Follow-up Case Report: Bumetanide Can Control Seizural Activity in Temporal Lobe Epilepsy Patient

Despite the infectiveness of conventional anti-epileptic drugs (AEDs) in refractory focal epilepsy, surgery along with medications, as the only treatment, was not successful in 30% of the cases. Recently, cysto- and histo-physiological investigations revealed the role of gamma-aminobutyric acid (GABA)-ergic system in etiopathology of temporal lobe epilepsy (TLE). Studies reported that the inhibitoryactionof GABAneurotransmitterduetoelevatedintracellularCl-concentrationthroughabnormalexpressionof Na-K-Cl cotransporter (NKCC)-1 became excessive in recurrent seizures. These primary results were confirmed in the brain tissue obtained frompatientswithTLE.Basedontheevidence,thecurrentstudysuggestedtheadministrationof bumetanide,anNKCC1inhibitor,as a potential candidatefor thetreatment of intractable TLE.The previousstudy byauthors showedasignificant reductionin seizural activityof 2outof 3patientswithTLEfollowingtheadministrationof bumetanide. However,resultof thecurrentstudyshowedthe controlof seizureinthe3rdcaseof previousstudybytheadministrationof bumetanideasanadjuvanttoAEDs. Moreover,hisAEDs dosage after discontinuation of Bumetanide tapered without any relapse.

[1]  Y. Ben-Ari,et al.  Treating Schizophrenia With the Diuretic Bumetanide: A Case Report. , 2016, Clinical neuropharmacology.

[2]  Sudhir Sivakumaran,et al.  Bumetanide reduces seizure progression and the development of pharmacoresistant status epilepticus , 2016, Epilepsia.

[3]  J. Rutka,et al.  Change in presurgical diagnostic imaging evaluation affects subsequent pediatric epilepsy surgery outcome , 2016, Epilepsia.

[4]  P. Damier,et al.  Bumetanide to Treat Parkinson Disease: A Report of 4 Cases. , 2016, Clinical neuropharmacology.

[5]  Christophe Bernard,et al.  Treatment during a vulnerable developmental period rescues a genetic epilepsy , 2015, Nature Medicine.

[6]  Simon-Shlomo Poil,et al.  Paradoxical Benzodiazepine Response: A Rationale for Bumetanide in Neurodevelopmental Disorders? , 2015, Pediatrics.

[7]  A. Cherubini,et al.  3‐T magnetic resonance imaging simultaneous automated multimodal approach improves detection of ambiguous visual hippocampal sclerosis , 2015, European journal of neurology.

[8]  A. Contestabile,et al.  Reversing excitatory GABAAR signaling restores synaptic plasticity and memory in a mouse model of Down syndrome , 2015, Nature Medicine.

[9]  E. Lemonnier,et al.  The effect of bumetanide treatment on the sensory behaviours of a young girl with Asperger syndrome , 2014, BMJ Case Reports.

[10]  W. Löscher,et al.  Cation-chloride cotransporters NKCC1 and KCC2 as potential targets for novel antiepileptic and antiepileptogenic treatments , 2013, Neuropharmacology.

[11]  M. Hadjighassem,et al.  Bumetanide reduces seizure frequency in patients with temporal lobe epilepsy , 2013, Epilepsia.

[12]  E. Cavalheiro,et al.  Temporal lobe epilepsy with mesial temporal sclerosis: hippocampal neuronal loss as a predictor of surgical outcome. , 2012, Arquivos de neuro-psiquiatria.

[13]  P. Schwartzkroin.  Why—and how—do we engage in basic epilepsy research? , 2010 .

[14]  R. Miles,et al.  Chloride homeostasis and GABA signaling in temporal lobe epilepsy , 2010 .

[15]  Maria Thom,et al.  Reliability of patterns of hippocampal sclerosis as predictors of postsurgical outcome , 2010, Epilepsia.

[16]  M. Goldenberg,et al.  Overview of drugs used for epilepsy and seizures: etiology, diagnosis, and treatment. , 2010, P & T : a peer-reviewed journal for formulary management.

[17]  K. Staley,et al.  The bumetanide-sensitive Na-K-2Cl cotransporter NKCC1 as a potential target of a novel mechanism-based treatment strategy for neonatal seizures. , 2008, Neurosurgical focus.

[18]  R. Miles,et al.  Perturbed Chloride Homeostasis and GABAergic Signaling in Human Temporal Lobe Epilepsy , 2007, The Journal of Neuroscience.