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1.
Figure 2

Figure 2. Probability of unprovoked seizures following severe lateral FPI. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

The cumulative probability of detecting epileptiform ECoG events in post-FPI (gray columns) and sham-operated (white columns) rats is plotted versus time after injury. Numerators indicate number of epileptic rats, while denominators indicate number of animals evaluated in the group.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
2.
Figure 7

Figure 7. Correlation between degree of glial reactivity and presence of epilepsy. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

Blind assessment of GFAP immunoreactivity at Bregma −3mm/−6.5mm ipsilateral to the injury site 9–16 weeks post-injury. All FPI animals (5 rats) with epileptic ECoG events showed a temporal focus of glial reactivity that was pronounced in 4, and mild in 1 of them. One FPI animal was not epileptic (4 months post-injury) and did not present a temporal focus of glial reactivity. The ratio of non epileptic vs. epileptic FPI animals in this study is different from the one shown in figure 2 because several epileptic rats were intentionally used for the slice physiology experiments.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
3.
Figure 4

Figure 4. Frontal-parietal and parietal-temporal ECoG. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

A) Representative recording of a spreading partial seizure originating from the frontal-parietal neocortex sampled by electrode 4 (central traces). Note it is first detected by electrode 4, and then by the other electrodes placed both ipsilaterally and contralaterally. A representative recording of generalized seizure appearing in multiple channels simultaneously, albeit with different amplitudes (right traces). B) Representative recording of a partial seizure limited to the frontal-parietal neocortex (middle traces). From the amplitude of the epileptic burst the focus can be estimated to be approximately at the site of FPI. Representative recording of partial seizures that originated at the site of FPI and were then propagated to the temporal cortex (right traces). Insets, left) Schematic of the location of the 7 cortical electrodes (filled circles) and of the injury site (hollow circle). The montage is indicated next to each ECoG traces. ECoG calibration bars are on the left. In all traces, vertical dotted lines mark the first detectable epileptiform activity.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
4.
Figure 3

Figure 3. Evolution of chronic seizures following lateral FPI. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

Electrical and behavioral correlates of PTE progression is assessed in 5 animals epileptic at week 2 post-injury. A) The proportions of events of grade 1, 2, and 3 are plotted over time from 2 to 8 weeks post-injury. Partial events (grade 1; filled square) were most frequently observed at 2 weeks post-injury. Spreading events (grade 2; filled circles) increased over time post-injury. Generalized events (grade 3; hollow triangle) remained constant up to 8 weeks post-injury. B) The increase in proportion of spreading epileptiform ECoG events was observed in all animals studies. C) The behavioral score during epileptiform ECoG events is plotted at 2 and 8 weeks post-injury. Sub-clinical seizures were only observed at 2 weeks, while facial automatisms, head-nodding and myoclonus were more frequently observed at 8 weeks post-injury. D) The increase in behavioral seizure score was observed in all animals studied. Each circle-diamond pair represents one animal evaluated at 2 and 8 weeks, respectively. Data are presented as mean±S.E.M. Statistics with paired t-test.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
5.
Figure 6

Figure 6. Cellular necrosis and reactive glial response after lateral FPI. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

Cresyl-violet staining (A through D) and GFAP immunoreactivity (E through H) in coronal sections from injured animals. From top to bottom, micrographs and inserts of representative regions are shown for stereotaxic coordinates Bregma 0 mm, Bregma −2mm, Bregma −3.5mm, and Bregma −6.5mm. Chronically following lateral FPI (6 to 16 weeks post-injury) there is a marked decrease in large cell bodies (neurons), and a marked increase in small cell bodies attributed to marked gliosis in the ipsilateral temporal lobe (C1). In addition, at the same time there is a marked increase in GFAP immunoreactivity of the hemisphere ipsilateral to the injury site. Clouds of GFAP+ reactive glial cells were observed from the white matter and gray/white matter interface of the right forelimb parietal cortex (E) throughout the cortical layers of the occipital/temporal cortex (G, H). Scale bars are 1 mm and 50 µm for all the low magnification and high magnification plates, respectively.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
6.
Figure 1

Figure 1. Post-FPI chronic seizures are partial in origin. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

Inset top, left) Schematic of the locations of the five cortical electrodes (filled circles) and of the injury site (hollow circle) in respect to the rat skull. From top to bottom, about 1.5 minutes of continuous ECoG recording from a posttraumatic rat, 2.5 months after severe lateral FPI, are shown. Frequent epileptiform events were recorded while the rat was fully awake and engaged in exploratory behavior. ECoG bursts were accompanied by pauses in ongoing behavior. Asterisks indicate partial epileptiform events (grade 1 and 2) all originating from the peri-lesion neocortical area. ECoG calibration bars are on the left. Dotted box highlights a typical grade 2 event. Bottom, middle inset) a grade 2 event at higher temporal resolution displaying its partial nature. Horizontal brackets delimit three areas of the top ECoG trace (channel 4–5) sampled for FFT analysis. Inset bottom, right) FFT analysis of three areas of the ECoG trace occurred immediately before, during and immediately after the epileptiform burst highlighted by the dotted box. FFT1 demonstrates the frequency components of the baseline ECoG immediately before the epileptic burst (1–9Hz). FFT 2 demonstrates the frequency components (5–30 Hz) during the epileptic burst, and the dramatic increase in the contribution of higher frequencies. FFT3 demonstrates the frequency components of the ECoG immediately after the epileptic burst. Note the disappearance of the theta activity at 7Hz immediately after the burst.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.
7.
Figure 5

Figure 5. Lateral FPI causes persistent neocortical hyperexcitability. From: Posttraumatic Epilepsy Following Fluid Percussion Injury in the Rat.

A map of neocortical excitability at Bregma 0 mm / −1 mm is constructed by assigning a black circle to each sub-region that displayed at least one slice with abnormal excitability. LFPs of population activities in layer V of coronal neocortical slices obtained from FPI animals (4 rats, 10 slices) and sham-operated (2 rats, 5 slices), 8–10 weeks after surgery. Representative LFPs are shown for each subregion of the neocortex and for each stimulation frequency tested. Negative DC shifts, typical of seizure precipitation and spreading-depression-like events, are zeroed for clarity. A) In slices obtained from sham-operated animals stimuli evoked typical field responses in layer V. Each neocortical subregion could sustain 1 to 3 minutes of stimulation at 0.1 Hz and 1Hz without generating afterdischarges. Normal layer V excitability was observed throughout. B) The hemisphere ipsilateral to the injury displayed widespread hyperexcitability when stimulated at 0.1 Hz, and 1Hz for 1 to 3 minutes (5 slices). The contralateral hemisphere had a lower tendency toward afterdischarge generation (5 slices) than the ipsilateral one. Fr: Frontal cortex; FL: Forelimb area of cortex; Par: parietal cortex, area I; Par II: parietal cortex, area II. Filled circles mark areas where stimulation could elicit afterdischarges or spreading depression. The configuration of stimulating and recording electrodes is representatively displayed at the left forelimb cortex. Artifacts of the stimuli were clipped for clarity. Calibration bars represent 0.5 mV and 20 ms throughout the figure. Note that each pair of LFPs acquired at 0.1–1Hz has different scale bars.

Raimondo D’Ambrosio, et al. Brain. ;127(Pt 2):304-314.

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