4. Temporal lobe atrophy: Frequent in elderly with epilepsy of unknown etiology. Issue 4 (April 2016)

• Record Type: Journal Article
• Authors: Lapointe, Emmanuelle; Deacon, Charles; Bocti, Christian; Royer-Perron, Louis; Cunnane, Stephen; Castellano, Alexandre
• Is Part Of: Clinical neurophysiology. Volume 127:Issue 4(2016:Apr.)
• Page Start: e161
• Publication Date: 2016-04
• Subjects: Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2015.10.055
• Languages: English
• ISSNs: 1388-2457

Abstract

Abstract : Objective: To evaluate the degree of temporal lobe atrophy (TLA) in elderly patients with new-onset epilepsy, and its relation to temporal epileptiform discharges. Background: No etiology can be identified in as much as 30% to 50% of cases of new-onset epilepsy in the elderly, despite adequate investigation. Degenerative diseases, notably Alzheimer's disease (AD), increase the risk of epilepsy, and are often underdiagnosed in routine clinical practice. Abnormal activity on electroencephalography (EEG) of demented epileptic individuals is most often found focally in temporal regions. Design/methods: We retrospectively reviewed neuroimaging and EEG results of a consecutive cohort of 322 elders with new-onset epilepsy. The > 65 year-old patients were evaluated at the Centre Hospitalier Universitaire de Sherbrooke (CHUS) between January 2001 and October 2010. On imaging, TLA was assessed visually on axial images and graded on a 0–3 scale estimating sulcal widening and temporal horn ventricular enlargement. Measurement of the temporal horn radial width (THRW) was also acquired as a quantitative estimate of TLA. TLA was compared between subjects with epilepsy of unknown etiology ( n = 127) and demented epileptic individuals of the same cohort ( n = 10), as well as a healthy elderly control group ( n = 31) and non-epileptic AD patients ( n = 10). EEG interpretations were also analyzed, looking for correlation between temporal lobe atrophy and temporal epileptiform discharges, in the whole epileptic cohort. Results: MRI (46%) or CT (93%) was available for 112 patients with epilepsy of unknown etiology. Thirty-eight percent of elderly with new-onset epilepsy of unknown cause had significant temporal atrophy, using the dichotomized 0–3 scale (0–1 vs 2–3) or THRW. This was significantly more than the healthy control group (0%) after adjustment for age and sex (p = 0.000). As expected, individuals of the same cohort with epilepsy attributed to dementia had higher prevalence of significant TLA using both THRW and the visual scale (70.4%, p = 0.026 and 76.9% p = 0.021) as did patients with established AD (70% p = 0.040 and 60% p = 0.077). EEG results were available for 297 of the 322 patients (92.2%), including 125 of the 127 subjects with epilepsy of unknown etiology. Epileptiform discharges were present in 111/297 (37.3%) and 45/125 (36%) individuals respectively, of which 68.5% and 55.5% were found in temporal leads. No correlation was found between the presence of temporal lobe atrophy, using either dichotomized THRW or the visual scale, and temporal epileptiform activity ( p = 0.312 and 0.469). Conclusions: A considerable proportion of elderly with new-onset epilepsy of unknown cause exhibit temporal lobe atrophy on brain imaging, which suggests that a degenerative disease such as AD could be underrecognized as a possible etiology. However, it appears there is no correlation between this atrophy and the temporal localization of epileptiform activity. Financial support: University Chair.