulopathies. The absence of T1 hyperintensities argues against both cavernoma hemorrhage and age older than 3 days

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At 6 months following the seizure, the patient presented to the epilepsy outpatient clinic at the Charité—Universitätsmedizin Berlin, Germany. He had been taking 1 g of levetiracetam daily since the seizure; no further seizures had occurred. He asked how long he should continue to take the medication and when he would be allowed to drive a car privately and drive a bus or truck professionally again. According to the neuroradiological re-evaluation performed at the authors’ hospital (E.S.) of the imaging carried out in the acute phase and during the follow-up, the hemorrhage can be classified as atraumatic and due to the intake of phenprocoumon (Marcumar-associated hemorrhage). According to the imaging, the hemorrhage was not older than 3 days at the time of the seizure; thus, according to the definition, the seizure was acute symptomatic.

Discussion

The distinction between acute symptomatic and unprovoked seizures is important for the prognostic assessment; furthermore, a differentiation needs to be made between structural and systemic seizures. Acute symptomatic seizures due to a structural brain lesion carry a probability of subsequent unprovoked seizures of 20–40% within 5–10 years (Fig. 2; [7, 10]). In some cases, it may be higher, e.g., after cerebral infarction with a very high SeLECT score [7]; seizures after acute cavernoma hemorrhage, which was initially discussed as a differential diagnosis in the present patient, are not considered acute symptomatic due to the high risk of further unprovoked seizures [13]. By contrast, acute symptomatic seizures due to transient systemic disturbances do not carry a relevant risk of subsequent unprovoked seizures according to unpublished data from the PROSA registry (prognosis of acute symptomatic seizures; Prognose akut-symptomatischer Anfälle; [9]) and the expert consensus opinion [2]. However, further acute symptomatic seizures may occur in around 30% of cases in 3 years, e.g., in the case of new alcohol withdrawal or renewed hypoglycemia [3].

Fig. 2
figure 2

Cumulative probability of recurrent unprovoked epileptic seizures depending on time (from [7,8,9,10, 12]). A risk of ≥ 60% in 10 years (dotted line) defines epilepsy [6]. TBI transient brain injury, CNS central nervous system, PROSA prognosis of acute symptomatic seizures (Prognose akut-symptomatischer Anfälle)

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If neither electroencephalography (EEG) nor imaging show pathological abnormalities after a first unprovoked seizure, this is referred to as an isolated unprovoked seizure. The risk of another unprovoked seizure in the next 5 years is then 30–40%. A second unprovoked seizure already carries a risk of further seizures of about 75% (Fig. 2); therefore, two separate unprovoked seizures define epilepsy. If, after a first unprovoked seizure, there is evidence from EEG or imaging of a similarly high seizure probability (> 60% in 10 years), this first unprovoked seizure already defines epilepsy [5].

The likelihood of unprovoked seizure recurrences influences the indication for seizure prophylaxis with medication. Clinical guidelines generally do not recommend long-term medication after acute symptomatic seizures due to the relatively low risk of further seizures [11] or see this as a case-by-case decision [5]. In addition, the likelihood of further seizures determines the duration of driving ineligibility for motor vehicles in group 1 (up to 3.5 t without professional passenger transport) and group 2 (from 3.5 t or professional passenger transport). The duration of driving ineligibility after epileptic seizures is specified in the BASt guidelines (Table 2; [4]). Acute symptomatic seizures without structural brain lesion, isolated unprovoked seizures, and epilepsy are addressed. Acute symptomatic seizures with a structural brain lesion are not included in the version that has remained unchanged since 2009.

Table 2 Duration of driving ineligibility (from [4])
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The risk of unprovoked seizure recurrence after acute symptomatic seizure with structural brain lesion is higher than after acute symptomatic seizure without structural lesion. Therefore, the duration of ineligibility to drive must be correspondingly longer. However, the risk is significantly lower than after an unprovoked seizure with a structural lesion, which defines epilepsy; accordingly, the duration of ineligibility to drive must be shorter. Statistically, the risk of seizure recurrence after a structurally induced acute symptomatic seizure is similar to that after an isolated unprovoked seizure (Fig. 2).

In this specific case, therefore, the authors applied the BASt guidelines recommendation on driving after isolated unprovoked seizures to their patient. He was informed that he would be allowed to use his car privately again from 6 months post-seizure (driving license group 1). Since seizure prevention with levetiracetam was stopped, the duration of the ineligibility to drive was prolonged by another 3 months. Regarding his eligibility to drive buses and trucks (group 2), the patient was informed that he must be seizure-free without medication for 2 years. He should regularly present for consultation in order to establish whether he is experiencing seizures that are less noticeable from a semiological perspective and that he may not perceive as epileptic.

The authors propose that for acute symptomatic seizures with structural brain lesion, the periods of ineligibility to drive of 6 months (group 1) or of 2 years (group 2) be included in future guidelines on the assessment of fitness to drive.

Practical conclusion

  • The duration of ineligibility to drive after acute symptomatic seizure in structural brain lesion is currently not defined.

  • The risk of seizure recurrence is approximately the same as after an isolated unprovoked seizure.

  • Therefore, the authors recommend a period of ineligibility to drive of 6 months for cars and 2 years for buses and trucks.