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.