ABSTRACT
A patient with chronic cerebral paragonimiasis began to have new motor seizures of the right face clonic contractions that occurred several hundred times a day resulting in the simple partial status epilepticus. The ictal EEG discharge started from the left frontal region and then spread to the left hemisphere. The ictal discharges were limited clearly to the left hemisphere. The brain MRI showed the multiple conglomerated round nodules with encephalomalacia in the left temporo-occipital lobes. Applying the ictal-interictal subtracted SPECT, we were able to localize the focal ictal hyperperfusion on the left precentral cortex adjacent to the lesions that correspond to the anatomical distribution of the left face motor area.
Subject(s)
Humans , Brain , Electroencephalography , Encephalomalacia , Epilepsies, Partial , Magnetic Resonance Imaging , Paragonimiasis , Seizures , Status Epilepticus , Subtraction Technique , Tomography, Emission-Computed, Single-PhotonABSTRACT
BACKGROUND: Although dystonic posturing (DP) during temporal lobe seizures is known to be related to basal ganglia activation, the mechanism of the dystonic posturing has not been investigated in greater details . METHODS: Thirty-two patients with mesial temporal lobe epilepsy (TLE) underwent ictal and interictal SPECTs. They were classified into two groups: 1) DP with ictal dystonia during ictal SPECT (N=15) and 2) Non-DP without dystonia (N=17). Ictal-interictal SPECT subtraction was performed as follows: co-registration, intensity normalization, subtraction, thresholding and then an overlay to SPGR MRI. The presence and intensity of ictal hyperperfusion were determined in frontal lobe, basal ganglia, temporal lobe and insular cortex. RESULTS: The incidences of ictal hyperperfusion in DP vs. Non-DP were caudate nucleus [80.0%(12/15 patients) vs. 0% (0/17), p=0.001], putamen [93.3% (14/15) vs. 48.2% (8/17), p=0.005], globus pallidus [53.3% (8/15) vs. 23.5% (4/17), p=0.082], thalamus [80.0% (12/15) vs. 41.2% (7/17), p=0.026], insular cortex [46.7% (7/15) vs.23.5% (4/17), p=0.051], orbitofrontal [46.7% (6/15) vs. 35.3% (7/17), p=0.053], medial frontal [6.7% (1/15) vs. 18.7% (2/17), p=0.621], dorsolateral frontal [13.3% (2/15) vs. 18.7%(2/17), p=0.737] in the hemisphere of epileptic side. In patients who showed ictal hyperperfusion in striatum and thalamus, the average intensity of hyperperfusion in DP vs. Non-DP was caudate nucleus 1.67 vs. 0.0, putamen 2.20 vs. 1.05, globus pallidus 1.2 vs. 0.65, thalamus 2.00 vs. 0.88 in the epileptic hemisphere. CONCLUSIONS: Caudate nucleus as well as putamen appeared to be important for producing ictal dystonia during TLE seizures. The greater intensity of ictal hyperperfusion in putamen, caudate nucleus and thalamus seems to be related to ictal dystonia.
Subject(s)
Humans , Basal Ganglia , Brain , Caudate Nucleus , Dystonia , Epilepsy, Temporal Lobe , Frontal Lobe , Globus Pallidus , Incidence , Magnetic Resonance Imaging , Putamen , Seizures , Temporal Lobe , Thalamus , Tomography, Emission-Computed, Single-PhotonABSTRACT
BACKGROUND: Although dystonic posturing (DP) during temporal lobe seizures is known to be related to basal ganglia activation, the mechanism of the dystonic posturing has not been investigated in greater details . METHODS: Thirty-two patients with mesial temporal lobe epilepsy (TLE) underwent ictal and interictal SPECTs. They were classified into two groups: 1) DP with ictal dystonia during ictal SPECT (N=15) and 2) Non-DP without dystonia (N=17). Ictal-interictal SPECT subtraction was performed as follows: co-registration, intensity normalization, subtraction, thresholding and then an overlay to SPGR MRI. The presence and intensity of ictal hyperperfusion were determined in frontal lobe, basal ganglia, temporal lobe and insular cortex. RESULTS: The incidences of ictal hyperperfusion in DP vs. Non-DP were caudate nucleus [80.0%(12/15 patients) vs. 0% (0/17), p=0.001], putamen [93.3% (14/15) vs. 48.2% (8/17), p=0.005], globus pallidus [53.3% (8/15) vs. 23.5% (4/17), p=0.082], thalamus [80.0% (12/15) vs. 41.2% (7/17), p=0.026], insular cortex [46.7% (7/15) vs.23.5% (4/17), p=0.051], orbitofrontal [46.7% (6/15) vs. 35.3% (7/17), p=0.053], medial frontal [6.7% (1/15) vs. 18.7% (2/17), p=0.621], dorsolateral frontal [13.3% (2/15) vs. 18.7%(2/17), p=0.737] in the hemisphere of epileptic side. In patients who showed ictal hyperperfusion in striatum and thalamus, the average intensity of hyperperfusion in DP vs. Non-DP was caudate nucleus 1.67 vs. 0.0, putamen 2.20 vs. 1.05, globus pallidus 1.2 vs. 0.65, thalamus 2.00 vs. 0.88 in the epileptic hemisphere. CONCLUSIONS: Caudate nucleus as well as putamen appeared to be important for producing ictal dystonia during TLE seizures. The greater intensity of ictal hyperperfusion in putamen, caudate nucleus and thalamus seems to be related to ictal dystonia.