Significance of different offending vessels and development of a potential screening tool for trigeminal neuralgia.

OBJECTIVES: This study was performed amongst trigeminal neuralgia (TN) patients with neurovascular contact (NVC) to 1) investigate the association of the demographic and radiologic factors/variables with TN occurrence, and 2) develop a screening tool for TN/TN-affected nerves based on the factors/variables associated with it. METHODS: Eighty-five TN patients were recruited, and 121 trigeminal nerves with NVC were derived from them. Based on MRI sequences, including balanced turbo field echo and enhanced T1 high-resolution isotropic volume excitation, radiologic factors/variables for each nerve, from the offending vessel to the presence of nerve displacement, were identified by a neuroradiologist and a neurosurgeon. Demographic and clinical data were obtained from clinical notes. Logistic regression was performed to assess the association of the factors/variables with TN occurrence (i.e., affected vs. unaffected nerves). RESULTS: Three factors/variables were significantly (p < 0.05) associated with TN occurrence amongst patients with NVC: nerve laterality, vertebral artery (VA) involvement, and the presence of nerve displacement. The nerves with VA involvement, those on the right side, and those with nerve displacement exhibited a significantly higher likelihood/odd of being affected by TN, compared to those without VA involvement, those on the left side, and those without nerve displacement, respectively. Based on these factors/variables, a screening tool/nomogram with acceptable accuracy was established (C-statistic/AUC = 0.80). CONCLUSIONS: This study revealed an association of the three radiologic factors/variables with TN occurrence. A screening tool for TN/TN-affected nerves was established based on them. The findings may lay a foundation for an improvement of the diagnosis and clinical management of TN. KEY POINTS: • VA involvement and nerve displacement could be identified using MRI, and are significantly associated with TN occurrence. • A potential objective screening tool/nomogram for TN/TN-affected nerves could be established based on the three radiologic factors/variables: VA involvement, the presence of nerve displacement, and nerve laterality. • The screening accuracy of the tool/nomogram is acceptable as the C-statistic is 0.80.

Prediction of trigeminal nerve position based on the main feeding artery in petroclival meningioma.

The trigeminal nerve is often displaced by petroclival meningioma (PCM) compression, making it difficult to locate during PCM surgery. This study investigated whether the deviated position of the trigeminal nerve could be easily predicted using the main tumor feeding artery. We retrospectively examined 32 patients who underwent surgery for primary PCM. The deviation of the trigeminal nerve was classified as either Type 1 (displacement toward the back of the cerebellar tentorium), Type 2 (toward the back of the superior petrosal sinus), Type 3 (toward the back of the petrous apex dura), Type 4 (toward the inferior aspect of the tumor), or Type 5 (toward the surface of the brain stem). The main feeding artery was determined by preoperative angiography. The trigeminal nerve was classified as Type 2 in 60% of cases where the proximal tentorial artery (TA) was the main feeding vessel. The nerve was Type 5 where the distal portion of the TA was the main feeding vessel (60% of the cases). The nerves were Type 3 and Type 4 where the proximal inferior lateral trunk (ILT) (60%) and distal ILT (75%), respectively, were the main feeding vessels. In 66.7% of the cases where the dorsal meningeal artery was the main feeding vessel, the nerve was Type 3. Type 1 classification applied in all cases where the ascending pharyngeal artery was the main feeding artery. The main feeding artery can be used to predict trigeminal nerve transposition during PCM surgery.

Safety profile of superior petrosal vein (the vein of Dandy) sacrifice in neurosurgical procedures: a systematic review.

OBJECTIVE Walter E. Dandy described for the first time the anatomical course of the superior petrosal vein (SPV) and its significance during surgery for trigeminal neuralgia. The patient's safety after sacrifice of this vein is a challenging question, with conflicting views in current literature. The aim of this systematic review was to analyze the current surgical considerations regarding Dandy's vein, as well as provide a concise review of the complications after its obliteration. METHODS A systematic review was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A thorough literature search was conducted on PubMed, Web of Science, and the Cochrane database; articles were selected systematically based on the PRISMA protocol and reviewed completely, and then relevant data were summarized and discussed. RESULTS A total of 35 publications pertaining to the SPV were included and reviewed. Although certain studies report almost negligible complications of SPV sectioning, there are reports demonstrating the deleterious effects of SPV obliteration when achieving adequate exposure in surgical pathologies like trigeminal neuralgia, vestibular schwannoma, and petroclival meningioma. The incidence of complications after SPV sacrifice (32/50 cases in the authors' series) is 2/32 (6.2%), and that reported in various case series varies from 0.01% to 31%. It includes hemorrhagic and nonhemorrhagic venous infarction of the cerebellum, sigmoid thrombosis, cerebellar hemorrhage, midbrain and pontine infarct, intracerebral hematoma, cerebellar and brainstem edema, acute hydrocephalus, peduncular hallucinosis, hearing loss, facial nerve palsy, coma, and even death. In many studies, the difference in incidence of complications between the SPV-sacrificed group and the SPV-preserved group was significant. CONCLUSIONS The preservation of Dandy's vein is a neurosurgical dilemma. Literature review and experiences from large series suggest that obliterating the vein of Dandy while approaching the superior cerebellopontine angle corridor may be associated with negligible complications. However, the counterview cannot be neglected in light of some series showing an up to 30% complication rate from SPV sacrifice. This review provides the insight that although the incidence of complications due to SPV obliteration is low, they can happen, and the sequelae might be worse than the natural history of the existing pathology. Therefore, SPV preservation should be attempted to optimize patient outcome.

Microvascular Decompression for Trigeminal Neuralgia Due to Venous Compression Alone.

Microvascular decompression (MVD) has been confirmed as an effective treatment of trigeminal neuralgia (TN); however, most previous reports just focused on MVD for TN caused by arterial conflict, there is a paucity of information about its use in venous compression causing TN. In the present study, the authors summarize 5-year experience of MVD for primary TN due to venous compression alone. Thirty-four patients with primary TN caused solely by veins underwent MVD. The presenting symptoms, key operative notes, surgical outcomes together with complications were reviewed. Of all the 34 patients, 19 (55.9%) patients occurred as typical TN. The V2 division was the most commonly affected area. Most of the venous conflicts were grade III (20/34, 58.8%). Deep superior petrosal venous system was the most frequent offending vessel (21/34, 61.8%). The venous conflicts were located at the trigeminal root entry zone in 10 (29.4%) patients, the mid cisternal zone in 18 (52.9%) patients, and the porus of Meckel's cave in 11 (32.4%) patients. At the last follow-up, excellent outcome was obtained in 26 (76.5%) patients, 7 (20.6%) patients got good outcome, fair outcome was achieved in 7 (20.6%) patients, and 1 patient unimproved (2.9%). Cerebrospinal fluid leakage was the most common complication (5.9%). In conclusion, MVD is a safe and effective surgical option for TN due to venous compression alone. It is noteworthy to explore the entire nerve and to protect veins as much as possible.

A human trigeminovascular biomarker for antimigraine drugs: A randomised, double-blind, placebo-controlled, crossover trial with sumatriptan.

Current antimigraine drugs are believed, besides their direct vasoconstrictive effect, to inhibit calcitonin gene-related peptide (CGRP) release from trigeminal nerve endings during migraine. Objective The objective of this report is to establish a biomarker for the CGRP-interfering effect of antimigraine drugs. Methods We quantified the effect of sumatriptan on the trigeminal nerve-mediated rise in forehead dermal blood flow (DBF), induced by capsaicin application (0.6 mg/ml) and electrical stimulation (0.2-1.0 mA), in a randomised, double-blind, placebo-controlled, crossover study in healthy male ( n = 11, age ± SD: 29 ± 8 years) and female ( n = 11, 32 ± 7 years) individuals. Results DBF responses to capsaicin were attenuated by sumatriptan (ΔDBF, mean ± SEM: 82 ± 18 AU, p = 0.0002), but not by placebo (ΔDBF: 21 ± 12 AU, p = 0.1026). Conclusion We demonstrated that sumatriptan inhibits increases in DBF, induced by the release of, most likely, CGRP. Thus, our model may be used as a biomarker to establish the trigeminovascular effects of (potential) antimigraine drugs, such as CGRP receptor antagonists or antibodies directed against CGRP or its receptor.

Nitric oxide synthase, calcitonin gene-related peptide and NK-1 receptor mechanisms are involved in GTN-induced neuronal activation.

BACKGROUND AND AIM: Infusion of glyceryltrinitrate (GTN), a nitric oxide (NO) donor, in awake, freely moving rats closely mimics a universally accepted human model of migraine and responds to sumatriptan treatment. Here we analyse the effect of nitric oxide synthase (NOS) and calcitonin gene-related peptide (CGRP) systems on the GTN-induced neuronal activation in this model. MATERIALS AND METHODS: The femoral vein was catheterised in rats and GTN was infused (4 µg/kg/min, for 20 minutes, intravenously). Immunohistochemistry was performed to analyse Fos, nNOS and CGRP and Western blot for measuring nNOS protein expression. The effect of olcegepant, L-nitro-arginine methyl ester (L-NAME) and neurokinin (NK)-1 receptor antagonist L-733060 were analysed on Fos activation. RESULTS: GTN-treated rats showed a significant increase of nNOS and CGRP in dura mater and CGRP in the trigeminal nucleus caudalis (TNC). Upregulation of Fos was observed in TNC four hours after the infusion. This activation was inhibited by pre-treatment with olcegepant. Pre-treatment with L-NAME and L-733060 also significantly inhibited GTN induced Fos expression. CONCLUSION: The present study indicates that blockers of CGRP, NOS and NK-1 receptors all inhibit GTN induced Fos activation. These findings also predict that pre-treatment with olcegepant may be a better option than post-treatment to study its inhibitory effect in GTN migraine models.

Neurostimulation at pterygopalatine fossa for cluster headaches and cerebrovascular disorders.

There are numerous neural structures (parasympathetic, sympathetic, and trigeminal sensory) that are compacted in a small well defined area of the pterygopalatine fossa (PPF). These targets can be readily accessed via minimally invasive neuromodulation techniques making the methods more desirable than neurosurgical deep brain or hypothalamic intervention. Recent research has shed light over the important role of the sphenopalatine ganglion (SPG), which is located within the PPF, in cerebrovascular autonomic physiology as well as in the pathophysiology of different headache disorders (cluster headache, migraine, and trigeminal autonomic cephalalgias). Accordingly, neuromodulation of the autonomic fibers (parasympathetic and sympathetic) may play a key role in the management of headaches, stroke, or cerebral vasospasm. Another important structure within the PPF is the maxillary nerve (V2), which passes through the roof of the fossa. Here the trigeminal system is accessible for a reliable neuromodulation by targeting its second branch -the maxillary nerve- and this could be utilized in various painful conditions of the head and face.

[Intraoperative decisions and surgical efficacies of trigeminal neuralgia responsible vessels].

OBJECTIVE: To explore the types of primary trigeminal neuralgia (TN) responsible vessels and curative efficacies of microscopic vascular decompression (MVD). METHODS: A total of 162 primary TN patients underwent MVD from August 2004 to the present at our hospital.Their clinical data were collected and analyzed. There were 69 males and 93 females with an age range of 22-88 years. RESULTS: The most common responsible vessels were superior cerebellar artery (n = 65, 40.12%), anteroinferior cerebellar artery (n = 45, 27.78%), multiple vessels (n = 26, 16.05%), posteroinferior cerebellar artery (n = 16, 9.88%), veins (n = 6, 3.70%) and vertebral artery (n = 4, 2.47%). And the pressure points were at the root of trigeminal nerve (n = 139, 85.80%), distal part (n = 16, 9.88%) and root and distal part (n = 7, 4.32%). Postoperatively pain disappeared in all patients (including one case on second surgery). Postoperative follow-ups were conducted for 132 cases.Two cases recurred over 8 years and the recurrence rate was 1.52%. CONCLUSION: MVD is preferred method for primary TN non-responsive to pharmacotherapy. Identification and treatment of responsible vessels remain a key. Venous and distal pressure points should be taken care.

Trigeminal neuralgia and persistent trigeminal artery.

We report a case of trigeminal neuralgia caused by persistent trigeminal artery (PTA) associated with asymptomatic left temporal cavernoma. Our patient presented unstable blood hypertension and the pain of typical trigeminal neuralgia over the second and third divisions of the nerve in the right side of the face. The attacks were often precipitated during physical exertion. MRI and Angio-MRI revealed the persistent carotid basilar anastomosis and occasionally left parietal cavernoma. After drug treatment of blood hypertension, spontaneous recovery of neuralgia was observed and we planned surgical treatment of left temporal cavernoma.

The pathophysiology of brain swelling associated with subdural hemorrhage: the role of the trigeminovascular system.

INTRODUCTION: This paper reviews the evidence in support of the hypothesis that the trigeminal system mediates brain swelling associated with subdural bleeding. The trigeminovascular system has been extensively studied in migraine; it may play an important but under-recognized role in the response to head trauma. Nerve fibers originating in trigeminal ganglion cells are the primary sensors of head trauma and, through their collateral innervation of the intracranial and dural blood vessels, are capable of inciting a cascade of vascular responses and brain swelling. The extensive trigeminal representation in the brainstem initiates and augments autonomic responses. Blood and tissue injury in the dura incite neurogenic inflammatory responses capable of sensitizing dural nerves and potentiating the response to trauma. DISCUSSION: The trigeminal system may provide the anatomo-physiological link between small-volume, thin subdural bleeds and swelling of the underlying brain. This physiology may help to explain the poorly understood phenomena of "second-impact syndrome," the infant response to subdural bleeding (the "big black brain"), as well as post-traumatic subdural effusions. Considerable age-specific differences in the density of dural innervation exist; age-specific responses of this innervation may explain differences in the brain's response to trauma in the young. An understanding of this pathophysiology is crucial to the development of intervention and treatment of these conditions. Antagonists to specific neuropeptides of the trigeminal system modify brain swelling after trauma and should be further explored as potential therapy in brain trauma and subdural bleeding.

Hemimasticatory spasm treated with microvascular decompression of the trigeminal nerve.

Hemimasticatory spasm is a very rare disorder of the trigeminal nerve characterized by paroxysmal involuntary contraction of the jaw-closing muscles. The mechanisms leading to hemimasticatory spasm are still unclear. Recently, injection of botulinum toxin has become the treatment of choice due to its excellent results. We report a case of a successful treatment of hemimasticatory spasm via microvascular decompression of the motor branch of the trigeminal nerve.

Effect of cortical spreading depression on basal and evoked traffic in the trigeminovascular sensory system.

AIM: To use an animal model to test whether migraine pain arises peripherally or centrally. METHODS: We monitored the spontaneous and evoked activity of second-order trigeminovascular neurons in rats to test whether traffic increased following a potential migraine trigger (cortical spreading depression, CSD) and by what mechanism any such change was mediated. RESULTS: Neurons (n = 33) responded to stimulation of the dura mater and facial skin with A-δ latencies. They were spontaneously active with a discharge rate of 6.1 ± 6.4 discharges s(-1). Injection of 10 µg lignocaine into the trigeminal ganglion produced a fully reversible reduction of the spontaneous discharge rate of neurons. Neuronal discharge rate returned to normal by 90 min. Lignocaine reduced the evoked responses of neurons to dural stimulation to 37% and to facial skin stimulation to 53% of control. Induction of CSD by cortical injection of KCl increased the spontaneous discharge rate of neurons from 2.9 to 16.3 discharges s(-1) at 20 min post CSD. Injection of 10 µg lignocaine into the trigeminal ganglion at this time failed to arrest or reverse this increase. Injection of lignocaine prior to the initiation of CSD failed to prevent the subsequent development of CSD-induced increases in discharge rates. CONCLUSIONS: These results suggest that there is a continuous baseline traffic in primary trigeminovascular fibres and that CSD does not act to increase this traffic by a peripheral action alone - rather, it must produce some of its effect by a mechanism intrinsic to the central nervous system. Thus the pain of migraine may not always be the result of peripheral sensory stimulation, but may also arise by a central mechanism.

Trigeminal neuralgia: assessment with T2 VISTA and FLAIR VISTA fusion imaging.

OBJECTIVE: To evaluate the neurovascular compression (NVC) in patients with trigeminal neuralgia (TN) using T2 VISTA and FLAIR VISTA fusion imaging. METHODS: Sixty-six consecutive patients with TN who underwent MR imaging at 3-T between April 2008 and December 2010 were retrospectively reviewed. Multiplanar reconstructions (MPR) of T2 VISTA and FLAIR VISTA fusion imaging were used for image interpretation. The frequency of vascular contact, the segment of compression and the type of vessel were compared between the ipsilateral symptomatic side and the contralateral asymptomatic side. RESULTS: The frequency of vascular contact on the ipsilateral side and the contralateral side were 95.5% (63/66) and 74.2% (49/66), respectively. The frequency of indentation on the ipsilateral side and contralateral side were 74.2% (49/66) and 21.2% (14/66), and showed a statistically significant difference (p < 0.05). The sensitivity, specificity and odds ratio were 77.8%, 71.4% and 10.7, respectively. There were no significant differences in the involved segment or type of vessel between the ipsilateral side and contralateral side. CONCLUSION: MPR of T2 VISTA and FLAIR VISTA fusion imaging is useful in the detection of NVC in patients with TN. Vascular indentation can predict the presence of symptoms in patients with TN. Key Points •Fusion MRI with multiplanar reconstruction can detect neurovascular compression in patients with trigeminal neuralgia •Vascular indentation can predict the presence of symptoms in patients with trigeminal neuralgia •In patients with trigeminal neuralgia, neurovascular indentation is commoner on the symptomatic side.

Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model.

Although the trigeminal nerve innervates the meninges and participates in the genesis of migraine headaches, triggering mechanisms remain controversial and poorly understood. Here we establish a link between migraine aura and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache. Cortical spreading depression caused long-lasting blood-flow enhancement selectively within the middle meningeal artery dependent upon trigeminal and parasympathetic activation, and plasma protein leakage within the dura mater in part by a neurokinin-1-receptor mechanism. Our findings provide a neural mechanism by which extracerebral cephalic blood flow couples to brain events; this mechanism explains vasodilation during headache and links intense neurometabolic brain activity with the transmission of headache pain by the trigeminal nerve.

Trigeminal neuralgia associated with the specific bridging pattern of transverse pontine vein: diagnostic value of three-dimensional multifusion volumetric imaging.

OBJECTIVES: We report the specific bridging pattern of a transverse pontine vein (TPV) associated with trigeminal neuralgia (TN), which was evaluated by 3-dimensional (3D) multifusion volumetric imaging (MFVI). METHODS: In 3 cases with TN (V1 or V1-2 territory), constructive interference in steady state (CISS) imaging confirmed no arterial compression but indicated a vein draining into Meckel's cave. Virtual endoscopic (VE) analysis for CISS images and 3D MFVI (in 2 cases) including venous information was obtained by a multidetector row computed tomography (MDCT) system. Additionally, we investigated the bridging pattern of veins around Meckel's cave on 3D MFVI of 50 cerebellopontine angle (CPA) regions without any lesions. RESULTS: In all 3 patients, VE of CISS or 3D MFVI identified a bridging vein from the TPV causing the focal deformity of the trigeminal nerve near Meckel's cave. All those patients achieved a pain-free state after surgically coagulating and cutting the vein. In investigating 3D MFVI of 50 CPA regions, this type of the bridging vein was found in 4 (8%) including the presented 2 cases. CONCLUSIONS: The specific bridging pattern of the TPV draining into Meckel's cave can be associated with TN. The 3D MFVI analysis using venous information obtained by MDCT was useful to evaluate surgical anatomy including the offending vein which can be missed.

Vasculature and neurovascular relationships of the trigeminal nerve root.

BACKGROUND: Specific microanatomical characteristics of the trigeminal nerve root (TNR) blood supply and close neurovascular relationships with surrounding vessels as well as their possible clinical significance were the main reasons for this study. METHOD: The vasculature of 25 adult and four fetal TNRs were microdissected and examined under the stereoscopic microscope, after injecting their arteries with India ink. RESULTS: The trigeminal vessels, which varied between two and five in number, arose from two or three of the following arteries: the superolateral pontine (92%), anterior inferior cerebellar (AICA) (88%), inferolateral pontine (72%), and superior cerebellar (SCA) (12%). The trigeminal vascular twigs had a mean diameter of 0.215 mm. A single vessel may supply either the motor portion of the nerve root or the sensory portion or both. The trigeminal vasculature formed the proximal and distal rings. The proximal ring was located at the trigeminal root entry zone. Its central branches extended along the TNR to the principal sensory and motor trigeminal nuclei while its peripheral longitudinal twigs followed the TNR fascicles. The incomplete distal arterial ring embraced the middle portion of the TNR before the level of its entrance into the arachnoid sleeve. The most frequent contact of the TNR was noticed with the SCA (20%), the petrosal or Dandy's vein (24%), and the AICA (12%). CONCLUSIONS: The observed characteristics of the TNR vasculature could be the anatomical basis for decompressive neurovascular surgery.

Giant, thrombosed, sellar-suprasellar internal carotid artery aneurysm with persistent, primitive trigeminal artery causing hypopituitarism.

A rare case of a giant, thrombosed, sellar-suprasellar paraclinoid internal carotid artery (ICA) aneurysm with persistent primitive trigeminal artery (PPTA) causing hypopituitarism that manifested as hypogonadism, hypothyroidism, and hypocortisolism is reported. There were no visual/neurological deficits, diabetes insipidus, or episodes of subarachnoid hemorrhage. The alteration in the flow dynamics of the circle of Willis due to the presence of PPTA may have been responsible for both the genesis of the giant aneurysm as well as for the induction of thrombogenesis within its lumen. As the digital subtraction angiogram showed complete thrombosis within the aneurysm and hormonal replacement therapy was effective in ensuring complete normalization of symptoms, the patient was unwilling to undergo surgical clipping of the aneurysm and removal of the suprasellar clot in an attempt to restore pituitary functions. Hypopituitarism recurred when the patient stopped her hormonal supplementation therapy after 7 years, and she again became symptom-free on restarting the therapy. To the best of the authors' knowledge, this represents the first reported case in the literature of hypopituitarism consequent to a giant, thrombosed, sellar-suprasellar ICA aneurysm with an associated PPTA on the side of the aneurysm.

Endoscopic vascular decompression of the trigeminal nerve.

BACKGROUND: Microvascular decompression is an effective method of treatment in trigeminal neuralgia. It may fail if a compressing vessel is overlooked during surgery. The endoscope has an edge over the microscope in visualizing such conflicts. MATERIALS AND METHODS: This is a prospective study of 51 patients. Preoperative computed tomography and magnetic resonance imaging scans were performed in all the cases. A 4 − 5 cm retroauricular skin incision was made and an about 3 cm craniectomy was performed. A 0° 4 mm telescope supported by the holder was used after the dural opening. A 2 by 6 cm sheet prepared from hand gloves was used to protect the brain. A Karl Storz 30° telescope was used for the visualization of the trigeminal nerve from the pons to Meckel's cave and dissection of the anterior conflict. Small pieces of dura patch were interposed between the nerve and the vessel. The microscope was not used at any stage. Post-operative infection, cerebrospinal fluid leak, cranial nerve deficit, failure of procedure in terms of pain relieves and recurrences of pain were recorded. The follow-up period ranged from 24 to 55 months with an average of 36 months. RESULTS: There was no mortality or any major permanent complications. The duration of stay ranged from 3 to 10 days with an average of 3.6 days. The pain was relieved in 48 patients. CONCLUSION: Endoscopic vascular decompression is an effective and safe alternative to endoscopic assisted microvascular decompression in trigeminal neuralgia.

Microvascular decompression of the trigeminal nerve in the treatment of SUNCT and SUNA.

BACKGROUND: Medical management of short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) syndrome and short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA) is often unsatisfactory. METHODS: The authors report nine cases of SUNCT/SUNA that failed medical treatment and had an aberrant arterial loop either in contact with or compressing the appropriate trigeminal nerve demonstrated on MRI. All underwent microvascular decompression of the ipsilateral trigeminal nerve for intractable pain. RESULTS: Immediate and complete relief of SUNCT and SUNA symptoms occurred in 6/9 (67%) cases. This was sustained for a follow-up period of 9-32 months (mean 22.2). In 3/9 (33%) cases, there was no benefit. Ipsilateral hearing loss was observed in one case. CONCLUSION: Medically intractable SUNCT and SUNA subjects with a demonstrable aberrant arterial loop impinging on the trigeminal nerve on neuroimaging may benefit from microvascular decompression.