The supersensitivity of chronically “isolated” cerebral cortex as a mechanism in focal epilepsy

Echlin, Francis A.; Peck, David M.; Schmer, Caryl; Brown, Lewis

doi:10.1016/0013-4694(59)90110-5

Cited by 162 publications

(36 citation statements)

References 40 publications

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“…These spikes do not likely reflect residual epileptogenic cortex, because there was no clinically apparent preoperative epileptogenic cortex and no preoperative EA. The possibility that these spikes resulted from cortical isolation is also unlikely, because the acute effect of cortical isolation in the absence of preresection EA is a burst suppression pattern (28,31,36). We also recorded spikes in a patient (R.R.)…”

Section: Discussionmentioning

confidence: 99%

Do Reactive Post‐Resection “Injury” Spikes Exist?

et al. 2000

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Summary:Purpose: New post-resection spikes on electrocorticography (ECoG) after lesionectomy in patients with seizures may represent residual epileptogenic tissue or presumed reactive injury spikes. We investigated the existence of postresection injury spikes by eliminating the possibility of residual epileptogenic tissue.Methods: Preresection and post-resection ECoG was performed on seven patients with an intra-axial neocortical tumor (glioblastoma multiforme or metastasis) and no history of seizures. All tumors were gross-totally resected.Results: The mean age of the patients was 59 years. The tumor location was frontal in four patients, parietal in two, and temporal in one. Two patients had preresection spikes with an average rate of 68 spikedmin that disappeared after surgery. Two different patients had new post-resection spikes, with an average firing rate of 4 spikedmin, despite normal preresection ECoG. In one of these patients, the new spikes were superimposed over a burst suppression pattern. Neither patient developed seizures after surgery.Conclusions: Surgical irritation of the neocortex is sufficient to produce reactive post-resection epileptogenic discharges surrounding an intra-axial neocortical tumor even in the absence of preoperative seizures and spikes. Injury spikes fire at a slow rate and are not predictive of clinical seizures.

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Section: Discussionmentioning

confidence: 99%

Do Reactive Post‐Resection “Injury” Spikes Exist?

et al. 2000

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“…Partially isolated "undercut" (UC) or "injured" neocortex is a well established in vivo model of posttraumatic epileptogenesis in cats and monkeys (Echlin and Battista 1963;Echlin and McDonald 1954;Grafstein and Sastry 1957;Sharpless 1969; reviewed in Halpern 1972). Spontaneous (s) and evoked (e) epileptiform activity persists in rodent neocortical slices cut through the UC neocortex and maintained in vitro (Hoffman et al 1994;Prince and Tseng 1993;Salin et al 1995; reviewed in Graber and Prince 2006).…”

Section: Introductionmentioning

confidence: 99%

Presynaptic Inhibitory Terminals Are Functionally Abnormal in a Rat Model of Posttraumatic Epilepsy

Faria

Prince

2010

Journal of Neurophysiology

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Faria LC, Prince DA. Presynaptic inhibitory terminals are functionally abnormal in a rat model of posttraumatic epilepsy. J Neurophysiol 104: 280-290, 2010. First published May 19, 2010 doi:10.1152/jn.00351.2010. Partially isolated "undercut" neocortex with intact pial circulation is a well-established model of posttraumatic epileptogenesis. Results of previous experiments showed a decreased frequency of miniature inhibitory postsynaptic currents (mIPSCs) in layer V pyramidal (Pyr) neurons of undercuts. We further examined possible functional abnormalities in GABAergic inhibition in rat epileptogenic neocortical slices in vitro by recording whole cell monosynaptic IPSCs in layer V Pyr cells and fast-spiking (FS) GABAergic interneurons using a paired pulse paradigm. Compared with controls, IPSCs in Pyr neurons of injured slices showed increased threshold and decreased peak amplitude at threshold, decreased input/output slopes, increased failure rates, and a shift from paired pulse depression toward paired pulse facilitation (increased paired pulse ratio or PPR). Increasing [Ca 2ϩ ] o from 2 to 4 mM partially reversed these abnormalities in Pyr cells of the epileptogenic tissue. IPSCs onto FS cells also had an increased PPR and failures. Blockade of GABA B receptors did not affect the paired results. These findings suggest that there are functional alterations in GABAergic presynaptic terminals onto both Pyr and FS cells in this model of posttraumatic epileptogenesis. I N T R O D U C T I O NPartially isolated "undercut" (UC) or "injured" neocortex is a well established in vivo model of posttraumatic epileptogenesis in cats and monkeys (Echlin and Battista 1963;Echlin and McDonald 1954;Grafstein and Sastry 1957;Sharpless 1969; reviewed in Halpern 1972). Spontaneous (s) and evoked (e) epileptiform activity persists in rodent neocortical slices cut through the UC neocortex and maintained in vitro (Hoffman et al. 1994;Prince and Tseng 1993;Salin et al. 1995; reviewed in Graber and Prince 2006). Alterations in glutamatergic excitatory synaptic activity/connectivity are present in this model and likely contribute to the development of hyperexcitability (Jin et al. 2006;Li and Prince 2002;Li et al. 2005;Salin et al. 1995).Results of anatomical and electrophysiological experiments in UC cortex indicate that decreases in GABAergic inhibitory activity/connectivity may also contribute to epileptogenesis. Biocytin-filled axons of fast-spiking (FS) GABAergic interneurons in the chronically epileptogenic cortex are structurally abnormal with decreased bouton size and marked reduction in axonal lengths ). Such alterations in presynaptic inhibitory terminals might be associated with functional abnormalities such as increased failure rate, decreased amplitude of inhibitory postsynaptic currents (IPSCs), and decreased probability of GABA release (Pr) that would make inhibitory transmission less effective (Harris and Sultan 1995;Pierce and Lewin 1994). There is also a decrease in the frequency of miniature inhibitory post synapt...

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“…Experiments with isolated cortex by E chlin [24] have shown the particular sensitivity of this preparation, especially to acetylcholine. Electrical coagulation and physical agents such as freezing techniques [25] have been studied also.…”

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confidence: 99%