Table 2.
Abnormality | F | T | Par | O | H | Peri | C | BS | G | ||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Volume loss | 10 | 3.6 | 11.5 | 3 | 2 | 4 | 3 | 2 | 1 | ||||
Leukomalacia/gliosis | 20 | 7.1 | 23.0 | 8 | 3 | 6 | 2 | 1 | 8 | 2 | |||
Other WML | 8 | 2.8 | 9.2 | 5 | 1 | 4 | 1 | 1 | |||||
Encephalomalacia | 5 | 1.8 | 5.7 | 3 | 2 | 3 | 2 | ||||||
Gray matter lesion - heterotopias | 4 | 1.4 | 4.6 | 3 | 1 | 2 | |||||||
Gray matter lesion-Cortical dysplasias | 3 | 1.1 | 3.4 | 3 | |||||||||
Other gray matter lesion | 4 | 1.4 | 4.6 | 1 | 1 | 2 | |||||||
Increased diffusion† | 2 | 0.7 | 2.3 | 2 | 2 | 1 | 1 | ||||||
Decreased diffusion† | 0 | ||||||||||||
Hemorrhage | 0 | ||||||||||||
Vascular lesion | 3 | 1.1 | 3.4 | 2 | 2 | ||||||||
Ventricular Enlargement | |||||||||||||
1.0–1.5 cm | 39 | 13.9 | 44.8 | 39 | |||||||||
1.6–2.5 cm | 5 | 1.8 | 5.7 | 5 | |||||||||
>2.5 | 0 | ||||||||||||
Extra-axial Spaces – width over frontal | |||||||||||||
0.5–1.0 cm | 3 | 1.1 | 3.4 | 3 | |||||||||
1.1–1.5 cm | 0 | ||||||||||||
>1.5 cm | 0 | ||||||||||||
Hippocampal Abnormality – Atrophy‡ | 4 | 1.4 | 4.6 | 4 | |||||||||
Hippocampal Signal Abnormality‡ | 3 | 1.1 | 3.4 | 3 | |||||||||
Other Structural Abnormality | |||||||||||||
Not Significant | 8 | 2.8 | 9.2 | 8 | |||||||||
Significant | 1 | 0.4 | 1.1 | 1§ | |||||||||
No. of Children by Location# | 44 | 23 | 13 | 17 | 3 | 1 | 11 | 11 | 1 | 2 | |||
% of 87 | 50.6 | 26.4 | 14.9 | 19.5 | 3.4 | 1.1 | 12.6 | 12.6 | 1.1 | 2.3 | |||
% of Total | 15.7 | 8.2 | 4.6 | 6.0 | 1.1 | 0.4 | 3.9 | 3.9 | 0.4 | 0.7 |
NLS = not location specific, F = frontal, T = temporal, Par = parietal, O = occipital, H = hemisphere, Peri = periventricular, C = cerebellar, BS = brainstem, G = generalized.
There were no extra axial spaces – cerebellar convex abnormalities.
For a given abnormality, a child can have more than one location, so the total number of abnormalities across locations for any given abnormality may be more than the number of children with that abnormality.
Diffusion was associated with other abnormalities in all three children and was not counted as a separate abnormality when reporting the number of children with multiple abnormalities.
A few scans were judged to be inadequate to assess hippocampal atrophy (8 scans) and hippocampal signal abnormality (7 scans).
The significant structural abnormality was agenesis of corpus callosum.
For a given location, a child can have more than one abnormality, so the total number of abnormalities across abnormalities for any given location may be more than the number of children with any abnormality at that location.
Note. Empty cells = 0. Shaded rows represent “significant abnormalities” (i.e., those that were judged to be etiologically related to the seizure condition).