The Occurrence and Evolution in the Eeg of a Lateralized Periodic Phenomenon

Schwartz, Martin S.; Prior, Pamela F.; Scott, D. F.

doi:10.1093/brain/96.3.613

Cited by 114 publications

(81 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The compound was dissolved in a vehicle mm thick) taken from the region beginning 1 mm from the of distilled, deionized water immediately prior to testing frontal pole and ending just rostral to the cortico-cerebeland administered in a volume of I mI/kg of body weight. temperature (36.7 ±0.7 'C, 35.6±0.4 'C and 35.7±0.6 C, temperature measurements from RS100642 treated animals respectively), which was similar to our earlier findings (Table 1) were not significantly different from the corre- [33,38].…”

Section: Neurological Testingsupporting

confidence: 91%

“…Glial cells then become unable to absorb an experimental model of ischemic brain injury and has extracellular glutamate, a process dependent on the Na+ proven to be highly sensitive to various neuroprotective gradient created by Na+-K+-ATPase pumps. Additionaldrug interventions [8,14,20,26,33,38,42]. In this study, ly, reverse operation of the glutamate transporter also post-injury treatment with RS100642 dose-dependently increases extracellular glutamate levels, leading to exreduced brain infarct volume, increased recovery in EEG citotoxicity or overstimulation of the post-synaptic neuron.…”

Section: Long Term Recovery (1 H Mcao172 H Recovery)mentioning

confidence: 74%

“…The the post-synaptic neurons become unable to pump out the correlation of increased EEG recovery with a reduction of brain infarction is similar to the effects seen with other rodotoxin (TTX)-sensitive channels of ce-subunits I, II, neuroprotective compounds in this model, including the IIA, III, and PNI, slow inactivating, TTX-resistant cehigh affinity N-methyl-D-aspartate antagonist conantokin-G subunits PN3 and NaN, and others including Na6 and NaG and an experimental anti-inflammatory agent PS519 [11,12,23]. Each of these subunits also exhibits different [26,38].…”

Section: Long Term Recovery (1 H Mcao172 H Recovery)mentioning

confidence: 99%

See 2 more Smart Citations

Neuronal Sodium Channels in Neurodegeneration and Neuroprotection

Tortella¹

2002

View full text Add to dashboard Cite

Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathe0 ng and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Infonnation Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and Approved for Public Release; Distribution Unlimited ABSTRACT (Maximum 200 Words)The purpose of this research project is to study the role of neuronal sodium channels in mechanisms of neuronal injury, neurodegeneration, and neuroprotection. The primary objective of this research project is to characterize the expression, and study the functional significance, of neuronal sodium channels during the process of injury and recovery. Also, the effects of sodium channel blockade (using antisense and channel blockers) on gene expression and neurodegeneration will be studies.The progress during our 3rd year of this project wss excellent. Several important and critical discoveries providing a greater understanding of the injury/neurodegeneration process and the role of brain NAChs in this process were elucidated. Our key observations were 1) using ASO for the Nal.1 NaCh it was demonstrated that functional blockade of this channel results in brain neuroprotection following injury; 2) our in situ hybridization experiments defined the regional anatomical distribution of Navl.1 sodium channel gene expression in normal and at various time-post MCAo and confirmed our QRT-PCR data showing the Nal .1 expression to be down-regulated in subcortical and cortical regions of injured and, to some degree of contralateral hemispheres. In addition, these in situ hybridization studies revealed that the expression of other NaCh gene appears not to be of significance to the brain injury process; 3) our preliminary results show that treatment of neurons with RS-1000642 at least partially reverses the down-regulation of Navl .1 caused by MCAo injury. Importantly, evidendc eindicates that this is an effect selective for the Nal.1 NaCh and not other NAChs; 4) Based upon our QRT-PCR resutls, it does not appear that sodium-calcium exhanger genes, namely NCXl, NCX2 and NCX3, re inolved in the NaCh mechanisms of ischemia brain injury, at least not at early time-points post-MCAo injury; 4) Finally, our comprehensive EEG studies have identified several non-convulsant (NCS) brain seizure events identical to the clinical brain injury and that of all the AEDs tested to date, only the sodium channel blocker RS-100642 significantly stops or attenuates the NCS neuropathology. received considerable attention, leading many, including our own laboratory, to propose the "calcium mechanism" of neuronal injury and neurodegeneration. However, of possibly equal consequence to t...

show abstract

Section: Neurological Testingsupporting

confidence: 91%

Section: Long Term Recovery (1 H Mcao172 H Recovery)mentioning

confidence: 74%

Section: Long Term Recovery (1 H Mcao172 H Recovery)mentioning

confidence: 99%

See 1 more Smart Citation

Neuronal Sodium Channels in Neurodegeneration and Neuroprotection

Tortella¹

2002

View full text Add to dashboard Cite

show abstract

“…Os achados mais específicos relatados nesses casos são as descargas epileptiformes paroxísticas lateralizadas (PLEDs), porém são pouco freqüentes 3,4,12,18,24 . Esses achados relacionaram-se a crises recorrentes nos estudos de Gupta et al 12 .…”

Section: Discussionunclassified

“…Já Blandin et al 3 concluiram que PLEDs foram específicas para a ocorrência de crises epilépticas após AVC, mas não foram preditivos para recorrência. Outros correlacionaram a presença de PLEDs a crises de difícil controle agudamente mas com bom prognóstico quanto a recorrência de crises 4,17,24 . Acredita-se que o EEG feito logo após a instalação do AVC tenha valor prognóstico para a recorrência de crises epilépticas tardiamente 13 .…”

Section: Discussionunclassified

Exames subsidiários preditivos de crises epilépticas após acidente vascular cerebral isquêmico

Fukujima¹,

Cardeal

1997

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

RESUMO -Na tentativa de detectar fatores preditivos para ocorrência de crises epilépticas após acidente vascular cerebral isquêmico (AVCI), estudamos exames laboratoriais de glicemia, hematócrito, colesterol total e frações e triglicérides, além de eletrocardiograma, eletrencefalograma (EEG), líquido cefalorraquiano e tomografia computadorizada do crânio (TC) em 35 pacientes com AVCI que evoluíram com crises epilépticas após pelo menos 24 horas a partir da instalação do AVCI (grupo 1 ou G1), que foram comparados a 35 pacientes com AVCI que evoluíram sem crises epilépticas (grupo 2 ou G2). Encontramos significância na análise EEG na comparação dos grupos, sendo a alteração mais freqüente o alentecimento focai da atividade elétrica cerebral no G1. A presença de lesão extensa na TC também associou-se ao G1. A associação de EEG anormal e lesão extensa na TC pode ser considerado elemento preditivo para ocorrência de crises epilépticas após AVCI com coeficiente de concordância de 34%. Os demais exames estudados não mostraram significância na comparação entre os grupos G1 e G2. PALAVRAS-CHAVE: doença cerebrovascular, infarto cerebral, epilepsia, eletrencefalograma, tomografia. Epileptic seizures after ischemic stroke: are there any preditive laboratory test?ABSTRACT -We studied subsidiary laboratorial tests such as serum glucose, red blood cell count, total cholesterol, HDL and LDL cholesterol and triglycerides, eletrocardiogram, eletroencephalogram (EEG), cerebrospinal fluid, and CT scan of 35 patients with cerebral infarction who developed epileptic seizures (group 1 or G1), and compared them to a group of 35 patients who had cerebral infarction but have not developed epileptic seizures (group 2 or G2). The EEG analysis showed significance in the comparison between the groups; focal lentification of the electrical cerebral activity was the most frequent abnormality found in G1. Extensive infarcts were also more frequent in G1. The association of abnormal EEG and extensive lesion on CT may be considered a preditive factor for occurrence of epileptic seizures after cerebral infarction. The analysis of the other tests showed no significance on the comparison between the groups. KEY WORDS: stroke, cerebral infarction, epilepsy, epileptic seizures, eletroencephalography, tomography.As crises epilépticas constituem importante complicação dos acidentes vasculares cerebrais (AVC), ocorrendo em 3,3 a 4,3% dos AVC na fase aguda, isto é, nos primeiros 14 dias desde sua instalação, e em 3 a 19% dos AVC na fase tardia, ou seja, após 14 dias da sua instalação 9,17,19,20,23,25 . Há dois principais mecanismos fisiopatológicos para explicar a ocorrência de crises epilépticas relacionadas ao AVC. As crises da fase aguda ocorreriam devido a alterações metabólicas citotóxicas conseqüentes à lesão cerebral, que poderiam induzir crises epilépticas por si só, ou poderiam ocorrer Este estudo faz parte da Tese de Mestrado "Crises epilépticas após acidente vascular cerebral por infarto cerebral: estudo de 35 pacientes" 10 , aprovada no Curso

show abstract

Periodic Lateralized Epileptiform Discharges With Preexisting Focal Brain Lesions

Chu¹

1980

Arch Neurol

View full text Add to dashboard Cite

The Occurrence and Evolution in the Eeg of a Lateralized Periodic Phenomenon

Cited by 114 publications

References 0 publications

Neuronal Sodium Channels in Neurodegeneration and Neuroprotection

Neuronal Sodium Channels in Neurodegeneration and Neuroprotection

Exames subsidiários preditivos de crises epilépticas após acidente vascular cerebral isquêmico

Periodic Lateralized Epileptiform Discharges With Preexisting Focal Brain Lesions

Contact Info

Product

Resources

About