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A
ABPE (atypical benign partial epilepsy), 128
Abscesses, cerebral, neuroimaging features of, 181
Absence status epilepticus (ASE), 91–104, 109, 113, 126
atypical, 92, 93, 96
diagnostic neuroimaging in, detection of structural brain lesions in diagnosis and, 188–189
treatment of, 518
clinical classification of, 13, 15, 93–94
clinical features of, 95–99
de novo, of late onset, 93, 97
diagnosis of, 99
neuroimaging in, 188–189
EEG in, 99–100, 117
epidemiology of, 94–95, 115
etiology of, 102–103
with focal features, 94, 98
historical background of, 91
natural history of, 103
neuroimaging in, 188–189
detection of structural brain lesions in diagnosis and, 188
pathophysiology and, 195–196
neuronal injury due to, 119
new cases of uncertain classification, 92–93
pathophysiology of, neuroimaging studies of, 195–196
petit mal, 91–92
situation-related, 93
treatment of, 100–102, 517–518
long-term, 103–104
typical, 92, 93, 95
Access to care, 618–619
research agenda for, 619
N-Acetylaspartate (NAA)
in CPSE, 193, 194
in EPC, 197
as marker of neuronal injury, 174
Acidemia, isovaleric, neonatal SE and, 507
Acidosis, 153–156
Acute symptomatic status epilepticus, sequelae of, 46
Adenosine, 315–321
as endogenous anticonvulsant, 316–317
formation of, 317
future research directions for, 320
mechanism for SE development and, 319–320
mediation of effects by adenosine receptors, 317–318
role in SE, 318–319
Adenosine agonists, as endogenous anticonvulsants, 320
Adenosine receptors, 317–318
AEDs. See Antiepileptic drugs (AEDs); specific drugs
Affective symptoms, nonconvulsive SPSE with, 75
Age
CPSE and, 76
epileptogenesis and, 426
mortality related to, 35
AIDs (anti-inflammatory drugs), epileptogenesis prevention by, 414–415
Airway management, in critical care, 607–608
Akinetic status epilepticus, 127
Ambulatory patients, electrographic SE in, 109–110
Ambulatory status epilepticus, 230
time course of brain damage following, 232–233, 234
Amidate. See Etomidate
Amino acid disturbances, neonatal SE and, 506
α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). See AMPA entries
Amnesia, in CPSE, 78
AMPA, inhaled anesthetics and, 572
AMPA receptor(s), 295
changes in, secondary to SE, 298
excitotoxicity and, 367
neuronal death related to, 466, 468
posttranslational editing for mRNA for GluR2 subunit of, 296–297
reactive synaptogenesis and, 450
role in delayed cell death, 381–383, 384
AMPA receptor antagonists, neuroprotection by, 472
Amygdala
basolateral
recruitment from, 241
status epilepticus originating from, 240
as kindling structure, 235
spread of SE to extensive limbic regions from, 243
Amygdalohippocampal nucleus, status epilepticus originating from, 240
Anesthesia, general, 498, 500. See also Inhaled anesthetics
for convulsive SE, 516
for GCSE, 486, 495
Angelmann's syndrome, NCSE associated with, 126
Angiomas, cavernous, neuroimaging features of, 182
Anoxic encephalopathy, acute, neuroimaging features of, 181
Anterograde amnesia, in CPSE, 78
Anticonvulsant(s), endogenous, 316
adenosine agonists as, 320
adenosine as, 316–317
Anticonvulsant agents. See Antiepileptic drugs (AEDs); specific drugs
Antiepileptic drugs (AEDs). See also specific drugs
adverse effects of, 484–485
anatomical effects of, 255, 257
ASE associated with, 103
controversies regarding antiepileptogenic effects of, 414
dosing of. See also specific drugs
inadequate, 482
focal perfusion of, 580–581, 582
glutamate antagonists as, 298–299
historical background of, 6
for neonatal seizures, 140–141
in subtle GCSE, 258
Anti-inflammatory drugs (AIDs), epileptogenesis prevention by, 414–415
Aphasic status epilepticus, 82–83
Apoptosis, 468–470. See also Neuronal death
bcl-2 gene family and, 158–159
necrosis versus, 331–333
Apraxia, in CPSE, 78
Area tempestas, spread of SE to extensive limbic regions from, 246–251
Arteriovenous malformations, neuroimaging features of, 182
ASE. See Absence status epilepticus (ASE)
Astrocytomas, neuroimaging features of, 181–182
Atonic status epilepticus, 127
Atypical benign partial epilepsy (ABPE), 128
Auditory hallucinations, in CPSE, 78
Auditory nonconvulsive simple partial status epilepticus, 74
Automatisms
in ASE, 97–98
in CPSE, 77
Axon sprouting. See Mossy fiber sprouting; Reactive synaptogenesis
B
Baclofen, seizure threshold and, 372, 373
BAPTA (1,2-bis-[2-amino-phenoxy]ethane-NτNτN′N′-tetraacetic acid), 472
Barbiturates. See also Pentobarbital; Phenobarbital
for emergency department treatment of SE, 601
for refractory SE, 610
Barbituric acid, 553
Basal forebrain, modulation of seizure susceptibility by, 249, 250
Basal ganglia, modulation of seizure susceptibility by, 247, 248–249
Basic model of status epilepticus, 229
Basolateral amygdala, recruitment from, 241
BCECS (benign childhood epilepsy with centrotemporal spikes), 128
bcl-2 gene family, apoptosis and, 158–159
BDNF (brain derived neurotrophic factor), 389, 391–392, 395–396
epileptogenesis and, 414
BDNF mRNA (brain derived neurotropic factor mRNA), SE induction of expression in developing brain, 393, 394, 395
Behavioral consequences of status epilepticus, 399–404
animal studies of, 400–404
cognitive deficits and, 403–404
mechanisms responsible for age-related differences in vulnerability to SE and, 401–403
morphologic, 400–401
clinical studies of, 399–400
Benign childhood epilepsy with centrotemporal spikes (BCECS), 128
Benzodiazepines, 525–533. See also specific drugs
for ASE, therapeutic trial of, 100–102
buccal/sublingual administration of, 530–531
chemistry of, 525, 526, 527
choice of, 495
for CPSE, 79
for emergency department treatment of SE, 599–600
as initial intravenous therapy, clinical efficacy of, 528–529
intramuscular administration of, 531–532
intranasal administration of, 532
pharmacokinetics and pharmacodynamics of, 526–528
pharmacology of, 525–526
prehospital treatment using, 532–533
rectal administration of, 530, 531
resistance to, 272–273
Bicuculline, seizure threshold and, 372, 373
Birth trauma, neonatal SE and, 504
1,2-bis-[2-amino-phenoxy]ethane-NτNτN′N′-tetraacetic acid (BAPTA), 472
Blood-brain barrier, transient breakdown of, CSF pleocytosis and, 153
Blood pressure. See Hypertension; Hypotension
BMPs (bone morphogenetic proteins), 390
Bone morphogenetic proteins (BMPs), 390
Brain. See also Neuronal entries
adenosine sources in, 317
consequences of generalized status epilepticus and, 3–4
energy metabolism in. See Cerebral energy metabolism
imaging of. See Neuroimaging; specific imaging modalities
neurotrophic factors in. See Neurotrophic factors
SE effects on growth of, 342
structural changes in, SE-induced, 391
synaptic plasticity in, 400
Brain derived neurotrophic factor (BDNF), 389, 391–392, 395–396
epileptogenesis and, 414
Brain derived neurotropic factor (BDNF) mRNA, SE induction of expression in developing brain, 393, 394, 395
Brain stem, 251–252
anatomy in rat seizure models, 251–252
modulation of seizure susceptibility by, 249
seizure propagation between forebrain and, 252
SE or seizure activity in humans and, 252
Brainstem release phenomena, 136
C
CAD (caspase-activated DNase), apoptosis and, 470
Caffeine, proconvulsant effects of, 318
Calcium channel antagonists, L-type, neuroprotective effect of, 472
Calcium chelators, cell-permeant, neuroprotective effect of, 472
Calpains
apoptosis and, 470
inhibition of, 472–473
Carbamazepine
for neonatal SE, 510
to reduce incidence or severity of chronic epilepsy following SE, 434
(S)4-Carboxy-3-hydroxyphenylglycine [(S)-4C3HPG], proconvulsant and anticonvulsant actions of, 308–309
Cardiac arrhythmias, drug-induced, 485
with phenytoin, 542
Caspase-3, apoptosis and, 469–470
Caspase-activated DNase (CAD), apoptosis and, 470
Catecholamines, in SE, 149, 151–154
Cathepsins, lysosomal, inhibition of, 472–473
Cell death
delayed
role of AMPA receptors in, 381–383, 384
role of enkephalins in, 383–384, 385
prevention of, by neurotrophins, 390
seizure-induced, resistance of immature brain to, 380, 381
Cerebellar nuclei, deep, modulation of seizure susceptibility by, 249
Cerebellum, modulation of seizure susceptibility by, 249
Cerebral abscess, neuroimaging features of, 181
Cerebral blood flow, local, SE effects on, in immature brains, 359–362
Cerebral edema, focal, foreign tissue lesions versus, neuroimaging for detection in CPSE, 186–188
Cerebral energy metabolism, 349–363
correlation with blood flow in developing brain under normal conditions, 350
glucose transport to brain and, 350
maturation under normal conditions, 349–350
in human brain, 349
in rat brain, 349–350
during seizures, 350–362
cerebral metabolic rates for glucose and, 351–359
SE effects on LCBF in immature brains and, 359–362
seizure effects on brain energy reserves and metabolites and, 350–351
Cerebral infarction, acute, neuroimaging features of, 181
Cerebrospinal fluid
lactate in, as marker of neuronal injury, 174
pleocytosis and, status-induced, 152–153
Cerebrovascular accident, as cause of SE, 28–29
Cerebyx. See Fosphenytoin
CGP35348, seizure threshold and, 372, 373
CHA (N6-Cyclohexyladenosine), 318, 319
Chlormethiazide, for GCSE, 495
Chlormethiazole
for convulsive SE, 516
as second-line agent, 496
(S)-4C3HPG ([S]4-Carboxy-3-hydroxyphenylglycine), proconvulsant and anticonvulsant actions of, 308–309
Ciliary neurotrophic factor (CNTF), 390
Circulatory support, in critical care, 608–609
Cisatracurium, for critical care, 608
Classification of status epilepticus, 13–15
clinical, 13–14
historical background of, 4
semiologic, 13, 14–15
description of seizure type and, 14–15
description of type of SE and, 14
Claustrum, spread of SE to extensive limbic regions from, 244
Clinical features of status epilepticus, 17
Clobazam, for ASE, 101–102
Clonazepam, 525. See also Benzodiazepines
chemical structure of, 525, 527
for convulsive SE, 516
intranasal administration of, 532
for neonatal SE, 510
pharmacokinetics of, 527, 528
rectal administration of, 531
Clonic convulsive status epilepticus, 239
CNTF (ciliary neurotrophic factor), 390
Cocaine, maternal use of, neonatal SE and, 507
Cognitive function
deficits following SE, 403–404
in ESES, 130
following febrile seizures, 339
nonconvulsive SPSE and, 74–75
sequelae of SE and, 44
Comatose patients, electrographic SE in, 110–112
Complex motor seizures, 14
Complex partial status epilepticus (CPSE), 75–82, 109, 113–114, 127
age and, 76
blood flow mapping of onset and propagation sites in
in experimental CPSE, 192
in human CPSE, 192–193
cerebral water diffusibility, edema, and neuronal injury imaging in
in experimental CPSE, 193
in human CPSE, 193–194
clinical characteristics of, 77–78
clinical classification of, 13, 15
clinical forms intermediate between SPSE and, 82–83
definition of, 75–76
diagnostic neuroimaging in, 185–190
detection of focal cerebral edema versus foreign tissue lesions and, 186–188
detection of structural brain lesions in diagnosis and, 185–186
emergency treatment of, 79
epidemiology of, 115
etiology of, 77, 115–116
following domoate intoxication, neuroimaging in, 194
frequency of cases of, 75
incidence of, 77
laboratory evaluation in, 78–79
neuronal injury due to, 119
NSE in, 172–173
pathophysiology of, neuroimaging studies of, 192–194
phenomenologic classification of, 75–76
prognosis of, 80–82
syndromes following, pathophysiology of, neuroimaging studies of, 194–195
terminology related to, 75
triggering factors for, 77
Computed tomography
in ASE, 196
in CPSE, 194
in GCSE, 191
etiologic diagnosis using, 183–184
pathophysiological studies using, 177
structural brain lesion detection using, 178, 179, 181–185, 189
in GCSE, 178, 179, 183–185
in spike-wave stupor of the elderly, 189
Consciousness, clouding of
in ASE, 95–98
in CPSE, 77
Continuous spike-and-wave discharges during slow-wave sleep (CSWS) syndrome, 127, 128
pathophysiology of, 131–132
Continuous status epilepticus, 252, 253
Convulsive status epilepticus (CSE), 163–167
clinical features of, 163–166, 167
hippocampal sclerosis in, 163, 165, 166
ischemic lesions in, 163
parenchymal necrosis in, 163, 166
refractory, treatment of, 517
treatment of, 515–517
Cortical dysplasia, neuroimaging features of, 182
Cortical lesions, epileptogenicity of, 423
Cortisol, serum, as marker of neuronal injury, 173–174
CPA (N6-Cyclopentyladenosine), 318
CPSE. See Complex partial status epilepticus (CPSE)
Critical care, 607–612
airway management in, 607–608
circulatory support and basic critical care management in, 608–609
drug therapy for refractory SE in, 609–612
maintenance of seizure control and, 612
mechanical ventilation in, 608
CSE. See Convulsive status epilepticus (CSE)
CSWS (continuous spike-and-wave discharges during slow-wave sleep) syndrome, 127, 128
pathophysiology of, 131–132
8-Cyclopentyl 1,3-dimethylxanthine (8-CPT), 315, 318–319
Cysticercosis, cerebral, neuroimaging features of, 181
Cytochrome c, translocation from mitochondria to cytosol, apoptosis and, 470
D
Definition of status epilepticus, 11–15, 125, 409
classification and, 13–15
conceptual basis for, 11
for impending SE, 11, 12, 13
need for reexamination of, 18
operational, for therapeutic purposes, 493–494
risk of overtreatment and, 13
seizure duration as basis of
clinical basis for, 11–12
experimental basis for, 12–13
Dendritic sprouting. See also Reactive synaptogenesis
epileptogenesis and, 431
Dentate granule cell GABA receptors. See Hippocampal GABAA receptors
Dentate gyrus
cell loss in, in PPS model, 342
mossy fiber sprouting in, 333, 391. See also Reactive synaptogenesis, in fascia dentata
neurogenesis of, increase after ictal events, 333
Desflurane, for refractory SE, 611
Development factors, neurologic sequelae of SE and, 417–419
DFF40 (DNA fragmentation factor 40), apoptosis and, 470
Diazepam, 495, 498. See also Benzodiazepines
chemical structure of, 525, 527
for convulsive SE, 516
for CPSE, 79
for emergency department treatment of SE, 600
GABAA receptor current enhancement by, 269, 270, 274–275
for GCSE, 486
as initial treatment, 483, 484
prehospital, 482
historical background of, 525
intranasal administration of, 532
lorazepam compared with, 496–497
for neonatal SE, 510
for out-of-hospital treatment of status epilepticus, 592–593
pharmacokinetics of, 527, 528
pharmacology of, 591
pharmacoresistance in SSSE and, 213–214
rectal administration of, 530, 531
for GCSE, 481–482
to reduce incidence or severity of chronic epilepsy following SE, 434
resistance to, 272–273, 276–277
Diazepam-phenytoin, 497
adverse effects of, 484
for GCSE, 485
as initial treatment, 483
Diffusion-weighted magnetic resonance imaging, 116
in CPSE, 193, 194
in GCSE, 190, 192, 195
structural brain lesion detection using, in neonates, 190
Dilantin. See Phenytoin
Discrete seizures, 252, 253
DNA fragmentation factor 40 (DFF40), apoptosis and, 470
Domoate intoxication, epilepsy following, 425
neuroimaging in CPSE and, 194
Dopamine, for critical care, 609
Dormant basket cell hypothesis, 411, 428
Dorsomedial thalamus, role in SE spread, 245
Dosing. See also specific drugs
inadequate, 482
Drug kinetics, in SE, 156
Duration of status epilepticus. See also Seizure duration
late development of epilepsy and, 415, 416
mortality related to, 36
Dysembryoplastic neuroepithelial tumors, neuroimaging features of, 182
E
EGF (epidermal growth factor), 390–391
Electroencephalogram, 599
in ASE, 99–100, 117
emergency, 99
spike-and-wave activity on, 99–100
in clinical diagnosis, 598
in CPSE, paroxysmal activity on, 78, 79
in CSWS, 131–132
etomidate and, 574–575
in GCSE, 62, 190–191
ictal discharges on, 58–61
inhaled anesthetics and, 573
lidocaine and, 576
with magnesium, 579
in NCSE, 117
in neonatal SE, 116
neonatal seizures and, 503
in neonates, 141–142
in older children, 116–117
propofol and, 571
Electrographic nonconvulsive status epilepticus, 109–112
in ambulatory patients, 109–110
in comatose inpatients, 110–112
Electrographic status epilepticus
clinical classification of, 13
encephalopathies associated with, pathophysiology of, neuroimaging studies of, 197–199
pathophysiology of, neuroimaging studies of, 197
Electrographic status epilepticus during slow-wave sleep (ESES) syndrome, 127–132
ABPE in, 128
comparison and relation of types of, 130
CSWS in, 128
pathophysiology of, 131–132
follow-up of, 130–131
negative myoclonus and, 128–130
NSENM in, 128
pathophysiology of, neuroimaging studies of, 197–198
prognosis of, 131, 132
Emergency department treatment, 597–606
clinical diagnosis and, 598–599
diagnostic testing and, 599–601
epidemiology of SE and, 597
initial management for, 598
patient management guidelines for, 601–602
prehospital treatment and, 597–598
research directions for, 602
therapies for, 599–601
Emotional disturbances, in CPSE, 78
Encephalitis
bihemispheric, acute, neuroimaging features of, 181
limbic
acute, neuroimaging features of, 181
paraneoplastic, neuroimaging features of, 183
Rasmussen's, 72–73
neuroimaging features of, 181
pathophysiology of, neuroimaging studies of, 196
Encephalitis syndrome, historical background of, 3
Encephalomalacia, neuroimaging features of, 181
Encephalopathy
anoxic, acute, neuroimaging features of, 181
epileptic, with suppression bursts. See Ohtahara syndrome
hypertensive, neuroimaging features of, 181
hypoxic-ischemic, neonatal SE and, 503–504
EndoG, apoptosis and, 470
Endopiriform nucleus, spread of SE to extensive limbic regions from, 245
Energy metabolism, cerebral. See Cerebral energy metabolism
Enkephalins, role in delayed cell death, 383–384, 385
Entopeduncular nucleus, modulation of seizure susceptibility by, 248
Entorhinal cortex
recruitment from, 241–242
status epilepticus originating from, 240
EPC. See Epilepsia partialis continua (EPC)
Epidemiology of status epilepticus, 17–29, 39–47, 114–115, 597
of ASE, 94–95, 115
clinical features and, 17
of CPSE, 115
etiology and, 24–26, 39–41
ethnic origin and, 24–25
past history of epilepsy and, 26
first population-based study of, 18–20
of GCSE, 56, 115
importance of prospective data collection for study of, 19–20
incidence and, 20–23, 34, 39, 40
genetic predisposition and, 29
occurrence of SE in United States and the world and, 21–23
recurrence of SE and, 23
long-term sequelae of SE in childhood and, 44–46
morbidity and, 43–44
mortality and, 26, 27, 43
of myoclonic SE, 115
of NCSE, 41
new advances through studies of, 28–29
outcome of SE and, 27–28
recurrence of SE and, 47
of recurrent SE, 47
risk for status epilepticus and, 42–43
seizure types and, 23–24, 41
Epidermal growth factor (EGF), 390–391
Epilepsia partialis continua (EPC), 70–73, 114
diagnostic neuroimaging in, detection of structural brain lesions in diagnosis and, 189
of nonspecific etiology, 70–72
pathophysiology of, neuroimaging studies of, 196–197
Rasmussen's encephalitis, 72–73
Epilepsy, future development of, with SE, 44–46
Epileptiform discharges, pseudoperiodic, persistent, neuroimaging studies of, 198–199
Epileptogenesis, SE-induced, 409, 423–436. See also Neurologic sequelae of status epilepticus
experimental attempts to prevent, 413–415
experimental evidence for, 423–424
neuropathology associated with, 424, 425
extrapolation of experimental evidence to humans, 425
in immature brain, 426
mechanisms of, 410–411, 413–415, 426–436
evidence for new excitatory connections and, 429, 431, 432
location of epileptogenic focus and, 426–427
loss of inhibition and, 428–429, 430, 431
patterns of neuronal injury resembling mesial temporal sclerosis and, 427–428
prevention, mitigation, or reversal of epileptogenesis and, 431, 434–436
neuropathology associated with
clinical evidence of, 425–426
experimental evidence of, 424, 425
EPSPs (excitatory postsynaptic potentials), 379
ESES. See Electrographic status epilepticus during slow-wave sleep (ESES) syndrome
Ethnic origin in status epilepticus, 24–25
Etiology of status epilepticus, 24–26, 39–41, 115–116
acute symptomatic, 40
of ASE, 102–103
cerebrovascular accident as cause and, 28–29
of CPSE, 77, 115–116
cryptogenic/idiopathic, 39
ethnic origin and, 24–25
febrile, 40
of GCSE, 56
genetic predisposition and, 29
mortality related to, 35–36
progressive encephalopathy and, 40
remote symptomatic, 40
seizure type correlated with, 41
Etomidate
for critical care, 607
for refractory SE, 574–575, 581, 611
adverse effects of, 575
animal models of seizures and, 574
clinical pharmacokinetics of, 574
clinical use of, 574
dosage and regimens for, 575
EEG effects of, 574–575
mechanisms of action of, 574
Excitatory postsynaptic potentials (EPSPs), 379
Excitotoxicity, 327–334. See also Neuronal damage
apoptosis versus necrosis and, 331–333
excitotoxic hypothesis and, 327
long-term changes and, 333–334
SE-induced, 327–331
silver impregnation methods to identify cell populations vulnerable to, 328
temporal pattern of, 328–331
Extravasation, of phenytoin, 541
F
Familial seizures, neonatal SE and, 507
Fascia dentata, reactive synaptogenesis in. See Reactive synaptogenesis, in fascia dentata
Febrile seizures, consequences of, 339
Febrile status epilepticus, 45–46
Felbamate, to reduce incidence or severity of chronic epilepsy following SE, 434
FGFs (fibroblast growth factors), 390
Fibroblast growth factors (FGFs), 390
Filter hypothesis, 429
Fluorofelbamate, to reduce incidence or severity of chronic epilepsy following SE, 434
Fluothane. See Halothane
Focal motor disturbances, in CPSE, 78
Focal neurologic deficits, in CPSE, 78
Foix-Chavany-Marie syndrome, 71
Forane. See Isoflurane
Forebrain
basal, modulation of seizure susceptibility by, 249, 250
generalization of limbic SE and, 246–251
seizure propagation between brain stem and, 252
Fosphenytoin, 495
adverse effects of, 484, 485
as alternative to phenytoin, 494–495, 542
animal studies of, 550
for convulsive SE, 516
for emergency department treatment of SE, 600–601
for GCSE, 485, 486, 497, 499
for continuing care, 487
intramuscular, 546–548
intravenous, clinical trials of, 548–550
for out-of-hospital treatment of status epilepticus, 593
parenteral, 545–546
pharmacoeconomic studies of, 550–551
pharmacology of, 592
phenytoin compared with, 498
to reduce incidence or severity of chronic epilepsy following SE, 435
Free radicals, postsynaptic generation of, reduction of, 472
Functional magnetic resonance imaging
in CPSE, 192, 194
pathophysiological studies using, 177
in PLEDs, 198–199
Furosemide, for refractory SE, 580, 581
G
GABA, potentiation of, by inhaled anesthetics, 572
GABAA antagonists, seizure duration and, 315
GABAA receptors
benzodiazepines and, 525–526
SE-induced decreases in function of, 285–286
SNR effects on seizures and, 372–373
GABAB receptors, SNR effects on seizures and, 372, 373
GABAergic basket cells, 411, 413
GABAergic inhibition, 281–289
development of, 282, 284
loss of, 428–429, 430, 431
mechanisms contributing to decreased release of GABA and, 284–285, 287
physiology of, 281–282
postsynaptic, 281–282, 283
presynaptic, 282, 283
propofol and, 569
SE-induced decreases in GABAA receptor function and, 285–286
SE-induced early changes in, 284, 285, 286
SE-induced long-term changes in, 286–289
GABAergic mechanisms, in seizure termination, 315
GABAergic system, reactive synaptogenesis and, 445, 448–449, 450, 452
Gabapentin, to reduce incidence or severity of chronic epilepsy following SE, 434
GABA receptors, 267–278
in GCSE, 57–58
hippocampal. See Hippocampal GABAA receptors
molecular mechanisms for altered function of, 277–278
plasticity of function during SE, 277
recombinant
pharmacology of, 267–268
properties and structure of, 267, 268
in SSSE, 213, 214–217, 219
Galanin, endogenous, 222–224
Gamma-aminobutyric acid (GABA). See also GABA entries
potentiation of, by inhaled anesthetics, 572
τ-Vinyl GABA (GVG), seizure threshold and, 372, 373
Gangliocytomas, neuroimaging features of, 182
Gangliogliomas, neuroimaging features of, 182
GCSE. See Generalized convulsive status epilepticus (GCSE)
GDNF (glial-cell-line-derived neurotrophic factor), 390
General anesthesia, 498, 500. See also Inhaled anesthetics
for convulsive SE, 516
for GCSE, 486, 495
Generalized convulsive status epilepticus (GCSE), 55–63, 113
clinical classification of, 13, 14
clinical diagnosis of, 598–599
clinical features of, 58–61
clonic, 113
definition of, 55–56
diagnosis of, 62
diagnostic neuroimaging in, 178–185
detection of structural brain lesions in diagnosis and, 178–183
etiologic diagnosis with CT versus MRI and, 183–184
myoclonic and subtle, 184–185
EEG in, 58–61
epidemiology of, 56, 115
etiology of, 56
functional neuroimaging studies after, in human GCSE, 191–192
historical background of, 3
mortality in, 62–63
myoclonic, 113
neuroimaging studies during and after, in experimental GCSE, 190–191
overt, 55
clinical features of, 58
pathology related to, 62
pathophysiology of, 56–58
neuroimaging studies of, 190–192
refractory, treatment of, 487–489
structural neuroimaging studies after, in human GCSE, 191
subtle, 55, 58, 113
neuroanatomy of, 255, 258
syndromes following, pathophysiology of, neuroimaging studies of, 194–195
time course of brain damage following, 234
tonic, 113
tonic-clonic, 113
treatment of, 481–489, 495, 497, 499, 500
adverse effects of drugs used for, 484–485
continuing care for, 487
environment of care and, 481
initial, 494–495
initiation of, 482–484
prehospital, 481–482
prevention of recurrence and, 487
for refractory SE, 487–489
sequences and protocols for, 485–486
types of, 13–14
Generalized nonconvulsive status epilepticus (GNCSE), 125, 126–127
akinetic, 127
ASE, 126
atonic, 127
with hypsarrhythmia, 126
minor epileptic SE, 126
myoclonic, 127
in myoclonic-astatic epilepsy and Lennox-Gastaut syndrome, 126
petit mal, 126
Generalized periodic eplileptiform discharges (GPEDs), in electrographic SE, 112
Generalized status epilepticus, 231
Genetic predisposition for status epilepticus, 29
Glial-cell-line-derived neurotrophic factor (GDNF), 390
Globus pallidus externa, modulation of seizure susceptibility by, 248
Globus pallidus interna, modulation of seizure susceptibility by, 248
Glucose
cerebral metabolic rates for, 351–359
SE effects on, in immature animals, 351–359
plasma levels of, elevation in SE, 151
transport to brain, 350
Glutamate
excitotoxicity and. See Neuronal damage
induction of seizures or SE by, 295
microdialysis and, 295–296
release of
calcium-dependent, blockade of, 473
sodium-dependent, reduction of, 473
resistance of immature brain to effects of, 402
Glutamate receptor(s), 295
changes in, as cause of seizures or SE, 296–298
in human focal epilepsy, 297–298
in kindled rats, 297
changes in, secondary to SE, 298
metabotropic. See Metabotropic receptors
neuronal death related to, 464, 466
Glutamate receptor antagonists
as antiepileptics, 298–299
neuroprotection by, 472
Glutamate transporters, change in, onset or maintenance of seizure activity and, 296
GNCSE. See Generalized nonconvulsive status epilepticus (GNCSE)
GPEDs (generalized periodic eplileptiform discharges), in electrographic SE, 112
G protein-coupled receptors, neuronal death related to, 466
Grand mal status epilepticus. See Generalized convulsive status epilepticus (GCSE)
Granule cell(s)
damage to, in PPS model, 342
hyperexcitability of, mossy fiber sprouting and, 452–454
loss of, in PPS model, 342
Granule cell GABA receptors. See Hippocampal GABAA receptors
Growth factors, neuroprotective effect of, 473
GVG (τ-vinyl GABA), seizure threshold and, 372, 373
H
Hallucinations, in CPSE, 78
Halothane, 572. See also Inhaled anesthetics
for refractory SE, 611
Hamartomas, glial, neuroimaging features of, 182
Handling test, 403
HEE (hemiconvulsion-hemiparesis-encephalomalacia) syndrome, following GCSE or CPSE, neuroimaging studies in, 194–195
Hemiconvulsion-hemiparesis-encephalomalacia (HHE) syndrome, following GCSE or CPSE, neuroimaging studies in, 194–195
Hemiconvulsion-hemiplegia-epilepsy syndrome, neuroimaging features of, 183
Hemimegalencephaly, neuroimaging features of, 182
Hepatotoxicity, of valproate, 565–566
Heterotopia
band, neuroimaging features of, 182
regional, neuroimaging features of, 182
Hilar cells
damage to, in PPS model, 342
loss of, in PPS model, 342
Hippocampal GABAA receptors, 268–270
different effects of SE and TLE on, 277
involvement in SE, 273–276
dentate granule cell GABAA receptor currents from rats undergoing SE and, 273–274
diminished diazepam enhancement of GABAA receptor currents in granule cells from rats undergoing SE and, 274–275, 276–277
diminished zinc sensitivity of GABAA receptor currents in granule cells from rats undergoing SE and, 275, 276
pentobarbital enhancement of GABAA receptor current cells from rats undergoing SE and, 275–276
pharmacology of, 269–270
Hippocampal sclerosis, 4, 118–119
in CSE, 163, 165, 166
following febrile seizures, 339
mesial TLE with, following GCSE or CPSE, neuroimaging studies in, 194–195
neuroimaging features of, 183
Hippocampus
epileptogenicity and, 423
lesions in, epileptogenesis and, 425, 426
neuronal damage in, 340
neuronal death in, 424, 425
recruitment from, 241–242
SE-induced epilepsy and, 410–411, 413–415
status epilepticus originating from, 240
time course following SE, sprouting visualized with Timm stain and, 234–236
vulnerability of, 379
History of status epilepticus, 3–6
of centralized conceptual issue, 4–5
of classification of types, 4
clinical, 3
of experimental studies, 5–6
of pathological consequences, 3–4
of therapy, 6
Hydrocephalus, acute, neuroimaging features of, 183
Hyperglycemia, nonketotic, EPC and, 71
Hyperglycinemia
ketotic, neonatal SE and, 506–507
nonketotic, neonatal SE and, 506
Hyperpyrexia, in GCSE, 61
Hypertension, in SE, 156–158
Hypertensive encephalopathy, neuroimaging features of, 181
Hyperthermia
historical background of, 3
with SE, 149, 150, 151
Hypnotics, withdrawal from, neonatal SE and, 507
Hypocalcemia, neonatal SE and, 505
Hypoglycemia, neonatal SE and, 505
Hypotension
avoiding, 497
drug-induced, 484–485
inhaled anesthetics and, 573
with phenobarbital, 558
phenytoin-induced, 541–542
with valproate, 566
Hypoventilation, drug-induced, 484
Hypoxic-ischemic encephalopathy, neonatal SE and, 503–504
Hypsarrhythmia, NCSE with, 126
I
Ictal activity, transition from interictal activity to, metabotropic receptors and, 310
Ideational apraxia, in CPSE, 78
Ideomotor apraxia, in CPSE, 78
Imaging studies. See Neuroimaging; specific imaging modalities
Immobile status epilepticus, 229–230, 239
time course of brain damage following, 232, 233
Impending status epilepticus, 11, 12, 13
Incidence of status epilepticus. See Epidemiology of status epilepticus
Infants. See also Neonatal entries
myoclonic epilepsy in, obtundation status epilepticus in, 127
Infections, neonatal SE and, 507
Inhaled anesthetics. See also Halothane; Isoflurane
for refractory SE, 572–574, 581, 611
adverse effects of, 573–574
animal models of seizures and, 572
clinical pharmacokinetics of, 572
clinical use of, 572–573
dosage and regimens for, 574
EEG effects of, 573
mechanisms of action of, 572
Inhibition. See GABAergic inhibition
Inhibitory postsynaptic potentials (IPSPs), 379
Initiation sites, 231–232
Injection site reactions, with valproate, 566
Interictal activity, transition to ictal activity from, metabotropic receptors and, 310
Intracranial hemorrhage, neuroimaging features of, 181
IPSPs (inhibitory postsynaptic potentials), 379
Isoflurane, 572. See also Inhaled anesthetics
for refractory SE, 611
Isovaleric acidemia, neonatal SE and, 507
K
Kainate receptors, 295
Kainic acid receptors, neuronal death related to, 367–368, 466
Kernicterus, neonatal SE and, 507
Ketamine, 496, 500
for convulsive SE, 516
neuroprotective effect of, 474
for refractory SE, 499, 611
Ketotic hyperglycinemia, neonatal SE and, 506–507
Kindling, 231–232, 399
in amygdala, 235
in perirhinal cortex, 235
in SSSE, 209
Kojewnikow syndrome. See Epilepsia partialis continua (EPC)
Kufs’ disease, in EPC, 71
L
Laboratory markers
CSF lactate as, 174
of SE-associated injury, 117, 173–174
cortisol as, 173–174
NAA as, 174
NSE as. See Neuron-specific enolase (NSE)
Laboratory testing, 599
Lactate, in CSF, as marker of neuronal injury, 174
Lamotrigine, to reduce incidence or severity of chronic epilepsy following SE, 434
Landau-Kleffner syndrome, 127
Language disturbances, in CPSE, 78
Lennox-Gastaut syndrome
hippocampal sclerosis in, 166
NCSE in, 126
tonic SE associated with, 14
Lethargic stupor, in ASE, 98
Leukemoid reactions, in SE, 151–152
Leukocyte demargination, in SE, 151–152
Levetiracetam, to reduce incidence or severity of chronic epilepsy following SE, 434
Lidocaine, 496
for convulsive SE, 516
for critical care, 607
for neonatal SE, 511
for refractory SE, 575–576, 581, 611–612
adverse effects of, 576
animal models of seizures and, 575
clinical pharmacokinetics of, 575–576
clinical use of, 576
EEG effects of, 576
mechanisms of action of, 575
Limbic encephalitis, paraneoplastic, neuroimaging features of, 183
Limbic regions, rostral, recruitment from, 242
Limbic status epilepticus, 239–251. See also Complex partial status epilepticus (CPSE)
early spread from highly restricted regions to restricted patterns, 241–243
epileptogenesis and, 426
forebrain generalization of, 246–251
highly restricted, 240–241
historical background of, 3
neuronal death and, 424, 425
spread to extensive limbic regions, 243–246
Lissencephaly, neuroimaging features of, 182
Local cerebral blood flow, SE effects on, in immature brains, 359–362
Locus ceruleus, modulation of seizure susceptibility by, 250
Long-term complications of status epilepticus, 118
Lorazepam, 495, 497, 498, 525. See also Benzodiazepines
chemical structure of, 525, 527
for convulsive SE, 516
for CPSE, 79
diazepam compared with, 496–497
for emergency department treatment of SE, 599–600
for GCSE, 485, 486
as initial treatment-6, 483
prehospital, 482
for neonatal SE, 510
neuroprotective effect of, 474–475
for out-of-hospital treatment of status epilepticus, 592, 593
pharmacokinetics of, 527, 528
pharmacology of, 592
rectal administration of, 531
M
Magnesium, for refractory SE, 578–580, 581
adverse effects of, 580
animal models of seizures and, 578, 579
clinical pharmacokinetics of, 578–579
clinical use of, 579–580
dosage and regimens for, 580
EEG effects of, 579
mechanisms of action of, 578
Magnetic resonance angiography, in CPSE, 192
Magnetic resonance imaging, 116
in ASE, 188, 189
in CPSE, 185–188, 194
in EPC, 189, 196–197
in ESES, 198
in GCSE, 178–179, 180, 183–184, 191, 195
in NCSE, 188, 189
in Ohtahara syndrome, 198
pathophysiological studies using, 177
structural brain lesion detection using, 178–179, 180, 181–184, 185–188, 189, 190
Magnetic resonance spectroscopy
in CPSE, 194
in EPC, 196, 197
in GCSE, 190, 191
in PLEDs, 199
Maple syrup urine disease, neonatal SE and, 506
Masticatory status epilepticus, 230–231, 239
time course of brain damage following, 233–234
Maximal dentate activation (MDA), 315
Mechanical ventilation, in critical care, 608
Medical complications, 117–118
MELAS syndrome
in EPC, 71
in GCSE, 178–179
Meningiomas, neuroimaging features of, 182
Meningitis, neuroimaging features of, 181
Mental regression, in ESES, 130
Metabotropic receptors, 295, 305–311
actions on excitotoxic brain damage, 309–310
agonists for, proconvulsant and anticonvulsant actions of, 307–308, 309
amygdaloid kindling in rat and, 309
antagonists for, proconvulsant and anticonvulsant actions of, 308–309
changes in, as consequence of SE, 310–311
classification of, 305–307
neuronal death related to, 466
pharmacologic approaches and, 307, 308
study methods for, 307
transition from interictal to ictal state and from seizures to SE and, 310
in in vitro models of epilepsy and SE, 309
Metastasis, cerebral, neuroimaging features of, 182
N-Methyl-D-aspartate (NMDA). See NMDA entries
Metrizamide, ASE associated with, 103
mGluRs. See Metabotropic receptors
Midazolam, 495, 498, 525. See also Benzodiazepines
buccal/sublingual administration of, 530–531
chemical structure of, 525, 527
for convulsive SE, 516
for emergency department treatment of SE, 600
for GCSE, 485, 486, 495, 497, 499
as initial treatment, 484
refractory, 488
intramuscular administration of, 531–532
intranasal administration of, 532
for neonatal SE, 510
for out-of-hospital treatment of status epilepticus, 593
pharmacokinetics of, 527, 528
pharmacology of, 591–592
rectal administration of, 531
for refractory SE, 610–611
as second-line agent, 496
Midbrain, dorsal, modulation of seizure susceptibility by, 248
Minor convulsive status epilepticus. See Masticatory status epilepticus
Minor epileptic status epilepticus, 126
MK-801, to reduce incidence or severity of chronic epilepsy following SE, 434–435
Morbidity, 36, 43–44
Morris water maze, 403
Mortality, 26, 27, 28, 34–36, 43, 118
with GCSE, 62–63
risk factors for
long-term, 35–36
short-term, 34–35
seizure duration related to, 119
short-term, 34
sudden death and, in SE, 158
time trends in, 36
Mossy fiber sprouting, 333, 413. See also Reactive synaptogenesis
electrophysiologic changes and, 452–454
epileptogenesis and, 429, 431, 432
neurotrophic factors and, 391, 395
visualized with Timm stain, time course following SE, 234–236
mRNA
BDNF, SE induction of expression in developing brain, 393, 394, 395
posttranslational editing for glutamate receptors, 296–297
Muscimol, seizure threshold and, 372, 373
Myoclonic-astatic epilepsy, NCSE in, 126
Myoclonic epilepsy, obtundation status epilepticus in, in infancy, 127
Myoclonic jerks, in EPC, 71–72
Myoclonic status epilepticus, 56, 127
diagnostic neuroimaging in, 184–185
epidemiology of, 115
treatment of, 564
Myoclonus
in ASE, 98
negative
ESES syndrome and, 128–130
NCSE with, 128
N
NAA. See N-Acetylaspartate (NAA)
NADH-coenzyme Q reductase deficiency, EPC and, 71
Narcotic withdrawal, neonatal SE and, 507
NCSE. See Nonconvulsive status epilepticus (NCSE)
N6-Cyclohexyladenosine (CHA), 318, 319
N6-Cyclopentyladenosine (CPA), 318
Necrosis, 468. See also Neuronal death
apoptosis versus, 331–333
Negative myoclonus
ESES syndrome and, 128–130
NCSE with, 128
Neocortex, SE originating from, 251
Neocortical status epilepticus, 251
Neonatal seizures, 135–142
classification of, 136–138
definition of SE and, 135
EEG and, 141–142
epidemiology of, 136
etiology of, 138–139
impact on prognosis, 139–140
predisposition to SE in, 135–136
treatment of, AEDs for, 140–141
Neonatal status epilepticus, 503–512
diagnosis of, 503, 508
EEG in, 503
neuroimaging in, 190
EEG in, 116
etiology of, 503–508
birth trauma and, 504
familial seizures and, 507
hypoxic-ischemic encephalopathy and, 503–504
kernicterus and, 507
metabolic, 505–507
toxins and, 507–508
outcome in, 511–512
prognosis of, 119
treatment of, 508–511
recommendation for, 511
Nerve growth factor (NGF), 389, 392. See also Neurotrophic factors
Neuroanatomy of status epilepticus, 239–258
anticonvulsant effects on, 255, 257
brain stem and, 251–252
status epilepticus originating from limbic sites and. See Limbic status epilepticus
status epilepticus originating from neocortex and, 251
subtle generalized status epilepticus and, 255, 258
temporal dynamics of territorial spread and, 252–255
Neurofibromatosis, neuroimaging features of, 182
Neurogenesis, of dentate gyrus, increase after ictal events, 333
Neuroimaging, 116, 177–200, 599
in CPSE, 78–79, 80
diagnostic
in CPSE, 185–190
in EPC, detection of structural brain lesions in diagnosis and, 189
in GCSE, 178–185
in myoclonic SE, 184–185
in NCSE, in elderly persons, 189
in neonatal SE, 190
in SPSE, nonmotor, putative diagnostic role of, 189–190
pathophysiology studied with, 190–199
in ASE, 195–196
in CPSE, 192–194
in encephalopathies associated with subclinical (electographic) SE, 197–199
in GCSE, 190–192
in SPSE, 196–197
in subclinical (electrographic) SE, 197
in syndromes following GCSE or CPSE, 194–195
Neurological abnormalities, as risk factor for status epilepticus, 42
Neurologic sequelae of status epilepticus, 399–400, 409–419. See also specific sequelae
animal models of TLE and, 409–410
developmental factors and, 417–419
mechanisms of SE-induced epileptogenesis and, 410–411, 413–415
SE duration and late development of epilepsy and, 415, 416
Neuromuscular junction blockade, for critical care, 607–608
Neuronal circuitry, neurotrophic factors and, 395
Neuronal damage, 339–345, 367–368, 400–401, 424, 425, 466
experimental data on, 340–344
extrahippocampal, 340
hippocampal, 340
markers of, 117
cortisol as, 173–174
CSF lactate as, 174
NAA as, 174
NSE as. See Neuron-specific enolase (NSE)
metabotropic receptor agonist actions on, 309–310
modulation during seizures, 158, 159
resembling mesial temporal sclerosis, 427–428
time course following SE, 232–236
in ambulatory SE, 232–233, 234
in GCSE, 234
in immobile SE, 232, 233
in masticatory SE, 233–234
sprouting visualized with Timm stain and, 234–236
Neuronal death. See also Apoptosis; Necrosis
axon sprouting as consequence of, 447
bcl-2 gene family and, 158–159
evidence for, 463–464
manipulation of cell-death-promoting or cell-death-inhibiting proteins and, 474
mechanisms of, 464, 466–468
AMPA receptor antagonists and, 468
excitotoxic hypothesis and, 466
NMDA receptor antagonists and, 466–468
neuroprotective strategies and, 470–475
blockade of pre- and postsynaptic neuronal depolarization with sodium channel blockers as, 473
blockade of presynaptic calcium-dependent, vesicular glutamate release as, 473
brief antecedent seizures as neuroprotectants and, 474
cell-permeant calcium chelators as, 472
growth factors as, 473
inhibition of calcium-sensitive proteases and lysosomal cathepsins as, 472–473
inhibition of poly (ADP-ribose) polymerase-1 as, 474
manipulation of cell-death-promoting or cell-death-inhibiting proteins as, 474
platelet-activating factor antagonists as, 473
postsynaptic blockade of calcium influx as, 472
postsynaptic glutamate receptor blockade as, 472
reduction of calcium-independent, sodium-dependent glutamate release as, 473
reduction of postsynaptic free radical generation as, 472
suggested first approach for, 474–475
region-specific, 391
time course of, 464, 465
types of, 468–470
Neuron-specific enolase (NSE), 169–173
detection of, 169
epileptic control values for, 170
in individual seizures, 171
limitations of, 174
as marker for neuronal injury, 117, 170–171
measurement of neurologic damage by, 340
mechanism of release of, 173
normal values of, 169–170
in SE, 171–173
in CPSE-5, 172
in NCSE, 172
Neuropeptides, in SSSE, 221–224
Neuroprotection. See also Neuronal death, neuroprotective strategies and
by glutamate antagonists, 298–299
by neurotrophic factors, 393, 395
by phenobarbital, 557
Neuropsychological testing, in ASE, 96–97
Neurosurgery, for refractory SE, 612
Neurotrophic factors, 389–396
neuromodulatory functions of, 390
to prevent axon sprouting, 414
receptors for, 390
seizure-induced expression of
in adult brain, 391–393
in developing brain, 393, 394, 395
functions of, 393, 395–396
structural changes in brain following SE and, 391
NGF (nerve growth factor), 389, 392. See also Neurotrophic factors
Nimodipine, neuroprotective effect of, 472
Nitrous oxide (NO), 318
NMDA, inhaled anesthetics and, 572
NMDA receptor(s), 295, 305
antagonists of, protective role of, 298–299
excitotoxicity and, 367, 368
hippocampal damage and, in PPS model, 342
neuronal death related to, 466–468
propofol and, 569
reactive synaptogenesis and, 450, 451
in SSSE, 213, 217–218, 220
NMDA receptor antagonists
neuroprotection by, 472
neuroprotective effect of, 473, 474
NO (nitrous oxide), 318
Nonconvulsive simple partial status epilepticus. See Simple partial status epilepticus (SPSE), nonconvulsive
Nonconvulsive status epilepticus (NCSE), 24, 55–56, 125–132
absence. See Absence status epilepticus (ASE)
clinical manifestations of, 125
complex partial. See Complex partial status epilepticus (CPSE)
confusional, 91
diagnostic neuroimaging in, 188–190
in elderly persons, 189
EEG in, 117
electrographic, 109–112
in ambulatory patients, 109–110
in comatose inpatients, 110–112
epidemiology of, 41
ESES syndrome. See Electrographic status epilepticus during slow-wave sleep (ESES) syndrome
frontal, 82, 83, 84
generalized. See Generalized nonconvulsive status epilepticus (GNCSE)
with hypsarrhythmia, 126
Landau-Kleffner syndrome, 127
nonconfusional, 91
NSE in, 172
obtundation, in severe myoclonic epilepsy in infancy, 127
partial
complex (focal). See Complex partial status epilepticus (CPSE)
simple. See Simple partial status epilepticus (SPSE), nonconvulsive
treatment of, 518–519
treatment of, 517–519, 564
Nonketotic hyperglycinemia, neonatal SE and, 506
Norepinephrine, elevation of, vasoconstriction and, 151
NSE. See Neuron-specific enolase (NSE)
O
Obtundation status epilepticus, in severe myoclonic epilepsy, in infancy, 127
Ohtahara syndrome, 507
neuroimaging studies of, 198
Olfactory bulb, status epilepticus originating from, 240
Oligodendromas, neuroimaging features of, 182
Open field test, 403
Opioid peptides, endogenous, in SSSE, 221, 222
Opioid receptors, 318
Outcome of status epilepticus, 27–28
Out-of-hospital treatment, 591–593
clinical studies of, 592–593
pharmacology of agents used for, 591–592
P
Pallidum, ventral, modulation of seizure susceptibility by, 248
Pancreatitis, with valproate, 566
Paraldehyde
for convulsive SE, 516
for GCSE, 495
for refractory SE, 576–578, 581
adverse effects of, 577
animal models of seizures and, 576–577
clinical pharmacokinetics of, 577
clinical use of, 577
dosage and regimens for, 577–578
mechanisms of action of, 576
as second-line agent, 496
Past history of epilepsy, as etiologic factor, 26
PEDs. See Periodic eplileptiform discharges (PEDs)
Pentobarbital, 500
for emergency department treatment of SE, 601
enhancement of GABAA receptor currents from rats undergoing SE, 275–276
for GCSE, 485, 486, 495
as initial treatment, 484
refractory, 487
for refractory SE, 499, 610
as second-line agent, 496
Pentothal, as second-line agent, 496
Perforant path stimulation (PPS) model
circuit modifications resulting from SE in, 428–429
epileptogenicity and, 423
neuronal damage and, 341–342, 343, 344
of SSSE, 210–214
Periaqueductal gray, modulation of seizure susceptibility by, 249
Periodic eplileptiform discharges (PEDs)
in GCSE, 58, 61
generalized, in electrographic SE, 112
Perirhinal cortex
as kindling structure, 235
spread of SE to extensive limbic regions from, 243–244
Perisylvian malformation, bilateral, neuroimaging features of, 182
Pertussis toxin (PTX), 318
Petit mal status epilepticus, 91–92, 126. See also Absence status epilepticus (ASE)
historical background of, 3
Pharmacoresistance, development of, 272–273
Phenobarbital, 496–497, 553–559
adverse effects of, 484, 558–559
chemistry of, 553–554
for convulsive SE, 516
dosage and clinical use of, 556–557
efficacy in SE, 555–556, 557
for emergency department treatment of SE, 601
for GCSE, 485, 486, 495, 497, 499
as initial treatment, 6, 483
mechanism of action of, 553, 554
for neonatal SE, 509
neuroprotective effects of, 557
pharmacokinetics of, 554–555
to reduce incidence or severity of chronic epilepsy following SE, 435
for refractory SE, 610
as second-line agent, 496
Phenytoin, 496, 539–542. See also Diazepam-phenytoin
adverse effects of, 484, 485
animal studies of, 550
for convulsive SE, 516
dosing for, 541
for emergency department treatment of SE, 600
fosphenytoin as alternative to, 494–495, 498, 542
for GCSE, 485, 486, 497
for continuing care, 487
as initial treatment, 6, 483
mechanism of action of, 539
for neonatal SE, 509–510
for out-of-hospital treatment of status epilepticus, 593
parenteral, 540–541, 545
Phenytoin (continued)
pharmacoeconomic studies of, 550–551
pharmacoresistance in SSSE and, 213–214
to reduce incidence or severity of chronic epilepsy following SE, 435
as second-line drug, 495–496
time course of action of, 539–540
toxicity of, 541–542
Phlebitis, drug-induced, 485
Physiologic responses to status epilepticus, 149–159. See also specific responses
Piriform cortex
central, spread of SE to extensive limbic regions from, 245
deep anterior, spread of SE to extensive limbic regions from, 245
spread of SE to extensive limbic regions from, 244–245
Platelet-activating factor (PAF) antagonists, neuroprotective effect of, 473
PLEDs (pseudoperiodic lateralized epileptiform discharges), neuroimaging studies of, 198–199
Polymicrogyria, focal, neuroimaging features of, 182
Poly(ADP-ribose) polymerase-1, inhibition of, neuroprotective effect of, 474
Pontine reticular formation, modulation of seizure susceptibility by, 248
Porencephaly, neuroimaging features of, 181
Positron-emission tomography
in ASE, 195–196
in CPSE, 192, 193, 194
in electrographic SE, 196
in EPC, 196
in ESES, 198
pathophysiological studies using, 177
in PLEDs, 198
in SPSE, 196
Postsynaptic receptors, reactive synaptogenesis and, 449–452
PPE (preproenkephalin), 383–384, 385
PPS model. See Perforant path stimulation (PPS) model
P75 receptors, in cell death regulation, 390
Precipitating factors, for CPSE, 77
Pregabalin, to reduce incidence or severity of chronic epilepsy following SE, 435
Prehospital treatment, 597–598
Preproenkephalin (PPE), 383–384, 385
Primates, nonhuman, cell death in, 341
Primidone, for neonatal SE, 510–511
Procaine derivatives, neonatal SE and, 507
Prognosis of status epilepticus, 118–119
of CPSE, 80–82
of ESES, 131, 132
after first episode, 33–37
incidence of SE and, 34
morbidity and, 36
mortality and, 34–36
recurrence of SE and, 36–37
Rochester, Minnesota study of, 33
impact of neonatal seizures on, 139–140
neonatal, 119
Propofol
for convulsive SE, 516
for CPSE, 79
for emergency department treatment of SE, 601
for GCSE, 485, 486, 495
as initial treatment, 484
refractory, 488–489
for out-of-hospital treatment of status epilepticus, 593
pharmacology of, 592
for refractory SE, 499, 569–572, 581, 611
adverse effects of, 571–572
animal models of seizures and, 569–570
clinical pharmacokinetics of, 570
clinical use of, 570–571
dosage and regimens for, 571–572
EEG effects of, 571
mechanisms of action of, 569
as second-line agent, 496
Propofol infusion syndrome, 498, 500
Propylene glycol, phenytoin toxicity due to, 541
Pseudoperiodic lateralized epileptiform discharges (PLEDs), neuroimaging studies of, 198–199
Psychiatric manifestations, in ASE, 99
Psychotropic medications, ASE associated with, 102–103
p53 tumor-suppressor gene, apoptosis and, 469
PTX (pertussis toxin), 318
Pulmonary vascular hypertension, in SE, 156–158
Purple glove syndrome, 485, 494, 541
Pyramidal cell damage, in PPS model, 342
Pyridoxine
for convulsive SE, 516
dependency of, neonatal SE and, 505–506
Q
Quality of care, 615–618
assessment of, 615–616
intervention research to improve, 616–618
research agenda for, 619
R
Race, as risk factor for status epilepticus, 42–43
Radioimmunoassay (RIA), for NSE detection, 169
Raphe nucleus, dorsal, modulation of seizure susceptibility by, 250
Rasmussen's encephalitis, 72–73
neuroimaging features of, 181
pathophysiology of, neuroimaging studies of, 196
Rat, as subject for study, 340
Reactive synaptogenesis, 441–454
axon and dendritic responses to partial synaptic loss and, 441–443
collateral sprouting and, 442
denervation-renervation process and, 443
in fascia dentata, 443–454
axon sprouting as consequence of SE-induced neuronal loss and, 447–449
functional consequences of, 449–454
loss of neuron following SE and, 447
mechanisms influencing axon sprouting and, 448, 449, 450
normal anatomy and, 443–447
paraterminal sprouting and, 443
Recurrent status epilepticus, 23, 36–37
convulsive, 119
epidemiology of, 47
prevention of, in GCSE, 487
Refractory status epilepticus
critical care for, 609–612
treatment of, 498, 499, 569–582
etomidate for, 570, 574–575, 581
focal perfusion of antiepileptic drugs and, 580–581, 582
furosemide for, 580, 581
inhaled anesthetics for, 572–574, 581
lidocaine for, 575–576, 581
magnesium for, 578–580, 581
paraldehyde for, 576–578, 581
propofol for, 569–572, 581
Research
on adenosine, future directions for, 320
on emergency department treatment, future directions for, 602
future directions for, 621–622
intervention, to improve quality of care, 616–618
on quality of care, agenda for, 618–619
Respiratory depression
phenobarbital and, 558
propofol and, 571
Retrograde amnesia, in CPSE, 78
RIA (radioimmunoassay), for NSE detection, 169
Rocuronium, for critical care, 608
S
Schizencephaly, neuroimaging features of, 181
Seizure(s)
antecedent, as neuroprotectants, 474
first, SE as, 45
prior, as risk factor for status epilepticus, 42
Seizure duration
definition of status epilepticus based on
clinical basis for, 11–12
experimental basis for, 12–13
GABAA antagonists and, 315
mortality related to, 119
Seizure susceptibility, 379–384
age-related differences in, mechanisms responsible for, 401–403
delayed cell death and. See Cell death, delayed
factors involved in age-dependent seizure-induced damage and, 380
increased, in immature brain, 379–380
resistance of immature brain to seizure-induced neuronal cell loss and, 380, 381
Seizure termination
in critical care, 609, 610
GABAergic mechanisms in, 315
Seizure types, 23–24, 28, 41
correlation with etiology, 41
mortality related to, 36
Self-sustaining status epilepticus (SSSE), 209–225
GABA receptors and, 213, 214–217, 219
maintenance of, 212
mechanism of transition from isolated seizures to SE and, 214–217, 219
mechanisms of, 224–225
models of, 209–214
neuronal circuitry subserving, 218, 220–221
autoradiographic studies using 2-DG and, 221
electrographic mapping of, 218, 220
immunostaining for fos protein and, 220
neuropeptides in, 221–224
NMDA receptors and, 213, 217–218, 220
NMDA receptor trafficking, synaptic potentiation, and maintenance phase of, 217–218, 220
ontogeny of, 224
pharmacologic distinctiveness of two phases of, 212–213
threshold for initiation of, 210–212
time-dependent development of pharmacoresistance and, 213–214
Semiologic classification of status epilepticus, 13, 14–15
description of seizure type and, 14–15
description of type of SE and, 14
Sensory seizures, 14–15
Simple partial status epilepticus (SPSE), 69–75, 114, 127
clinical forms intermediate between CPSE and, 82–83
convulsive, 69–73
epilepsia partialis continua, 70–73
somatomotor, 69–70, 71
nonconvulsive, 73–75
with affective symptoms, 75
auditory, 74
with cognitive symptoms, 74–75
somatosensory, 74
with vegetative symptoms, 74
visual, 74
nonmotor, diagnostic neuroimaging in, putative diagnostic role of, 189–190
pathophysiology of, neuroimaging studies of, 196–197
Single-photon emission computed tomography, 116
in CPSE, 192
in Ohtahara syndrome, 198
pathophysiological studies using, 177
in PLEDs, 198
in SPSE, 196
structural brain lesion detection using, 190
SNC (substantia nigra pars compacta), 371, 372
SNL (substantia nigra pars lateralis), 371
SNR. See Substantia nigra pars reticulata (SNR)
Sodium channel blockers, blockade of pre- and postsynaptic neuronal depolarization with, 473
Solitary tract, nucleus of, modulation of seizure susceptibility by, 250
Somatomotor simple partial status epilepticus, 69–70, 71
Somatosensory nonconvulsive simple partial status epilepticus, 74
SP (substance P), endogenous, 224
Spike-wave index, in ESES, 130
Spike-wave stupor, 91, 126. See also Absence status epilepticus (ASE)
pathophysiology of, neuroimaging studies of, 196
Spontaneous seizures, fascia dentata synaptic reorganization and, 452
Spread of status epilepticus
to extensive limbic regions, 243–246
from amygdala, 243
from claustrum, 244
from endopiriform nucleus, 245
from perirhinal cortex, 243–244
from piriform cortex, 244–245
role of thalamic nuclei in, 245–246
between forebrain and brain stem, 252
temporal dynamics of, 252–255
SPSE. See Simple partial status epilepticus (SPSE)
SSSE. See Self-sustaining status epilepticus (SSSE)
Staring status epilepticus. See Immobile status epilepticus
Striatum, modulation of seizure susceptibility by, 248
Stupor, lethargic, in ASE, 98
Sturge-Weber syndrome, neuroimaging features of, 182
Substance P (SP), endogenous, 224
Substantia nigra pars compacta (SNC), 371, 372
Substantia nigra pars lateralis (SNL), 371
Substantia nigra pars reticulata (SNR), 371–375
anatomy and connectivity of, 371–372
developmental profile of “anticonvulsant” region of, 374–375
modulation of seizure susceptibility by, 247–248
role in seizures in adult animals, 372–374
role in seizures in young animals, 374
Subthalamus, modulation of seizure susceptibility by, 248
Succinylcholine, for critical care, 607–608
Sudden death, in SE, 158
Synaptic connections, SE effects on, 342–343
Synaptic plasticity, in adult brain, 400
Synaptogenesis, reactive. See Reactive synaptogenesis
T
Tachykinins, endogenous, 224
Tegmental reticular nucleus, laterodorsal, modulation of seizure susceptibility by, 249
Temporal lobe epilepsy (TLE)
animal models of, 409–410
hippocampal GABAA receptors and, 277
mesial
evolution to, 119
with hippocampal sclerosis, following GCSE or CPSE, neuroimaging studies in, 194–195
with mesial temporal sclerosis, following febrile seizures, 339
natural history of, 410, 411, 412
SE in, 166, 167
Temporal sclerosis, mesial
following SE, 425–426
patterns of neuronal injury resembling, 427–428
with prolonged febrile seizures, 45–46
temporal lobe epilepsy with. See Temporal lobe epilepsy (TLE), with mesial temporal sclerosis
4,5,6,7-Tetrahydroisoxazolo[5,5-c]pyridin-3-ol (THIP), seizure threshold and, 372, 373
Thalamic nuclei, role in SE spread, 245–246
Thalamus, modulation of seizure susceptibility by, 247
Theophylline, proconvulsant effects of, 318
Thiopental
for convulsive SE, 516
for critical care, 607
for GCSE, 495
refractory, 487
for neonatal SE, 511
for refractory SE, 610
as second-line agent, 496
THIP (4,5,6,7-tetrahydroisoxazolo[5,5-c]pyridin-3-ol), seizure threshold and, 372, 373
Thrombocytopenia, with valproate, 566
Tiagabine, nonconvulsive SE associated with, 518
Tissue necrosis, drug-induced, 485
TLE. See Temporal lobe epilepsy (TLE)
Todd's paresis, 82
Tonic status epilepticus
associated with Lennox-Gastaut syndrome, 14
treatment of, 518
Topiramate
to reduce incidence or severity of chronic epilepsy following SE, 435
for refractory SE, 612
Toxicity. See also specific drugs
of valproate, 565–566
Treatment of status epilepticus, 515–520. See also specific drugs and types of status epilepticus
acute changes in, 270, 272–273
during acute period, 436
benzodiazepines for, choice of, 495, 497–498
for convulsive SE, 515–517
critical care and. See Critical care
emergency, for CPSE, 79
in emergency department. See Emergency department treatment
future of, 622
general anesthesia for, choice of, 498, 500
hydantoins for, comparison of, 498
initial
choice of benzodiazepine for, 495, 497–498
fosphenytoin versus phenytoin for, 494–495
one versus two drugs for, 494, 497
protocols for, 495
initiation of, 482–484
dosing considerations for, 482
in hospital, controlled clinical trials of, 482–483
uncontrolled case studies of, 483–484
VA cooperative study of, 483
during latent period, 436
for neonatal seizures, AEDs for, 140–141
in neonates, 508–511
for nonconvulsive SE, 517–519
out-of-hospital, 591–593
clinical studies of, 592–593
pharmacology of agents used for, 591–592
prehospital, 532–533, 597–598
for refractory SE, 609–612
therapeutic algorithms for, 496–500
therapeutic attitudes and, 493–496
initial treatment of GCSE and, 494–495
management of treatment failures and, 495–496
operational definition of SE for therapeutic purposes and, 493–494
timing of, 515
for treatment failures, 495–496
second-line drugs for, 495–496
vigor of, 496
Tuberous sclerosis, neuroimaging features of, 183
Tyrosine kinases, as neurotrophic factor receptors, 390
U
Ulegyria, neuroimaging features of, 181
Unilateral status epilepticus, clinical classification of, 13
Urea cycle abnormalities, neonatal SE and, 506
V
Vagal nerve stimulation, for refractory SE, 612
Valproate, 496, 561–566
ASE associated with, 103
for convulsive SE, 516
dosage and administration of, 565
efficacy in SE, 562–565
adult studies of, 562–564
pediatric studies of, 564–565
for emergency department treatment of SE, 601
for GCSE, 485, 497, 499
refractory, 489
indications for, 561
mechanism of action of, 561
for myoclonic SE, 564
for nonconvulsive SE, 564
for out-of-hospital treatment of status epilepticus, 593
rapid infusions of, tolerability of, 562
to reduce incidence or severity of chronic epilepsy following SE, 435
for refractory SE, 498, 499, 612
safety trials of, 561–562
side effects of, 565–566
Valproic acid, for neonatal SE, 511
Vasoconstriction, in SE, 151
Vecuronium, for critical care, 608
Vegetative signs, in CPSE, 78
Vegetative symptoms, nonconvulsive SPSE with, 74
Ventromedial thalamus, role in SE spread, 246
Vigabatrin, to reduce incidence or severity of chronic epilepsy following SE, 435
τ-Vinyl GABA (GVG), seizure threshold and, 372, 373
Visual hallucinations, in CPSE, 78
Visual nonconvulsive simple partial status epilepticus, 74
W
Waxing-and-waning seizures, 252, 253
West's syndrome, historical background of, 3
Z
ZAPA ([Z]-3-[(aminoiminomethyl)thio] prop-2-enoic acid), seizure threshold and, 372, 373
Zinc
diminished sensitivity of GABAA receptor currents from rats undergoing SE, 275, 276
GABAA receptor current reduction by, 270, 271
Zolpidem, GABAA receptor current enhancement by, 269–270, 271
