Perirhinal cortical lesion suppresses the secondary generalization in kainic acid‐induced limbic seizure

Fukumoto, Shin-ichiro; Tanaka, Shigeya; Tojo, Hideshi; Akaike, Koichi; Takigawa, Morikuni

doi:10.1046/j.1440-1819.2002.01055.x

Cited by 10 publications

(3 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, if epileptiform activity is present here it can be severe [ 32 ]. It has been shown to be a highly sensitive area for intervention for seizure propagation and resistance to kindling [ 33 , 34 ] but is rarely removed in epilepsy surgery [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Electrographic Waveform Structure Predicts Laminar Focus Location in a Model of Temporal Lobe Seizures In Vitro

Adams

Traub

et al. 2015

PLoS ONE

View full text Add to dashboard Cite

Temporal lobe epilepsy is the most common form of partial-onset epilepsy and accounts for the majority of adult epilepsy cases in most countries. A critical role for the hippocampus (and to some extent amygdala) in the pathology of these epilepsies is clear, with selective removal of these regions almost as effective as temporal lobectomy in reducing subsequent seizure risk. However, there is debate about whether hippocampus is ‘victim’ or ‘perpetrator’: The structure is ideally placed to ‘broadcast’ epileptiform activity to a great many other brain regions, but removal often leaves epileptiform events still occurring in cortex, particularly in adjacent areas, and recruitment of the hippocampus into seizure-like activity has been shown to be difficult in clinically-relevant models. Using a very simple model of acute epileptiform activity with known, single primary pathology (GABAA Receptor partial blockade), we track the onset and propagation of epileptiform events in hippocampus, parahippocampal areas and neocortex. In this model the hippocampus acts as a potential seizure focus for the majority of observed events. Events with hippocampal focus were far more readily propagated throughout parahippocampal areas and into neocortex than vice versa. The electrographic signature of events of hippocampal origin was significantly different to those of primary neocortical origin – a consequence of differential laminar activation. These data confirm the critical role of the hippocampus in epileptiform activity generation in the temporal lobe and suggest the morphology of non-invasive electrical recording of neocortical interictal events may be useful in confirming this role.

show abstract

Section: Discussionmentioning

confidence: 99%

Electrographic Waveform Structure Predicts Laminar Focus Location in a Model of Temporal Lobe Seizures In Vitro

Adams

Traub

et al. 2015

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…In line with this view, in vivo studies have shown that kindling within the perirhinal cortex promotes seizure activity more rapidly than stimulation of the piriform cortex, amygdala or dorsal hippocampus (McIntyre et al, 1993, 1999; Sato et al, 1998). Moreover, lesioning the perirhinal cortex (Kelly and McIntyre, 1996; Fukumoto et al, 2002) or applying glutamatergic receptor antagonists (Tortorella et al, 1997) or adenosine A1 receptor agonists (Mirnajafi-Zadeh et al, 1999) to the perirhinal cortex attenuated and even prevented the appearance of seizure activity following amygdala kindling.…”

Section: Epileptiform Synchronization In Vitromentioning

confidence: 99%

Perirhinal cortex and temporal lobe epilepsy

Biagini¹,

D’Antuono²,

Benini³

et al. 2013

Front. Cell. Neurosci.

View full text Add to dashboard Cite

The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures. Both features may be relevant to the pathophysiology of mesial temporal lobe epilepsy that represents the most refractory adult form of epilepsy with up to 30% of patients not achieving adequate seizure control. Compared to other limbic structures such as the hippocampus or the entorhinal cortex, the perirhinal area remains understudied and, in particular, detailed information on its dysfunctional characteristics remains scarce; this lack of information may be due to the fact that the perirhinal cortex is not grossly damaged in mesial temporal lobe epilepsy and in models mimicking this epileptic disorder. However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability. In this review we: (i) highlight the fundamental electrophysiological properties of perirhinal cortex neurons; (ii) briefly stress the mechanisms underlying epileptiform synchronization in perirhinal cortex networks following epileptogenic pharmacological manipulations; and (iii) focus on the changes in neuronal excitability and cytoarchitecture of the perirhinal cortex occurring in the pilocarpine model of mesial temporal lobe epilepsy. Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

show abstract

“…The kainic acid dose (an average of 0.07 lg kainic acid/g body weight among ages) is similar to the dosage of kainic acid injected into the perirhinal or occipital cortex that causes seizures in adult rodents (0.004-0.010 lg kainic acid/g body weight). [32][33][34] Kainic acid was either injected 5-7 mm deep into the cortical parenchyma of the rostral gyrus leaving the needle in place for 5 min (to prevent egress) or kainic acid was mixed into the blood that was placed under the dura at one time. One piglet that received kainic acid in the cortical parenchyma developed an intraparenchymal hematoma and was excluded.…”

Section: Protocol Specific To Experimental Phasementioning

confidence: 99%

Development of a Model of Hemispheric Hypodensity (“Big Black Brain”)

Costine-Bartell

McGuone

Price

et al. 2019

Journal of Neurotrauma

View full text Add to dashboard Cite

Subdural hematoma (SDH) is the most common finding after abusive head trauma (AHT). Hemispheric hypodensity (HH) is a radiological indicator of severe brain damage that encompasses multiple vascular territories, and may develop in the hemisphere(s) underlying the SDH. In some instances where the SDH is predominantly unilateral, the widespread damage is unilateral underlying the SDH. To date, no animal model has successfully replicated this pattern of injury. We combined escalating severities of the injuries and insults commonly associated with HH including SDH, impact, mass effect, seizures, apnea, and hypoventilation to create an experimental model of HH in piglets aged 1 week (comparable to human infants) to 1 month (comparable to human toddlers). Unilateral HH evolved over 24 h when kainic acid was applied ipsilateral to the SDH to induce seizures. Pathological examination revealed a hypoxic-ischemic injury-type pattern with vasogenic edema through much of the cortical ribbon with relative sparing of deep gray matter. The percentage of the hemisphere that was damaged was greater on the ipsilateral versus contralateral side and was positively correlated with SDH area and estimated seizure duration. Further studies are needed to parse out the pathophysiology of this injury and to determine if multiple injuries and insults act synergistically to induce a metabolic mismatch or if the mechanism of trauma induces severe seizures that drive this distinctive pattern of injury.

show abstract

Perirhinal cortical lesion suppresses the secondary generalization in kainic acid‐induced limbic seizure

Cited by 10 publications

References 18 publications

Electrographic Waveform Structure Predicts Laminar Focus Location in a Model of Temporal Lobe Seizures In Vitro

Electrographic Waveform Structure Predicts Laminar Focus Location in a Model of Temporal Lobe Seizures In Vitro

Perirhinal cortex and temporal lobe epilepsy

Development of a Model of Hemispheric Hypodensity (“Big Black Brain”)

Contact Info

Product

Resources

About