TY  - CHAP
M1  - Book, Section
TI  - Seizure Disorders
A1  - Nestler, Eric J.
A1  - Kenny, Paul J.
A1  - Russo, Scott J.
A1  - Schaefer, Anne
PY  - 2020
T2  - Nestler, Hyman & Malenka’s Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 4e
AB  - KEY  CONCEPTSA  seizure  is  a  transient  alteration  in  behavior  or  perception  caused  by  abnormal  synchronous  firing  of  large  ensembles  of  neurons  in  the  brain.  Epilepsy  refers  to  a  collection  of  diverse  disorders  that  are  characterized  by  an  enduring  predisposition  to  repeated  seizures.Epileptic  activity  in  the  brain  can  be  detected  by  the  electroencephalogram  (EEG),  a  noninvasive  test  that  records  electrical  activity  from  numerous  surface  electrodes  on  the  scalp.At  onset,  hypersynchronous  neuronal  activity  in  focal  seizures  remains  confined  largely  to  a  specific  brain  region  within  one  hemisphere  of  the  brain.  In  contrast,  generalized  seizures  refer  to  those  that  rapidly  engage  a  bilateral  network  of  numerous  brain  regions.Seizures  typically  occur  because  of  a  focal  or  more  generalized  imbalance  between  excitatory  and  inhibitory  synaptic  processes  in  the  brain.  This  change  can  be  caused  by  any  number  of  different  developmental  abnormalities  as  well  as  acquired  brain  insults,  including  tumors,  strokes,  head  injury,  and  autoimmune  processes.An  area  of  the  brain  that  generates  epileptic  activity  is  called  a  seizure  focus.  Such  epileptic  activity  can  remain  localized  or  spread  and  become  generalized.While  many  monogenic  causes  of  epilepsy  have  been  identified  and  characterized,  in  most  patients,  the  inheritance  of  epilepsy  is  complex  and  polygenic.Most  anticonvulsants  work  by  suppressing  the  function  of  Na+  or  Ca2+  channels  or  by  enhancing  GABA–mediated  inhibitory  synaptic  transmission.Other  known  actions  of  a  smaller  number  of  anticonvulsants  include  potentiation  of  K+  channels  or  inhibition  of  glutamatergic  transmission  mediated  through  several  mechanisms  including  decreased  glutamate  release  via  binding  a  synaptic  vesicle–associated  protein  termed  synaptic  vesicle  protein  2A  (SV2A).Other  therapeutic  targets  not  involving  ion  channels  or  glutamatergic  and  GABAergic  neurotransmission  include  cannabidiol  (CBD),  which  has  been  approved  for  the  specific  treatment  of  seizures  in  patients  with  Lennox–Gastaut  syndrome  and  Dravet  syndrome.  
SN  - 
PB  - McGraw-Hill
CY  - New York, NY
Y2  - 2024/04/16
UR  - neurology.mhmedical.com/content.aspx?aid=1174975244
ER  -