Nonconvulsive seizures after traumatic brain injury are associated with hippocampal atrophy

Abstract

Objective: To determine if posttraumatic nonconvulsive electrographic seizures result in long-term brain atrophy.

Methods: Prospective continuous EEG (cEEG) monitoring was done in 140 patients with moderate to severe traumatic brain injury (TBI) and in-depth study of 16 selected patients was done using serial volumetric MRI acutely and at 6 months after TBI. Fluorodeoxyglucose PET was done in the acute stage in 14/16 patients. These data were retrospectively analyzed after collection of data for 7 years.

Results: cEEG detected seizures in 32/140 (23%) of the entire cohort. In the selected imaging subgroup, 6 patients with seizures were compared with a cohort of 10 age- and GCS-matched patients with TBI without seizures. In this subgroup, the seizures were repetitive and constituted status epilepticus in 4/6 patients. Patients with seizures had greater hippocampal atrophy as compared to those without seizures (21 +/- 9 vs 12 +/- 6%, p = 0.017). Hippocampi ipsilateral to the electrographic seizure focus demonstrated a greater degree of volumetric atrophy as compared with nonseizure hippocampi (28 +/- 5 vs 13 +/- 9%, p = 0.007). A single patient had an ictal PET scan which demonstrated increased hippocampal glucose uptake.

Conclusion: Acute posttraumatic nonconvulsive seizures occur frequently after TBI and, in a selected subgroup, appear to be associated with disproportionate long-term hippocampal atrophy. These data suggest anatomic damage is potentially elicited by nonconvulsive seizures in the acute postinjury setting.

Figure 1 Comparison of the PET images for 1 patient seizing during PET (ictal), the interictal state in the seizure group, and nonseizure group The global brain metabolism in each group is compared with the regional metabolism in the hippocampus (hippo). (A) Glucose metabolism (mg/100 mg/min); (B) oxidative metabolism (mg/100 mg/min); (C) cerebral blood flow (cc/100 mg/min). The seizure PET shows regionally increased glucose metabolism in the absence of an increase in blood flow or oxidative metabolism.

Figure 2 Long-term brain atrophy in hippocampal regions are shown for the seizure and nonseizure groups Bars are labeled by group (seizure, black; nonseizure, white) and by hippocampus location (right, left, ipsilateral or contralateral to the EEG seizure focus). There is greatest hippocampal atrophy in the seizure patients' hippocampi ipsilateral to the EEG seizure focus. The right hemisphere was ipsilateral to seizures more commonly than the left. Late hippo atrophy = percentage atrophy at 6 months as compared with the acute image.

Figure 3 Hippocampal atrophy ipsilateral to the seizure focus Composite of acute PET scan and acute and chronic MRI volumetric scans on seizure subject 4. The patient has increased glucose metabolism in the right hippocampus without a similar increase in CMRO2. The hyperintensity on the fluid-attenuated inversion recovery (FLAIR) sequence was due to acute seizure activity and not traumatic hemorrhage. MRI at 6 months shows right hippocampal atrophy and also right temporal lobe atrophy. CMRO2 = oxidative metabolism PET; FDG = fluorodeoxyglucose PET; PIH = postinjury hour.