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NEUROLOGY 2004;62:1729-1735
© 2004 American Academy of Neurology

Temporal lobe volumes in patients with hippocampal sclerosis with or without cortical dysplasia

B. Diehl, MD, I. Najm, MD, E. LaPresto, MS, R. Prayson, MD, P. Ruggieri, MD, A. Mohamed, FRACP, Z. Ying, PhD, M. Lieber, MS, T. Babb, PhD, W. Bingaman, MD and H. O. Lüders, MD PhD

From the Departments of Neurology (Drs. Diehl, Najm, Mohamed, and Lüders), Neurosurgery (Dr. Bingaman, E. LaPresto), Biostatistics and Epidemiology (M. Lieber), Radiology (Dr. Ruggieri), Pathology (Dr. Prayson), and Neurosciences (Drs. Ying and Babb), The Cleveland Clinic Foundation, OH.

Address correspondence and reprint requests to Dr. B. Diehl, Department of Neurology, The Cleveland Clinic Foundation, 9500 Euclid Ave., Desk S51, Cleveland, OH 44195; e-mail: diehlb{at}ccf.org

Background: Recent MRI-based volume reconstruction studies in intractable temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS) suggested atrophy that extends to the adjacent neocortical areas.

Objective: To study the extent of temporal lobe volume (TLV) abnormalities in patients with pathologically confirmed HS (with or without cortical dysplasia [CD]) who underwent anterior temporal lobectomy for the treatment of drug-resistant TLE.

Methods: Fifty patients (right TLE: n = 24; left TLE: n = 26) were found to have HS (hippocampal cell loss of >30%). Associated neocortical CD was seen in 20 patients (43%). MRI-based TLVs and hippocampal and hemispheric volume reconstructions in all patients were compared between pathologic groups and with volumes acquired from 10 age-matched control subjects.

Results: TLVs ipsilateral to the epileptogenic zone in patients with TLE were smaller than TLVs in control subjects (p < 0.01). In patients with left TLE, TLVs ipsilateral to the epileptogenic zone were smaller than contralateral TLVs (left: 66.6 ± 8.3 cm3, right: 74.9 ± 10.0 cm3; p < 0.001). In patients with right TLE, there were no significant asymmetries. The contralateral TLVs (regardless of the side of surgery) were smaller in the HS + CD group than the HS group (HS + CD group: 74.9 ± 8.6 cm3, HS group: 79.7 ± 6.6 cm3; p < 0.05). Patients with HS + CD had a tendency to have less hippocampal atrophy and slightly smaller TLVs ipsilateral to the epileptogenic zone, accounting for significantly smaller TLV/hippocampal volume ratios compared with patients with HS alone.

Conclusions: Drug-resistant TLE due to HS is associated with extrahippocampal temporal lobe atrophy. The presence of bilateral temporal lobe atrophy is suggestive of a more widespread (bilateral) temporal lobe involvement in patients with HS and CD.


Received December 4, 2001. Accepted in final form January 24, 2004.

The current address of Dr. Mohamed is Department of Neurology, Royal Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, Camperdown, Australia. The current address of Dr. Babb is Department of Pediatric Neurology, Children’s Hospital of Michigan, Wayne State University, Detroit, MI.




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