Neuroimaging Biomarkers of Experimental Epileptogenesis and Refractory Epilepsy

Abstract

This article provides an overview of neuroimaging biomarkers in experimental epileptogenesis and refractory epilepsy. Neuroimaging represents a gold standard and clinically translatable technique to identify neuropathological changes in epileptogenesis and longitudinally monitor its progression after a precipitating injury. Neuroimaging studies, along with molecular studies from animal models, have greatly improved our understanding of the neuropathology of epilepsy, such as the hallmark hippocampus sclerosis. Animal models are effective for differentiating the different stages of epileptogenesis. Neuroimaging in experimental epilepsy provides unique information about anatomic, functional, and metabolic alterations linked to epileptogenesis. Recently, several in vivo biomarkers for epileptogenesis have been investigated for characterizing neuronal loss, inflammation, blood-brain barrier alterations, changes in neurotransmitter density, neurovascular coupling, cerebral blood flow and volume, network connectivity, and metabolic activity in the brain. Magnetic resonance imaging (MRI) is a sensitive method for detecting structural and functional changes in the brain, especially to identify region-specific neuronal damage patterns in epilepsy. Positron emission tomography (PET) and single-photon emission computerized tomography are helpful to elucidate key functional alterations, especially in areas of brain metabolism and molecular patterns, and can help monitor pathology of epileptic disorders. Multimodal procedures such as PET-MRI integrated systems are desired for refractory epilepsy. Validated biomarkers are warranted for early identification of people at risk for epilepsy and monitoring of the progression of medical interventions.

Exploring with [18F]UCB-H the in vivo Variations in SV2A Expression through the Kainic Acid Rat Model of Temporal Lobe Epilepsy

“…Thus, studying the underlying pathophysiology of this disease is essential for the discovery of more efficient treatments [ 2 , 3 ]. In this regard, the development and preclinical evaluation of new positron emission tomography (PET) radiotracers has provided new longitudinal insights on the neurobiological processes affected by epilepsy [ 4 , 5 ]. Among them, two have been extensively investigated: (1) alterations in the glucose metabolism of the brain, quantified through [ 18 F]-fluoro-2-deoxy-D-glucose ([ 18 F]FDG) radiotracer [ 6 , 7 ], and (2) neuroinflammatory processes, detected with different translocator protein (TSPO) markers [ 8 – 10 ].…”

The Biochemical Profile of Post-Mortem Brain from People Who Suffered from Epilepsy Reveals Novel Insights into the Etiopathogenesis of the Disease

“…However, AEDs are highly impactful, have adverse effects and are ineffective in large populations of those people who suffer from epilepsy [11,12]. Due to the unknown multifactorial etiology and the necessity for early intervention in ENOS, current research focuses on the early detection [13][14][15][16] and prevention of ENOS [17][18][19], as well as increasing our understanding of the etiopathogenesis of the disease [20][21][22].…”

Cognitive Impairments and Associated Structural Brain Changes in Metabolic Syndrome and Implications of Neurocognitive Intervention

“…For example, brain metabolism plays a major role in pathogenesis of some neurological disorders such as Alzheimer’s disease 17 - 19 by hypometabolismpromoted Aβ deposition. 20 Furthermore, the findings based on proton magnetic resonance spectroscopy have shown the alteration of metabolite concentration in various areas of the brain in different neurometabolic disorders such as multiple sclerosis, 21 brain tumors, 22 , 23 epilepsy, 24 , 25 Alzheimer disease, 26 - 28 and dementia 29 is significantly correlated with cognitive decline. Based on the abovementioned studies, metabolic diseases of the brain can lead to changes in the structure and function of brain areas associated with cognition; most metabolic diseases of the brain cause changes in neuronal structure and cognitive decline.…”