| Trigeminal neuralgia, or tic douloureux, is relatively uncommon but should be considered when facial pain is a part of a patient's complaint. It has an annual occurrence rate of 3 to 5 per 100,000 people. The pain is described as sudden, sharp, shocklike, or burning. The pain is found in the distributions of 1 or more of the branches of the trigeminal nerve, which supplies sensation to the skin of the face and anterior half of the head, and has a limited motor component supplying the masseter and pterygoid masticatory muscles. Trigeminal neuralgia is most commonly found in the maxillary and mandibular division or the maxillary branch alone. A small percentage of cases affect the ophthalmic division alone.A subdivision in an idiopathic and a symptomatic type is non-essential. In a part of the cases microvascular compression of the sensory root may be the cause of trigeminal neuralgia but there are some good arguments against this concept. Other causes such as multiple sclerosis, acoustic neuroma or carotid aneurysm are well known. The principle of neurosurgical procedures is either an interruption of the pain-conducting fibres or a non-specific manipulation at the Gasserian ganglion or the sensory root with the result of an interruption of abnormal ephapses and short-circuits which may recur later on. So microvascular decompression should not be considered to be a specific and causal therapeutic approach as well as the therapy of first choice for all cases.Classical trigeminal neuralgia has an annual incidence of 4.5 per 100 000. It is characterized by recurrent episodes of intense, lancinating pain localized to small areas of the face. The onset is usually in middle or old age, but youngadults and children can also be affected. Attacks usually last only seconds but may recur repeatedly within a short period of time. The attacks are often, but not always, precipitated by mild sensory stimulation of so-called trigger zones, which may be located anywhere within the territory of the affected trigeminal nerve. Typical antecedent stimuli include light touching, draughts of wind, eating, drinking, washing, shaving and applying make-up. The neuralgia tends to occur in bouts over a period of weeks or months, with subsequent spontaneous remission that may last months or years. In time, however, attacks usually become more frequent and the pain more sustained. Although not usually significant clinically, the cutaneous perception of temperature and light touch is slightly impaired within the affected trigeminal divisions.Trigeminal neuralgia is found more often in women than in men (age-adjusted ratio, 1.74:1) and is most common from age 50 to 69 years, and attacks are more commonly seen on the right. The attacks can occur during the day or night but rarely during sleep. Attacks are usually triggered by nonpainful stimuli such as touch, movement, wind exposure, eating, brushing teeth, shaving, washing, talking, or swallowing. Patients have multiple clusters of pain that last from a few seconds to several minutes. Patients have often seen several providers, including dentists, before their diagnosis. The name tic douloureux comes from the ticlike muscle cramps caused by the pain.PathologyEarly ultrastructural studies concentrated on the morphology of the trigeminal ganglion and nerve and described a range of abnormalities of myelin sheaths, including proliferative degenerative changes and myelin disintegration. However, most of these changes were probably artefactual and similar findings were present in some of the control cases. These studies antedated the observations of Jannetta and others on the association of trigeminal neuralgia with vascular compression of the nerve root.1. Compression of the trigeminal nerve root The first detailed description of ultrastructural abnormalities in the nerve root in the region of vascular compression was by Hilton and colleagues. The authors observed focal loss of myelin and close apposition of demyelinated axons. There were fewresidual oligodendrocytes and no inflammatory cells. Immunoelectron microscopy for glial fibrillary acid protein revealed that astrocyte processes were largely confined to the periphery of the lesion. Of a further six trigeminal rhizotomy specimens from patients with trigeminal neuralgia in the absence of detectable vascular compression of the nerve root, only one, from a patient with multiple sclerosis, showed demyelination, but in that case astrocyte processes separated many of the demyelinated axons and the lesion contained perivascular clusters of perivascular lymphocytes and scattered lipid-laden macrophages.The findings in relation to vascular compression of the nerve root were confirmed in a subsequent electron microscope study of trigeminal rhizotomy specimens from two further patients with medically intractable trigeminal neuralgia, in whom, because of the local vascular anatomy, the compressing artery or vein could not safely be repositioned. In both specimens, examination revealed a circumscribed zone of chronic demyelination immediately beneath the region of indentation. As in cases we have seen subsequently, the demyelination was restricted to proximal (CNS) tissue but occurred close to the junction of this part of the root with distal (PNS) tissue. Adjacent to the zone of demyelination were small numbers of thinly myelinated axons, reflecting either demyelination and remyelination, or partial demyelination of the affected fibres. In some cases a single thin myelin sheath encircled several adjacent axons that were still in close apposition, a finding that was interpreted as suggesting that aberrant remyelination had occurred. Similar findings were described by Rappaport and colleagues. However, although Rappaport and colleagues illustrated disrupted myelin in the proximal, CNS part of the trigeminal root, they also described (but did not illustrate) the presence of large numbers of collagen fibrils in the extracellular matrix, suggesting that the abnormalities in their cases also involved the distal part of the nerve root.Since our initial reports, we have demonstrated demyelination in several further trigeminal rhizotomy specimens from patients with vascular compression of the nerve root. In rhizotomy specimens large enough to allow assessment of the size of the zone of demyelination, this zone has been limited to the immediate vicinity of the point of vascular indentation, extending no more than 2 mm in any direction. Foci of apposition of demyelinated axons and a paucity of glial and inflammatory cells have been relatively consistent ultrastructural features in thesebiopsies, although in one specimen we did find a focal infiltrate of lipid-laden macrophages, suggesting that there had been recent demyelinating activity. It should also be noted that we have found the trigeminal rhizotomy specimen from a small number of patients with visible vascular compression of the nerve root on neuroimaging or at craniotomy to be ultrastructurally normal, without demyelination. However, as the region of demyelination has rarely been visible macroscopically in the cases of vascular compression and a typical rhizotomy specimen measures no more than a few millimetres in diameter, it seems likely that the lack of abnormality in a small proportion of specimens reflects sampling error rather than heterogeneity in the pathology and pathogenesis of the disorder.In several of the reports of trigeminal neuralgia associated with tumours, the nerve root was described as stretched or attenuated, but none of the resected specimens was subjected to detailed histological assessment with reference to the possibility of demyelination. However, it is of note that demyelination has been demonstrated in several experimental models of acute or chronic compression of central white matter. Both Fish and Blakemore and Clifford-Jones and colleagues commented on the occurrence of partial demyelination after chronic compression of white matter. The most persuasive evidence of this was the finding of variations in the thickness of the myelin sheath along individual internodes. In trigeminal rhizotomy specimens from patients with trigeminal neuralgia, the distribution and extent of changes are more variable than in the experimental animals and the thinly myelinated fibres, in particular, tend to be distributed quite unpredictably. In consequence, we have had only limited opportunity for detailed assessment of these fibres in longitudinal section. To date, we have not been able to demonstrate convincing variations in the thickness of myelin sheaths along individual internodes in our specimens, but this may simply reflect the limitations of our examinations. None of the reports on experimental compression of white matter refers to demyelinated axons in direct apposition or to the encirclement of occasional groups of apposed axons by a single, thin myelin sheath. This may reflect several differences between these experimental models and trigeminal neuralgia, including the greater chronicity of the compression in the human disorder and the fact that the compression is likely to be pulsatile in nature, particularly if an artery is involved rather than a vein.2. Primary demyelinating disorders We have been able to examine trigeminal rhizotomy specimens from several patients with multiple sclerosis and intractable trigeminal neuralgia in the absence of a compressive lesion. As noted in two other case reports, demyelination has been found to extend along the proximal part of the trigeminal nerve root, in some cases right up to the junction with the PNS. The appearances have tended to differ slightly from those in vascular compression in that astrocyte processes have usually been more numerous and widely distributed within the regions of demyelination in the multiple sclerosis patients. Furthermore, the rhizotomy specimens from these patients have more often shown disease activity, as evidenced by the presence of lipid-laden macrophages. However, as in the compressed nerve roots, groups of juxtaposed axons have been a consistent finding in all of the specimens from multiple sclerosis patients. The specimens have also all contained variable numbers of thinly myelinated fibres, both within and immediately adjacent to the regions of demyelination.3. Infiltrative disorders The pathological findings in these conditions depend on the nature of the infiltrative process, which is usually carcinoma. Like infiltration by carcinoma, infiltration by amyloid may be very extensive, involving the trigeminal nerve, gasserian ganglion and both the distal and proximal parts of the nerve root.4. Changes secondary to Iesioning of the nerve root or gasserian ganglion Although microvascular decompression is now widely regarded as the treatment of choice in medically intractable trigeminal neuralgia, ablative procedures are still used to treat patients in whom (i) no compressing blood vessel is demonstrable; (ii) symptoms persist despite adequate microvascular decompression; (iii) a compressing blood vessel is present but not technically amenable to safe repositioning; (iv) there are medical contraindications to surgery under general anaesthesia; and (v) appropriate surgical expertise is not available. Numerous types of ablative procedure have been used in the past. The ablative techniques most commonly used nowadays are partial rhizotomy, and Iesioning at the level of the gasserian ganglion by percutaneous radio-frequency thermocoagulation, injection of glycerol or balloon compression. The precise pathological findings in such cases depend on the site of Iesioning but includeWallerian-type degeneration in the part of the nerve root that is proximal to the lesion and in the affected intrapontine trigeminal fibres. If the nerve root is examined soon after the ablative lesion has been made, fibres will show acute degenerative changes associated with accumulation of myelin debris and infiltration by macrophages. Older lesions result in patchy depletion of nerve fibres, astrocytic gliosis and, if the lesion is sufficiently distal (e.g. after radio-frequency lesioning), fibrosis of affected fascicles in the distal, PNS part of the nerve root. If the ganglion itself is damaged, there is also degeneration of peripheral trigeminal nerve fibres.Pathogenesis of trigeminal neuralgiaThe pathophysiology of trigeminal neuralgia has been much debated, the pain being ascribed variously to hyperactivity or abnormal discharges arising from the gasserian ganglion, the "injured' nerve root and the trigeminal nucleus within the brainstem. Any credible explanation of the pathophysiology has to account for both the abnormal generation of sensory impulses and their spread from fibres subserving light touch to pathways involved in the perception of pain in non-congruous regions of the face. The explanation has also to be reconciled with the observation that the pathological substrate of this condition in the great majority of cases appears to be demyelination, especially in the trigeminal root entry zone.We suggest that both the abnormal generation of sensory impulses and their subsequent spread to pathways subserving the perception of pain can be accounted for by the pathological findings. There is good experimental evidence that ectopic impulses can arise from demyelinated axons. Smith and McDonald demonstrated that many experimentally demyelinated nerve fibres in the dorsal spinal white matter of the cat were spontaneously active, discharging either in small bursts or steadily at 15-45 impulses per second for many hours. Small deformations of the spinal cord in the region of demyelination not only increased the level of activity in fibres already discharging, but also transiently induced activity in fibres that had previously been electrically silent. In the context of vascular compression of the trigeminal nerve root, these observations raise the possibility that pulsatilecompression of demyelinated axons by an overlying blood vessel may be responsible for initiating the aberrant impulses in some patients.Insofar as the subsequent spread of impulses is concerned, we have previously argued that the close apposition of demyelinated axons in regions of vascular compression should facilitate the ephaptic transmission of nerve impulses, as has been demonstrated between immediately adjacent non-myelinated axons in experimental studies. Ephaptic cross-talk between fibres mediating light touch and those involved in the generation of pain may account for the precipitation of attacks of neuralgia by light tactile stimulation of facial trigger zones. The frequency of involvement of the trigeminal nerve root entry zone in multiple sclerosis patients with trigeminal neuralgia as well as in patients with vascular compression probably reflects the fact that fibres subserving light touch and those involved in the generation of pain are in closest proximity in this region, so that ephaptic cross-talk between the two pathways is most likely to occur when the demyelination is in this region.Other evidence for the roles of focal demyelination and ephaptic transmission in the production of trigeminal neuralgia come from observations in patients with multiple sclerosis. Soustiel and colleagues documented a correlation between abnormal brainstem trigeminal evoked potentials and presentation with trigeminal neuralgia or dysaesthesiae in patients with multiple sclerosis, and Hartmann and colleagues described a patient with a plaque involving the right lateral lemniscus and right trigeminal tract in whom right-sided trigeminal neuralgia was precipitated by auditory stimuli to the right ear, strongly suggesting ephaptic spread of impulse activity within the pontine lesion.An objection that has been raised to a central role for demyelination in the development of trigeminal neuralgia relates to the rapid clinical and electrophysiological recovery that usually occurs after surgical decompression of the affected nerve root. Many patients experience complete relief of symptoms immediately after operation, and electrophysiological monitoring of conduction through the compressed nerve root has shown very substantial recovery of conduction almost immediately after microvascular decompression in manypatients. The explanation, we suggest, is that the clinical improvement and recovery of conduction reflect two distinct processes.1. The rapid relief of clinical symptoms probably reflects the cessation of the ectopic generation of impulses and of their ephaptic spread to adjacent fibres. Experimental studies indicate that reversal of the focal indentation and distortion of demyelinated axons is likely to reduce spontaneous impulse activity within the region of demyelination. Release from compression should also lead to the separation of demyelinated axons that were previously compacted together, and this would be expected to prevent ephaptic cross-talk. Reperfusion through previously compressed endoneurial capillaries and venules and endoneurial oedema resulting from the trauma of surgical manipulation may further contribute to separation of the demyelinated fibres.2. The recovery of conduction probably reflects rapid reversal of conduction block in relatively large-calibre, fast-conducting fibres that are not demyelinated. Reversible conduction block is a well-documented manifestation of nerve fibre compression. Although most extensively investigated in the PNS, several studies have demonstrated compression-induced conduction block within the CNS. This is most likely to occur during the conduction of high-frequency trains of impulses. In compression of low-to-moderate severity, large-calibre myelinated fibres seem to be more susceptible than smaller fibres to conduction block. Reversal of conduction block in these larger fibres would account for the rapid fall in conduction latencies across the trigeminal nerve root as soon as it is decompressed. Compression-induced conduction block in a proportion of the larger myelinated fibres may also explain the mild reduction in the perception of light touch over a more extensive area of trigeminal innervation than could be attributed to the impairment of conduction across the relatively small zone of nerve root demyelination.The fact that clinical improvement appears to be dissociated from recovery of conduction in some patients after microvascular decompression supports the concept that these are two distinct processes that are simply related by their common aetiology: nerve root compression.The pathogenesis of some phenomena related to trigeminal neuralgia remains unclear. These include the very occasional triggering of attacks by stimuli outside of the field of innervation of the trigeminal nerve, and even by bright lights or loud noises, which must involve central pathways. Another well-documented finding in some patients is the occurrence of a refractory period of seconds to minutes after an attack of trigeminal neuralgia, during which further attacks cannot be provoked. Experimental studies have shown the length of time for which nerve fibres are refractory to further excitation to be increased after demyelination in both the PNS and the CNS, but the duration of the refractory period in these experimental studies is much shorter than that in patients with trigeminal neuralgia. However, factors other than the demyelination per se could conceivably delay the restoration of membrane potentials and excitability after an episode of trigeminal neuralgia. These include impaired mitochondrial generation of ATP in an environment of focal endoneurial ischaemia due to the nerve root compression, with resulting delay in the restoration of ionic gradients after a burst of discharges, and the paucity of extracellular fluid and increased longitudinal resistance to ionic current between closely juxtaposed demyelinated axons.The role, if any, of remyelination in initial symptomatic recovery after microvascular decompression is unclear. Clearly, remyelination cannot account for the immediate relief from neuralgia. In the longer term, however, it is possible that remyelination helps to ensure that relief of symptoms is sustained. Remyelination may also be responsible for spontaneous remission of trigeminal neuralgia in some patients. Failure of microvascular decompression to relieve symptoms is most common in patients with very long-standing disease, in whom severe local depletion of oligodendrocytes and astrocytes may prevent effective remyelination after decompressive surgery. A further possibility is that the aberrant remyelination that is occasionally seen in the compressed nerve root may, by preventing the separation of groups of apposed axons after decompression, contribute to the failure of this procedure in a few patients.DiagnosisSeveral authors have used a slightly different approach by classifying TGN patients into subgroups depending on how 'pure' the pain is. We agree with thisviewpoint, because our own experience reflects the general conclusion that the outcome is dependent on the nature of the pain. We have also frequently witnessed, both over- and under-diagnosing of TGN, which seems to reflect difficulties in interpreting the painful symptoms in the context of an unnecessarily restrictive 'official' definition.We use it as guidance, rather than a fixed set of rules. While arbitrary, it has worked well in our hands and greatly helped communication between various specialists. It is obvious that, in some cases, pain slowly evolves from one category to another. A typical form of TGN may, in prolonged cases, develop atypical signs, as observed by Burchiel. By contrast, many cases of TGN start with pain lacking the typical characteristics of TGN, but respond well to carbamazepine, and later developing all the hallmark signs of TGN ('pre-TGN').Difficultal DiagnosisThe diagnosis of TN is based on clinical findings, but a careful history and examination can distinguish between TN and other disorders that cause facial pain. The classification scheme of the International Headache Society divides facial pain into 2 groups—pain from local facial structures and pain from neuralgia. Local examination findings may indicate otitis media, sinusitis, temporomandibular joint disease, herpes zoster, dental caries, or eye disease. Neurologic deficits, especially those involving the eye, are useful in diagnosis. Tolosa-Hunt syndrome is characterized by ocular pain and ophthalmoplegia, and is caused by nonspecific idiopathic granuloma in the area of the cavernous sinus or superior orbital fissure. Raeder paratrigeminal neuralgia (or Raeder syndrome) is a paroxysm of throbbing pain in the first division of the trigeminal nerve, associated with ptosis and miosis. Optic neuritis, which appears as acute loss of vision and mild pain with eye movement, may indicate multiple sclerosis. Two percent to 4% of patients with TN also have multiple sclerosis. Eye pain and third-nerve palsy may be seen with diabetes mellitus. Cluster headache can cause closely spaced attacks of headache, ptosis, lacrimation, and conjunctival congestion. With any neurologic deficit, there should be suspicion of a structural lesion, including aneurysm, neural fibroma, meningioma, or other intracranial lesion. Magnetic resonance imaging can be useful in examining patients with neurologic abnormalities. Patients with normalresults of physical examination can be divided into those with persistent and those with episodic pain. Persistent pain can be caused by compression or distortions of a cranial nerve before nerve deficit. Intracranial lesions should be excluded in this case. Giant cell arteritis causes persistent temporal headache, and postherpetic neuralgia may cause persistent pain even after the characteristic herpetic rash is gone. The most frustrating type of persistent facial pain is atypical facial pain. Atypical facial pain does not follow a nerve distribution and often occurs after local trauma, such as tooth extraction. Atypical facial pain is far less responsive to treatment than TN. Finally, episodic pain is helpful in the history. Cluster headaches cause paroxysms of unilateral periorbital pain. Trigeminal neuralgia causes lancinating paroxysms of pain associated with triggers. Other neuralgias may cause episodic pain, may be associated with triggers, and can be differentiated by their distribution. Glossopharyngeal neuralgia causes severe pain in the tonsils, the base of the tongue, the ear, and the posterior pharynx. It can be triggered by swallowing, talking, yawning, or coughing. Occipital neuralgia causes less severe pain in the occipital area. Superior laryngeal neuralgia causes laryngeal pain triggered by swallowing. Geniculate neuralgia is characterized by pain deep within the ear.Treatment1. PharmacologicalHistorically, the treatment of choice has been the anticonvulsant carbamazepine, but most of the evidence for medical treatment of TN is based on noncontrolled studies from the 1960s. Evaluation of medical treatments is difficult because of the high rate of spontaneous remission. The mechanism of action for these drug treatments is not clear. Common adverse effects are listed in.Carbamazepine is an effective and well-tolerated treatment. Initial dose of carbamazepine is 100 mg twice daily, then increased to 3 times per day. The dose may then be increased by 100 mg/d (on a 3-times-daily schedule) until pain relief is achieved or 1200 mg/d is reached. A serum level should be determined 2 to 3 weeks after beginning therapy, and again every 1 to 3 months. A complete blood cell count and liver function tests should be done periodically on patients treated for longer periods. After the pain has been controlled for 6 to 8 weeks, the dosageshould be decreased to the lowest level that maintains pain control or withdrawn completely. Some drugs, such as erythromycin, cimetidine, diltiazem hydrochloride, and terfenadine, can increase the plasma concentration of carbamazepine. Carbamazepine may also interact with other anticonvulsants and can decrease the effectiveness of oral contraceptives.The anticonvulsant phenytoin has also been used to relieve TN pain. A form of phenytoin can be used intravenously in patients in acute neurologic crisis.Baclofen is a 1-aminobutyric acid receptor agonist that has the least serious adverse effects. A double-blind crossover study by Fromm et al showed a significant decrease in the number of TN attacks when treated with baclofen, even in patients who had become unresponsive to carbamazepine.Several other medications with central nervous system effects have been used to treat TN, with varied success.Pimozide is a neuroleptic that has shown significant relief of pain when compared with carbamazepine in a double-blind crossover trial by Lechin et al. Patients in this study had been diagnosed as having TN for at least 2 years and were treated with carbamazepine or pimozide. Adverse effects were common with pimozide, but mild, and no patients stopped the treatment because of side effects.Lamotrigine is an anticonvulsant with an action similar to that of carbamazepine, but with fewer side effects. A small noncontrolled study of patients who could not tolerate carbamazepine showed response without the side effects associated with carbamazepine. A controlled trial is needed to confirm this benefit.Tizanidine hydrochloride has neurochemical activity similar to that of baclofen and carbamazepine. A double-blind crossover study by Fromm et al evaluated its efficacy in patients with TN who were not responding to carbamazepine and found short-term improvement, with recurrence of pain in 1 to 3 months.Other drugs include valproate sodium, racemic ketamine, proparacaine hydrochloride, and topical capsaicin cream. Valproate sodium was beneficial in a small group of patients studied by Peiris et al. Racemic ketamine, an anesthetic, showed some benefit when treating acute pain but was ineffective for pain lasting more than 5 years. The use of topical ophthalmic anesthetics, such as proparacaine, has been reported to relieve TN pain in some patients, but a randomized trial by Kondziolka et al showed no change in the frequency or severity of attacks. Topical capsaicin cream showed improvement in 60% of patients using it in an open trial.If an initial trial of medications fails or the patient has atypical symptoms or any neurologic deficits, magnetic resonance imaging should be performed. This modality is preferred over computed tomography and cerebral angiography because of better resolution and visualization of the entire course of the trigeminal nerve.Trigeminal neuralgia is the most common neurologic cause of facial pain. The first step is to make the correct diagnosis. Initial therapy should be low-dose carbamazepine, with upward titration of the dose to relief of pain. Baclofen is a good choice for second-line therapy. Most patients will respond to anticonvulsant therapy, but its effectiveness decreases with time. Newer medications have shown promise, but none has been shown to be more effective than carbamazepine and need not be used for first-line therapy. Effective surgical options are available for cases that do not respond to medical treatment. There are serious risks associated with the surgical procedures, which should be reserved for the most resistant cases ofTN.For patients who do not respond to pharmacological therapy or have worsening symptoms or more frequent recurrence, a surgical procedure may be appropriate. These procedures have variable success rates and different definitions of success; they have been reported as case series data and thus are difficult to compare objectively.Peripheral approaches, including cryotherapy and alcohol injection, act to block the peripheral branches of the trigeminal nerve. These are effective initially but have a high rate of pain recurrence. Repeated blocks are not recommended because of the risk of permanent facial anesthesia.Central procedures can be divided into percutaneous and open approaches. Percutaneous destruction of the trigeminal ganglion is accomplished through administration of radiofrequency lesions (thermal rhizotomy), glycerol injection, or balloon microcompression. Thermal rhizotomy is most commonly performed but has the risk of cornea] anesthesia, keratitis, masticatory weakness, and temporary oculomotor paresis. Glycerol injection (into the arachnoid cistern of Meckel cavern) and balloon microcompression are less painful procedures, simpler to perform than thermal rhizotomy, but also less effective.2. Open surgical treatmentsOpen surgical treatments for TN include microvascular decompression and partial trigeminal rhizotomy. Microvascular decompression is very effective but involves a suboccipital craniotomy and has serious risks, such as hearing loss, permanent facial anesthesia, brainstem infarction, cerebellar injury, ataxia, meningitis, headaches, and death. A partial sensory trigeminal rhizotomy at the pons has shown success in some cases, but with similar operative risks.2.1 Procedures 2.1.1 MVDSince the original theory, outlined by Dandy in 1925, of vascular compression as a prominent feature of TGN, it took almost half a century until MVD was accepted as one of the major surgical methods for treating this condition. Advances in neuroanaesthesia, adoption of the operation microscope and developments in surgical techniques during this time helped to make the procedure safer and more effective.In MVD, the target area lies at the nerve-pons junction. The posterior fossa is approached through a suboccipital craniotomy. After aspiration of the cerebrospinal fluid, the operator advances toward the nerve by gently retracting the superolateral margin of the cerebellum. The most common finding is a segment of the superior cerebellar artery compressing the nerve at the root entry zone. Less frequently, the anterior inferior cerebellar artery or the superior petrosal veins are the cause of the compression. After the arachnoid is dissected and the vessel freed,the operator places a piece of shredded Teflon felt between the vessel and the nerve to separate them.There is no age limit for the procedure as long as the patient is fit for general anaesthesia. In our recent retrospective study in patients over 70 yr of age, pain relief and complications were no different from those seen in a group of patients under the age of 50. There are anecdo... |
PDF Full Text Request