Treatment for trigeminal neuralgiaBMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7079.519a (Published 15 February 1997) Cite this as: BMJ 1997;314:519
Pathophysiological mechanisms of trigeminal neuralgia need to be explored
- Turo Nurmikko, Consultant in pain managementa,
- John Miles, Consultant neurosurgeona,
- Paul Eldridge, Consultant neurosurgeona,
- David Bowsher, Director of medical researchb
- a Walton Centre for Neurology and Neurosurgery NHS Trust, Liverpool L9 1AE
- b Pain Relief Foundation, Liverpool L9 1AE
- c Pain Management Unit, Montagu Hospital, Mexborough, South Yorkshire S64 0AZ
- d St Bartholomew's and the Royal London School of Medicine and Dentistry, Department of Oral Medicine, London E1 2AD
- e Regional Maxillofacial Unit, Walton Hospital, Liverpool L9 1AE
Editor—R Walchenbach and J H C Voormolen highlight the difficulties inherent in choosing treatment for patients with trigeminal neuralgia and suggest a prospective randomised comparison between percutaneous ablation of the gasserian ganglion and microvascular decompression.1 We believe that the problem is greater than simply the treatment of pain: it is our limited understanding of the pathophysiology of trigeminal neuralgia and the lack of a diagnostic gold standard.
Several hypotheses exist to explain the characteristics of the disorder, ranging from peripheral neural ectopic pacemakers to central disinhibition.2 Although unproved, they can be used to justify a variety of treatments, which usually result in excellent early improvement. Logically, any prospective randomised trial should therefore have an arm for pharmacological treatment and an arm for peripheral procedures (for example, cryotherapy), while the outcome measures should assess not only pain and its recurrence but also quality of life.
In our opinion, the authors err in their suggestion that surgery is warranted only after medical treatment has failed. We have shown that abnormal vascular contact can be detected in most patients with trigeminal neuralgia by use of a new technique, magnetic resonance tomoangiography, and that in these cases microvascular decompression leads to excellent results.3 Why should people have to fail a drug trial to qualify for surgery that not only is safe and effective but also results in the restitution of preoperative sensory status?4 Similarly, how would one justify disregarding evidence of vascular compression from magnetic resonance tomoangiography, or deciding against performing this simple imaging, and proceeding to produce a lesion in the nerve that might …