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1 us network inhibition in the initiation of a focal seizure.
2 h of excitation contributes to terminating a focal seizure.
3  and the differences between generalized and focal seizures.
4 ly 65 million people worldwide, and 60% have focal seizures.
5 hat cortical GABAergic networks may initiate focal seizures.
6  synchronization can arise from the start of focal seizures.
7 rolling seizures in patients presenting with focal seizures.
8  adequate model using clinical recordings of focal seizures.
9 E, suggesting a common lateralized effect of focal seizures.
10 n account for major elements common to human focal seizures.
11 und in patients with limbic encephalitis and focal seizures.
12 del groups of connected neuronal networks or focal seizures.
13 ported focal seizures; (iii) locally induced focal seizures.
14 n of caged GABA to quickly terminate intense focal seizures.
15 increases of brain excitability resulting in focal seizures.
16 al resection for alleviation of uncontrolled focal seizures.
17 eatment option in patients with uncontrolled focal seizures.
18 cemia may be associated with exacerbation of focal seizures.
19 upper age limit) with two or more unprovoked focal seizures.
20    Procedures were generally well tolerated; focal seizures (9.2%) were the most frequent side effect
21                        The onset patterns of focal seizure activity have been studied intensively, an
22 n postoperative day 5, 7 or 14 had recurrent focal seizures after a latent period of 4-13 days, and s
23  with encephalitis who present with frequent focal seizures and a pattern of amnesia consistent with
24 epsy syndrome, characterized by self-limited focal seizures and cognitive symptoms.
25 g [a serious adverse reaction] and increased focal seizures and decreased consciousness considered to
26 oes it delay onset or lower the incidence of focal seizures and drug-resistant epilepsy at 24 months.
27 ental impairment, as well as generalized and focal seizures and EEG abnormalities for patients with g
28               Interictal spikes in models of focal seizures and epilepsies are sustained by the synch
29  variants (n = 30) had an increased risk for focal seizures and ongoing seizures after the first year
30 ing all these into account, benign childhood focal seizures and related epileptic syndromes would nee
31 es who presented in infancy with intractable focal seizures and severe developmental delay.
32 s include epilepsy of infancy with migrating focal seizures and sleep-related hypermotor epilepsy.
33 ilepsy, number of seizures before remission, focal seizures, and epileptiform abnormality on EEG befo
34 TERPRETATION: Underlying pathology, repeated focal seizures, and global insults each contribute to at
35 syndrome, epilepsy of infancy with migrating focal seizures, and intellectual disability or autism wi
36                                              Focal seizures appear to start abruptly and unpredictabl
37          Pathophysiology of basal ganglia in focal seizures appears to be much more interlinked with
38 es, lends weight to the hypothesis that even focal seizures are a network phenomenon that involve wid
39                                              Focal seizures are assumed to arise from a hypersynchron
40 ation and development.SIGNIFICANCE STATEMENT Focal seizures are believed to result from enhanced exci
41                                              Focal seizures are episodes of pathological brain activi
42 ible clinical phenotypes of benign childhood focal seizures are likely to be linked together by a gen
43        Our findings support the concept that focal seizures are terminated by the simultaneous and op
44 livery of phenobarbital and valproate had on focal seizures, as well as adverse effects, and compared
45            Now there are new means to induce focal seizures, as with magnetic seizure therapy (MST),
46 g our chronic implants significantly reduced focal seizures at all doses given.
47                                  Intractable focal seizures began in early childhood, after which lan
48 ion of individuals with medically refractory focal seizures being considered for surgical treatment.
49 endent cell death pathways has been shown in focal seizures, but whether this occurs in prolonged gen
50 and ictal haemodynamic changes in refractory focal seizures can non-invasively localize seizure onset
51 he electrographic pattern of a typical human focal seizure characterized by low voltage fast activity
52 ce seizure frequency in infantile spasms and focal seizures compared to other treatment options, whil
53     Fifty-five patients with >/=2 refractory focal seizures/day, and who had undergone long-term vide
54       Adult patients (aged 18-70 years) with focal seizures despite treatment with 1-3 antiepileptic
55  of early-onset seizures (median 24 months), focal seizures, developmental delay and macrocephaly sim
56 implanted cerebellar electrodes demonstrated focal seizure discharges in the region of the mass.
57 emporal lobe epilepsy (TLE), the most common focal seizure disorder in adults, can be instigated in e
58 ilepsy to epilepsy of infancy with migrating focal seizures (EIMFS) and include developmental and epi
59 result in epilepsy of infancy with migrating focal seizures (EIMFS) and several other forms of epilep
60 syndrome, epilepsy of infancy with migrating focal seizures (EIMFS).
61 NFLE) and epilepsy of infancy with migrating focal seizures (EIMFS).
62 yer directional network interactions between focal seizures either with or without secondary generali
63 y cortex in vivo to reconstruct the onset of focal seizures elicited by local injection of the chemoc
64    Systemic administration of CNO suppresses focal seizures evoked by two different chemoconvulsants,
65 amics in the range of tens of seconds govern focal seizure evolution.
66 ologically inhibiting SD occurrence during a focal seizure facilitated seizure generalization.
67 ive impairment and infantile onset epilepsy (focal seizures, fever sensitivity, and electroencephalog
68  to the human condition, chronic spontaneous focal seizures follow a single episode of traumatic brai
69 cy outcomes were percentage change in 28-day focal seizure frequency (focal aware motor, focal impair
70 cranial electroencephalography (iEEG) during focal seizures from patients diagnosed with pharmacoresi
71    In particular, the R1667P mutation causes focal seizures, generalized hypotonia, dysarthria, conge
72 e supports a role of interneuron activity in focal seizure generation.SIGNIFICANCE STATEMENT The pape
73 , who had epilepsy of infancy with migrating focal seizures, had 80% reduction in seizure frequency a
74 hese three classes are: (i) globally induced focal seizures; (ii) globally supported focal seizures;
75 uced focal seizures; (ii) globally supported focal seizures; (iii) locally induced focal seizures.
76 ses of dynamical mechanisms for the onset of focal seizures in a unified framework.
77                         Therefore, modelling focal seizures in human neuronal networks is now possibl
78                                 The onset of focal seizures in humans and in different animal models
79 cross the six layers of the neocortex during focal seizures in humans.
80                 We pharmacologically induced focal seizures in primary visual cortex (V1) of awake mi
81                                              Focal seizures in rats were induced by neocortical injec
82 lopathy with poor prognosis, presenting with focal seizures in the first year of life.
83 imol can prevent acetylcholine (Ach)-induced focal seizures in the rat neocortex without causing cess
84 susceptibility to generalized (as opposed to focal) seizures in AD vs controls.
85  to the neural activation threshold and more focal seizure induction, which could potentially reduce
86 suggest that INs have a preferential role in focal seizure initiation and development.SIGNIFICANCE ST
87 diverse insight into the mechanisms of human focal seizure initiation and propagation.
88 suggest that the secondary generalization of focal seizures is regulated by numerous within- and cros
89  known as epilepsy of infancy with migrating focal seizures, is a rare early infantile epileptic ence
90                    We conclude that although focal seizures might have different patient-specific aet
91               We found that in this in vitro focal seizure model, all IN types contribute to seizure
92 possible mechanisms underlying the different focal seizure onset patterns in the model.
93 s have shown that interneurons are active at focal seizure onset.
94 an (SD) probability cutoff for identifying a focal seizure-onset zone of 37.6 (3.5).
95 atients where SEEG is unlikely to identify a focal seizure-onset zone.
96 ogical Institute were analyzed to identify a focal seizure-onset zone.
97 odes implanted in the hamartoma demonstrated focal seizure origin from the hamartoma in 1 patient.
98 emonstrate at cellular resolution that acute focal seizures originate as increasingly synchronized lo
99  alterations are generally more prominent in focal seizures originating from the temporal lobe, demon
100 million people with drug-resistant epilepsy, focal seizures originating in dysfunctional brain networ
101 diac arrhythmias in patients with refractory focal seizures over an extended period.
102    We describe here a novel, region-specific focal seizure pattern that mimics seizure activity obser
103 1 or CASPR2 antibodies that include frequent focal seizures, prominent amnesia, dysautonomia, neuromy
104 ed in our in vitro experiments, but also for focal seizures recorded in different syndromes, brain re
105 al toward seizure end was confirmed in human focal seizures recorded with intracerebral electrodes in
106 latory networks constrain the propagation of focal seizures remains unclear.
107 ma inactivated 1 (LGI1) is the very frequent focal seizure semiologies, including faciobrachial dysto
108 wn if this in vivo gene transfer could alter focal seizure sensitivity in the inferior colliculus.
109 de, however, the promoter determined whether focal seizure sensitivity was significantly attenuated o
110 nin peptide significantly attenuated in vivo focal seizure sensitivity, even with different promoters
111 flects propagated activity from a relatively focal seizure source, even during later time points when
112 represent travelling waves propagated from a focal seizure source.
113  seizure "generalization" stages (3-6) from "focal" seizure stages (1-2).
114   Human and animal EEG data demonstrate that focal seizures start with low-voltage fast activity, evo
115 een established in conditions with primarily focal seizures, such as tuberous sclerosis complex (TSC)
116 even more prominent role of basal ganglia in focal seizures, the mode of interaction between cortical
117 biomarkers that may mark the transition from focal seizures to the more severe form of TLE (FBTCS +).
118 ed with febrile and multiple afebrile, often focal seizure types, multifocal epileptiform discharges
119      Specifically, we find that although all focal seizures typically appear to arise from localised
120                                The effect of focal seizures was inferred from lateralized atrophy com
121  of 6 months, and presentation with afebrile focal seizures were significantly associated with geneti
122 pose a two-step model for the progression of focal seizures, where neuronal ensembles activate first,
123 lepsy surgery is indicated for patients with focal seizures who do not respond to appropriate antiepi
124 uliar of the olfactory cortex that resembles focal seizures with low-voltage fast activity at onset o
125       In the UK, driving is not permitted if focal seizures with no impairment of awareness (auras, s
126 day) continued to experience reading-induced focal seizures with preserved consciousness.
127 pilepsy syndrome clinically characterized by focal seizures with prominent auditory symptoms.
128                                              Focal seizures with secondary generalization are traditi
129                 Among the cohort as a whole, focal seizures, with or without progression to bilateral

 
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