Hypothesis | Summary |
Pharmacokinetic Hypothesis [13] | Anticonvulsant levels are reduced when drug efflux vectors are over expressed in peripheral organs. |
Transport Hypothesis [14] | Anticonvulsant levels are reduced when drug efflux vectors are over expressed in the blood brain barrier. |
Neural Network Hypothesis [15] | The brain’s seizure control mechanism is suppressed by neuron loss and synaptic network reorganization, preventing drug access to targets. |
Intrinsic Severity Hypothesis [16] | Both the severity of epilepsy and drug resistance are influenced by neurobiological variables. |
Genetic Variants Hypothesis [17] | Drug resistance develops because of genetic polymorphisms related to pharmacodynamics, metabolic pathways, enzymes, ion channels, and neurotransmitter receptors, which may inhibit drug binding, metabolism, and transport. |
Epigenetic Hypothesis [18] | Drug resistance patterns may be influenced by epigenome alterations. |
Target Hypothesis [19] | Drug efficacy is reduced because of quantitative and qualitative alterations in potential-dependent ion channels and neurotransmitter receptors. |
Neuroinflammation Hypothesis [20] | Neuroinflammation can cause blood brain barrier disruption leading to decreased transport of antiepileptic drugs. |