Magnetic resonance spectroscopy reveals an epileptic network in juvenile myoclonic epilepsy.
OBJECTIVE
To investigate the cerebral metabolic differences between patients with juvenile myoclonic epilepsy (JME) and normal controls and to evaluate to what extent these metabolic alterations reflect involvement of an epileptic network.


METHODS
Sixty patients with JME were submitted to multi-voxel proton spectroscopy (1H-MRS) at 1.5 T over medial prefrontal cortex (MPC), primary motor cortex (PMC), thalamus, striatum, posterior cingulate gyrus (PCG), and insular, parietal, and occipital cortices. We determined ratios for integral values of N-acetyl-aspartate (NAA) and glutamate-glutamine (GLX) over creatine-phosphocreatine (Cr). The control group (CTL) consisted of 30 age- and sex-matched healthy volunteers.


RESULTS
The NAA/Cr ratio, a measure of neuronal injury, was reduced in PMC, MPC, and thalamus among patients. In addition, they had an altered GLX/Cr ratio, which is involved in excitatory activity, on PMC, MPC, and PCG, where it was reduced, whereas it was increased on insula and striatum. Multiple regression analysis revealed the strongest correlation between thalamus and MPC, but the thalamus was also correlated with insula, occipital cortex, and striatum among patients. Lower NAA/Cr was observed with advancing age and duration of epilepsy, regardless of frequency of seizures and antiepileptic drug therapy in thalamus and frontal cortex.


CONCLUSIONS
The identification of a specific network of neurochemical dysfunction in patients with JME, with diverse involvement of particular structures within the thalamocortical circuitry, suggests that cortical hyperexcitability in JME is not necessarily diffuse, supporting the knowledge that the focal/generalized distinction of epileptogenesis should be reconsidered. Furthermore, evidence is provided toward progressive neuronal dysfunction in JME.
Lin
Katia
K
Unidade de Pesquisa e Tratamento das Epilepsias (UNIPETE), Universidade Federal de São Paulo (UNIFESP/EPM), São Paulo, SP, Brazil. linkatia@uol.com.br
Carrete
Henrique
H
Lin
Jaime
J
Peruchi
Mirella Maccarini
MM
de Araújo Filho
Gerardo Maria
GM
Guaranha
Mirian Salvadori Bittar
MS
Guilhoto
Laura Maria Figueiredo Ferreira
LM
Sakamoto
Américo Ceiki
AC
Yacubian
Elza Márcia Targas
EM
D000328:Adult; D000704:Analysis of Variance; D000927:Anticonvulsants / Q000494:pharmacology / Q000627:therapeutic use; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D001923:Brain Chemistry / Q000502:physiology; D016022:Case-Control Studies; D003401:Creatine / Q000378:metabolism; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D008875:Middle Aged; D020190:Myoclonic Epilepsy, Juvenile / Q000175:diagnosis* / Q000188:drug therapy / Q000378:metabolism*; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D011522:Protons; D055815:Young Adult
D000927:Anticonvulsants; D011522:Protons; D005973:Glutamine; D001224:Aspartic Acid; D018698:Glutamic Acid; C000179:N-acetylaspartate; D003401:Creatine