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Tissue hypoxia correlates with intensity of interictal spikes.

ABSTRACT: Interictal spikes (IISs) represent burst firing of a small focal population of hypersynchronous, hyperexcitable cells. Whether cerebral blood flow (CBF) is adequate to meet the metabolic demands of this dramatic increase in membrane excitability is unknown. Positron emission tomography, single photon emission computed tomography, and functional magnetic resonance imaging studies have shown increases in CBF and hypometabolism, thus indicating the likelihood of adequate perfusion. We measured tissue oxygenation and CBF in a rat model of IIS using oxygen electrodes and laser-Doppler flowmetry. A ?3-second dip in tissue oxygenation was shown, followed by more prolonged tissue hyperoxygenation, in spite of a 25% increase in CBF. Increases in the number of spikes, as well as in their amplitude and spike width further amplified these responses, and a decrease in interspike interval decreased the CBF response. Altering the anesthetic did not influence our results. Taken together, these findings indicate that frequent, high-amplitude IISs may produce significant tissue hypoxia, which has implications for patients with epilepsy and noninvasive techniques of seizure localization.

SUBMITTER: Geneslaw AS

PROVIDER: S-EPMC3130319 | biostudies-literature | 2011 Jun

REPOSITORIES: biostudies-literature

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Tissue hypoxia correlates with intensity of interictal spikes.

Geneslaw Andrew S AS Zhao Mingrui M Ma Hongtao H Schwartz Theodore H TH

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 20110223 6

Interictal spikes (IISs) represent burst firing of a small focal population of hypersynchronous, hyperexcitable cells. Whether cerebral blood flow (CBF) is adequate to meet the metabolic demands of this dramatic increase in membrane excitability is unknown. Positron emission tomography, single photon emission computed tomography, and functional magnetic resonance imaging studies have shown increases in CBF and hypometabolism, thus indicating the likelihood of adequate perfusion. We measured tiss ...[more]

PMID: 21343943

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Project description:The location of interictal spikes is used to aid surgical planning in patients with medically refractory epilepsy; however, their spatial and temporal dynamics are poorly understood. In this study, we analysed the spatial distribution of interictal spikes over time in 20 adult and paediatric patients (12 females, mean age = 34.5 years, range = 5-58) who underwent intracranial EEG evaluation for epilepsy surgery. Interictal spikes were detected in the 24 h surrounding each seizure and spikes were clustered based on spatial location. The temporal dynamics of spike spatial distribution were calculated for each patient and the effects of sleep and seizures on these dynamics were evaluated. Finally, spike location was assessed in relation to seizure onset location. We found that spike spatial distribution fluctuated significantly over time in 14/20 patients (with a significant aggregate effect across patients, Fisher's method: P < 0.001). A median of 12 sequential hours were required to capture 80% of the variability in spike spatial distribution. Sleep and postictal state affected the spike spatial distribution in 8/20 and 4/20 patients, respectively, with a significant aggregate effect (Fisher's method: P < 0.001 for each). There was no evidence of pre-ictal change in the spike spatial distribution for any patient or in aggregate (Fisher's method: P = 0.99). The electrode with the highest spike frequency and the electrode with the largest area of downstream spike propagation both localized the seizure onset zone better than predicted by chance (Wilcoxon signed-rank test: P = 0.005 and P = 0.002, respectively). In conclusion, spikes localize seizure onset. However, temporal fluctuations in spike spatial distribution, particularly in relation to sleep and post-ictal state, can confound localization. An adequate duration of intracranial recording-ideally at least 12 sequential hours-capturing both sleep and wakefulness should be obtained to sufficiently sample the interictal network.

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Project description:In organotypic hippocampal slice cultures, principal neurons form aberrant excitatory connections with other principal cells in response to slicing induced deafferentation, similar to mechanisms underlying epileptogenesis in posttraumatic epilepsy. To investigate the consequences of this synaptogenesis, the authors recorded field-potential activity from area CA3 during perfusion with the complete growth medium used during incubation. At 7 days in vitro, slice cultures only displayed multiunit activity. At 14 days in vitro, the majority displayed population bursts reminiscent of interictal-like spikes, but sustained synchronous activity was rare. Band-pass filtering of interictal discharges revealed fast ripple-like complexes, similar to in vivo recordings. Spontaneous ictal-like activity became progressively more prevalent with age: at 21 days in vitro, 50% of organotypic hippocampal slice cultures displayed long-lasting, ictal-like discharges that could be suppressed by phenytoin, whereas interictal activity was not suppressed. The fraction of cultures displaying ictal events continually increased with incubation time. Quantification of population spike activity throughout epileptogenesis using automatic detection and clustering algorithms confirmed the appearance of interictal-like activity before ictal-like discharges and also revealed high-frequency pathologic multiunit activity in slice cultures at 14 to 17 days in vitro. These experiments indicate that interictal-like spikes precede the appearance of ictal-like activity in a reduced in vitro preparation. Epileptiform activity in cultures resembled in vivo epilepsy, including sensitivity to anticonvulsants and steadily increasing seizure incidence over time, although seizure frequency and rate of epileptogenesis were higher in vitro. Organotypic hippocampal slice cultures comprise a useful model system for investigating mechanisms of epileptogenesis as well as developing antiepileptic and antiepileptogenic drugs.

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Tissue hypoxia correlates with intensity of interictal spikes.

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Tissue hypoxia correlates with intensity of interictal spikes.

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