Phosphorus magnetic resonance spectroscopy in the investigation of temporal lobe epilepsy: ‘reading between the lines’ of metabolic abnormalities

Abstract

T he natural course of mesial temporal lobe epilepsy (MTLE) is usually associated with a precipitating injury in childhood, which later develops to become the most common form of focal epilepsy in adulthood 1 . Hippocampal sclerosis (HS) is the main underlying lesion detected in both histopathology and magnetic resonance imaging (MRI) evaluation of these patients. A significant proportion of patients MTLE become refractory to antiepileptic drugs (AEDs). Surgery is the most effective treatment in this scenario, with the majority of patients becoming seizure free postoperatively. However, there are many open questions about the neurobiology of MTLE. Focusing on brain imaging, for example, most MTLE patients present with HS although in some the MRI is negative 2 . Moreover, not only the hippocampus seems to be involved in the physiopathology of TLE but also extratemporal regions 2,3 . Besides, for surgical treatment to succeed is mandatory to correctly lateralize seizure focus, which is more complex in MRI negative patients. Magnetic resonance spectroscopy (MRS) ist an important tool in the investigation of these broader and subtle changes that are missed by structural MRI techniques. Exploiting the magnetic properties of several nuclei, MRS is a useful tool when it comes to provide metabolic information in vivo without invasive intervention. The most common is proton magnetic resonance spectroscopy (1H-MRS), due to 1 H natural abundance in biological tissues 2 . Phosphorus MRS ( 31 P-MRS) is not so commonly employed in brain tissue evaluation; nevertheless, it is able to add important information about energy metabolism. The metabolites visible in a high resolution spectrum from 31 P-MRS are basically phosphorus compounds: total adenosine triphosphate (total ATP, composed by γ-+ α-+ β-ATP, according to the position of the three phosphate groups), inorganic phosphate (Pi), PCr (phosphocreatine), phosphodiesters (PDE, the sum of glycerophosphocholine plus glycerophosphoethanolamine) and phosphomonoesters (PME, composed by phosphocholine plus phosphoethanolamine) 4 . These metabolites are mainly involved in mitochondrial processes and cellular membrane turnover. Fewer studies addressed the issue of metabolic changes in epilepsy using 31 P-MRS than those using 1 H-MRS. Data from 1 H-MRS show a decrease in N-acetyl aspartate (NAA) referred as a result of neuronal loss and/or neuronal mitochondrial dysfunction, in other words, energy metabolism disturbance. NAA decrease is a key finding in several types of epilepsy, often associated with the lateralization of seizure focus and AED response 2 . Since mitochondria are the energetic engine of the cell, further evaluation of brain energy metabolism may help to shed lights on seizures underlying mechanisms. In spite of having less spatial resolution than 1 H-MRS, studies on 31 P-MRS show that it is able to lateralize the seizure focus and also to characterize the role of brain energy metabolism alterations in MTLE 5,6 . In this issue of Arquivos de Park et al. 7 showed a...

Magnetic Resonance Spectroscopy and its Clinical Applications: A Review

“…Several studies revealed the reduction of NAA levels and trivial changes or mild increment of tCho signal. A decrease of NAA concentration accompanied with the presence of Lac in the temporal lobe is the marker of the epileptogenic zone ( Figures 5 and 10) [118][119][120][121].…”