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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 26:319-332, February 2005
© 2005 American Society of Neuroradiology

BRAIN

MR Volumetric Analysis of The Piriform Cortex and Cortical Amygdala in Drug-Refractory Temporal Lobe Epilepsy

Pedro M. Gonçalves Pereira^a,b,c, Ricardo Insausti^d, Emilio Artacho-Pérula^d, Tuuli Salmenperä^e, Reetta Kälviäinen^e and Asla Pitkänen^f

^a Department of Neuroradiology, Pedro Hispano Hospital, Matosinhos, Portugal
^b Department of Medical Science, Medical School, University of Beira Interior, Covilhã, Portugal
^c Institute of Electronics Engineering and Telematics of Aveiro, University of Aveiro, Aveiro, Portugal
^d Department of Health Sciences and Regional Center for Medical Investigations, Human Neuroanatomy Laboratory, School of Medicine, University of Castilla-la Mancha, Albacete, Spain
^e Department of Neurology, Kuopio University Hospital, Kuopio, Finland
^f Epilepsy Research Laboratory, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, Kuopio, Finland

Address reprint requests to Asla Pitkänen, MD, PhD, Epilepsy Research Laboratory, A.I. Virtanen Institute for Molecular Sciences, University of Kuopio, P. O. Box 1627, FIN-70 211 Kuopio, Finland, E-mail: asla.pitkanen{at}uku.fi.

BACKGROUND AND PURPOSE: The assessment of patients with temporal lobe epilepsy (TLE) traditionally focuses on the hippocampal formation. These patients, however, may present structural abnormalities in other brain areas. Our purpose was to develop a method to measure the combined volume of the human piriform cortex and cortical amygdala (PCA) by using MR imaging and to investigate PCA atrophy.

METHODS: The definition of anatomic landmarks on MR images was based on histologic analysis of 23 autopsy control subjects. Thirty-nine adults with chronic TLE and 23 age-matched control subjects were studied. All underwent high-spatial-resolution MR imaging at 1.5T, including a tilted T1-weighted 3D dataset. The PCA volumes were compared with the control values and further correlated with hippocampal, amygdale, and entorhinal cortex volumes.

RESULTS: The normal volume was 530 ± 59 mm³ (422–644) [mean ± 1 SD (range)] on the right and 512 ± 60 mm³ (406–610) on the left PCA (no asymmetry, and no age or sex effect). The intraobserver and interobserver variability were 6% and 8%, respectively. In right TLE patients, the mean right PCA volume was 18% smaller than in control subjects (P < .001) and 15% smaller than in left TLE (P < .001). In left TLE, the mean left PCA volume was 16% smaller than in control subjects (P < .001) and 19% smaller than in right TLE (P < .001). Overall, 46% (18/39) of the patients had a greater than 20% volume reduction in the ipsilateral PCA. There was bilateral atrophy in 18% (7/39). Patients with hippocampal volumes of at least 2 SDs below the control mean had an 18% reduction in the mean PCA volume compared with patients without hippocampal atrophy (P < .001). Ipsilaterally, hippocampal (r = 0.756, P < .01), amygdaloid (r = 0.548, P < .01), and entorhinal (r = 0.500, P < .01) volumes correlated with the PCA volumes.

CONCLUSION: The quantification of PCA volume with MR imaging showed that the PCA is extensively damaged in chronic TLE patients, particularly in those with hippocampal atrophy.