Cause Of Trigeminal Neuralgia Research Articles

Microstructural abnormalities of the trigeminal nerve by diffusion-tensor imaging in trigeminal neuralgia without neurovascular compression.

Microstructural changes of the trigeminal nerve in trigeminal neuralgia due to neurovascular compression have been reported by using diffusion tensor imaging. Other aetiologies such as primary demyelinating lesions, brain stem infarction and nerve root infiltration by tumour affecting the trigeminal pathway may also present as trigeminal neuralgia. The aim of this study was to evaluate the microstructural tissue abnormalities in the trigeminal nerve in symptomatic trigeminal neuralgia not related to neurovascular compression using diffusion tensor imaging. Mean values of the quantitative diffusion parameters of trigeminal nerve, fractional anisotropy and apparent diffusion coefficient, were measured in a group of four symptomatic trigeminal neuralgia patients without neurovascular compression who showed focal non-enhancing T2-hyperintense lesions in the pontine trigeminal pathway. These diffusion parameters were compared between the affected and unaffected sides in the same patient and with four age-matched healthy controls. Cranial magnetic resonance imaging revealed hyperintense lesions in the dorsolateral part of the pons along the central trigeminal pathway on T2-fluid-attenuated inversion recovery sequences. The mean fractional anisotropy value on the affected side was significantly decreased (P = 0.001) compared to the unaffected side and healthy controls. Similarly, the mean apparent diffusion coefficient value was significantly higher (P = 0.001) on the affected side compared to the unaffected side and healthy controls. The cause of trigeminal neuralgia in our patients was abnormal pontine lesions affecting the central trigeminal pathway. The diffusion tensor imaging results suggest that microstructural tissue abnormalities of the trigeminal nerve also exist even in non-neurovascular compression-related trigeminal neuralgia.

Occurrence of Herpes Simplex Virus Reactivation Suggests a Mechanism of Trigeminal Neuralgia Surgical Efficacy

Common to the types of surgery that are effective for the treatment of trigeminal neuralgia (TN) is reactivation of herpes simplex virus (HSV). It is likely that such HSV reactivation following surgery indicates altered trigeminal ganglion neuron function, which was caused by the surgery. It is not thought that HSV infection is related to the cause of TN or that HSV reactivation is important for surgical treatment efficacy. Rather, it is thought that HSV reactivation is a marker of altered trigeminal ganglion neuron function resulting from the TN surgery. It is suggested that HSV reactivation is a surrogate marker of ganglion neuron injury. The correlation between effective types of surgery and evidence that they alter ganglion neuron function suggests that altered trigeminal ganglion neuron function may be the basis of the surgical efficacy.

MRI-based Volumetry in Trigeminal Neuralgia

Objective A noticeable contact between a blood vessel and the root entry zone (REZ) of the trigeminal nerve (CN V) is considered as the major cause of trigeminal neuralgia (TN) known as neurovascular compression (NVC). Earlier volumetric studies using magnetic resonance imaging (MRI) attempted to prove an atrophy of the affected trigeminal nerves in comparison to the unaffected contralateral trigeminal nerves. They described lower volumes on the affected sides in all their cases and criteria for diagnostics and surgery were concluded from these results. The goal of this study was to verify the difference in volume of the symptomatic and asymptomatic trigeminal nerves. Methods 100 patients with TN were prospectively examined using highresolution MRI and segmentation of the cisternal portion of the trigeminal nerve by defining a region of interest in the transversal sections. The resulting nerve volumes were compared by intra individual, bilateral comparison (t-test for paired samples, p < 0.05). Results 63% of the examined patients showed a lower volume of the cisternal portion of CN V on the affected sides. In 35% of the investigated individuals the volumes of the affected trigeminal nerves were larger than the nerve volumes on the unaffected sides. 2% of the examined patients showed identical volumes on either side. Conclusion In comparison to previous studies the described atrophy of CN V based on NVC could be reproduced in 63% of patients with TN and not in all patients with high-resolution MRI. Consequently the difference in nerve volume between the affected and unaffected trigeminal nerves cannot be proved for all cases of trigeminal neuralgia.

Diffusion tensor imaging of the trigeminal nerve in patients with trigeminal neuralgia due to multiple sclerosis.

Neurovascular compression (NVC) is the most common cause of trigeminal neuralgia (TN), leading to microstructural changes in the affected nerve detectable using diffusion tensor imaging (DTI). But TN may also emerge as a symptom of multiple sclerosis (MS). The aim of this study was to evaluate if patients with MS-related TN feature the same DTI characteristics as patients with TN caused by NVC. Twelve patients with MS-related TN, 12 age-matched patients with NVC-related TN, and 12 healthy controls were included. Using 3T-DTI, mean fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were calculated for each affected and contralateral trigeminal nerve in patients with MS and NVC-related TN as well as healthy controls. Furthermore, presence of NVC was evaluated for patients with TN. There was no significant difference concerning FA or ADC when comparing the affected and the non-affected sides in patients with MS. FA was significantly lower and ADC higher in patients with MS on the TN affected as well as on the non-affected side compared to the non-affected side of patients with idiopathic TN or healthy controls. Likewise, FA was significantly lower on the affected side compared to the non-affected side in patients with idiopathic TN or healthy controls. NVC was evident in 41.7/0% on the affected/contralateral side in MS patients and 100/8% in the patients with NVC-related TN. In patients with MS-related TN, DTI reveals microstructural changes within the trigeminal nerve not only on the affected side but also on the clinically non-affected side.

Trigeminal neuralgia: differences in magnetic resonance imaging characteristics of neurovascular compression between symptomatic and asymptomatic nerves.

Neurovascular compression (NVC) of the trigeminal nerve is the primary cause of trigeminal neuralgia (TN) but is known to occur in both symptomatic and asymptomatic nerves. The purposes of this study were to evaluate the relationship between the magnetic resonance imaging (MRI) findings regarding the site of NVC and the manifestation of TN symptoms. In 147 patients with unilateral TN, the presence or absence of NVC was evaluated on MRI in both symptomatic and asymptomatic nerves. In cases with NVC, the shortest distance from the trigeminal nerve root to the responsible vessel was measured. The mean distance from the trigeminal nerve root to the site of NVC in asymptomatic nerves (3.85 ± 2.69 mm) was significantly greater than that in symptomatic nerves (0.94 ± 1.27 mm). When the distance was 3 mm or less, the rate of the manifestation of TN symptoms was 83.1% (103/124). On the other hand, it was only 19.6% (9/46) in cases with a distance of greater than 3 mm. Whether or not NVC of the trigeminal nerve was symptomatic was closely related to the distance from the trigeminal nerve root to the responsible blood vessel.

Tentorial dural arteriovenous fistula manifesting as contralateral trigeminal neuralgia: resolution after transarterial Onyx embolization

Tentorial dural arteriovenous fistula (DAVF) as a cause of trigeminal neuralgia is extremely rare. Although less than 10 cases have been reported in the literature, all cases presented with ipsilateral...

Trigeminal Neuralgia Caused by Nerve Compression by Dilated Superior Cerebellar Artery Associated with Cerebellar Arteriovenous Malformation: Case Report

Intracranial arteriovenous malformation (AVM) is a rare cause of trigeminal neuralgia (TGN). In this presented case, successful resolution of AVM-related TGN following embolization and gamma knife radiosurgery (GKRS) was obtained. A patient suffered from TGN on the left side, which was thought to be caused by root entry zone compression by dilated superior cerebellar artery (SCA) associated with cerebellar AVM. The cerebellar vermis AVM was embolized in endovascular surgery. The AVM was reduced in size and TGN was partially relieved. The patient subsequently underwent GKRS for the residual nidus. TGN was completely resolved within one year and a half. GKRS following embolization of the nidus improved the flow-related dilation of the SCA and completely relieved TGN.

Arterial compression of nerve is the primary cause of trigeminal neuralgia

Whether arterial or venous compression or arachnoid adhesions are primarily responsible for compression of the trigeminal nerve in patients with trigeminal neuralgia is unclear. The aim of this study was to determine the causes of trigeminal nerve compression in patients with trigeminal neuralgia. The surgical findings in patients with trigeminal neuralgia who were treated by micro vascular decompression were compared to those in patients with hemifacial spasm without any signs or symptoms of trigeminal neuralgia who were treated with microvascular decompression. The study included 99 patients with trigeminal neuralgia (median age, 57 years) and 101 patients with hemifacial spasm (median age, 47 years). There were significant differences between the groups in the relationship of artery to nerve (p < 0.001) and the presence of arachnoid adhesions (p < 0.001) but no significant difference in relationship of vein to nerve. After adjustment for age, gender, and other factors, patients with vein compression of nerve or with artery compression of nerve were more likely to have trigeminal neuralgia (OR = 5.21 and 42.54, p = 0.026 and p < 0.001, respectively). Patients with arachnoid adhesions were less likely to have trigeminal neuralgia (OR = 0.15, p = 0.038). Arterial compression of the trigeminal nerve is the primary cause of trigeminal neuralgia and therefore, decompression of veins need not be a priority when performing microvascular dissection in patients with trigeminal neuralgia.

Trigeminal Neuralgia Due to Dandy-Walker Syndrome

Trigeminal neuralgia (TN) is a common pain in the orofacial region. Dandy-Walker syndrome (DWS) is a congenital malformation of the cerebellar and the fourth ventricle foramina atresia. Dandy-Walker syndrome is rarely found in patients with TN. This article presents a 36-year-old man with the symptoms of typical TN. His physical examination was entirely normal. An enhanced magnetic resonance imaging was taken. Magnetic resonance imaging revealed the bilateral lateral ventricle, the fourth and third ventricle significantly enlarged with severe obstructive hydrocephalus, a huge posterior fossa cyst connected with the fourth ventricle, and hypoplastic vermis. The pain was controlled by Tegretol. The reported case suggests that DWS is an unusual cause of TN.

Microvascular Decompression for Trigeminal Neuralgia: Does the Type of Vascular Contact Impact Outcome?

Although the precise mechanism of the pathogenesis of trigeminal neuralgia (TN) is not completely understood, vascular compression of the trigeminal nerve is the most widely accepted etiology. Although an arterial contact is believed to be the most common cause of TN, venous compression can also cause it. In this study, we examine the association between the type of vascular compression and its presentation (TN type I or II) and patient outcomes following microvascular decompression (MVD). We used a validated outcome tool, Brief Pain Inventory (BPI)-Facial, an 18-item instrument that measures pain in three different categories to gauge outcomes in a systematic, numeric format: pain intensity (1-4), general interference (1-7), and facial-specific interference (1-7).

Interactive virtual simulation using a 3D computer graphics model for microvascular decompression surgery

The purpose of this paper is to report on the authors' advanced presurgical interactive virtual simulation technique using a 3D computer graphics model for microvascular decompression (MVD) surgery. The authors performed interactive virtual simulation prior to surgery in 26 patients with trigeminal neuralgia or hemifacial spasm. The 3D computer graphics models for interactive virtual simulation were composed of the brainstem, cerebellum, cranial nerves, vessels, and skull individually created by the image analysis, including segmentation, surface rendering, and data fusion for data collected by 3-T MRI and 64-row multidetector CT systems. Interactive virtual simulation was performed by employing novel computer-aided design software with manipulation of a haptic device to imitate the surgical procedures of bone drilling and retraction of the cerebellum. The findings were compared with intraoperative findings. In all patients, interactive virtual simulation provided detailed and realistic surgical perspectives, of sufficient quality, representing the lateral suboccipital route. The causes of trigeminal neuralgia or hemifacial spasm determined by observing 3D computer graphics models were concordant with those identified intraoperatively in 25 (96%) of 26 patients, which was a significantly higher rate than the 73% concordance rate (concordance in 19 of 26 patients) obtained by review of 2D images only (p < 0.05). Surgeons evaluated interactive virtual simulation as having "prominent" utility for carrying out the entire surgical procedure in 50% of cases. It was evaluated as moderately useful or "supportive" in the other 50% of cases. There were no cases in which it was evaluated as having no utility. The utilities of interactive virtual simulation were associated with atypical or complex forms of neurovascular compression and structural restrictions in the surgical window. Finally, MVD procedures were performed as simulated in 23 (88%) of the 26 patients . Our interactive virtual simulation using a 3D computer graphics model provided a realistic environment for performing virtual simulations prior to MVD surgery and enabled us to ascertain complex microsurgical anatomy.

Clinicopathological review of patients with and without multiple sclerosis treated by partial sensory rhizotomy for medically refractory trigeminal neuralgia: A 12-year retrospective study

BackgroundTrigeminal nerve root entry zone demyelination has been implicated as a cause of trigeminal neuralgia (TN) in multiple sclerosis (MS) and patients with nerve root vascular compression. We have examined the relationship between pathology and treatment outcome in patients with and without MS, treated for intractable TN by partial sensory rhizotomy (PSR). MethodsWe reviewed the operative records, electron microscopic biopsy findings and post-operative satisfaction and pain scores of 23 MS and 47 non-MS patients who underwent PSR between 1992 and 2004. ResultsThe MS and non-MS patients had similar ages of onset of TN, duration of symptoms, age at surgery and proportions with typical and atypical symptoms. Demyelination was present in 16 MS and 23 non-MS patients (p=0.129), and a compressing vessel in 5 MS and 23 non-MS patients (p=0.039). Of those with demyelination, vascular compression was documented in 3 MS and 15 non-MS patients (p=0.008). Pain and satisfaction scores were similar in both groups. Recurrent TN was more commonly associated with a compressing vessel (p=0.019). ConclusionsTN is frequently associated with nerve root entry zone demyelination in MS and patients with nerve root vascular compression. The characteristics of the TN and response to PSR are similar in both groups. Persistent vascular compression increases the risk of recurrent TN after PSR.

Outcomes of Gamma Knife surgery for trigeminal neuralgia secondary to vertebrobasilar ectasia

Vertebrobasilar ectasia (VBE) is an unusual cause of trigeminal neuralgia (TN). The surgical options for patients with medically refractory pain include percutaneous or microsurgical rhizotomy and microvascular decompression (MVD). All such procedures can be technically challenging. This report evaluates the response to a minimally invasive procedure, Gamma Knife surgery (GKS), in patients with TN associated with severe vascular compression caused by VBE. Twenty patients underwent GKS for medically refractory TN associated with VBE. The median patient age was 74 years (range 48-95 years). Prior surgical procedures had failed in 11 patients (55%). In 9 patients (45%), GKS was the first procedure they had undergone. The median target dose for GKS was 80 Gy (range 75-85 Gy). The median follow-up was 29 months (range 8-123 months) after GKS. The treatment outcomes were compared with 80 case-matched controls who underwent GKS for TN not associated with VBE. Intraoperative MR imaging or CT scanning revealed VBE that deformed the brainstem in 50% of patients. The trigeminal nerve was displaced in cephalad or lateral planes in 60%. In 4 patients (20%), the authors could identify only the distal cisternal component of the trigeminal nerve as it entered into the Meckel cave. After GKS, 15 patients (75%) achieved initial pain relief that was adequate or better, with or without medication (Barrow Neurological Institute [BNI] pain scale, Grades I-IIIb). The median time until pain relief was 5 weeks (range 1 day-6 months). Twelve patients (60%) with initial pain relief reported recurrent pain between 3 and 43 months after GKS (median 12 months). Pain relief was maintained in 53% at 1 year, 38% at 2 years, and 10% at 5 years. Some degree of facial sensory dysfunction occurred in 10% of patients. Eventually, 14 (70%) of the 20 patients underwent an additional surgical procedure including repeat GKS, percutaneous procedure, or MVD at a median of 14 months (range 5-50 months) after the initial GKS. At the last follow-up, 15 patients (75%) had satisfactory pain control (BNI Grades I-IIIb), but 5 patients (25%) continued to have unsatisfactory pain control (BNI Grade IV or V). Compared with patients without VBE, patients with VBE were much less likely to have initial (p = 0.025) or lasting (p = 0.006) pain relief. Pain control rates of GKS in patients with TN associated with VBE were inferior to those of patients without VBE. Multimodality surgical or medical management strategies were required in most patients with VBE.

Editorial

High blood pressure affects nearly 25% of the world’s population, and is a major risk factor for stroke, myocardial infarction, heart failure, kidney failure, and aortic aneurysm. In 5%–10% of hypertensive individuals, an endocrine, renal, or neoplastic cause is found, but the vast majority of cases are idiopathic. Because the medulla is responsible for control of blood pressure, brainstem pathological conditions may be responsible for essential hypertension in some patients. Bilateral lesions in the middle third of the nucleus solitarius produce persistent hypertension in pigeons, 8 and pulsatile compression of the lateral medulla in nonhuman primates is able to produce reversible hypertension. 4 In humans, certain tumors of the inferior cerebellum have led to refractory hypertension that resolves after resection, 5 and arterial decompression of the brainstem in hypertensive patients undergoing microvascular decompression for other indications has been observed to normalize blood pressure postoperatively. 3 Based on the theory that hypertension may result from neurovascular compression (NVC) through mechanisms similar to trigeminal neuralgia and hemifacial spasm, it has been postulated that a subset of patients with medically refractory hypertension may benefit from surgical exploration of the lateral brainstem to resolve compression by the vertebral artery or one of its branches. This idea has failed to gain much traction in the neurosurgical and medical communities. The discovery of NVC as the putative cause of trigeminal neuralgia was based on Walter Dandy’s observations among 215 patients with trigeminal neuralgia. 2 In 1934, Dandy observed the following: In the routine treatment of trigeminal neuralgia by division of the posterior root, either totally or subtotally, and using the sub-cerebellar approach, I have been impressed with the frequency of certain anatomical findings which, I believe, must have a bearing on the production of this pain.… These are the arteries and veins which impinge upon and frequently distort the sensory root.

Arteriovenous malformation: a rare cause of trigeminal neuralgia identified by magnetic resonance imaging with constructive interference in steady state sequences

A 64-year-old female presented with a 4-year history of right-sided facial pain. She described an ‘electric shock-type’ pain starting on the right side of her chin that radiated along the lower lip, upper lip and into the lower cheek, in the mandibular division of the trigeminal nerve. The pain was triggered by speaking, eating, drinking, brushing her teeth or touching her chin. These attacks occurred daily and lasted for 3 months before resolving spontaneously, consistent with classical trigeminal neuralgia (TN). Systemic and neurological examinations were normal. In particular, trigeminal sensation was intact bilaterally and trigeminal reflexes were normal. A diagnosis of right-sided, mandibular division TN was made. She had four similar episodes of pain over the following 4 years, each lasting ∼3 months, with each episode becoming more severe. She did not want any analgesic medication for the first two episodes. However, during the most recent episode, carbamazepine (300 mg twice a day) and, subsequently, adjunctive amitriptyline (10 mg at night) were prescribed, although these failed to control the symptoms. Therefore the patient underwent investigation to assess for a structural cause amenable to neurosurgical intervention. The patient underwent a cranial MRI with constructive interference in steady state (CISS) sequences, which demonstrated several small blood vessels surrounding the right trigeminal nerve and a very large mass, thought likely to be a venous aneurysm, lying just behind the root entry zone into the trigeminal nerve (Figure 1). A contrast-enhanced computed tomography angiogram (CTA) confirmed the previous MRI findings and was highly suggestive of an underlying arteriovenous malformation (AVM) (Figure 2). For the pre-surgical work-up a digital subtraction angiogram was organized. This demonstrated a definite AVM during contrast injection in the right vertebral artery with rapid filling of the straight sinus during the early arterial phase (Figure …

Review on the causes of trigeminal neuralgia symptomatic to other diseases

Trigeminal neuralgia, also called tic douloureux, causes extreme, sporadic, sudden burning or shock-like face pain that lasts from few seconds to several minutes and can be physically and mentally incapacitating. Most cases are still referred to as idiopathic, although many are associated with vascular compression of the trigeminal nerve. A minority of cases are symptomatic to other diseases. The aim of this review is to show rare causes of trigeminal neuralgia described so far in the medical literature.

Case series: non vascular considerations in trigeminal neuralgia

An abnormal vascular course of the superior cerebellar artery is often cited as the cause for trigeminal neuralgia. However, among patients with TN-like symptoms, 6% to 16% are variously reported to have intracranial tumours. Aneurysms, tumours, or other lesions may impinge or irritate the trigeminal nerve along its course. Uncommonly, an area of demyelination from multiple sclerosis may be the precipitant. We would like to present a series of unusual lesions, all of which initially presented with neuralgic-like symptoms and were refractory to treatment. Collated case series with photographs and imaging are reviewed in this paper. Discussion of case presentation and management are done for evaluation. A wide range of other compressive lesions can cause trigeminal neuralgia. This paper illustrates the clinical presentation of atypical trigeminal neuralgia and emphasises the value of diagnostic imaging in trigeminal neuralgia patient. Suggested algorithm for management of trigeminal neuralgia.

Microvascular Decompression in the Treatment of Trigeminal Neuralgia Caused by Vertebrobasilar Ectasia

Vertebrobasilar ectasia (VBE) is a rare cause of trigeminal neuralgia (TN). It occurs in about 2% of all patients. This study reviewed the clinical features, radiological concomitants, and surgical findings of VBE and evaluate the microsurgical decompression procedure as a surgical line of treatment of the associated TN. Ten patients with TN caused by VBE and treated by microvascular decompression are the subject of this study. The study consisted of 6 men and 4 women with a mean age of 54 years. The mean duration of symptoms was 4.5 years. TN was the only symptom in 6 patients; it was associated with hemifacial spasm in 4. Arterial hypertension was present in 6 patients. Multiplanar high-resolution magnetic resonance imaging showed the accurate location and course of the ectatic vessel. Magnetic resonance angiography and digital subtraction angiography confirmed the diagnosis. Surgery demonstrated fifth nerve compression by an ectatic and tortuous vertebrobasilar artery in all cases and seventh nerve compression in 4 cases. Teflon felt was placed between the ectatic artery and compressed nerves. There was complete resolution of TN in 8 patients (80%) and hemifacial spasm in 3 (75%) without medication. Four of 6 hypertensive patients (66.7%) achieved normotension without medication. There was no recurrence of symptoms in the mean follow-up period of 7.8 years. Microvascular decompression is recommended for the treatment of TN caused by VBE if medical treatment has failed, if the patient is suitable for general anesthesia, and if there is evidence of vascular compression of the trigeminal nerve on magnetic resonance imaging.

Clues for Previously Undiagnosed Connective Tissue Disease in Patients With Trigeminal Neuralgia

Connective tissue diseases (CTD) may be associated with idiopathic trigeminal neuralgia (TN). The prevalence and diagnostic implications of this association are, however, not well established. The objective of this study was to evaluate, in TN patients, if rheumatologic clinical and laboratory findings could contribute to the early diagnosis of rheumatic diseases. Forty-six consecutive TN patients, 67% female, mean disease duration 8.78 +/- 7.25 years, and 47 controls were initially interviewed using a standard questionnaire based on common signs/symptoms of systemic lupus erythematosus, Sjögren syndrome, mixed CTD, and systemic sclerosis. Autoantibodies were detected by standard techniques. Those with rheumatologic complaints or positive autoantibodies were referred to the Rheumatology Outpatient Clinic for a more detailed evaluation. Secondary causes of TN were excluded. The frequency of Raynaud phenomenon (P = 0.026) and ANA reactivity (P = 0.04) were significantly higher in TN patients compared with controls. Fourteen TN patients were ANA positive. Seven of them reported concomitant rheumatic complaints, and interestingly, diffuse CTD was diagnosed in 4 (57%) of these patients: 1 systemic lupus erythematosus; 2 Sjögren syndrome; and 1 undifferentiated disease with scleritis and positive parotid scintigraphy. In all cases, TN preceded by at least 10 months the rheumatologic signs/symptoms. Moreover, these 4 TN patients with CTD had a higher frequency of sicca symptoms (P = 0.001) and higher titers of ANA (>or=1:320) (P = 0.006) than the remaining 42 TN patients without CTD diagnoses. Sixteen patients had isolated laboratory or clinical abnormalities, and none of them had CTD diagnoses. The concomitant presence of sicca symptoms and high titer ANA are clues for the early investigation of rheumatic diseases in TN patients.

Trigeminal Neuralgia Caused by a Choroid Plexus Papilloma of the Cerebellopontine Angle: Case Report and Review of the Literature

This report describes a 59-year old woman with a rare choroid plexus papilloma of the cerebellopontine angle presenting with trigeminal neuralgia. The patient was admitted complaining of a 12-year history of paroxysmal lancinating pain throughout the right side of her face. Treatment with carbamazepine, Chinese medicine and a peripheral neurectomy had not relieved the pain. At operation, a 0.5 x 0.5 x 0.5 cm neoplasm was found in the cerebellopontine angle, which was firmly adherent to the roots of the seventh and eighth cranial nerves and the brainstem. There was no apparent tumour bulk or vascular compression around the trigeminal nerve root entry zone. Subtotal tumour excision and selective partial rhizotomy were performed. The patient's facial pain gradually resolved. Involvement of the trigeminal nucleus in the brainstem by the cerebellopontine angle tumour is suggested as the possible cause for trigeminal neuralgia in this case.