Introduction
Group | Target | Radioligand |
---|---|---|
GABA | GABAA receptor | [11C]flumazenil-PET |
[18F]flumazenil-PET | ||
Glutamate | NMDA receptor | [18F]GE-179 |
Drug transporters | P-glycoprotein | [11C]verapamil |
Inflammation | TSPO | [11C]PBR28 |
[18F]PBR111 | ||
[11C](R)-PK11195 | ||
Serotonin, inflammation | Tryptophan metabolism | α-[11C]methyl-l-tryptophan |
Serotonin | 5-HT1A receptor | [18F]MPPF |
[11C]WAY-100635 | ||
[18F]FCWAY | ||
Serotonin transporter | [11C]DASB | |
Dopamine | Presynaptic dopamine | [18F]fluoro-l-DOPA |
D2/D3 receptor | [18F]fallypride | |
D1 receptor | [11C]SCH23390 | |
Dopamine transporter | [11C]PE2I | |
Cannabinoids | CB1 receptor | [18F]MK-9470 |
[11C]MePPEP | ||
Opioids | μ, δ and κ opioid receptors | [11C]diprenorphine |
μ opioid receptors | [11C]carfentanil | |
δ opioid receptors | [11C]methylnaltrindole | |
Acetylcholine | Nicotinic ACh receptor | [18F]fluoro-A-85380 |
γ-Aminobutyric Acid
Glutamate
[18F]GE-179 PET
Multidrug transporters
[11C]verapamil PET
Inflammation
Translocator protein positron emission tomography
Serotonin
α-[11C]methyl-l-tryptophan positron emission tomography
5-HT1A Receptor Ligands and Tracer for Serotonin Transporter
Dopamine
Cannabinoids
Opioids
[11C]diprenorphine
Acetylcholine
Conclusions
Group | Target | Main findings in epilepsy patients | Author’s interpretation |
---|---|---|---|
GABA | GABAA receptor | Inverse correlation of seizure frequency with uptake in the frontal piriform cortex in patients with different sites of seizure onset [4]. | The prepiriform cortex might represent a common epileptogenic area independent of the localization of seizure onset. |
Glutamate | NMDA receptor | Increased global uptake in patients not on antidepressants. [13••] | Global increase of NMDA receptor activation might reflect ongoing epileptogenesis. |
Multidrug transporters | P-glycoprotein | Increased P-glycoprotein activity could contribute to multidrug resistance by reducing the intracellular concentration of antiepileptic drugs. | |
Inflammation | TSPO | Increased TSPO expression points to activation of microglia and an inflammatory reaction in epilepsy patients that could induce epileptogenesis. | |
Serotonin, inflammation | Tryptophan metabolism | [11C]AMT-PET adds valuable information on the location of the epileptic focus. It might reflect increased tryptophan metabolism that indicates the local production of proconvulsants. | |
Serotonin | 5-HT1A receptor | Adds lateralizing information with higher specificity than FDG-PET. A widespread reduction of serotonin receptors extending beyond the temporal lobe might indicate a pathomechanism of comorbid depression. | |
Serotonin transporter | Reduced uptake in ipsilateral insula in epilepsy patients with depression [49•] | Decreased serotonin reuptake might represent a compensatory mechanism for low serotonin levels in comorbid depression. | |
Dopamine | Presynaptic dopamine, D1/D2/D3 receptor, dopamine transporter | An altered dopaminergic neurotransmission might impair termination of seizures. | |
Cannabinoids | CB1 receptor | Increased uptake in ipsilateral temporal lobe; decreased uptake in bilateral insula [82] | Supports dysregulation of cannabinoids in epilepsy that could represent a pro or anticonvulsive phenomenon. |
Opioids | μ, δ. and κ opioid receptors | Opioid release during seizures might contribute to seizure termination. This is likely followed by an early interictal overexpression of opioid receptors. | |
Acetylcholine | Nicotinic ACh receptor | Increased uptake in epithalamus, ventral mesencephalon, and cerebellum in ADNFLE patients. Decreased uptake in prefrontal cortex [90] | Thalamic and mesencephalic findings may indicate a unique mechanism of nocturnal seizures in ADNFLE. Reduced prefrontal receptor density could be due to neuronal loss. |