Trigeminal neuralgia is a severe, recurrent (episodic, but otherwise chronic) facial pain syndrome which affects chiefly older patients. The pain of trigeminal neuralgia is unique in its paroxysmal nature, excruciating intensity, lancinating quality, and confinement to the trigeminal nervous system. Various medical and surgical treatments are available for this disorder, but none is uniformly and permanently effective. It appears that a substantial improvement in the long-term treatment of trigeminal neuralgia may be hindered by the lack of basic understanding of the neurological basis of this disorder. Theories involving abnormal sensory input from the peripheral nervous system and/or alteration of synaptic processing in the central nervous system have been invoked in the past, but thus far there is no direct experimental evidence to support them. In the absence of an adequate animal model of trigeminal neuralgia, theories of genesis have to be tested in symptomatic human patients. The goal of this research proposal is to apply a novel micro-neurographic recording technique to study directly the neurophysiological characteristics of trigeminal ganglion neurons in patients with trigeminal neuralgia. The technique, which we have developed, allows intra-operative microelectrode recordings in the trigeminal ganglion before the patients undergo percutaneous gangliolysis for treatment of the pain. The proposed study will examine if light mechanical stimulation of the trigger zone elicits abnormal (self-sustained) action potential discharge in trigeminal primary afferent neurons. Electrical stimulation of the axons will be used to detect auto-rhythmic activity in the roots or somata of trigeminal ganglion neurons. Finally, an attempt will be made to identify action potential discharges which may occur in trigeminal gang!ion neurons concurrent with patient's experience of trigeminal neuralgic pain. It is anticipated that intra-operative recordings will provide, for the first time, direct evidence that trigeminal neuralgia is associated with abnormal sensory input from the peripheral nervous system. Choral made observations of impulse traffic in the nerve or ganglion during paroxysms of pain should greatly illuminate the neural mechanism of trigeminal neuralgia, allow for modelling of the syndrome in experimental animals, and direct research toward better medical and surgical treatment of pain paroxysms in this and other neuropathic pain disorders.
|Baumann, Thomas K; Burchiel, Kim J (2004) A method for intraoperative microneurographic recording of unitary activity in the trigeminal ganglion of patients with trigeminal neuralgia. J Neurosci Methods 132:19-24|
|Baumann, Thomas K; Chaudhary, Priya; Martenson, Melissa E (2004) Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic pain. Eur J Neurosci 19:1343-51|
|Burchiel, Kim J; Baumann, Thomas K (2004) Pathophysiology of trigeminal neuralgia: new evidence from a trigeminal ganglion intraoperative microneurographic recording. Case report. J Neurosurg 101:872-3|
|Chaudhary, Priya; Baumann, Thomas K (2002) Expression of VPAC2 receptor and PAC1 receptor splice variants in the trigeminal ganglion of the adult rat. Brain Res Mol Brain Res 104:137-42|