Orofacial sensory conditions associated with trigeminal nerve injury have been speculated to be driven by shifts in the levels of an array of molecules in trigeminal ganglion (TG) neurons. Since TG is the primary site of aberration in trigeminal neuralgia (TN), it serves as a crucial location for modifying afferent input. We have shown that diminishing TG neuronal activity will reduce brainstem TNC (trigeminal nucleus caudalis) function and have postulated that this inhibition might contribute to the pain-relieving outcome following trigeminal nerve injury.