✓ In his 1756 text, Observations pratiques sur les maladies de l'urèthre et sur plusiers faits convulsifs, Nicolas André coined the term “tic douloureux.” He believed that this pain originated from compression of facial sensory peripheral nerves. Using scientific observation and experimentation to confirm this hypothesis, he reproduced the tic pain and treated it by using careful efforts to remove adhesions from the nerve with a caustic solution of mercury water. Believing that recurrence of the pain was a result of early closure of the wound, with recompression of the nerve being the direct cause, André prevented recompression by ensuring open wound drainage. André's surgical technique of using cauterizing stones ensured that there was minimal blood loss and little danger of rebleeding and recompression of the nerve by an accumulated blood clot. His case reports include lengthy follow-up periods that documented the benefits of his procedures, which were confirmed by testimonials from uninvolved colleagues. Although remembered for the two words, “tic douloureux,” Nicolas André has long been ignored for his prescient treatment and scientific analysis of a disease for which the modern standard of care has only been defined during the last generation.
Jeffrey A. Brown, Catherine Coursaget, Mark C. Preul, and Devdutta Sangvai
Mark C. Preul, Phillip B. Long, Jeffrey A. Brown, Manuel E. Velasco, and Michael T. Weaver
✓ The histopathological and autonomic effects of percutaneous trigeminal ganglion compression for trigeminal neuralgia were studied in New Zealand White rabbits. Drops in mean arterial blood pressure of 38% and in heart rate of 30% were observed during compression (p < 0.0001). Corneal reflex, pinprick sensation, and mastication strength were intact in 13 of 14 rabbits after compression. These findings resembled the effects of percutaneous compression in humans and suggested that the New Zealand White rabbit is a useful model for the study of percutaneous compression.
Trigeminal sensory roots and ganglia from 14 rabbits killed at intervals from 1 to 84 days after percutaneous compression were sectioned and stained using immunoperoxidase for neurofilaments, hematoxylin and eosin, luxol fast blue, and cresyl echt violet. Focal axonal damage and demyelination were present 7 days after compression. No difference could be detected in the perikaryonal distribution of neurofilaments between compressed and control trigeminal ganglia. Focal demyelination and Schwann cell proliferation preceding remyelination were present in the trigeminal sensory root at 84 days. Differential injury of axons compared to trigeminal ganglion cell bodies suggests that axonal regeneration is possible and may contribute to the recovery of motor and sensory function in patients after percutaneous compression.
Experience in 22 patients and review of the literature
Jeffrey A. Brown and Mark C. Preul
✓ Between 1983 and 1988, a percutaneous trigeminal ganglion compression (PTGC) procedure for trigeminal neuralgia was performed on 22 patients. All patients were initially relieved of their pain. There were three recurrences (14%); two of these patients underwent a second PTGC procedure and one a partial trigeminal nerve root section. Follow-up examination 3 to 53 months after the procedure showed that all patients were free of pain. Morbidity included persistent minor hypesthesia in five patients, persistent minor dysesthesias in three, persistent minor weakness in three, aseptic meningitis in one, transient sixth nerve palsy in one, and transient otalgia in three. None of the patients had either anesthesia dolorosa or an absent corneal reflex.