Tapani Keränen

University of Eastern Finland, Kuopio, Eastern Finland Province, Finland

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Publications (106)249.73 Total impact

  • Acta Neurologica Scandinavica 04/2009; 69:87-88. DOI:10.1111/j.1600-0404.1984.tb02399.x · 2.44 Impact Factor
  • Acta Neurologica Scandinavica 04/2009; 69:99-100. DOI:10.1111/j.1600-0404.1984.tb02405.x · 2.44 Impact Factor
  • Acta Neurologica Scandinavica 04/2009; 69:89-90. DOI:10.1111/j.1600-0404.1984.tb02400.x · 2.44 Impact Factor
  • Acta Neurologica Scandinavica 04/2009; 69:93-94. DOI:10.1111/j.1600-0404.1984.tb02402.x · 2.44 Impact Factor
  • Acta Neurologica Scandinavica 03/2009; 65:208-209. DOI:10.1111/j.1600-0404.1982.tb03456.x · 2.44 Impact Factor
  • European Journal of Neurology 03/2009; 16(4):e75. DOI:10.1111/j.1468-1331.2009.02557.x · 3.85 Impact Factor
  • Acta Neurologica Scandinavica 03/2009; 65:190-190. DOI:10.1111/j.1600-0404.1982.tb03446.x · 2.44 Impact Factor
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    ABSTRACT: Previous studies have associated coeliac disease (CD) and gluten sensitivity (defined as the presence of anti-gliadin antibodies and positive immunogenetics) with cerebellar degeneration and epilepsy with occipital calcifications. Hippocampal sclerosis (HS) in temporal lobe epilepsy (TLE) is a potentially progressive disorder with unknown aetiology; however, autoimmunity has been implicated as one of the possible mechanisms leading to HS. The purpose of this study is to analyze CD-associated antibodies and gluten sensitivity in a well-characterised group of patients with refractory focal epilepsy. We measured anti-gliadin, anti-tissue-transglutaminase and anti-endomysium antibodies, and coeliac-type human leukocyte antigen (DQ2 and DQ8), in 48 consecutive patients with therapy-resistant, localisation-related epilepsy. The patients were categorised into the following three groups on the basis of ictal electro-clinical characteristics and the findings of high resolution MRI: TLE with HS (n = 16), TLE without HS (n = 16) and extratemporal epilepsy (n = 16). Patients with suspected CD or gluten sensitivity underwent duodenal biopsies. Seven patients in total were gluten sensitive; all of these patients fell in the TLE with HS group. On the other hand, none of the TLE without HS patients or those with extratemporal epilepsy were gluten sensitive (p<0.0002). The results of duodenal biopsies showed that three of the seven gluten-sensitive patients had histological evidence of CD and four had inflammatory changes consistent with early CD without villous atrophy. Four of the patients with gluten sensitivity had evidence of dual pathology (HS+another brain lesion), whereas none of the remaining patients did (p<0.0002). The present study demonstrates a previously unrecognised link between gluten sensitivity and TLE with HS. This association was very robust in this well-characterised group of patients; thus gluten sensitivity should be added to the list of potential mechanisms leading to intractable epilepsy and HS.
    Journal of neurology, neurosurgery, and psychiatry 02/2009; 80(6):626-30. DOI:10.1136/jnnp.2008.148221 · 5.58 Impact Factor
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    ABSTRACT: Status epilepticus is a medical emergency. Most epileptic seizures last for 1-4 minutes and seizures lasting over five minutes, should be treated as status epilepticus. EEG is essential for diagnostics and the monitoring of treatment effect. The treatment for status epilepticus, irrespective of aetiology, can be divided into first-aid medications, such as buccal midazolam or rectal diazepam, first-line medications such as intravenous diazepam or lorazepam, and second-line medications such as fosphenytoin and valproate for adults and phenobarbital for children. Third-line treatment is suppressive general anaesthesia, monitored by continuous EEG. Antiepileptic medication of patients with epilepsy should be carefully re-evaluated after episode of status epilepticus.
    Duodecim; lääketieteellinen aikakauskirja 01/2009; 125(22):2469-71.
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    ABSTRACT: Established markers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100), may increase after status epilepticus, but whether a single tonic-clonic or complex partial seizure induces elevation of these markers is not known. Furthermore, it is unclear whether the risk of seizure-related neuronal damage in temporal lobe epilepsy (TLE) differs from that in extratemporal lobe epilepsies (XTLE). The aim of this study was to analyze NSE and S-100 in patients with TLE and XTLE after acute seizures. The levels of NSE and S-100 were measured in serum before (0h) and at 3, 6, 12, and 24h after acute seizures in 31 patients during inpatient video-EEG monitoring. The patients were categorized into the TLE and the XTLE group based on video-EEG recordings and MRI findings. Fifteen patients had TLE and 16 XTLE. Index seizures were mainly complex partial seizures (n=21). In TLE mean+/-S.D. values for NSE levels (mug/L) were 8.36+/-2.64 (0h), 11.35+/-3.84 (3h), 13.48+/-4.49 (6h), 12.95+/-5.46 (12h) and 10.33+/-3.13 (24h) (p=0.006, ANOVA). In XTLE the changes were not significant (p=0.3). There was less increase in the levels of S-100 in TLE (p=0.05) and no significant change in XTLE (p=0.4). The levels of markers of neuronal damage were increased in patients with TLE, not only after tonic-clonic but also after complex partial seizures. These data suggest that TLE may be associated with brain damage.
    Epilepsy Research 07/2008; 81(2-3):155-60. DOI:10.1016/j.eplepsyres.2008.05.006 · 2.19 Impact Factor
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    ABSTRACT: This aim of the study was to ascertain the importance of clinical parameters on the response to treatment in refractory epilepsy patients on levetiracetam (LEV). We retrospectively evaluated medical records of 132 patients aged 17-78 years with refractory epilepsy (defined as a failure of at least two antiepileptic drugs due to the lack of efficacy) exposed to LEV. We analyzed the response (seizure freedom or continuing LEV) using logistic regression. Of 132 patients exposed to LEV, 103 cases continued the drug. Of the discontinuations (29/132), 75% were for lack of efficacy and 25% for tolerability problems. Twenty-three percent of the previously refractory patients achieved seizure freedom for at least 1 year with LEV in combination therapy. The dose of LEV in 80% of seizure-free patients was 1000 mg/day or less. The duration of epilepsy, age and sex were not associated with response to LEV. Seizure freedom was associated with epileptic syndrome or etiology. If no specific syndrome was recognized, there was a significantly greater chance for response compared with temporal lobe epilepsy (OR 20.76; 95% CI 2.12-203.61). Our study was based on the careful clinical evaluation of the patients with extensive use of video EEG (50%) and MRI scans (95%). These clinical predictors were evasive in previous studies. This study showed that they are worth pursuing but significantly larger groups of patients need to be investigated to reach significant findings.
    Acta Neurologica Scandinavica 06/2008; 117(5):332-6. DOI:10.1111/j.1600-0404.2007.00956.x · 2.44 Impact Factor
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    ABSTRACT: We evaluated long-term retention rates of newer antiepileptic drugs (AED) in adults with localization-related epilepsy retrospectively. We estimated retention rates by Kaplan-Meier method in all 222 patients (age > or = 16) with localization-related epilepsy exposed to new AED at the Tampere University Hospital. There were 141 patients exposed to lamotrigine, 78 to levetiracetam, 97 to topiramate, 68 to gabapentin, and 69 to tiagabine. Three-year retention rate for lamotrigine was 73.5%, levetiracetam 65.4%, topiramate 64.2%, gabapentin 41.7%, and tiagabine 38.2%. The most common cause for withdrawal of these AED was lack of efficacy. Our study suggests that there are clinically significant differences among gabapentin, lamotrigine, levetiracetam, tiagabine, and topiramate as treatment for focal epilepsy in everyday practice. Gabapentin and tiagabine seem to be less useful than the other three AED. Furthermore, our study supports the value of retention rate studies in assessing outcome of the drugs in clinical practice.
    Acta Neurologica Scandinavica 06/2008; 119(1):55-60. DOI:10.1111/j.1600-0404.2008.01062.x · 2.44 Impact Factor
  • Source
    T Keränen, M Tuhkasaari, H Kuusisto
    European Journal of Neurology 05/2008; 15(4):e30. DOI:10.1111/j.1468-1331.2008.02068.x · 3.85 Impact Factor
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    ABSTRACT: Electroconvulsive therapy (ECT) is regarded as an effective treatment of drug-resistant depression, but its mechanism of action is mostly unknown. We have previously reported that epileptic seizures result in cerebral production of cytokines, which are also reflected in the plasma. In this study, we tested whether ECT is associated with similar acute release of cytokines. The plasma levels of cytokines interleukin (IL) 1beta, IL-1 receptor antagonist, and IL-6 were measured using enzyme-linked immunosorbent assay at several time points after ECT. The study included 9 patients who met the diagnostic criteria of major depression (mean age, 55 years; mean Montgomery-Asberg Depression Rating Scale score, 30). Our results demonstrate that cytokines IL-1beta and IL-6 are increased at 3- and 6-hour time points after ECT. IL-6 release also correlated to the stimulus dose used, suggesting neuronal depolarization as a mechanism of cytokine release. These results indicate that ECT is associated with rapid induction of inflammatory cytokines most likely in the central nervous system, which are also measurable in the peripheral blood.
    Journal of Ect 04/2008; 24(1):88-91. DOI:10.1097/YCT.0b013e3181571abb · 1.39 Impact Factor
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    ABSTRACT: We analyzed the effect of combination therapy on seizure frequency in all adult patients (N=193) with focal epilepsy followed at a single institution in a cross-sectional study. One hundred and thirty-five patients were on two AEDs, of them, 37 (27%) were seizure-free, 50 patients were on three AEDs including 5 (10%) seizure-free patients (p<0.01 for seizure-freedom with two AEDs versus three AEDs). Thirty-five different combinations were used in patients on two AEDs and 40 combinations on patients on three drugs emphasizing the difficulties involved in evaluation of the efficacy and tolerability of specific combinations. The significant proportion of seizure-free cases (27%) on duotherapy is suggesting the usefulness of combination therapy in achieving seizure-freedom in epilepsies refractory to single drug treatment. The material in the study was not from a randomized trial and therefore the comparability of patients on different AEDs is uncertain, but on the other hand the clinical practice followed provides a natural experiment suitable for comparative, non-randomized assessment of treatment outcomes.
    Seizure 04/2008; 17(3):276-80. DOI:10.1016/j.seizure.2007.08.001 · 2.06 Impact Factor
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    ABSTRACT: Twenty ambulatory outpatients with generalized tonic-clonic seizures with primary generalized discharges and photoconvulsive reponse on electroencephalogram (EEG) and 11 ambulatory outpatients with partial complex seizures with or without secondary generalization were studied with pattern-reversal light-emitting diode (LED) stimulator visual evoked potential (VEPs) and short-latency median nerve cortical somatosensory evoked potentials (SEPs). The patients with primary generalized epilepsy had significantly prolonged latencies of VEP components P2 and N3 and SEP component P22. The patients with partial epilepsy had significantly prolonged latency of VEP component N3. It is concluded that both functional and structural factors may cause a slowing of central impulse conduction.RÉSUMÉChez 20 sujets consultants ayant des crises généralisées tonico-cloniques, et sur l'EEG des décharges généralisées primaires et une réponse photoconvulsive, et chez 11 sujets consultants ayant des crises partielles complexes avec ou sans généralisation secondaire ont étéétudiés les PEV obtenus avec une stimulation LED par damier réversible et les PES à courte latence (par stimulation du nerf médian). Les patients ayant une épilepsie généralisée primaire avaient une latence significativement allongée des composants P2 et N3 du PEV et P22 du PES. Les patients ayant une épilepsie partielle avaient une latence significativement allongée avec les composants N3 du PEV. II est conclu que des facteurs fonctionnels et structurels peuvent provoquer un ral-entissement de la conduction cérébrale.RESUMENMediante la utilización de un estimulador LED de patrón-inverso, se han estudiado los VETs y los SETs de corta latencia del nervio mediano a la corteza en 20 pacientes ambulatorios que padecían ataques tónico-clónicos generalizados con descargas generalizadas primarias y respuestas fotoconvulsivas en el EEG y en 11 pacientes ambulatorios con ataques parciales complejos con o sin generalización secundaria. Los pacientes con epilepsía generalizada primaria tenían latencias significativamente prolongadas de los componentes E2 y N3 de los VET y del componente T22 de los SET. Los pacientes con epilepsia parcial demostraron una latencia significativamente prolongada del componente N3 de los VET. Se concluye que factores funcionales y también estructurales pueden ser causa de una lentificación de la conducción de impulsos centrales.ZUSAMMENFASSUNGBei 20 ambulanten Patienten mit generalisierten tonischklonischen Anfällen bei primär generalisierten Entladungen und fotokonvulsiver Antwort im EEG und bei 11 ambulanten Patienten mit komplexen Partialanfällen mit oder ohne sekundäre Generalisation wurden die VEP mit Hilfe des Muster-Umkehr LED-Stimulators und die frühen corticalen SEP nach Stimulation des N. medianus untersucht. Die Patienten mit primär generalisierter Epilepsie zeigten signifikant verlängerte Latenzen der VEP-Komponenten P2 und N3 und der SEP Komponente P 22. Die Patienten mit Partialepilepsie hatten signifikant verlängerte Latenzen der VEP Komponente N3. Es ist zu folgern, daß sowohl funktionelle wie strukturelle Faktoren eine Verlangsamung der zentralen Erregungsleitung bewirken können.
    Epilepsia 11/2007; 26(5):441 - 445. DOI:10.1111/j.1528-1157.1985.tb05677.x · 4.58 Impact Factor
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    ABSTRACT: Experimental studies suggest increased cerebral production of inflammatory cytokines after prolonged seizures. Whether a single non-prolonged seizure in human patients is associated with activation of cytokine network is still unknown. We studied the levels of interleukin-1beta (IL-1beta), interleukin-1 receptor antagonist (IL-1ra), interlukin-6 (IL-6) and soluble IL-6 receptors (sIL-6R and Gp130) in plasma after single seizures during video-EEG recordings in patients with chronic localization-related epilepsy. The levels of IL-1ra and IL-6 were increased after seizures, whereas IL-1beta and IL-6 cytokine receptors remained unchanged. These results show that only single seizures cause activation of cytokine cascade and associated inflammatory signals. In the case of recurrent seizures, these signals may result in structural changes in the nervous tissue, which are generally associated with drug refractory epilepsy.
    Acta Neurologica Scandinavica 11/2007; 116(4):226-30. DOI:10.1111/j.1600-0404.2007.00882.x · 2.44 Impact Factor
  • European Urology Supplements 03/2007; 6(2):203-203. DOI:10.1016/S1569-9056(07)60719-2 · 3.37 Impact Factor
  • Duodecim; lääketieteellinen aikakauskirja 02/2007; 123(9):1096-102.
  • Source
    Journal of Postgraduate Medicine 01/2007; 53(4):277-8. DOI:10.4103/0022-3859.37528 · 0.97 Impact Factor

Publication Stats

2k Citations
249.73 Total Impact Points


  • 2011–2014
    • University of Eastern Finland
      • School of Pharmacy
      Kuopio, Eastern Finland Province, Finland
  • 1994–2011
    • Tampere University Hospital (TAUH)
      Tammerfors, Province of Western Finland, Finland
  • 1994–2010
    • University of Tampere
      • • Department of Neurosurgery
      • • Department of Neurology and Rehabilitation
      • • Department of Pharmacological Sciences
      • • Department of Neurology
      Tammerfors, Pirkanmaa, Finland
  • 1987–2009
    • University of Kuopio
      • Department of Neurology
      Kuopio, Northern Savo, Finland
  • 1983–2009
    • Kuopio University Hospital
      • Department of Neurology
      Kuopio, Eastern Finland Province, Finland
  • 2002–2004
    • University of Turku
      • Department of Neurology
      Turku, Province of Western Finland, Finland
  • 2003
    • Pirkanmaa Hospital District
      Tammerfors, Province of Western Finland, Finland
  • 1993
    • Kemira Espoo Research Center
      Esbo, Uusimaa, Finland