Eugen Trinka
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Eugen Trinka has a total of 26 co-authors. Here are the top co-authors by number of shared publications:
Iris Unterberger
Department of Neurology, Innsbruck Medical University, Innsbruck, Austria
3 shared publicationsJudith Dobesberger
Departments of Neurology
3 shared publicationsThaddaeus Gotwald
3 shared publicationsGerald Walser
Department of Neurology, Innsbruck Medical University, Innsbruck, Austria
2 shared publicationsGerhard Bauer
Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria
2 shared publicationsGiorgi Kuchukhidze
Department of Neurology, Innsbruck Medical University, Innsbruck, Austria
2 shared publications
Latest Publications
- 9 August 2025
- Published by BMJ in BMJ Case Reports
- Vol. 2009
Bilateral mesial temporal polymicrogyria: a case report
Polymicrogyria is a malformation of cortical organisation morphologically marked by an irregular brain surface with multiple excessively folded small gyri. Cortical thickness is reduced but appears increased in some areas as a result of the fusion of small gyri. On magnetic resonance imaging polymicrogyria is delineated by an abnormal gyral pattern, increased cortical thickness and irregularity of the cortical–white matter junction.
- 9 August 2025
- Published by BMJ in BMJ Case Reports
- Vol. 2009
Bilateral mesial temporal polymicrogyria: a case report
Polymicrogyria is a malformation of cortical organisation morphologically marked by an irregular brain surface with multiple excessively folded small gyri. Cortical thickness is reduced but appears increased in some areas as a result of the fusion of small gyri. On magnetic resonance imaging polymicrogyria is delineated by an abnormal gyral pattern, increased cortical thickness and irregularity of the cortical–white matter junction.
- Open Access
Status epilepticus—Making progress
- 1 February 2011
- Published by Elsevier in Clinical Neurology and Neurosurgery
- Vol. 113 (2) , 136-138
Selective amygdalo-hippocampectomy as a potential trigger for disease progression in multiple sclerosis
- 1 February 2011
- Published by Elsevier in Clinical Neurology and Neurosurgery
- Vol. 113 (2) , 136-138
Selective amygdalo-hippocampectomy as a potential trigger for disease progression in multiple sclerosis
- Open Access
Nonconvulsive status epilepticus and coma
Summary: Nonconvulsive status epilepticus (NCSE) in a comatose patient cannot be diagnosed without electroencephalography (EEG). In many advanced coma stages, the EEG exhibits continuous or periodic EEG abnormalities, but their causal role in coma remains unclear in many cases. To date there is no consensus on whether to treat NCSE in a comatose patient in order to improve the outcome or to retract from treatment, as these EEG patterns might reflect the end stages of a dying brain. On the basis of EEG, NCSE in comatose patients may be classified as generalized or lateralized. This review aims to summarize the ongoing debate of NCSE and coma and to critically reassess the available literature on coma with epileptiform EEG pattern and its prognostic and therapeutic implications. The authors suggest distinguishing NCSE proper and comatose NCSE, which includes coma with continuous lateralized discharges or generalized epileptiform discharges (coma‐LED, coma‐GED). Although NCSE proper is accompanied by clinical symptoms suggestive of status epilepticus and mild impairment of consciousness, such as in absence status or complex focal status epilepticus, coma‐LED and coma‐GED represent deep coma of various etiology without any clinical motor signs of status epilepticus but with characteristic epileptiform EEG pattern. Hence coma‐LED and coma‐GED can be diagnosed with EEG only. Subtle or stuporous status epilepticus and epilepsia partialis continua–like symptoms in severe acute central nervous system (CNS) disorders represent the borderland in this biologic continuum between NCSE proper and comatose NCSE (coma‐LED/GED). This pragmatic differentiation could act as a starting point to solve terminologic and factual confusion.
Open AccessNonconvulsive status epilepticus and coma
Summary: Nonconvulsive status epilepticus (NCSE) in a comatose patient cannot be diagnosed without electroencephalography (EEG). In many advanced coma stages, the EEG exhibits continuous or periodic EEG abnormalities, but their causal role in coma remains unclear in many cases. To date there is no consensus on whether to treat NCSE in a comatose patient in order to improve the outcome or to retract from treatment, as these EEG patterns might reflect the end stages of a dying brain. On the basis of EEG, NCSE in comatose patients may be classified as generalized or lateralized. This review aims to summarize the ongoing debate of NCSE and coma and to critically reassess the available literature on coma with epileptiform EEG pattern and its prognostic and therapeutic implications. The authors suggest distinguishing NCSE proper and comatose NCSE, which includes coma with continuous lateralized discharges or generalized epileptiform discharges (coma‐LED, coma‐GED). Although NCSE proper is accompanied by clinical symptoms suggestive of status epilepticus and mild impairment of consciousness, such as in absence status or complex focal status epilepticus, coma‐LED and coma‐GED represent deep coma of various etiology without any clinical motor signs of status epilepticus but with characteristic epileptiform EEG pattern. Hence coma‐LED and coma‐GED can be diagnosed with EEG only. Subtle or stuporous status epilepticus and epilepsia partialis continua–like symptoms in severe acute central nervous system (CNS) disorders represent the borderland in this biologic continuum between NCSE proper and comatose NCSE (coma‐LED/GED). This pragmatic differentiation could act as a starting point to solve terminologic and factual confusion.
Asymmetric seizure termination in primary and secondary generalized tonic–clonic seizures
Summary: Purpose: In temporal lobe epilepsies an asymmetric termination (AST) of the clonic phase of secondary generalized tonic–clonic seizures (sGTCS) reliably lateralizes the side of seizure onset. The last clonic activity occurs ipsilateral to the side of the seizure onset zone. We compared the prevalence and lateralizing value of AST in sGTCS of frontal and temporal lobe origin as well as in primary generalized tonic–clonic seizures (pGTCS).Methods: We analyzed 177 seizures in 84 consecutive patients. Forty‐one patients had temporal lobe epilepsy (TLE), 24 frontal lobe epilepsy (FLE), and 19 had nonfocal (primary) generalized epilepsies (GE). All patients underwent intensive video‐EEG (electroencephalography) monitoring, high‐resolution magnetic resonance imaging (MRI), neuropsychological testing, and single photon emission computed tomography/positron emission tomography (SPECT/PET) when feasible. Two investigators blinded for diagnosis, EEG, and imaging data assessed frequency and side of the last clonic jerk.Results: AST occurred in 63% of patients with TLE (47% of seizures), in 71% with FLE (60% of seizures), and in 42% with GE (21% of seizures). These results were not significant for patients, but significant for seizures in TLE versus GE and in FLE versus GE (p < 0.001). The positive predictive value (PPV) for the side of seizure onset was 74% (p = 0.003) in TLE and 75% (p = 0.008) in FLE.Discussion: AST in sGTCS lateralizes the side of seizure onset in TLE and in FLE to the ipsilateral hemisphere with a high PPV. However, AST was also observed in GE. Therefore, asymmetric clinical signs should not inevitably lead to the assumption of focal epilepsy syndromes.
Asymmetric seizure termination in primary and secondary generalized tonic–clonic seizures
Summary: Purpose: In temporal lobe epilepsies an asymmetric termination (AST) of the clonic phase of secondary generalized tonic–clonic seizures (sGTCS) reliably lateralizes the side of seizure onset. The last clonic activity occurs ipsilateral to the side of the seizure onset zone. We compared the prevalence and lateralizing value of AST in sGTCS of frontal and temporal lobe origin as well as in primary generalized tonic–clonic seizures (pGTCS).Methods: We analyzed 177 seizures in 84 consecutive patients. Forty‐one patients had temporal lobe epilepsy (TLE), 24 frontal lobe epilepsy (FLE), and 19 had nonfocal (primary) generalized epilepsies (GE). All patients underwent intensive video‐EEG (electroencephalography) monitoring, high‐resolution magnetic resonance imaging (MRI), neuropsychological testing, and single photon emission computed tomography/positron emission tomography (SPECT/PET) when feasible. Two investigators blinded for diagnosis, EEG, and imaging data assessed frequency and side of the last clonic jerk.Results: AST occurred in 63% of patients with TLE (47% of seizures), in 71% with FLE (60% of seizures), and in 42% with GE (21% of seizures). These results were not significant for patients, but significant for seizures in TLE versus GE and in FLE versus GE (p < 0.001). The positive predictive value (PPV) for the side of seizure onset was 74% (p = 0.003) in TLE and 75% (p = 0.008) in FLE.Discussion: AST in sGTCS lateralizes the side of seizure onset in TLE and in FLE to the ipsilateral hemisphere with a high PPV. However, AST was also observed in GE. Therefore, asymmetric clinical signs should not inevitably lead to the assumption of focal epilepsy syndromes.
- Open Access
- 1 March 2009
- Published by SAGE Publications in Therapeutic Advances in Neurological Disorders
- Vol. 2 (2) , 79-91
Review: New treatment options in status epilepticus: a critical review on intravenous levetiracetam
The effectiveness of levetiracetam (LEV) in the treatment of focal and generalised epilepsies is well established. LEV has a wide spectrum of action, good tolerability and a favourable pharmacokinetic profile. An injectable formulation has been released as an intravenous (IV) infusion in 2006 for patients with epilepsy when oral administration is temporarily not feasible. Bioequivalence to the oral preparation has been demonstrated with good tolerability and safety enabling a smooth transition from oral to parenteral formulation and vice versa. Although IV LEV is not licensed for treatment of status epilepticus (SE), open-label experience in retrospective case series is accumulating. Until now (August 2008) 156 patients who were treated with IV LEV for various forms of SE have been reported with an overall success rate of 65.4%. The most often used initial dose was 2000—3000 mg over 15 minutes. Adverse events were reported in 7.1%, and were mild and transient. Although IV LEV is an interesting alternative for the treatment of SE due to the lack of centrally depressive effects and low potential of drug interactions, one has to be aware of the nonrandomised retrospective study design, the heterogenous patient population and treatment protocols, and the publication bias inherent in these type of studies. Only a large randomised controlled trial with an adequate comparator will reveal the efficacy and effectiveness of this promising new IV formulation.
- 1 March 2009
- Published by SAGE Publications in Therapeutic Advances in Neurological Disorders
- Vol. 2 (2) , 79-91
Open AccessReview: New treatment options in status epilepticus: a critical review on intravenous levetiracetam
The effectiveness of levetiracetam (LEV) in the treatment of focal and generalised epilepsies is well established. LEV has a wide spectrum of action, good tolerability and a favourable pharmacokinetic profile. An injectable formulation has been released as an intravenous (IV) infusion in 2006 for patients with epilepsy when oral administration is temporarily not feasible. Bioequivalence to the oral preparation has been demonstrated with good tolerability and safety enabling a smooth transition from oral to parenteral formulation and vice versa. Although IV LEV is not licensed for treatment of status epilepticus (SE), open-label experience in retrospective case series is accumulating. Until now (August 2008) 156 patients who were treated with IV LEV for various forms of SE have been reported with an overall success rate of 65.4%. The most often used initial dose was 2000—3000 mg over 15 minutes. Adverse events were reported in 7.1%, and were mild and transient. Although IV LEV is an interesting alternative for the treatment of SE due to the lack of centrally depressive effects and low potential of drug interactions, one has to be aware of the nonrandomised retrospective study design, the heterogenous patient population and treatment protocols, and the publication bias inherent in these type of studies. Only a large randomised controlled trial with an adequate comparator will reveal the efficacy and effectiveness of this promising new IV formulation.
Successful surgical treatment of insular epilepsy with nocturnal hypermotor seizures
Summary: Nocturnal hypermotor seizures (NHSs) suggest seizure onset in the frontal lobe. We present a patient with NHSs and insular seizure onset who underwent successful surgical treatment. A 29‐year‐old right‐handed man suffered from intractable NHSs since the age of 12 years. High‐resolution MRI, [18F]FDG‐PET, and neuropsychological examination gave normal results, ictal EEG was obscured by artifacts. Ictal [99mTc]HMPAO‐SPECT revealed hyperperfusion in the right anterior part of the insula and right frontal operculum. The seizure onset zone was localized in the right anterior insula based on invasive recordings. Electrical stimulation in that area elicited habitual seizures. A limited resection of the anterior part of the right insula and the right frontal operculum was performed rendering the patient seizure‐free (follow‐up 1 year). To our knowledge, this is the first reported nonlesional patient with an insular seizure onset and NHSs who underwent successful epilepsy surgery.
Successful surgical treatment of insular epilepsy with nocturnal hypermotor seizures
Summary: Nocturnal hypermotor seizures (NHSs) suggest seizure onset in the frontal lobe. We present a patient with NHSs and insular seizure onset who underwent successful surgical treatment. A 29‐year‐old right‐handed man suffered from intractable NHSs since the age of 12 years. High‐resolution MRI, [18F]FDG‐PET, and neuropsychological examination gave normal results, ictal EEG was obscured by artifacts. Ictal [99mTc]HMPAO‐SPECT revealed hyperperfusion in the right anterior part of the insula and right frontal operculum. The seizure onset zone was localized in the right anterior insula based on invasive recordings. Electrical stimulation in that area elicited habitual seizures. A limited resection of the anterior part of the right insula and the right frontal operculum was performed rendering the patient seizure‐free (follow‐up 1 year). To our knowledge, this is the first reported nonlesional patient with an insular seizure onset and NHSs who underwent successful epilepsy surgery.