Abstracts

Rationale: Ictal SPECT studies have demonstrated hyperperfusion of the brainstem, cerebellum, basal ganglia, thalamus, and cortex. This study’s purpose was to determine the relationship between regional brain activation, and seizure secondary generalization. Methods: We retrospectively reviewed all SISCOM (subtraction ictal SPECT co-registered to MRI) data from the Medical College of Georgia from 1998 to 2009. Using Analyze 2.5, 5.0 and 8.1 (Mayo BIR, Rochester, MN), we reviewed 312 SISCOM studies (187 studies from 158 children, and 125 studies from 121 adults); 30 patients had more than one study. The SISCOM interpreters were blinded to seizure type, lateralization, and surgical history. We identified ictal hyperperfusion in 4 brain regions: brainstem, cerebellum, basal ganglia, and thalamus. Using the Chi-square test for each brain region, we determined if hyperperfusion was more likely during secondary generalized tonic-clonic (SGTC) seizures as compared to complex partial (CP) seizures without secondary generalization. Results: Brainstem hyperperfusion occurred for 34% (29/86) of SGTC seizures compared to 18% (40/226) of CP seizures without secondary generalization (p=0.002). Cerebellar hyperperfusion occurred for 64% (55/86) of SGTC seizures compared to 30% (67/225) of CP seizures without secondary generalization (p=0.001). Thalamic hyperperfusion occurred for 49% (42/86) of SGTC seizures compared to 36% (81/226) of CP seizures without secondary generalization (p=0.035). No significant relationship occurred for basal ganglia hyperperfusion. This relationship occurred for both children and adults. This relationship also occurred for both ablative surgery cases and non-ablative surgery cases. Correspondence analysis revealed that an increased number of hyperperfused regions, and cerebellar hyperperfusion were linked to secondary generalized seizures. Conclusions: In conclusion, this study delineates the subcortical network linked to secondary seizure generalization. This study confirms the role of the superior cerebellum in secondary seizure generalization (Blumenfeld et al., 2009).