Epileptiform activity initiated by pial iontophoresis of ferrous and ferric chloride on rat cerebral cortex

Willmore, L. James; Hurd, R.W.; Sypert, George W.

doi:10.1016/0006-8993(78)90273-1

Cited by 71 publications

(24 citation statements)

References 9 publications

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“…Alternatively, an epileptic mechanism would be consistent with the stereotyped, repeated and short-lived paresthetic episodes. Blood is known as a potent epileptogenic agent, and animal studies have demonstrated that epileptic seizures can be induced by ferrous or ferric chloride injections into the cerebral cortex [15,16,17]. The normality of electroencephalograms does not rule out such a hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Focal Cortical Subarachnoid Hemorrhage Revealed by Recurrent Paresthesias: A Clinico-Radiological Syndrome Strongly Associated with Cerebral Amyloid Angiopathy

et al. 2013

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Background: Focal subarachnoid hemorrhage (SAH) is often revealed by transient and recurrent focal neurological episodes. This cause is important to identify because it carries a high risk of intracerebral hemorrhage (ICH). We report the clinical, imaging and prognostic data of 17 patients with focal SAH revealed by short episodes of paresthesias mimicking transient ischemic attacks. Methods: The medical records and imaging data of patients with focal acute SAH at the cerebral convexity and at least one episode of focal paresthesia having attended the Neurology Department of Caen University Hospital in the last 10 years were retrospectively reviewed. Hemorrhagic lesions, ischemic lesions, cerebral microbleeds (CMBs), superficial siderosis, white matter changes (leukoaraiosis) and modified Boston criteria for cerebral amyloid angiopathy (CAA) were assessed. All patients or relatives were contacted after a median delay of 16 months in order to seek for new events (death, stroke, recurrent focal symptoms, ICH and dementia) that occurred since hospital discharge. Results: Seventeen patients (12 men) aged 69-96 years were identified. All but 1 had multiple, repeated, stereotyped and brief attacks of paresthesias, associated in some of them with motor and/or speech difficulties, but only 1 had a headache. SAHs were seen on CT scans in 15/17 patients and on T2* gradient-echo magnetic resonance imaging (MRI) in all patients. They were multiple SAHs in 14/17 patients, including at least 1 SAH in the central or pre- or postcentral sulcus contralateral to the symptoms in all patients. Five patients had punctate cortical hyperintensities on diffusion-weighted MRI. Eleven patients had CMBs, and 4 of them had more than 5 CMBs. Seven patients met the modified Boston criteria for probable and 10 for possible CAA. At follow-up, 5 patients had a subsequent ICH, 4 of whom had received antithrombotic treatments. Five patients died (1 from ICH). Six patients developed dementia. Conclusion: The combination of transient, repeated and stereotyped attacks of unilateral paresthesias with a contralateral sulcal SAH seems to preferentially occur in elderly people and is often indicative of CAA.

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Section: Discussionmentioning

confidence: 99%

Focal Cortical Subarachnoid Hemorrhage Revealed by Recurrent Paresthesias: A Clinico-Radiological Syndrome Strongly Associated with Cerebral Amyloid Angiopathy

et al. 2013

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“…A single stereotaxic injection of microliter quantities of ferrous or ferric chloride into rat or cat sensorimotor cortex results in chronic recurrent focal paroxysmal electroencephalographic discharges as well as behavioral seizures [21,55,56 ]. Focal epileptiform discharges are induced within 15 min.…”

Section: Iron Salts Model Of Epilepsymentioning

confidence: 99%

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Willmore

Ueda

2008

Neurochem Res

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Traumatic brain injury causes development of posttraumatic epilepsy. Bleeding within neuropil is followed by hemolysis and deposition of hemoglobin in neocortex. Iron from hemoglobin and transferring is deposited in brains of patients with posttraumatic epilepsy. Iron compounds form reactive free radical oxidants. Microinjection of ferric ions into rodent brain results in chronic recurrent seizures and liberation of glutamate into the neuropil, as is observed in humans with epilepsy. Termination of synaptic effects of glutamate is by removal via transporter proteins. EAAC-1 is within neurons while GLT-1 and GLAST are confined to glia. Persistent down regulation of GLAST production is present in hippocampal regions in chronic seizure models. Down regulation of GLAST may be fundamental to a sequence of free radical reactions initiated by brain injury with hemorrhage. Administration of antioxidants to animals causes interruption of the sequence of brain injury responses induced by hemorrhage, suggesting that such a strategy needs to be evaluated in patients with traumatic brain injury.

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“…O outro mecanismo refere-se à recorrência crônica de crises, associada a fase tardia, que seria causada pela lesão estrutural decorrente do AVC 5,15,16,29 . Apesar da associação entre crises epilépticas e AVC isquêmico (AVCI) ser bem estabelecida e ser motivo de extensos estudos, não foram ainda bem delineadas as características do grupo de pacientes com AVCI que evoluem com essas crises, diferenciando-o do grupo que não as apresenta.…”

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Exames subsidiários preditivos de crises epilépticas após acidente vascular cerebral isquêmico

Fukujima¹,

Cardeal

1997

Arq. Neuro-Psiquiatr.

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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

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Epileptiform activity initiated by pial iontophoresis of ferrous and ferric chloride on rat cerebral cortex

Cited by 71 publications

References 9 publications

Focal Cortical Subarachnoid Hemorrhage Revealed by Recurrent Paresthesias: A Clinico-Radiological Syndrome Strongly Associated with Cerebral Amyloid Angiopathy

Focal Cortical Subarachnoid Hemorrhage Revealed by Recurrent Paresthesias: A Clinico-Radiological Syndrome Strongly Associated with Cerebral Amyloid Angiopathy

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Exames subsidiários preditivos de crises epilépticas após acidente vascular cerebral isquêmico

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