ライフサイエンスコーパス: epileptiform

1 Smartphone Brain Scanner-2 (SBS2), to detect epileptiform abnormalities compared to standard clinical

2 between cortisol levels and the incidence of epileptiform abnormalities in the electroencephalogram o

3 a viable supportive test for the capture of epileptiform abnormalities, and extend EEG access to new

4 izures before remission, focal seizures, and epileptiform abnormality on EEG before withdrawal.

5 epilepsy syndrome, developmental delay, and epileptiform abnormality on electroencephalogram (EEG) b

6 8, 1.05-1.11), electroencephalogram results (epileptiform abnormality vs normal, 1.26, 1.07-1.50), se

7 t to inhibit action potential generation and epileptiform activities in vitro.

8 ivity of Pv interneurons enhances or opposes epileptiform activities.

9 rcuits govern generation and spread of focal epileptiform activities.

10 tivity is a condition in which lights induce epileptiform activities.

11 myoclonus, less frequently in myoclonus with epileptiform activity (2% vs 15%; p < 0.001).

12 ound activity (unsynchronized oscillations), epileptiform activity (highly synchronized oscillations)

13 ation of seizure onset, bilateral interictal epileptiform activity (p = 0.017), secondary generalizat

14 ersistent increases in spontaneous bursts of epileptiform activity (spike-wave discharges) that occur

15 The long-lasting epileptiform activity after CTZ washout may also make it

16 Patients with AD who had subclinical epileptiform activity also had an early onset of cogniti

17 omes, usually in patients without associated epileptiform activity and after prolonged hospitalizatio

18 ital malformations, intellectual impairment, epileptiform activity and autism spectrum disorder.

19 hat VU0422465 is an agonist PAM that induces epileptiform activity and behavioral convulsions in rode

20 c levels can significantly attenuate ongoing epileptiform activity and prophylactically dampen subseq

21 electrographic biomarkers in the absence of epileptiform activity and provide a potential network co

22 K(+)-ATPase alpha3 isoform in the control of epileptiform activity and seizure behavior.

23 he band heterotopia in generating interictal epileptiform activity and seizures in brains with SBH.

24 rious neurological disorders associated with epileptiform activity and seizures.

25 ippocampal infusion of Zn(2+) elicited rapid epileptiform activity and significantly blocked the anti

26 of synaptic conductances from neurons during epileptiform activity and then replayed them in pharmaco

27 kinase 2 (Plk2) was induced during prolonged epileptiform activity and was required for the activity-

28 ung adult male rats and mice, we report that epileptiform activity at CA3-CA1 synapses, generated by

29 s supported by our finding that synaptic and epileptiform activity at SynII(-) and wild-type synapses

30 and a reduced threshold for the induction of epileptiform activity by 4-aminopyridine (4-AP).

31 e studies have shown that chemically induced epileptiform activity can lead to elevated astrocytic Ca

32 strong activation of GABAergic inputs during epileptiform activity can switch GABA(A) receptor (GABA(

33 At the time of monitoring, AD patients with epileptiform activity did not differ clinically from tho

34 followed by prolonged suppression of ongoing epileptiform activity during light exposure.

35 dazolam or normocapnia, the risk of inducing epileptiform activity during spontaneous respiration is

36 Epileptiform activity evoked by zero Mg(2+) incubation d

37 followed by local inflammatory response and epileptiform activity ex vivo.

38 The avalanches collected during interictal epileptiform activity had not only a stereotypical size

39 Inhibition of epileptiform activity has been demonstrated in hippocamp

40 e upon loss of the eyelash reflex to prevent epileptiform activity has not been shown to reduce the r

41 oencephalography demonstrated myoclonus with epileptiform activity in 209 of 374 (55%), including sta

42 ut electroencephalography demonstrated ictal epileptiform activity in 7 patients (24%).

43 Extended monitoring detects subclinical epileptiform activity in a substantial proportion of pat

44 Here, we sought to identify the origin of epileptiform activity in a targeted genetic model of SBH

45 However, the incidence of subclinical epileptiform activity in AD and its consequences are unk

46 ed higher than expected rates of subclinical epileptiform activity in AD with deleterious effects on

47 Kbeta4 was sufficient to normalize excessive epileptiform activity in an in vitro model of seizure ac

48 to mediate the majority of SST inhibition of epileptiform activity in CA1.

49 cally, it has also been reported to increase epileptiform activity in clinical and experimental studi

50 xacerbated behavioral deficits and increased epileptiform activity in hAPP mice.

51 Here we report that CTZ induces robust epileptiform activity in hippocampal neurons both in vit

52 maintain synapses in a plastic state during epileptiform activity in hippocampal slice cultures.

53 regulating synaptic strengthening following epileptiform activity in hippocampal slices.

54 togenetics and study their impact on ongoing epileptiform activity in mouse acute hippocampal slices.

55 und that tau reduction prevented spontaneous epileptiform activity in multiple lines of hAPP mice.

56 d molecules in the dentate gyrus and CA1 and epileptiform activity in parietal cortex.

57 hyperactivity states in general, and during epileptiform activity in particular, is unclear.

58 Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disea

59 izure onset zone, suggesting that interictal epileptiform activity in patients with epilepsy is not a

60 Igf2(-/-) mice exhibited attenuated epileptiform activity in response to KA and were less su

61 lar mechanism, has been reported to increase epileptiform activity in several clinical and experiment

62 minant-negative SNARE domain in mice reduced epileptiform activity in situ, delayed seizure onset aft

63 mes inhibitory with maturation and can block epileptiform activity in the adult brain.

64 alpha(2) adrenergic receptors (ARs) inhibits epileptiform activity in the hippocampal CA3 region.

65 y associated with synaptic transmission, but epileptiform activity in the hippocampus can propagate w

66 ultures with CTZ (5 microM, 48 h) results in epileptiform activity in the majority of neurons (80%).

67 enesis of periods of network 'up' states and epileptiform activity in the neocortex.

68 (LFS) is an alternative tool for controlling epileptiform activity in these patients.

69 stitute a primary origin for interictal-like epileptiform activity in vitro and is dispensable for ge

70 Here, we have taken advantage of a model of epileptiform activity in vitro to quantify the charge tr

71 cytes is not necessary for the generation of epileptiform activity in vitro, although we cannot exclu

72 e to 4-aminopyridine (4-AP)-induced seizures/epileptiform activity in vivo and in vitro and investiga

73 Epileptiform activity induced by high potassium and low

74 and chronically epileptic rats and find that epileptiform activity is associated with increased synap

75 Synaptic strengthening produced by epileptiform activity may contribute to seizure progress

76 Because mounting evidence suggests that epileptiform activity may play an important role in the

77 inhibition suppresses action potentials and epileptiform activity more robustly than perisomatic inh

78 olazine was able to significantly reduce the epileptiform activity of the neuronal cultures, suggesti

79 acterised by several seizure types, frequent epileptiform activity on EEG, and developmental slowing

80 evidence argues against the hypothesis that epileptiform activity per se contributes to focal brain

81 robust release of glutamate during sustained epileptiform activity requires that neurons be provided

82 These abnormalities resemble the epileptiform activity seen in children with Batten disea

83 However, patients with subclinical epileptiform activity showed faster declines in global c

84 the TGF-beta pathway by TGF-beta1 results in epileptiform activity similar to that after exposure to

85 ffusion coupling is crucial for establishing epileptiform activity similar to that generated experime

86 port key features of AD-related seizures and epileptiform activity that are instructive for clinical

87 ne reduces hippocampal cornu ammonis 3 (CA3) epileptiform activity through alpha(2) adrenergic recept

88 l lobes or the effects of the propagation of epileptiform activity through the network of brain regio

89 nanolone reverted the threshold for inducing epileptiform activity to virgin levels.

90 inhibitory effect of EPI on hippocampal CA3 epileptiform activity uses an alpha(2A)AR/Galpha(o) prot

91 xamination (3.9 points/year in patients with epileptiform activity vs 1.6 points/year in patients wit

92 Subclinical epileptiform activity was assessed, blinded to diagnosis

93 where the occurrence of interictal and ictal epileptiform activity was confirmed by either stereo-ele

94 Subclinical epileptiform activity was detected in 42.4% of AD patien

95 Epileptiform activity was induced by arterial perfusion

96 The inhibition of epileptiform activity was less pronounced if only parval

97 Consistent with this, epileptiform activity was observed in hippocampal and co

98 Hippocampal CA3 epileptiform activity was then examined using field pote

99 orders characterized by seizures, interictal epileptiform activity with a disorganized electroencepha

100 The algorithm identified epileptiform activity with high fidelity compared to vis

101 od for quantification of multiple classes of epileptiform activity within the murine EEG and is tunab

102 TTX blocked both ictal- and interictal-like epileptiform activity without affecting SICs or SIC-medi

103 At low levels of KA, generating epileptiform activity without seizures, we indeed found

104 rger doses and sevoflurane appear to support epileptiform activity, although the clinical significanc

105 titative electrographic biomarkers free from epileptiform activity, and provide a potential network c

106 uoronorepinephrine caused a reduction of CA3 epileptiform activity, as measured by decreased frequenc

107 Although both models trigger epileptiform activity, astrocytic Ca2+ oscillations were

108 The devices detect normal physiologic and epileptiform activity, both in acute and chronic recordi

109 wnregulation of membrane excitability during epileptiform activity, but also unmasked a slow and prog

110 bility that, rather than being initiators of epileptiform activity, fast ripples may be markers of a

111 separate experiments, during high-K+ induced epileptiform activity, glutamine (0.5 mM) did not affect

112 GABA delivery stopped epileptiform activity, recorded simultaneously and coloc

113 ainly in neuronal ictal- and interictal-like epileptiform activity, respectively.

114 gies as well as beta-amyloid (Abeta)-induced epileptiform activity, some of the mechanisms that event

115 By contrast, we detected no epileptiform activity, spontaneous behavioral seizures,

116 igate this paradox during realistic neuronal epileptiform activity, we developed a method, activity c

117 Using in vitro and in vivo models of epileptiform activity, we show that acutely increasing O

118 By opposing synaptic strengthening caused by epileptiform activity, we suggest that neuregulin may re

119 astrocytes are observed to alkalinize during epileptiform activity, whereas neurons are observed to a

120 hibit distinct pH dynamics during periods of epileptiform activity, which has relevance to multiple p

121 that Sema4D rapidly and dramatically alters epileptiform activity, which is consistent with a Sema4D

122 circuit dynamics underlie this phase of the epileptiform activity.

123 hood substantially delayed the appearance of epileptiform activity.

124 ty and changes in GABAergic signaling during epileptiform activity.

125 information about interictal or sub-clinical epileptiform activity.

126 EEG at detecting interictal and subclinical epileptiform activity.

127 ed a burst-suppression pattern or multifocal epileptiform activity.

128 h neurotransmitter glutamate during enhanced epileptiform activity.

129 used voltage-clamp waveforms that replicated epileptiform activity.

130 nhanced excitatory synaptic connectivity and epileptiform activity.

131 onal changes and prevented the generation of epileptiform activity.

132 e of synaptic responses and plasticity after epileptiform activity.

133 M-channels is critical to its inhibition of epileptiform activity.

134 n paired-pulse responses and high-K+ induced epileptiform activity.

135 e specific alpha(2)AR subtype inhibiting CA3 epileptiform activity.

136 uppression of hypersynchrony associated with epileptiform activity.

137 auing or regression associated with frequent epileptiform activity.

138 the second action potential in each burst of epileptiform activity.

139 cute ex vivo rat hippocampal slice models of epileptiform activity.

140 r avalanches, particularly during interictal epileptiform activity.

141 brain dynamics, particularly during abnormal epileptiform activity.

142 ions at the transition from resting-state to epileptiform activity.

143 ors almost completely abolished this form of epileptiform activity.

144 nation for the paradoxical effects of CBZ on epileptiform activity.SIGNIFICANCE STATEMENT The effects

145 mGlu1 ago-PAMs/PAMs do not possess the same epileptiform adverse effect liability as mGlu5 ago-PAMs/

146 nule cell paired-pulse inhibition, decreased epileptiform afterdischarge durations during 8 hours of

147 eals a clinically underappreciated burden of epileptiform and epileptic activity in patients with pri

148 the direction of pH change, the kinetics of epileptiform-associated intracellular pH transients are

149 hich blocks inhibitory GABA(A) receptors, an epileptiform burst consisting of a series of PSs was evo

150 Taken together, our data suggest that epileptiform burst firing generated in the CA3 region by

151 itical role in the generation of spontaneous epileptiform burst firing in cornu ammonis (CA) 3 pyrami

152 with long-form Homers enhanced mGluR-induced epileptiform burst firing in wild-type (WT) animals, rep

153 arizing plateau potential that underlies the epileptiform burst firing induced by metabotropic glutam

154 were classified as isoelectric, low voltage, epileptiform, burst-suppression, diffusely slowed, or no

155 esis was based on the finding that prolonged epileptiform bursting (repetitive bursts of prolonged de

156 mice, and contributes to the development of epileptiform bursting activity in the TSC2(+/-) CA3 regi

157 xposure to 10 mM potassium chloride produced epileptiform bursting and potentiation of CA1 synapses a

158 that TRPC1/4 double-knockout (DKO) mice lack epileptiform bursting in lateral septal neurons and exhi

159 dependence to LTD, and significantly reduces epileptiform bursting in TSC2(+/-) hippocampal slices.

160 Interestingly, epileptiform bursting induced by agonists for metabotrop

161 2DG (10mM) reduced interictal epileptiform bursts induced by 7.5mM [K(+)](o), 4-aminop

162 onged activation of GABA(A) receptors during epileptiform bursts may even initiate a shift in GABAerg

163 Epileptiform bursts with an underlying plateau potential

164 se using recordings of mouse hippocampal CA3 epileptiform bursts.

165 also reduced the EPI-mediated inhibition of epileptiform bursts.

166 asured by decreased frequency of spontaneous epileptiform bursts.

167 of epilepsy in vitro by comparing GABAergic epileptiform currents and their sensitivity to gap junct

168 d amplitude, frequency and half-width of the epileptiform currents both in wild-type and in knockout

169 Furthermore, epileptiform currents propagated similarly across hippoc

170 leculare interneurons from knockout animals, epileptiform currents were not eliminated.

171 pectomy (ATL), but the utility of interictal epileptiform discharge (IED) identification and its role

172 Furthermore, mutant LGI1 promoted epileptiform discharge in vitro and kindling epileptogen

173 c currents with strikingly long duration and epileptiform discharge patterns, similar to waveforms ob

174 glutamatergic neurons resulted in recurrent epileptiform discharge, which provoked cognitive dysfunc

175 itute a trigger for pathological synchronous epileptiform discharge.

176 ); (3) prior seizure (1 point); (4) sporadic epileptiform discharges (1 point); (5) frequency greater

177 tisol was positively related to incidence of epileptiform discharges (beta = 0.26, P = 0.002) in peop

178 he seizure onset zone and surface interictal epileptiform discharges (IED).

179 Interictal epileptiform discharges (IEDs) identify epileptic brain

180 Interictal epileptiform discharges (IEDs) were identified on intra-

181 stimulation for 3 hours evoked granule cell epileptiform discharges and convulsive status epilepticu

182 ith a cerebral infarct developed spontaneous epileptiform discharges and recurrent seizures (100%); i

183 stimulation of the fornix reduces interictal epileptiform discharges and seizures in patients with in

184 equency stimulation is tolerable and reduces epileptiform discharges and seizures in patients with in

185 expression of convulsive and non-convulsive epileptiform discharges and seizures.

186 long been recognized to influence interictal epileptiform discharges and seizures.

187 nt patterns of neuronal circuit activity and epileptiform discharges at the network level.

188 mmonly associated with widespread interictal epileptiform discharges but not with locally generated '

189 relationship between cortisol levels and the epileptiform discharges distinguishing persons with from

190 EG of Emx-Cre; Clock(flox/flox) mice reveals epileptiform discharges during sleep and also seizures a

191 ars, 6 males) with known frequent interictal epileptiform discharges had an [(18)F]GE-179 PET scan, i

192 was a significant decrease in the number of epileptiform discharges immediately after (p = 0.01) and

193 trode by measuring the magnetic signature of epileptiform discharges in a rat model of epilepsy.

194 ATPA also specifically activates epileptiform discharges in BLA slices in vitro via GluK1

195 Here, we show that prolonged high-frequency epileptiform discharges in cultured hippocampal neurons

196 exin36 is not critical for the generation of epileptiform discharges in GABAergic networks and that t

197 ng neurons manifested spontaneous, recurrent epileptiform discharges in neural networks, characterize

198 cortisol levels and incidence of interictal epileptiform discharges in people with stress-sensitive

199 The number of epileptiform discharges in the electroencephalogram and

200 reases cortical excitability, culminating in epileptiform discharges in vitro and spontaneous seizure

201 Moreover, the speed of propagation of epileptiform discharges in vivo and in vitro can vary ov

202 the effects of such repetitive activation on epileptiform discharges induced by 4-aminopyridine.

203 Conducting polymer electrodes recorded epileptiform discharges induced in mouse hippocampal pre

204 GLUT-1+/- mice have epileptiform discharges on electroencephalography (EEG),

205 te analysis showed that localized interictal epileptiform discharges on scalp EEGs were associated wi

206 seizures (100%); in contrast, no spontaneous epileptiform discharges or seizures were detected with c

207 The conversion is long lasting in that epileptiform discharges persist after washout of the ind

208 brile, often focal seizure types, multifocal epileptiform discharges strongly activated by sleep, mil

209 of the GABA(A) receptors transforms GDPs to epileptiform discharges suggesting dual, both excitatory

210 s, and were longer when preceded by periodic epileptiform discharges than by continuous delta (0.5-4.

211 wn of stx1b showed seizure-like behavior and epileptiform discharges that were highly sensitive to in

212 We test this in the 0 Mg(2+) model of epileptiform discharges using slices from healthy and ch

213 The relationship between cortisol and epileptiform discharges was positively associated only w

214 In both cases, prolonged epileptiform discharges were blocked by group I mGluR an

215 ticipants (54% female, median age 24 years), epileptiform discharges were detected on 14% of SBS2 and

216 Interictal epileptiform discharges were determined in the same time

217 Spontaneous epileptiform discharges were initially lateralized to ip

218 Epileptiform discharges were recorded in layer V-VI pyra

219 ir implications in pharmacologically-induced epileptiform discharges were studied in the same slices.

220 94.8% specificity (95% CI 90.0%, 97.7%) for epileptiform discharges with positive and negative predi

221 sure, synaptic stimulation induced prolonged epileptiform discharges with properties similar to those

222 scharges (also known as periodic lateralized epileptiform discharges), subjects with focal nonrhythmi

223 apses, effective in eliciting mGluR-mediated epileptiform discharges, also induced long-lasting I(mGl

224 In these patients, interictal epileptiform discharges, also termed spikes, are seen ro

225 ta receptor antagonist, were investigated on epileptiform discharges, brain inflammation, and BBB dam

226 recordings in hAPP mice revealed spontaneous epileptiform discharges, indicating network hypersynchro

227 Similar to group I mGluR-mediated prolonged epileptiform discharges, persistent I(mGluR(V)) was no l

228 exclusively connected to brief intervals at epileptiform discharges, strengthening the association b

229 s Blue we found that, at time of BBB-induced epileptiform discharges, WBCs populated the perivascular

230 ruitment of group I mGluR-mediated prolonged epileptiform discharges.

231 uit deficient in rhythmogenesis and prone to epileptiform discharges.

232 Cre; Clock(flox/flox) mouse have spontaneous epileptiform discharges.

233 ity with frequent generalized and multifocal epileptiform discharges.

234 ning (BBBD) leads to the occurrence of acute epileptiform discharges.

235 ield potential amplitudes and produces focal epileptiform discharges.

236 scale events were associated with interictal epileptiform discharges.

237 sociated with group I mGluR agonist-elicited epileptiform discharges.

238 orms normal neuronal activity into prolonged epileptiform discharges.

239 ls were preceded by spontaneous granule cell epileptiform discharges.

240 ed slowing to bilateral periodic lateralized epileptiform discharges.

241 2+) conditions induced unremitting recurrent epileptiform discharges.

242 the mouse dorsal hippocampus rapidly caused epileptiform discharges.

243 sociated with (i) isoelectricity or periodic epileptiform discharges; (ii) prolonged depression of sp

244 ures on CEEG decays to <5% by 24 hours if no epileptiform EEG abnormalities emerge, independent of in

245 In the absence of epileptiform EEG abnormalities, the duration of monitori

246 rtex or hippocampus reversibly can attenuate epileptiform EEG activity and seizures, but engineering

247 clinical seizures; more commonly, it causes epileptiform EEG activity that only weakly portends seiz

248 ion of the seizure network to the forebrain, epileptiform electrocorticographic activity, and prolong

249 based on the clinical practice of observing epileptiform electrocorticography and simultaneous ictal

250 rief (<2 s) focal, recurrent and spontaneous epileptiform electrocorticography events (EEEs) that are

251 taxia accompanied by epilepsy and/or clearly epileptiform electroencephalograms (EEGs).

252 s among the pharmacokinetics of sevoflurane, epileptiform electroencephalographic (EEG) activity and

253 Ictal epileptiform electroencephalographic changes were presen

254 Bicuculline evoked high-amplitude rhythmic epileptiform events at the site of injection which resem

255 It is still poorly understood how epileptiform events can recruit cortical circuits.

256 the wide range of propagation velocities of epileptiform events observed in vitro and in vivo.

257 etween injection and the occurrence of first epileptiform events were 3.93 +/- 2.76 (+/-STD) min for

258 ry required to capture these very infrequent epileptiform events.

259 could exercise voluntary control over these epileptiform events.

260 alography variables (reactivity, continuity, epileptiform features, and prespecified "benign" or "hig

261 Spontaneous and evoked epileptiform field potentials occurred at multiple sites

262 If epileptiform findings developed, the seizure incidence w

263 If there were no epileptiform findings on EEG, the risk of seizures withi

264 and optical recordings showed glutamatergic epileptiform hyperexcitability that spread into adjacent

265 There was a decreased threshold to induce epileptiform local field potentials in slices from pregn

266 nt role in the generation of a novel type of epileptiform nonsynaptic activity.

267 ve rates for mortality were less than 5% for epileptiform or nonreactive early electroencephalography

268 are unknown and unexpected because thalamic epileptiform oscillatory activity requires AMPARs.

269 standard EEG for the epileptiform versus non-epileptiform outcome was kappa = 0.40 (95% CI 0.25, 0.55

270 EEG risk state is defined by emergence of epileptiform patterns.

271 on was the prime determinant of the speed of epileptiform propagation.

272 ony can limit information coding and lead to epileptiform responses.

273 on of focal brain lesions or the presence of epileptiform rhythms, do not necessarily predict the bes

274 al inhibitory feedback is necessary to avoid epileptiform runaway activity (an "inhibition-stabilized

275 s in hippocampal circuitries can manifest in epileptiform seizures, and impact specific behavioral tr

276 dent neuroprotection from chemically induced epileptiform seizures.

277 However, quantitative analyses of epileptiform spatial dynamics with cellular resolution h

278 ature dependence and frequency of interictal epileptiform spike activity.

279 ocal field potential dynamics and interictal epileptiform spike generation.

280 Interictal epileptiform spike rate correlated with spectral band po

281 re was a significant reduction in interictal epileptiform spike rate in the amygdala, hippocampus, an

282 redicted significant reduction in interictal epileptiform spike rate.

283 nd age dependence of seizures and interictal epileptiform spike-and-wave activity in mSMEI.

284 We conclude that interictal epileptiform spikes are modulated by the patterns of net

285 d clinically silent hippocampal seizures and epileptiform spikes during sleep, a period when these ab

286 ous recurrent convulsive seizures in 45% and epileptiform spikes in 100%, of the rats.

287 synchronization 200 ms before the interictal epileptiform spikes that arose during this period of enc

288 Interictal epileptiform spikes were manually marked and their rate

289 During the latent pre-seizure period, epileptiform spikes were more frequent in epileptic comp

290 e examined, in addition to the daily rate of epileptiform spikes, the relative power of five frequenc

291 We previously showed how epileptiform spread in neocortical slices is opposed by

292 When this feedforward inhibition is intact, epileptiform spreads very slowly (approximately 100 micr

293 ss, its degree of functional activity during epileptiform synchronization has not been thoroughly inv

294 tion in the recurrent CA3 network preventing epileptiform synchronization.

295 tex in the in vitro 4-aminopyridine model of epileptiform synchronization.

296 ge but also to control excitation to prevent epileptiform synchronization.

297 Although the temporal dynamics of epileptiform synchronizations are well described at the

298 a) for the SBS2 EEG and standard EEG for the epileptiform versus non-epileptiform outcome was kappa =

299 rages of inhibitory inputs in advance of the epileptiform wave.

300 Mild sleep abnormalities and abnormal epileptiform waveforms were found in the electroencephal