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Other indirect ways to stimulate the antiepileptic effects of KD may lay in the alterations of the metabolism of neurotransmitters such as glutamate and gamma-amino butyric acid (GABA), and the activation of energy-sensing signaling pathways such as the PPAR, mammalian target of rapamycin (mTOR), and adenosine monophosphate-(AMP)-activated kinase (AMPK) pathways (71, 72)

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Lesioning is slow, and it can take several weeks to months for the facial pain to begin to subside

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