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Idiopathic trigeminal neuralgia (ITN) is increasingly regarded as being due to microvascular compression of the trigeminal sensory root, either by an artery or a vein close to the brainstem.1 Yet vascular contacts are found in entirely asymptomatic cases, no vascular contacts are found in some asymptomatic patients, and, most importantly, ITN suddenly switches off, even for years, only to return later, in the face of continuing vascular compression.2 Despite this, microvascular decompression produces immediate virtually complete (98–100%) relief in 82% of the cases and 64% after 10 years.3 Adams has suggested that, ITN being a hyperfunctional disorder of the brainstem, microvascular decompression “produces chronic trauma to a sensitive zone of the cranial nerve... by the dissection necessary and by the manipulation required microvascular decompression produces sufficient trauma to achieve interference of normal functioning of that nerve”, thus dampening the abnormal brainstem activity responsible for ITN.2 Failure to achieve an initial result or early recurrence would imply insufficient surgical trauma.2 We evaluated this hypothesis in our patients submitted to microvascular decompression. Forty one out of 410 patients with ITN have had keyhole microvascular decompression in the posterior fossa from December 1986 to February 1996 at the neurosurgical pain relief unit of the University of Turin. Twenty six patients showed pronounced arterial or arterovenous compression, three distally (group 1), three mild or disputable contacts (group 2), two slight and three pronounced venous compressions (group 3), five with arachnoiditis, two with a sharp root kink, four distally (group 4). In four cases (group 5), no anomaly whatsoever could be found, despite adequate magnification and careful exploration; vessels were noted close to the root, but no contact or groove could be seen. Thus the root was gently “massaged” with a microdissector; no other manoeuvre was attempted. These four patients included one woman and three men, with a mean age of 59 (range 54–66). All had typical ITN which at some point could no longer be controlled by drugs at adequate dosage. In all other cases, the vessels were separated from the root by interposing Surgicel; the arachnoiditis was dissected to free the root and, in one patient with slight venous compression partial (25%) rhizotomy was also carried out. In several patients, “massage” of the trigeminal root was performed.
All patients were relieved by surgery. Follow up disclosed the following recurrences: two in group 1 (follow up 4 months-9 years), none in group 2 (follow up 2.3–5 years), none in group 3 (follow up 1.1–5 years), two in group 4 (follow up 1–6 years), one in group 5 six years postoperatively (follow up 6 months-8 years). Importantly, one of the group 1 recurrences was operated on and no vascular contact whatsoever could be found (partial rhizotomy was elected). The only group 5 recurrence could be controlled by drugs. Whereas this was seen in other groups as well, all four group 5 patients showed transient slight to moderate hypaesthesia in two to three branches after surgery, a hallmark of trauma.
In 1961, Taarnhøj reported that simple manipulation of the trigeminal root by running a nerve hook along the root obtained 60% long term pain free results over a mean of 6.5 years (longest follow up 10 years).4 Gardner and Miklos also obtained 67% pain free results over 4.5 years by manipulating the trigeminal sensory root at the point of crossing the apex of the petrous bone,5suggesting that manipulation not at the root entry zone (as suggested by Jannetta), but peripherally at the petrous apex produces as good results as microvascular decompression. As no other report considered the problem, the microvascular compression hypothesis for ITN gained favour. Our data suggest that (1) trauma alone can ensure long term relief; (2) this relief is similar between patients showing microvascular compression and those without; it should be stressed that several patients of the microvascular compression group were “massaged” to ensure a control with the group without.
The trigeminal nerve root is surrounded by many arteries. In 60% of the roots, the trigeminal vessels form arterial rings encircling at least half of the root or its entry zone in asymptomatic patients,6 justifying the frequency of vascular contacts at large. Despite a plethora of vessels reported to compress the trigeminal nerve in a recent series,3 initial relief could not be achieved in 18% of the patients. Recently, a group reported electrophysiological data supporting the concept of trauma during microvascular decompression, despite attempts to limit the procedure to simply moving the vessel.7 The trauma hypothesis would explain recurrences of successful microvascular decompression in which no new compression is found (for example, our case and see Yamakiet al 8) at re-exploration.
Adam’s contention is being appreciated in the case of hemifacial spasm. Payner and Tew,9 discussing their results with microvascular decompression for this disorder, stated that “...perhaps there is truth that the early success in most patients results from minor trauma... to support this theory, additional analysis is needed of the long term follow up in patients without vascular compression and...treated by “manipulation” alone”. This is what has been done in this study. Microvascular decompression entails a risk of death (although this is small) and other serious complications requiring surgery (much more often) in the face of a painful, but benign disorder. Perhaps, “trauma surgery” would be best to ensure equal results with a much lower complication rate. A minimally invasive approach (endoscopy) could be studied in this regard.
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