Figure 7.

Coronal slices from T2-weighted magnetic resonance imaging 11 months after 8 hours of perforant pathway stimulation in Long-Evans rats that exhibited convulsive status epilepticus (CSE) (B), or non-convulsive satatus epilepticus (NCSE) (C). A1,A2: Naïve images acquired from the same animal seen in row B, prior to electrode implantation. B1,B2: Images acquired 11 months after 8 hours of perforant path stimulation (10 sec- long-20 Hz stimulus trains delivered once per minute for 8 hours) that caused mild (non-lethal) status epilepticus for the duration of the 8 hours of perforant pathway stimulation as a result of increased ambient temperature (see text). Arrows denote an elevated signal in extra-hippocampal areas. C1,C2: Images acquired 11 months after identical stimulation at normal ambient temperature, which did not cause convulsive status epilepticus. Note the lack of apparent injury in extra-hippocampal areas compared to the section in (B1). A3-C3: Nissl-stained coronal sections from rats subjected to convulsive vs. non-convulsive SE. A3: Nissl-stained section from a sham-stimulated rat. B3: Nissl-stained coronal section of the rat shown in B1 and B2. Note that the enhanced T2 signal reflected a pan-necrosis and loss of brain tissue presumably filled in vivo with cerebrospinal fluid. C3: Nissl-stained section from a stimulated rat that did not exhibit convulsive status epilepticus. Note the corresponding lack of extra-hippocampal damage in (A3) compared to panel (A2), but also greater pyramidal cell loss and hippocampal atrophy after non-convulsive status epilepticus (C3) than after convulsive status epilepticus (C3). Images were obtained in animals in which all metal electrodes had been removed within 24 hours of the end of stimulation or sham stimulation. Scale bar = 1 mm.