Seizures and CNS Hemorrhage

Gilmore, Emily; Choi, H. Alex; Hirsch, Lawrence J.; Claassen, Jan

doi:10.1097/nrl.0b013e3181c7cd0b

Cited by 61 publications

(11 citation statements)

References 101 publications

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“…The proportion of patients with late post-haemorrhagic seizures was higher in our study than in previous surveys (Claassen et al , 2003; Buczacki et al , 2004; Gilmore et al , 2010). This was presumably due to the severity of the initial haemorrhage, a high rate of intracerebral haemorrhage, the high proportion of delayed cerebral ischaemia, the prospective design of the study and the fact that the indication for neurosurgical intervention was an inclusion criterion (Gilmore et al , 2010).…”

Section: Discussioncontrasting

confidence: 86%

“…This was presumably due to the severity of the initial haemorrhage, a high rate of intracerebral haemorrhage, the high proportion of delayed cerebral ischaemia, the prospective design of the study and the fact that the indication for neurosurgical intervention was an inclusion criterion (Gilmore et al , 2010). The only statistically significant finding associated with the development of late post-haemorrhagic seizures was a higher peak number of spreading depolarizations in the electrocorticography monitored, subacute phase after aneurismal SAH.…”

Section: Discussionmentioning

confidence: 99%

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Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

Dreier

Major

Pannek

et al. 2011

Brain

218

243

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Spreading depolarization of cells in cerebral grey matter is characterized by massive ion translocation, neuronal swelling and large changes in direct current-coupled voltage recording. The near-complete sustained depolarization above the inactivation threshold for action potential generating channels initiates spreading depression of brain activity. In contrast, epileptic seizures show modest ion translocation and sustained depolarization below the inactivation threshold for action potential generating channels. Such modest sustained depolarization allows synchronous, highly frequent neuronal firing; ictal epileptic field potentials being its electrocorticographic and epileptic seizure its clinical correlate. Nevertheless, Leão in 1944 and Van Harreveld and Stamm in 1953 described in animals that silencing of brain activity induced by spreading depolarization changed during minimal electrical stimulations. Eventually, epileptic field potentials were recorded during the period that had originally seen spreading depression of activity. Such spreading convulsions are characterized by epileptic field potentials on the final shoulder of the large slow potential change of spreading depolarization. We here report on such spreading convulsions in monopolar subdural recordings in 2 of 25 consecutive aneurismal subarachnoid haemorrhage patients in vivo and neocortical slices from 12 patients with intractable temporal lobe epilepsy in vitro. The in vitro results suggest that γ-aminobutyric acid-mediated inhibition protects from spreading convulsions. Moreover, we describe arterial pulse artefacts mimicking epileptic field potentials in three patients with subarachnoid haemorrhage that ride on the slow potential peak. Twenty-one of the 25 subarachnoid haemorrhage patients (84%) had 656 spreading depolarizations in contrast to only three patients (12%) with 55 ictal epileptic events isolated from spreading depolarizations. Spreading depolarization frequency and depression periods per 24 h recording episodes showed an early and a delayed peak on Day 7. Patients surviving subarachnoid haemorrhage with poor outcome at 6 months showed significantly higher total and peak numbers of spreading depolarizations and significantly longer total and peak depression periods during the electrocorticographic monitoring than patients with good outcome. In a semi-structured telephone interview 3 years after the initial haemorrhage, 44% of the subarachnoid haemorrhage survivors had developed late post-haemorrhagic seizures requiring anti-convulsant medication. In those patients, peak spreading depolarization number had been significantly higher [15.1 (11.4–30.8) versus 7.0 (0.8–11.2) events per day, P = 0.045]. In summary, monopolar recordings here provided unequivocal evidence of spreading convulsions in patients. Hence, practically all major pathological cortical network events in animals have now been observed in people. Early spreading depolarizations may indicate a risk for late post-haemorrhagic seizures.

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Section: Discussioncontrasting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

Dreier

Major

Pannek

et al. 2011

Brain

218

243

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“…[10] The existing literature has mainly focused on clinically overt focal or generalized tonic-clonic seizure activity despite the fact that as many as 95% of seizures in ntSAH patients are nonconvulsive and can only be detected with EEG. [6] Electrographic seizures detected by continuous EEG have been independently associated with poor outcomes. The incidence of status epilepticus among ntSAH patients with nonconvulsive seizures may be as high as 70%.…”

Section: Discussionmentioning

confidence: 99%

The spectrum of management practices in nontraumatic subarachnoid hemorrhage: A survey of high-volume centers in the United States

Tomycz

Shekhawat²,

Forbes³

et al. 2011

Surg Neurol Int

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Background:There is a considerable variety of management practices for nontraumatic subarachnoid hemorrhage (ntSAH) across high-volume centers in the United States. We sought to design a survey which would highlight areas of controversy in the modern management of ntSAH and identify specific areas of interest fo further study.Methods:A questionnaire on management practices in ntSAH was formulated using a popular web-based survey tool (SurveyMonkey™, Palo Alto, CA) and sent to endovascular neurointerventionists and cerebrovascular surgeons who manage a high volume of these patients annually. Two-hundred questionnaires were delivered electronically, and after a period of 2 months, the questionnaire was resent to nonresponders.Results:Seventy-three physicians responded, representing a cross-section of academic and other high-volume centers of excellence from around the country. On average, the responding interventionists in this survey each manage approximately 100 patients with ntSAH annually. Over 57% reported using steroids to treat this patient population. Approximately 18% of the respondents use intrathecal thrombolytics in ntSAH. Over 90% of responding physicians administer nimodipine to all patients with ntSAH. Over 40% selectively administer antiepileptic drugs to patients with ntSAH. Several additional questions were posed regarding the methods of detecting and treating vasospasm, as well as the indications for CSF diversion in patients with ntSAH further demonstrating the great diversity in management.Conclusion:This survey illustrates the astonishing variety of treatment practices for patients with ntSAH and underscores the need for further study.

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“…Most seizures are associated with hemorrhagic stroke (Sun et al 2001;Herman 2002;Silverman et al 2002;Balami and Buchan 2012) and occur within the first 24 hours of injury (Gilmore et al 2010;Löscher and Brandt 2010). In cortical and hippocampal (Lehohla et al 2001;Russell 2001), as well as in olfactory cortex slices (Khama-Murad and Mokrushin 2007), the functional activity of the ionotropic receptors in rats with hypertension (SHRs) is modified due to a functional predominance of NR2B subunit of NMDA receptors (Jensen et al 2009).…”

Section: Effects Of Whole and Diluted Autologous Blood On Synaptic Acmentioning

confidence: 99%

“…A widening of the early neuronal damage in the different brain regions during ICH is a result of increasing excitotoxicity mediated by glutamate activation of NMDA or AMPA receptors in brain tissue (Qureshi et al 2003;Ardizzone et al 2004;Liu et al 2007;Lau and Tymianski 2010;Lai et al 2011). Early acute hypersynchronous glutamatergic activation of cortical neurons leads to acute seizures and epilepsy (Herman 2002;DeLorenzo et al 2007;Gilmore et al 2010;Balami and Buchan 2012). Extravasated blood plasma components are toxic for brain neurons (Qureshi et al 2003;Wagner 2007;Aronowski and Zhao 2011) and may induce the neuronal network failure.…”

Section: Introductionmentioning

confidence: 99%

Effects of the blood components on the AMPA and NMDA synaptic responses in brain slices in the onset of hemorrhagic stroke

Mokrushin¹,

Pavlinova²

2013

gpb

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Abstract. Blood-borne events play a major role in post bleeding disturbances of the neuronal network. However, very little is known about the early effects of blood plasma, leucocytes, and the red blood cells on the AMPA and NMDA-mediated synaptic responses in the onset of experimental intracranial hemorrhage (ICH). In this study, we used the technique of on-line monitoring of electrophysiological parameters referred to synaptic activity in piriform cortex of SHR rat slice. We exposed the olfactory cortex slices to diluted autologous blood or its components and compared with effects of ferric chloride. Whole blood exerted a total inhibition of synaptic activity in piriform cortex within first 5 min. Dilution of blood induced prolonged epileptic synaptic activation of NMDA receptors. Blood plasma and fraction of leucocytes induced hyperactivation of neurons transforming to epileptiform discharges. Fraction of red blood cells acted biphasic, an initial sharp activity of AMPA-and NMDAmediated receptors replaced by a following total depression. Our slice-based models of experimental stroke revealed the mechanism of the earliest pathophysiologic events occur in brain tissue during bleeding that may be relevant to the human ICH.

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Seizures and CNS Hemorrhage

Cited by 61 publications

References 101 publications

Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

The spectrum of management practices in nontraumatic subarachnoid hemorrhage: A survey of high-volume centers in the United States

Effects of the blood components on the AMPA and NMDA synaptic responses in brain slices in the onset of hemorrhagic stroke

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