During that procedure, he observed that the nerve was being compressed by vascular loops. In , Dandy theorized that trigeminal neuralgia was caused by a blood vessel compressing the nerve. With the advent of the operative microscope, Peter Jannetta was finally able to further confirm this theory in Jannetta pioneered a procedure in which he moved the offending blood vessel and placed a sponge to prevent the vessel from returning to its native position.
Microvascular decompression is now regarded by many as one of the most important modern breakthroughs in the treatment of neurological disease. Skip to main content. Clev Clin Q 20 2 — J Neurosurg 19 3 — Jannetta PJ Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia.
J Neurosurg 26 1part2 — Jannetta PJ Outcome after microvascular decompression for typical trigeminal neuralgia, hemifacial spasm, tinnitus, disabling positional vertigo, and glossopharyngeal neuralgia honored guest lecture. Clin Neurosurg — Jannetta PJ Trigeminal neuralgia. Neurosurg Focus 18 5 Oxford University Press, Oxford. Neurosurg Clin N Am 15 3 — Neurol Res 20 8 — Neurosurgery 16 5 — Olivecrona H Cholesteatomas of the cerebello-pontine angle.
Acta Psychiatr Scand 24 — Neurosurg Clin N Am 27 3 — Neurosurgery 14 5 — Provost J, Hardy J Trigeminal microsurgery: functional anatomy. Neurochirurgie 16 6 — Rand RW The Gardner neurovascular decompression operation for trigeminal neuralgia. Acta Neurochir 58 3—4 — Shelton ML Working in a very small place: the making of a neurosurgeon. Vintage Books, New York. Sindou M, Leston J, Decullier E, Chapuis F Microvascular decompression for primary trigeminal neuralgia: long-term effectiveness and prognostic factors in a series of consecutive patients with clear-cut neurovascular conflicts who underwent pure decompression.
J Neurosurg 6 — Charles C Thomas Publisher, Springfield. J Neurosurg 9 3 — J Neurosurg 11 3 — Certain conclusions can be drawn from these prospective and retrospective series. The procedure can be done under local anaesthesia in fully awake patients, although mild sedation is usually used. The needle is inserted into the trigeminal cistern through the foramen ovale using similar trajectories as in radiofrequency lesioning and balloon compression.
Needle positioning must be precise to ensure the tip lies in the ganglion and not the subarachnoid space beneath the temporal lobe. Once the needle is optimally placed, the patient is brought into a sitting position and a small test dose of sterile anhydrous glycerol injected. This is followed by small dose increments up to a total of 0.
Patients are usually able to perceive the effect of the injection as a tingling or burning sensation in the affected divisions. They remain in the sitting position for 2 h after the injections. Alhough pain relief is usually immediate, it may take up to 7 days to occur in some patients. Patients with atypical TGN or painful trigeminal neuropathy are likely to have less favourable results.
This method is generally well tolerated and mortality is negligible. There are anecdotal reports of meningitis, cranial nerve palsies, and local haematomas. Activation of herpes labialis occurs in one third and permanent masseter weakness is seen in a small proportion of patients. This variability may, in part, be a result of many authors including in their series patients previously treated with neuroablative procedures. Glycerol rhizolysis has probably caused more controversy than any other procedure with strong views expressed by both proponents and critics.
In the s, several groups reported that compression of the ganglion seemed to produce similar, if not better, results compared with the techniques used at the time for root decompression. Using fluoroscopic control, a guide needle is inserted into the foramen ovale, but not beyond it. Total compression times vary from 1—6 min.
Interestingly, masseter weakness is very common although, in most cases, there is complete recovery in a matter of weeks. Troublesome dysaesthesiae following the procedure are reported in all series. Many had atypical TGN with dysaesthesia possibly as a result of previous surgery and this dysaesthesia was not relieved by balloon compression.
Among the first patients he treated were two with TGN. However, it took decades before the technique had been refined and imaging developed sufficiently to allow precision targeting for the procedure. However, in recent years, the target has been the proximal trigeminal root near the pons, with a much improved outcome. The Gamma Knife is a focused array of intercepting beams of gamma radiation, produced by separate cobalt sources.
Radiosurgery is carried out with the patient supine with the head under the collimator helmet. Local anaesthesia is used for securing the frame and irradiation is frequently carried out under mild oral or i. The dose used is 70—90 Gy. Pain relief is usually not immediate. The mean time to pain relief in two series was approximately one month.
This appears to correlate with contrast enhancement seen on MRI months after radiosurgery. No changes in the ganglion were seen. In , the first systematic study on the use of stereotactic radiosurgery in TGN was published. In both studies, side effects were minimal. Currently, the limiting factor for this treatment is the small number of centres capable of providing this service.
Neurectomies of the affected branches were attempted for the first time in the 18th century with variable success. However, he makes a point that, in this retrospective analysis, careful selection of patients was employed conforming to the strictest of TGN criteria.
Recently, a small retrospective series was published on 40 patients with typical TGN who underwent this procedure. The majority had previously undergone radiofrequency lesions. Surprisingly, none of the above authors discuss adverse effects at all. In their series, neurectomy as well as alcohol block compared unfavourably with radiofrequency lesioning. All branches are divided and avulsed under magnification. The relevant foramen is blocked by bone wax, wooden sticks or silicone plugs.
The remnant of the nerve may also be cauterized. Despite these efforts, remnants may be found on re exploration and dealing with them in the same way is said to lead to pain relief. From the existing scarce literature, it cannot be concluded how this procedure sits on the map of TGN management. It does not appear to offer any benefit over other well established surgical procedures, but it may be useful in cases where other treatments have failed and the patient or doctor are reluctant to consider procedures aimed at the ganglion or root.
Although well tolerated by patients, the results are modest. Although improvement in individual nerves was better, from the pain point of view, cryosurgery falls short of results obtained either with procedures aimed at the ganglion or the root. Peripheral and ganglionic alcohol blocks have been used since the beginning of the last century but have fallen into disrepute within the neurosurgical and neurological community, mainly because of capricious results and reports of adverse effects.
Unfortunately, there is little documentation on the sensory aftermaths of this procedure. Alcohol injections must be administered directly into the nerve and they are painful and cause local oedema. In our view, the high risk of recurrence of pain combined with a moderate risk of dysaesthetic and other complications exclude this procedure from routine use, except in frail or medically unfit patients, or those who refuse more extensive surgery.
Other methods of producing controlled peripheral neural trauma include radiofrequency lesions and injections using glycerol, phenol, high concentration tetracaine or a mixture of lignocaine and streptromycin. Authors advocating the use of these measures frequently quote failure rates or complications from other, more invasive treatments that do not accurately reflect the current literature.
In general agreement, pharmacotherapy remains the mainstay of treatment of TGN despite the fact that only few randomized controlled trials have been conducted. These drugs include tizanidine, baclofen, pimozide, tocainade, and oxcarbazepine. Table 4 lists the drugs most commonly used in this condition. Considering the complexities of the pathophysiology of TGN atypical TGN included and the narrow mechanism of action of the drugs available, combination treatments seem a natural choice.
However, there are no published studies comparing directly polytherapy with monotherapy. Using these drugs requires a good understanding of their pharmacokinetics, metabolism, and interactions. There are several good reviews available. It is, therefore, imperative for the doctor to have an understanding of the relative efficacy of various treatments, including complications and recurrence rates. Our policy is to view requests of early surgical treatment with sympathy, even if the patient responds well to pharmacotherapy, but to ensure that he has a realistic view of what it entails.
Table 5 summarizes our current thinking with respect to preferred treatments in individual cases. We emphasize that it reflects only our experience and conclusions we have drawn from the often conflicting literature. Fig 2 MRTA, sagittal reconstruction, showing the trigeminal nerve star and the artery compressing it from above arrow.
Same patient as in Figure 1. Fig 3 Microscopic view of the trigeminal nerve star showing an arterial loop triangle compressing it. A vein cross is seen in close proximity to the nerve as well. Fig 4 Lateral radiograph of radiofrequency needle inserted into the gasserian ganglion. Fig 5 Balloon compression in TGN. Differential diagnosis of TGN. Summary of drugs commonly used in TGN. Stereotact Funct Neurosurg ; 68 : —5. Microvascular compression: an alternative view and hypothesis.
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