Can Intractable Temporal Lobe Epilepsy be Determined Early in the Course of the Disease?
Abstract & Commentary
By Cynthia L. Harden, MD, Professor of Neurology and Neuroscience, Comprehensive Epilepsy Center, Weill Medical College of Cornell University. Dr. Harden reports no financial relationship relevant to this field of study.
Synopsis: The presence of hippocampal sclerosis, by itself, does not predict the clinical course of temporal lobe epilepsy.
Source: Briellmann RS, et. al. Hippocampal sclerosis: MR prediction of seizure intractability. Epilepsia. 2007;48(2):315-323.
Using 3 tesla magnetic resonance (MR) imaging, these investigators compared brain MR characteristics of 24 subjects with intractable temporal lobe epilepsy (TLE) with 17 subjects with mild TLE, and 60 normal controls. Specifically, the MR parameters studied were hippocampal volumes, T2 relaxometry in the hippocampus, amygdala, thalamus and white matter of the anterior temporal lobe (ATL) and frontal lobe, as well as proton MR spectroscopy (MRS) of the temporal lobe. The authors differentiated the intractable TLE from the mild TLE groups by seizure frequency; the intractable patients had an average of 3 complex partial seizures per week, while most of the mild TLE patients had no seizures for 3 months before the investigation, and the remainder had one mild complex partial seizure per month.
The rather surprising results showed no difference in hippocampal volumes or hippocampal T2 signal increase between the 2 epilepsy groups, and age at onset and duration of epilepsy were the same across the epilepsy groups. The MR characteristics that differentiated the high vs the low seizure frequency groups were T2 signal abnormality in the ATL white matter, and hippocampal N-acetylaspartate concentration determined by MRS in the temporal lobe ispilateral to the seizure focus; both were significantly more abnormal in the high seizure frequency group. The authors speculate that hippocampal T2 signal increase and decreased hippocampal volume, a complex known as hippocampal sclerosis (HS), and often present in temporal lobe epilepsy, is conferred by the presence of epilepsy but not by intractable epilepsy. However, abnormal T2 signal in the ATL white matter and abnormal MRS seizure-producing hippocampus are associated with intractable epilepsy, as defined by high complex partial seizure frequency.
Commentary
These interesting results provide insight into how recurrent temporal lobe seizures affect brain structures, and perhaps provide a "surrogate marker" for intractable epilepsy. The findings would be useful for aiding in the decision to offer temporal lobe resection for persons with TLE; the presence of these markers may indicate ongoing temporal lobe injury and dysfunction in TLE whereas the findings associated with HS only support the diagnosis of TLE. It is now well appreciated that not all persons with HS have intractable epilepsy and may have only rare seizures throughout their lives. The ATL T2 increased signal and MRS information would also be potentially useful for managing patients who have difficulty reporting their seizure frequency since they may be amnestic for the events.
One limitation of this study is that data were obtained using a 3 Tesla MR scanner, which is not in widely available at this time. Further, although MRS N-acetylaspartate values are also not standardized, the findings suggest that reliable temporal lobe MRS N-acetylaspartate values as a fraction of normal control values may be useful in the MR evaluation of TLE patients and should further developed.
Although the authors make a clear case for how their intractable TLE patients were differentiated from their "mild" TLE group, the usefulness of self- and observer-reporting of seizure frequency can be questioned. The MR findings that differentiated these 2 groups really only differentiates between high and low seizure frequency reporting. It may be that these parameters do not differentiate between an intractable or nonintractable epileptic syndrome. This may be especially applicable to the MRS findings, which are known to be very dynamic in their representation of brain function. However, the ATL signal abnormality is likely a more reliable reflection of ongoing temporal lobe injury and intractable epilepsy itself.
The presence of hippocampal sclerosis, by itself, does not predict the clinical course of temporal lobe epilepsy.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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