Benzodiazepines in the Treatment of Epilepsy A Review

Browne, Thomas R.; Penry, J. Kiffin

doi:10.1111/j.1528-1157.1973.tb03965.x

Cited by 230 publications

(71 citation statements)

References 118 publications

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“…We know of no other reports of de novo ENM secondary to AED discontinuation. Discontinuation of AEDs, including CLB (13) and VPA (14) is believed to cause an increase in seizures frequency, which in turn augments interictal spiking activity (15) but has no influence on their electroclinical patterns, usually analogous to those observed with full therapy (16,17). The part played by the rate of AED discontinuation in our patients remains unknown, since either fast or slow tapering of AEDs typically does not affect the pattern of seizures (14).…”

Section: Discussionmentioning

confidence: 92%

Negative Myoclonic Status Due to Antiepileptic Drug Tapering: Report of Three Cases

Gambardella¹,

Aguglia²,

Oliveri³

et al. 1997

Epilepsia

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Summary: Purpose: Epileptic negative myoclonus (ENM) has been increasingly recognized in different epilepsies, but the reasons for its appearance and prognosis remain uncertain. We report 3 patients who developed de novo, almost continuous ENM, triggered by antiepileptic drug (AED) tapering, that resolved with treatment.Methods: Three patients aged 16, 19, and 65 years with a 13-to 36-year history of partial epilepsy were receiving a therapeutic dosage of carbamazepine or phenobarbital plus either clobazam (CLB) or valproate (VPA). None had previously had ENM. Forty-eight to 72 h after CLB or VPA withdrawal, the habitual seizures recurred. The patient also began to report repetitive postural lapses of one or more limbs that interfered with eating or writing. At this time, each patient underwent polygraphy with simultaneous surface electromyography (EMG) of deltoid, biceps, and triceps muscles and of the wrist extensor and flexor bilaterally.Results: In all patients, EEGs demonstrated almost continuous epileptiform discharges whose spatial distribution was similar to that observed before ENM appearance. Polygraphic recordings showed repetitive loss of postural EMG activity in one or more limbs, 100400 ms in duration, which occurred in conjunction with the spike-waves. One milligram of clonazepam intravenously always terminated ENM status, which has not recurred in the ensuing 9-36 months.Conclusions: ENM may emerge as a new type of seizure due to tapering of AED therapy. This effect is possibly related to the great activation of epileptiform activity with consequent interference with cortical activity.

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Section: Discussionmentioning

confidence: 92%

Negative Myoclonic Status Due to Antiepileptic Drug Tapering: Report of Three Cases

Gambardella¹,

Aguglia²,

Oliveri³

et al. 1997

Epilepsia

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“…HEK-293 cell medium also contained 1 mmol/L sodium pyruvate and 0.1 mmol/L nonessential amino acids. Cells were plated on collagen-coated (COS-7) or poly-d-lysine-coated (HEK-293) 24-well plates at 0.6 × 10 5 cells per well and mental and neurologic outcomes. We focused on antiseizure treatment to identify harmful and helpful treatment strategies.…”

Section: Introductionmentioning

confidence: 99%

Mutations in the Na+/Citrate Cotransporter NaCT (SLC13A5) in Pediatric Patients with Epilepsy and Developmental Delay

Klotz

Porter

Colas

et al. 2016

Mol Med

125

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Mutations in the SLC13A5 gene that codes for the Na + /citrate cotransporter, NaCT, are associated with early onset epilepsy, developmental delay and tooth dysplasia in children. In this study, we identify additional SLC13A5 mutations in nine epilepsy patients from six families. To better characterize the syndrome, families with affected children answered questions about the scope of illness and the treatment strategies. Currently, there are no effective treatments, but some antiepileptic drugs targeting the γ-aminobutyric acid system reduce seizure frequency. Acetazolamide, a carbonic anhydrase inhibitor and atypical antiseizure medication, decreases seizures in four patients. In contrast to previous reports, the ketogenic diet and fasting resulted in worsening of symptoms. The effects of the mutations on NaCT transport function and protein expression were examined by transient transfections of COS-7 cells. There was no transport activity from any of the mutant transporters, although some of the mutant transporter proteins were present on the plasma membrane. The structural model of NaCT suggests that these mutations can affect helix packing or substrate binding. We tested various treatments, including chemical chaperones and low temperatures, but none improved transport function in the NaCT mutants. Interestingly, coexpression of NaCT and the mutants results in decreased protein expression and activity of the wild-type transporter, indicating functional interaction. In conclusion, this study has identified additional SLC13A5 mutations in patients with chronic epilepsy starting in the neonatal period, with the mutations producing inactive Na + /citrate transporters.online address: http://www.molmed.org

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“…Embora o tratamento mais eficaz para o paciente fotossensivel seja evitar condições estimulantes que provocam crises epilépticas, dependendo do tipo e freqüência de crises, pode-se prescrever profilaticamente drogas anti-epilépticas, como fenobarbital, fenitoina 2 > 17 , valproate 11 ou benzodiazepines 3 . Em nossos casos instituímos o uso do fenobarbital e obtivemos controle das crises epilépticas durante o tempo de seguimento.…”

Section: Comentáriosunclassified

Epilepsia fotossensível: relato de dois casos

Lauda

Albuquerque²,

Nascimento³

et al. 1990

Arq. Neuro-Psiquiatr.

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RESUMO -Epilepsia fotossensível é tema ainda pouco descrito. Os autores revisam a literatura pertinente e descrevem dois casos de epilepsia fotossensível, dando ênfase à assim chamada epilepsia da televisão.Photosensitive epilepsy: report of two cases.SUMMARY -Reports on photosensitive epilepsy are uncommon. The authors review the literature, and special attention is given to television epilepsy. Two cases are reported and discussed.A epilepsia reflexa ou de indução sensorial caracteriza-se pelo aparecimento de crises epilépticas induzidas por estímulos ambientais específicos. Estímulos visuais, auditivos, olfatórios, gustativos, somestésticos e viscerais podem precipitar tais crises 1.5.8,12, A epilepsia fotossensível foi descrita inicialmente por Gowersio, em 1885 e, em seu conceito atual, incluem-se pacientes com crises epilépticas e fotossensibilidade, caracterizada pela presença da «resposta fotoparaxistica» (RFP) ao exame eletrencefalográfico (EEG)6. A RFP consiste de descarga generalizada, geralmente de pontas ou complexos poli-ponta-onda, registrada em todas as regiões do cérebro durante a foto-estimulação intermitente (FEI) 14 . As respostas localizadas em regiões anteriores (resposta fotomioclônica ou fotomiogênica) ou posteriores («driving» fótico) são consideradas fisiológicas e são excluídas do conceito de RFP 1 4 -19 . Segundo Jeavons e Harding 12, a epilepsia fotossensível pode ser de dois tipos: 1. Epilepsia fotossensível pura -forma rara de epilepsia reflexa, na qual as crises epilépticas são precipitadas somente pela estimulação luminosa 7 ; 2. Epilepsia com fotossensibilidade -pacientes com crises epilépticas não relacionadas ao estímulo luminoso, porém com fotossensibilidade ao EEG 6 >20. A epilepsia fotossensível tem prevalência estimada em I para 10000 pessoas 13, sendo as mulheres duas vezes mais acometidas que os homens 20. A fotossensibilidade tem sido descrita em pacientes de ambos os sexos, com idade compreendida entre 7 meses e 65 anos e com maior freqüência entre os II e 15 anos de idade 16. Jeavons e Harding 12 relatam nítida predisposição à epilepsia fotossensível em gêmeos monozigóticos. Na revisão de Newmark e Penryis, até 39% dos pacientes fotossensíveis apresentam história familiar positiva para epilepsia. Os pacientes usualmente respondem à FEI com crises mioclônicas, tônico-clônicas ou ausências, embora crises parciais possam também estar presentes 8. O tipo de apresentação mais comum da epilepsia fotossensível pura é a chamada epilepsia da televisão 4.9,18.

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Benzodiazepines in the Treatment of Epilepsy A Review

Cited by 230 publications

References 118 publications

Negative Myoclonic Status Due to Antiepileptic Drug Tapering: Report of Three Cases

Negative Myoclonic Status Due to Antiepileptic Drug Tapering: Report of Three Cases

Mutations in the Na+/Citrate Cotransporter NaCT (SLC13A5) in Pediatric Patients with Epilepsy and Developmental Delay

Epilepsia fotossensível: relato de dois casos

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