Perirhinal cortex and temporal lobe epilepsy

Abstract

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.

Object and spatial memory after neonatal perirhinal lesions in monkeys

“…Yet, a recent review of the literature [55] indicated a volumetric reduction of the perirhinal cortex in a subset of patients affected by temporal lobe epilepsy in spite of normal hippocampal volumes as well as a presence of selective neuronal loss and synaptic reorganization in the perirhinal cortex in the absence of hippocampal sclerosis. Interestingly, Guedj and colleagues [15] showed that performance on recognition tests in patients with temporal lobe epilepsy was correlated with interictal metabolism of entorhinal/perirhinal cortex but not with the hippocampus.…”

Blockade of in vitro ictogenesis by low-frequency stimulation coincides with increased epileptiform response latency

“…Biagini et al, 2013), the onset of the ictal discharge recorded from the PC was charac-154 terized either by a series of 3-4 events that progressively increased in their rate of occurrence 155(Fig. 1Ca, arrows)or by a single, large amplitude transient (Fig.…”

Adenosine A2A receptor and ecto-5′-nucleotidase/CD73 are upregulated in hippocampal astrocytes of human patients with mesial temporal lobe epilepsy (MTLE)

“…This disorder is characterized by irreversible biochemical and structural changes in the hippocampus and several neocortical regions [2][3][4]. In spite of the extensive research of last decades resulting in the discovery of new antiepileptic drugs available for clinical practice, up to 80 % of MTLE patients remain refractory to medication [5].…”