Journal articles: 'Posttraumatic epilepsy'

1

Willmore, L. James. "Posttraumatic Epilepsy." Neurologic Clinics 10, no. 4 (November 1992): 869–78. http://dx.doi.org/10.1016/s0733-8619(18)30184-1.

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Kharatishvili, Irina, and Asla Pitkänen. "Posttraumatic epilepsy." Current Opinion in Neurology 23, no. 2 (April 2010): 183–88. http://dx.doi.org/10.1097/wco.0b013e32833749e4.

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Rinaldi, A., and L. Conti. "Posttraumatic epilepsy." Neurological Sciences 24, no. 4 (November 1, 2003): 229–30. http://dx.doi.org/10.1007/s10072-003-0144-9.

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Mazarati, Andrey. "Is Posttraumatic Epilepsy the Best Model of Posttraumatic Epilepsy?" Epilepsy Currents 6, no. 6 (November 2006): 213–14. http://dx.doi.org/10.1111/j.1535-7511.2006.00149.x.

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Kennedy, Colin R., and John M. Freeman. "Posttraumatic seizures and posttraumatic epilepsy in children." Journal of Head Trauma Rehabilitation 1, no. 4 (December 1986): 66–73. http://dx.doi.org/10.1097/00001199-198612000-00012.

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Chen, James W. Y., Robert L. Ruff, Roland Eavey, and Claude G. Wasterlain. "Posttraumatic epilepsy and treatment." Journal of Rehabilitation Research and Development 46, no. 6 (2009): 685. http://dx.doi.org/10.1682/jrrd.2008.09.0130.

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7

Sandyk, R., and C. R. Bamford. "Baclofen Responsive Posttraumatic Epilepsy." International Journal of Neuroscience 37, no. 3-4 (January 1987): 183–85. http://dx.doi.org/10.3109/00207458708987146.

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Heikkinen, E. R., H. S. Rönty, U. Tolonen, and J. Pyhtinen. "Development of Posttraumatic Epilepsy." Stereotactic and Functional Neurosurgery 54, no. 1-8 (1990): 25–33. http://dx.doi.org/10.1159/000100186.

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9

Brissos, Sofia, Vasco Videira Dias, and Teresa Paiva. "Posttraumatic Parieto-Occipital Epilepsy." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 2 (April 2007): 200–201. http://dx.doi.org/10.1176/jnp.2007.19.2.200.

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10

Schubert-Bast, S. "Posttraumatic Epilepsy: An Update." Neuropediatrics 48, S 01 (April 26, 2017): S1—S45. http://dx.doi.org/10.1055/s-0037-1602881.

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Khiari, H. Mrabet, M. Kechaou, A. Banasr, B. Zouari, M. Hamdoun, and A. Mrabet. "Posttraumatic epilepsy in Tunisia." Epilepsy & Behavior 21, no. 4 (August 2011): 417–19. http://dx.doi.org/10.1016/j.yebeh.2011.05.016.

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12

Parko, Karen, and Vikram Rao. "Clinical Approach to Posttraumatic Epilepsy." Seminars in Neurology 35, no. 01 (February 25, 2015): 057–63. http://dx.doi.org/10.1055/s-0035-1544239.

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13

Christensen, Jakob. "The Epidemiology of Posttraumatic Epilepsy." Seminars in Neurology 35, no. 03 (June 10, 2015): 218–22. http://dx.doi.org/10.1055/s-0035-1552923.

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14

Jabbari, Bahman. "Posttraumatic Brain Damage and Epilepsy." American Journal of EEG Technology 27, no. 4 (December 1987): 213–22. http://dx.doi.org/10.1080/00029238.1987.11080236.

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15

Pitkänen, Asla, Samuli Kemppainen, Xavier Ekolle Ndode-Ekane, Noora Huusko, Joanna K. Huttunen, Olli Gröhn, Riikka Immonen, Alejandra Sierra, and Tamuna Bolkvadze. "Posttraumatic epilepsy — Disease or comorbidity?" Epilepsy & Behavior 38 (September 2014): 19–24. http://dx.doi.org/10.1016/j.yebeh.2014.01.013.

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Zimmermann, Lara L., Ryan M. Martin, and Fady Girgis. "Treatment options for posttraumatic epilepsy." Current Opinion in Neurology 30, no. 6 (December 2017): 580–86. http://dx.doi.org/10.1097/wco.0000000000000505.

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Jensen, Frances E. "Introduction Posttraumatic epilepsy: Treatable epileptogenesis." Epilepsia 50 (February 2009): 1–3. http://dx.doi.org/10.1111/j.1528-1167.2008.02003.x.

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Grinenko, Olesya Aleksandrovna, O. S. Zaitsev, L. B. Oknina, S. Urakov, A. L. Golovteyev, and A. A. Potapov. "Posttraumatic epilepsy: Diagnosis and treatment." Neurology, neuropsychiatry, Psychosomatics, no. 3 (September 13, 2011): 13. http://dx.doi.org/10.14412/2074-2711-2011-160.

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Cho, Sung‐Joon, Eugene Park, Tamar Telliyan, Andrew Baker, and Aylin Y. Reid. "Zebrafish model of posttraumatic epilepsy." Epilepsia 61, no. 8 (June 27, 2020): 1774–85. http://dx.doi.org/10.1111/epi.16589.

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20

Atabaevich, Kasimov Arslanbek. "DYNAMICS OF CLINICAL AND NEUROPHYSIOLOGICAL CHANGES AGAINST THE BACKGROUND OF COMPLEX MEDICAL THERAPY IN PATIENTS WITH POSTTRAUMATIC EPILEPSY WITH CONCOMITANT SOMATIC DISEASES." Frontline Medical Sciences and Pharmaceutical Journal 02, no. 03 (March 1, 2022): 78–87. http://dx.doi.org/10.37547/medical-fmspj-02-03-08.

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Posttraumatic epilepsy can be characterized as a variant of the consequences of craniocerebral trauma (CMT) with a leading epileptic syndrome, which is manifested, respectively, by systematically repeated epileptic seizures, most often of convulsive nature.The leading etiological factor of symptomatic epilepsy of young age is craniocerebral trauma, which takes 30-50% of all types of injuries in peace time. The incidence of post-traumatic epilepsy in cases of previously suffered traumatic brain injury ranges from 5 to 50%, according to numerous studies, and its course is often progredient. The problem of diagnosis and drug treatment of posttraumatic epilepsy remains one of the most difficult tasks of clinical neurology [1,3,5].

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Kurihara, Mana, Atsushi Shishido, Manabu Yoshihashi, Hiroyuki Fujita, and Toshitaka Kohagizawa. "Prognosis of Posttraumatic Epilepsy in Children." Journal of the Japan Epilepsy Society 29, no. 3 (2012): 460–69. http://dx.doi.org/10.3805/jjes.29.460.

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Kryukova, K. K., E. V. Aleksandrova, O. N. Voskresenskaya, A. G. Bragin, V. V. Podlepich, E. Yu Sokolova, K. N. Lapteva, E. M. Troshina, A. V. Oshorov, and A. A. Potapov. "Early predictive biomarkers of posttraumatic epilepsy." Voprosy neirokhirurgii imeni N.N. Burdenko 85, no. 5 (2021): 110. http://dx.doi.org/10.17116/neiro202185051110.

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23

Servit, Z. "Pharmacological prevention of posttraumatic epilepsy. (Czech)." Plastic and Reconstructive Surgery 75, no. 1 (January 1985): 150. http://dx.doi.org/10.1097/00006534-198501000-00114.

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24

Pohlmann-Eden, B., and J. Bruckmeir. "Predictors and dynamics of posttraumatic epilepsy." Acta Neurologica Scandinavica 95, no. 5 (May 1997): 257–62. http://dx.doi.org/10.1111/j.1600-0404.1997.tb00206.x.

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25

Eid, T. "A Cool Intervention for Posttraumatic Epilepsy." Science Translational Medicine 5, no. 182 (April 24, 2013): 182ec69. http://dx.doi.org/10.1126/scitranslmed.3006347.

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26

Dildora Kadirovna, Khaydarova, Khodjieva Dilbar Tadjiyevna, and Khaydarov Nodirjon Kadirovich. "DIAGNOSIS AND TREATMENT OF POSTTRAUMATIC EPILEPSY." Journal of Research in Health Science 1, no. 2 (April 4, 2018): 45–51. http://dx.doi.org/10.26739/2523-1243/-2017-1-2-7.

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27

D'Alessandro, R., R. Ferrara, G. Benassi, P. L. Lenzi, and L. Sabattini. "Computed Tomographic Scans in Posttraumatic Epilepsy." Archives of Neurology 45, no. 1 (January 1, 1988): 42–43. http://dx.doi.org/10.1001/archneur.1988.00520250048019.

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28

Aarabi, Bizhan, Musa Taghipour, Ali Haghnegahdar, Majidreza Farokhi, and Lloyd Mobley. "Prognostic factors in the occurrence of posttraumatic epilepsy after penetrating head injury suffered during military service." Neurosurgical Focus 8, no. 1 (January 2000): 1–6. http://dx.doi.org/10.3171/foc.2000.8.1.155.

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In this retrospective study, the authors evaluated confounding risk factors, which are allegedly influential in causing unprovoked posttraumatic epilepsy, in 489 patients from the frontlines of the Iran–Iraq War. Four hundred eighty-nine patients were followed for 6 to154 months (mean 39.4 months, median 23 months), and important factors precipitating posttraumatic epilepsy were evaluated using uni- and multivariate regression analysis. One hundred fifty-seven (32%) of 489 patients became epileptic during the study period. The results of univariate analysis indicated a significant relationship between epilepsy and Glasgow Outcome Scale (GOS) score (X2 = 76.49, p < 0.0001, df = 2), Glasgow Coma Scale score at admission (X2 = 19.48, p < 0.0001, df = 3), motor deficit (X2 = 11.79, p < 0.001, df = 1), mode of injury (X2 = 10.731, p < 0.05), transventricular injury (X2 = 6.9, p < 0.008, df = 1), dysphasia (X2 = 5.3, p < 0.02), central nervous system infections (X2 = 5.3, p < 0.02), and early-onset seizures (X2 = 4.1, p < 0.04, df = 1). The results of multivariate analysis, on the other hand, indicated that the GOS score and motor deficit were of greater statistical importance (X2 = 35.24, p < 0.0001; and X2 = 7.1, p < 0.07, respectively). Factors that did have much statistically significant bearing on posttraumatic epilepsy were the projectile type, site of injury on the skull, patient age, number of affected lobes, related hemorrhagic complications, and retained metallic or bone fragments. Glasgow Outcome Scale score and focal motor neurological deficit are of particular importance in predicting posttraumatic epilepsy after missile head injury.

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29

Maslov, N. E., A. A. Litvinova, P. S. Kovalev, N. N. Maslova, N. V. Yuryeva, and E. I. Khamtsova. "Posttraumatic epilepsy: clinical, diagnostic and therapeutic features." Epilepsy and paroxysmal conditions 13, no. 4 (January 18, 2022): 377–92. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2021.100.

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According to 2019 statistics records, traumatic brain injuries (TBI) are the most common type of injuries and one of the main causes for disability in Russia. Every year 200 people per 10,000 subjects around the world suffer from serious brain injuries. Severe TBI can result in long-term disability. Posttraumatic epilepsy (PTE) is one of the most dramatic consequences of TBI with an estimated incidence rate ranging from 2% to 50% based on severity of injury. Conducting studies on PTE poses numerous challenges because epilepsy never develops in many patients with TBI or it may occur more than 10 years after TBI.In this review, which includes data from studies conducted by Russian researchers, including us, and foreign colleagues over the last few years (mainly 2017–2022), we analyzed and generalized currently known risk factors, clinical and diagnostic features of PTE in order to increase the awareness about modern methods of laboratory and instrumental diagnostics related to this disease (including electroencephalography and routine/special neuroimaging techniques that allow to identify PTE biomarkers). We also aimed to promote development of preventive strategies for patient management. It has been proved that no clear algorithms for PTE diagnostics and treatment are currently available, which often leads to insufficient patient care.

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30

Prokhorova, Anna. "Clinical features of posttraumatic epilepsy in children." Medical and Health Science Journal 7 (April 29, 2011): 69–74. http://dx.doi.org/10.15208/mhsj.2011.135.

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31

Beghi, Ettore. "Overview of Studies to Prevent Posttraumatic Epilepsy." Epilepsia 44 (September 26, 2003): 21–26. http://dx.doi.org/10.1046/j.1528-1157.44.s10.1.x.

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32

Frey, Lauren C. "Epidemiology of Posttraumatic Epilepsy: A Critical Review." Epilepsia 44 (September 26, 2003): 11–17. http://dx.doi.org/10.1046/j.1528-1157.44.s10.4.x.

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33

Timofeev, Igor, Maksim Bazhenov, Sinziana Avramescu, and Dragos A. Nita. "Posttraumatic Epilepsy: The Roles of Synaptic Plasticity." Neuroscientist 16, no. 1 (April 9, 2009): 19–27. http://dx.doi.org/10.1177/1073858409333545.

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34

Pollicino, P. "Incidence of epilepsy in posttraumatic vegetative state." Electroencephalography and Clinical Neurophysiology 103, no. 1 (July 1997): 216. http://dx.doi.org/10.1016/s0013-4694(97)89045-5.

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35

van Emde Boas, W. "Prevention of posttraumatic epilepsy: fiction or fact?" European Journal of Paediatric Neurology 12 (May 2008): S13. http://dx.doi.org/10.1016/s1090-3798(08)70042-4.

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36

Statler, K. D., P. Scheerlinck, W. Pouliot, M. Hamilton, H. S. White, and F. E. Dudek. "A potential model of pediatric posttraumatic epilepsy." Epilepsy Research 86, no. 2-3 (October 2009): 221–23. http://dx.doi.org/10.1016/j.eplepsyres.2009.05.006.

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37

Armstrong, K. K., V. Sahgal, R. Bloch, K. J. Armstrong, and A. Heinemann. "Rehabilitation outcomes in patients with posttraumatic epilepsy." Journal of Head Trauma Rehabilitation 6, no. 1 (March 1991): 93–94. http://dx.doi.org/10.1097/00001199-199103000-00016.

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38

Blume, Warren T. "Hippocampal Cell Loss in Posttraumatic Human Epilepsy." Epilepsy Currents 7, no. 6 (November 2007): 156–58. http://dx.doi.org/10.1111/j.1535-7511.2007.00177.x.

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39

Kelly, Kevin M. "Modeling Traumatic Brain Injury and Posttraumatic Epilepsy." Epilepsy Currents 4, no. 4 (July 2004): 160–61. http://dx.doi.org/10.1111/j.1535-7597.2004.44015.x.

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40

Gupta, Rakesh K., Sona Saksena, Atul Agarwal, Khader M. Hasan, Mazhar Husain, Vikas Gupta, and Ponnada A. Narayana. "Diffusion Tensor Imaging in Late Posttraumatic Epilepsy." Epilepsia 46, no. 9 (September 2005): 1465–71. http://dx.doi.org/10.1111/j.1528-1167.2005.01205.x.

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41

Swartz, Barbara E., Carolyn R. Houser, Uwami Tomiyasu, Gregory O. Walsh, Antonio DeSalles, J. Ronald Rich, and Antonio Delgado-Escueta. "Hippocampal Cell Loss in Posttraumatic Human Epilepsy." Epilepsia 47, no. 8 (August 2006): 1373–82. http://dx.doi.org/10.1111/j.1528-1167.2006.00602.x.

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42

Weiss, G. H., A. M. Salazar, S. C. Vance, J. H. Grafman, and B. Jabbari. "Predicting Posttraumatic Epilepsy in Penetrating Head Injury." Archives of Neurology 43, no. 8 (August 1, 1986): 771–73. http://dx.doi.org/10.1001/archneur.1986.00520080019013.

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43

Walker, A. Earl. "Posttraumatic epilepsy in world war II veterans." Surgical Neurology 32, no. 3 (September 1989): 235–36. http://dx.doi.org/10.1016/0090-3019(89)90185-7.

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44

Dwyer, Brigid. "Posttraumatic Headache." Seminars in Neurology 38, no. 06 (December 2018): 619–26. http://dx.doi.org/10.1055/s-0038-1673692.

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AbstractPosttraumatic headaches are among the most challenging complaints after mild traumatic brain injury (mTBI). They are a debilitating problem experienced by patients after TBI of all severities. Up to 90% of mild TBI patients experience headache, particularly if female and with a premorbid history of primary headache. Tension headache has classically been the most common subtype, but in military populations migraine has dominated. Posttraumatic headache encompasses a spectrum of headache types that overlap heavily with common primary headache disorders, but also autonomic cephalgias as well as several secondary headache conditions. It is important to understand the evolution of postconcussion syndrome as a concept, and the challenges associated with diagnosing and treating multidomain drivers effectively. The first-line treatments for posttraumatic headache are typically the same as those used in nontraumatic headache, with additional considerations for cognitive side effects, posttraumatic epilepsy, and coexisting injuries resulting in neuropathic pain or medication overuse.

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45

Hakimian, Shahin, Amir Kershenovich, John W. Miller, Jeffrey G. Ojemann, Adam O. Hebb, Raimondo D'Ambrosio, and George A. Ojemann. "Long-term outcome of extratemporal resection in posttraumatic epilepsy." Neurosurgical Focus 32, no. 3 (March 2012): E10. http://dx.doi.org/10.3171/2012.1.focus11329.

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Object Posttraumatic epilepsy (PTE) is a common cause of medically intractable epilepsy. While much of PTE is extratemporal, little is known about factors associated with good outcomes in extratemporal resections in medically intractable PTE. The authors investigated and characterized the long-term outcome and patient factors associated with outcome in this population. Methods A single-institution retrospective query of all epilepsy surgeries at Regional Epilepsy Center at the University of Washington was performed for a 17-year time span with search terms indicative of trauma or brain injury. The query was limited to adult patients who underwent an extratemporal resection (with or without temporal lobectomy), in whom no other cause of epilepsy could be identified, and for whom minimum 1-year follow-up data were available. Surgical outcomes (in terms of seizure reduction) and clinical data were analyzed and compared. Results Twenty-one patients met inclusion and exclusion criteria. In long-term follow-up 6 patients (28%) were seizure-free and an additional 6 (28%) had a good outcome of 2 or fewer seizures per year. Another 5 patients (24%) experienced a reduction in seizures, while only 4 (19%) did not attain significant benefit. The presence of focal encephalomalacia on imaging was associated with good or excellent outcomes in 83%. In 8 patients with the combination of encephalomalacia and invasive intracranial EEG, 5 (62.5%) were found to be seizure free. Normal MRI examinations preoperatively were associated with worse outcomes, particularly when combined with multifocal or poorly localized EEG findings. Two patients suffered complications but none were life threatening or disabling. Conclusions Many patients with extratemporal PTE can achieve good to excellent seizure control with epilepsy surgery. The risks of complications are acceptably low. Patients with focal encephalomalacia on MRI generally do well. Excellent outcomes can be achieved when extratemporal resection is guided by intracranial EEG electrodes defining the extent of resection.

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46

Unalp, Aycan, Elcin Bora, Tufan Cankaya, Ozlem Giray Bozkaya, Derya Ercal, Aysel Ozturk, and Ayfer Ulgenalp. "Lack of Association of Childhood Partial Epilepsy with Brain Derived Neurotrophic Factor Gene." Scientific World Journal 2012 (2012): 1–5. http://dx.doi.org/10.1100/2012/414797.

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Brain-derived factor (BDNF) is a member of neurotrophin family and is localized and upregulated in areas implicated in epileptogenesis. Several lines of evidence make the BDNF gene a plausible candidate gene for predisposition to epilepsy. In this study, we tested that BDNF might be involved in the etiology of childhood PE. To assess whether BDNF gene C270T polimorphism could be implicated in vulnerability to PE, we conducted a case-control association analysis (112 partial epileptic and 100 controls) in Turkish children. Epileptic children were divided into two groups: 1—idiopathic (n=85) and 2—symptomathic epilepsy (n=27). There was no significant difference in genotypic distribution and allelic frequencies of the BDNF gene C270T polimorphism between the PE and control groups. However, the BDNF gene TT genotype was more frequently seen in the epileptic children (15 versus 11 patients, resp.). Interestingly, in the epilepsy group, both two children with TT genotype have posttraumatic epilepsy. The data indicate a possible association with the 270T genotype of the BDNF gene with a posttraumatic epilepsy. To draw any conclusion, further studies using larger sample sizes should be carried out in various ethnic populations in childhood epilepsies.

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47

Benardo, Larry S. "Insights into the Cellular Basis of Posttraumatic Epilepsy." Epilepsy Currents 2, no. 2 (March 2002): 59. http://dx.doi.org/10.1111/j.1535-7597.2002.00021.x.

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Physiological and Structural Evidence for Hippocampal Involvement in Persistent Seizure Susceptibility after Traumatic Brain Injury Golarai G, Greenwood AC, Feeney DM, Connor JA J Neurosci 2001;21:8523–8537 Epilepsy is a common outcome of traumatic brain injury (TBI), but the mechanisms of posttraumatic epileptogenesis are poorly understood. One clue is the occurrence of selective hippocampal cell death after fluid-percussion TBI in rats, consistent with the reported reduction of hippocampal volume bilaterally in humans after TBI and resembling hippocampal sclerosis, a hallmark of temporal-lobe epilepsy. Other features of temporal-lobe epilepsy, such as long-term seizure susceptibility, persistent hyperexcitability in the dentate gyrus (DG), and mossy fiber synaptic reorganization, however, have not been examined after TBI. To determine whether TBI induces these changes, we used a well studied model of TBI by weight drop on somatosensory cortex in adult rats. First, we confirmed an early and selective cell loss in the hilus of the DG and area CA3 of hippocampus, ipsilateral to the impact. Second, we found persistently enhanced susceptibility to pentylenetetrazole-induced convulsions 15 weeks after TBI. Third, by applying GABAA antagonists during field-potential and optical recordings in hippocampal slices 3 and 15 weeks after TBI, we unmasked a persistent, abnormal APV-sensitive hyperexcitability that was bilateral and localized to the granule cell and molecular layers of the DG. Finally, using Timm histo-chemistry, we detected progressive sprouting of mossy fibers into the inner molecular layers of the DG bilaterally 2–27 weeks after TBI. These findings are consistent with the development of posttraumatic epilepsy in an animal model of impact head injury, showing a striking similarity to the enduring behavioral, functional, and structural alterations associated with temporal-lobe epilepsy. Long-Term Hyperexcitability in the Hippocampus After Experimental Head Trauma Santhakumar V, Ratzliff AD, Jeng J, Toth Z, Soltesz I Ann Neurol 2001;50:708–717 Head injury is a causative factor in the development of temporal lobe epilepsy. However, whether a single episode of concussive head trauma causes a persistent increase in neuronal excitability in the limbic system has not been unequivocally determined. This study used the rodent fluid percussion injury (FPI) model, in combination with electrophysiological and histochemical techniques, to investigate the early (1 week) and long-term (1 month or longer) changes in the hippocampus after head trauma. Low-frequency, single-shock stimulation of the perforant path revealed an early granule cell hyperexcitability in head-injured animals that returned to control levels by 1 month. However, there was a persistent decrease in threshold to induction of seizure-like electrical activity in response to high-frequency tetanic stimulation in the hippocampus after head injury. Timm staining revealed both early- and long-term mossy fiber sprouting at low to moderate levels in the dentate gyrus of animals that experienced FPI. There was a long-lasting increase in the frequency of spontaneous inhibitory postsynaptic currents in dentate granule cells after FPI, and ionotropic glutamate receptor antagonists selectively decreased the spontaneous inhibitory postsynaptic current frequency in the head-injured animals. These results demonstrate that a single episode of experimental closed head trauma induces long-lasting alterations in the hippocampus. These persistent structural and functional alterations in inhibitory and excitatory circuits are likely to influence the development of hyperexcitable foci in posttraumatic limbic circuits.

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48

Steinmetz, Sonja, Andrea Tipold, and Wolfgang Löscher. "Epilepsy after head injury in dogs: A natural model of posttraumatic epilepsy." Epilepsia 54, no. 4 (January 7, 2013): 580–88. http://dx.doi.org/10.1111/epi.12071.

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49

Fierain, Alexane, Aileen McGonigal, Stanislas Lagarde, Hélène Catenoix, Luc Valton, Sylvain Rheims, Anca Nica, Agnes Trebuchon, Romain Carron, and Fabrice Bartolomei. "Stereoelectroencephalography (SEEG) and epilepsy surgery in posttraumatic epilepsy: A multicenter retrospective study." Epilepsy & Behavior 112 (November 2020): 107378. http://dx.doi.org/10.1016/j.yebeh.2020.107378.

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50

Carrazana, Enrique J. "Portrait of My Father: Frida Kahlo’s Intimate Relation to Epilepsy." European Neurology 84, no. 4 (2021): 295–99. http://dx.doi.org/10.1159/000516321.

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The painting <i>Portrait of My Father</i> (1951) by the Mexican painter, Frida Kahlo, is discussed by the author within the context of epilepsy and biographical events in the lives of both Frida and her father, the German Mexican photographer Guillermo Kahlo. The biographical accounts of the photographer’s seizures are suggestive of juvenile absence epilepsy but cannot discount the possibility of posttraumatic epilepsy of mesial frontal origin.

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Journal articles on the topic 'Posttraumatic epilepsy'

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