Signal Changes In Epilepsy

AT, anterior temporal lobe.

AT, anterior temporal lobe.

FIG. 4.49. This is a severe example of signal change in the anterior temporal lobe and temporal pole. The T2-weighted image (A) shows high signal in the temporal white matter, in this case even greater than the gray matter (long arrow). The heavily T1 -weighted IR sequence (B) shows decreased signal in temporal white matter. Abnormal signal is also in the atrophic hippocampus and was proved to be typical hippocampal sclerosis. There was no developmental abnormality in the resected temporal lobe.

temporal white matter. In common with Mitchell's study, no convincing pathologic abnormality was observed in Meiners's reports (327, 330, 343) of these findings.

In the absence of gliosis or minor dysplasia as an explanation of these MRI findings, it is tempting to attribute them to defective myelination, failure of myelination, or loss of myelin, due either to seizures or to an early childhood event.

Abnormal temporal lobe myelination is unlikely to be the whole explanation, as the signal change involves the cortical gray matter in some cases. We now believe these changes are due to an arrest in development of the temporal lobes and persistence of immature cell types (465) and myelin. The immature temporal lobe does indeed look remarkably like the changes we describe (Fig. 4.52).

FIG. 4.49. This is a severe example of signal change in the anterior temporal lobe and temporal pole. The T2-weighted image (A) shows high signal in the temporal white matter, in this case even greater than the gray matter (long arrow). The heavily T1 -weighted IR sequence (B) shows decreased signal in temporal white matter. Abnormal signal is also in the atrophic hippocampus and was proved to be typical hippocampal sclerosis. There was no developmental abnormality in the resected temporal lobe.

Temporal Lobe Abnormalities

FIG. 4.50. This is a subtle example of anterior temporal lobe abnormality seen on heavily T1 -weighted IR images. Careful examination of the white matter shows decreased signal in the right temporal lobe core (A). There is also subtle atrophy, particularly of the superior and middle temporal gyrus on the right (B). The left image shows abnormal signal in the mesial gray matter, which is more obviously in the hippocampal

FIG. 4.50. This is a subtle example of anterior temporal lobe abnormality seen on heavily T1 -weighted IR images. Careful examination of the white matter shows decreased signal in the right temporal lobe core (A). There is also subtle atrophy, particularly of the superior and middle temporal gyrus on the right (B). The left image shows abnormal signal in the mesial gray matter, which is more obviously in the hippocampal

FIG. 4.51. Subtle changes in the anterior temporal lobe seen on T2-weighted images. The left image shows increased signal in a small hippocampal head consistent with hippocampal sclerosis (short arrow). The anterior temporal lobe white matter core is poorly defined compared to the contralateral side (long arrow, B).

FIG. 4.51. Subtle changes in the anterior temporal lobe seen on T2-weighted images. The left image shows increased signal in a small hippocampal head consistent with hippocampal sclerosis (short arrow). The anterior temporal lobe white matter core is poorly defined compared to the contralateral side (long arrow, B).

The anterior temporal lobe abnormality is present in children with the same frequency as adults (about 66% of cases with HS), suggesting that it is not the consequence of longstanding seizures (138). It is the arrested myelination that most probably gives these signal changes. Atrophy, on the other hand, is likely to be a combination of arrest of growth and secondary damage from seizures. The temporal pole is the last part of the cortex to fully develop and myelination and other developmental changes occur here up to 80 months after birth.

FIG. 4.52. A. A 10-year-old boy with TLE and definite and classical HS on the left side. The anterior temporal lobe shows marked signal change similar to that see in Figure 4.49. This extends through the temporal lobe and can involve the insula, as in this case. B. A normal 12-month-old boy. Note the similarity of this normal developmental stage with the persistent features in our patient with HS and TLE.

FIG. 4.52. A. A 10-year-old boy with TLE and definite and classical HS on the left side. The anterior temporal lobe shows marked signal change similar to that see in Figure 4.49. This extends through the temporal lobe and can involve the insula, as in this case. B. A normal 12-month-old boy. Note the similarity of this normal developmental stage with the persistent features in our patient with HS and TLE.

The finding, in a children cohort, that an initial precipitating event before the age of 2 almost always leads to this change, suggests that the injury that causes hippocampal damage causes changes in the immature AT that arrests its development. There is no correlation between the presence of AT changes on MRI and length of seizure history or age of onset of epilepsy. There is no difference in seizure-free outcome between the groups with and without AT changes. The temporal pole is virtually the last area of the brain to mature, and this may make it vulnerable to the effects of seizures.

In the patients with HS, there is an association between AT signal abnormality and the severity of HS as determined by a higher T2-relaxation time within the hippocampus. Severity of insult as a cause of this change is supported by the significant twofold increase in the incidence of febrile convulsions in the patients with AT changes.

There appears to be few consequences of anterior temporal abnormality (138, 252). Neuropsychologic findings appear to be identical in patients with and without this, seizure outcome is the same, and postoperative memory deficit in left-sided operations was the same in both groups (138, 252). Overall it seems that the AT MR changes do not determine functionality of tissue.

One must always be careful not to assume that all anterior temporal changes in signal are due to the same process; other causes must be recognized. True developmental abnormality, if severe, can give this appearance (Fig. 4.53).

FIG. 4.53. An example of a focal cortical dysplasia, which can give a similar appearance in the anterior temporal lobe. Coronal T2 image showing increased signal from the left temporal lobe, which has a more focal distribution than is the case for the more diffuse anterior temporal lobe change. No mass effect Is seen.

Was this article helpful?

0 0
Relaxation Audio Sounds Babbling Brook

Relaxation Audio Sounds Babbling Brook

This is an audio all about guiding you to relaxation. This is a Relaxation Audio Sounds with sounds from the Babbling Brooks.

Get My Free MP3 Audio


Post a comment