Compression Of Trigeminal Nerve Research Articles

VASONEURAL COMPRESSION: RELATIONS BETWEEN VESSEL AND REZ IN PАTIENTS WITH TRIGEMINAL NEURALGIA

Trigeminal neuralgia in most cases caused by compression of trigeminal nerve or its branches with vessels. Compression may locate in root entry zone (REZ) or in a distance from it. The aim of the study is to compare distances from REZ of trigeminal nerve to offending vessel on the symptomatic side to distance to the same vessel on asymptomatic side. Comparing this distances showed significantly shorter distance on symptomatic side. Thus, it could be concluded that this factor has its part in development of trigeminal neuralgia.

静脈血管腫のdrainerが三叉神経を貫通し圧迫していた特発性三叉神経痛の1例

静脈血管腫のdrainerが三叉神経を貫通し圧迫していた特発性三叉神経痛の1例

Sacrificing the superior petrosal vein during microvascular decompression. Is it safe? Learning the hard way. Case report and review of literature.

Background:Venous infarction as a complication of microvascular decompression (MVD) is a recognized but extremely rare occurrence in an otherwise standard neurosurgical procedure. Sacrificing one or more veins is considered safe by majority of experienced surgeons and authors. However, in the recent years, there has been growing debate about the management of venous trigeminal compression and/or superior petrosal complex (separation vs. coagulation and cutting of the vein), with few papers describing mild to severe complications related to venous sacrifice.Case Description:We report our dramatic experience during re-exploration for MVD on a male who developed massive cerebellar, brainstem, and brain infarction. Extensive analysis of surgical planning and literature debate about this topic is also reported.Conclusion:Despite rare, venous infarction after venous sacrifice in MVD is possible and can have catastrophic consequences. We would advise: (1) To try preserving the vein anytime this is possible, especially if it is large in size; (2) if it is decided to sacrifice the vein temporary occlusion while observing changed in the neurophysiology might be safer; (3) when planning an MVD for suspected venous compression, possible alternative forms of treatment should also be considered.

Refractory cluster headache

Introduction: Cluster headache is classified as unilateral primary headache characterized by intense pain associated with ipsilateral autonomic symptoms. Typically it occurs with short periods of crises, called clusters. It is included in the group of trigeminal autonomic headache. It affects 0.1 to 0.4% of the population, being more prevalent in men in the ratio of 3:1 compared to women. Report atypical and refractory to drug treatment table with various therapeutic attempts to neurosurgical approach of a case of cluster headache. Clinical case men,white, 55 years, hypertension, bearer of cluster headache, with daily recurrent pain crises, initially with five daily episodes, lasting 30–240 min. Continuous intense pain on periorbital region to the left associated with conjunctival hyperemia, eyelid ptosis and ipsilateral hyaline rhinorrhea. Significant pain relief with oxygen. Already in use of Topiramate 150 mg/day, Verapamil 240 mg/day, Prednisone 30 mg/day, in addition to naproxen and Tramadol. Admitted for pain control, had cardiac contraindication to increasing the dose of Verapamil due to risk of AVB. Despite the adjustment Lithium 300 to 600 mg/day and increased to Topiramate 200 mg/day, held 10 and 25 episodes per day with an average duration of 20–80 min. There was no clinical response to a therapeutic trial with Indomethacin 150 mg/day. After 04 months of clinical treatment without success and on the refractory and incapacitating nature of pain, we opted for neurosurgical intervention. Performed Gasserian Trigeminal ganglion balloon compression rhizotomy of V1 and V2 roots to the left. In the immediate post-operative patient developed left facial anesthesia without new episodes of pain.After three months remained with significant improvement in pain intensity. Discussion: Chronic cluster headache occurs in less than 8 a 10% of cases. The rhizotomy of the trigeminal nerve compression with Fogarty balloon. The literature describes a frequency of 83% relief of at least 53% pain after the procedure. In the long term the rate drops to about 50% of cases.

Compressive Trigeminal Neuropathy after Caldwell-Luc Operation

Most postoperative maxillary cysts develop more than 10 years after a Caldwell-Luc operation. They can manifest with cheek pain, swelling and dental and visual symptoms. Brain imaging should be performed to distinguish trigeminal nerve compression from various other possible causes. It should be treated by surgical intervention to relieve the above-mentioned symptoms. We report a patient who presented with compressive trigeminal neuropathy caused by a postoperative maxillary cyst. Key Words: Caldwell-Luc operation, Trigeminal neuropathy, Maxillary sinus mucocele

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.

The persistent trigeminal artery: development, imaging anatomy, variants, and associated vascular pathologies

The persistent trigeminal artery (PTA) is the most common and most cephalad-located embryological anastomosis between the developing carotid artery and vertebrobasilar system to persist into adulthood. As such, it is frequently reported as an incidental finding in computed tomography angiography and magnetic resonance angiography studies. Here, we review the embryology, anatomy, and angiographic imaging findings, including important variants of this commonly encountered cerebrovascular anomaly (reported incidence of PTA/PTA variants ranges from 0.1% to 0.76%). Further, the aim is to present the range of associated arterial anomalies or syndromes, as well as pathologies that are associated with a PTA: aneurysms, trigeminal cavernous fistulas, and trigeminal nerve compression. Besides summarizing the risks and clinical presentation of such pathologies, their management is discussed with endovascular strategies mostly being the primary choice for aneurysms and trigeminal cavernous fistulas. Symptomatic trigeminal nerve compression can be treated with microvascular decompression surgery. As an illustrative example, a case of a trigeminal cavernous fistula on a PTA variant is included, mainly to emphasize the importance of understanding the variant anatomy for treatment planning in such pathologies. Finally, recommendations on how to manage patients with PTA-associated vascular pathologies are advanced.

Painful tic convulsif syndrome due to vertebrobasilar dolichoectasia

Combined clinical presentation of hemifacial spasm and ipsilateral trigeminal neuralgia is also known as painful tic convulsif (PTC). It is a rare condition and the most common cause is vascular compression. Vertebrobasilar dolichoectasia (VBD) is characterized by dilated and tortuous vertebral and basilar arteries. VBD is an uncommon and rarely reported cause of PTC. Magnetic resonance imaging (MRI), due to its inherent excellent contrast resolution, is an excellent modality for demonstrating the nerve compression by dilated and tortuous vessels seen in this condition. For this purpose, 3D MRI sequences are especially useful like constructive interference in steady state (CISS) and MR angiography. Both of these have been reported to be helpful in the diagnosis of this condition. We report a case of PTC in which we were able to document facial and trigeminal nerve compression by VBD on MRI, using CISS and time-of-flight MR angiography.

Progressive hemi facial atrophy - Parry Romberg syndrome presenting as severe facial pain in a young man: a case report

We present a 30-year-old South Indian man who presented with complaints of left sided headache and facial pain for past 3 months, severe for past 10 days. On physical examination, right side of the face appeared normal. Left side of the face showed signs of hemi atrophy with minimal drooping of left eyelid. All Systems were found to be normal. Routine blood and urine investigations results were within normal limits. X-ray chest revealed no abnormalities and x-ray skull showed both sides equal. Computerized tomogram of the brain showed left minimal sub dural hygroma with no midline shift, and no evidence of cerebral edema or cerebral atrophy. Nerve conduction study showed features suggestive of trigeminal neuralgia. MRI of the skull base was also normal and showed no evidence of trigeminal nerve compression. Interestingly, he had minimal response to analgesics, steroids, and propranolol, but showed immediate response to carbamazepine. Hence this patient indeed had Parry Romberg syndrome: Hemi facial atrophy with trigeminal neuralgia.

Vascular Decompression of Trigeminal and Facial Nerves in the Posterior Fossa under Endoscope-Assisted Keyhole Conditions

The aim of this study was to determine the use and safety of the endoscope as an adjunct during trigeminal and facial nerve decompression procedures performed under keyhole conditions in the posterior fossa. We performed 67 surgeries in 65 patients with symptomatic trigeminal and facial nerve compression syndromes. The diagnosis was made mainly on the basis of clinical history, examination, and magnetic resonance imaging scans. Surgery was performed in all cases under endoscope-assisted keyhole conditions. The follow-up was 1 week postoperatively, 6 months, and then yearly up to 7 years. All 34 patients with trigeminal neuralgia received preoperative medication treatment and experienced failure with it. Eighteen patients out of 30 with hemifacial spasm had been previously treated with botulinum toxin injections. One patient suffered from both trigeminal neuralgia and facial spasm, because of a megadolichobasilar and vertebral artery with compression of both cranial nerves. Sixty-four of the 65 patients became symptom free after surgical treatment; one revision surgery was necessary because of disappearance of the decompression muscle piece. No mortalities or minor morbidities were observed in this series. A precise planned keyhole craniotomy and the simultaneous use of the microscope and the endoscope render the procedure of the decompression less traumatic.

Microvascular decompression is effective method for treatment of trigeminal neuralgia in elderly patients

Background: The study aimed to determine the possible differences in the effectiveness of microvascular decompression for the treatment of trigeminal neuralgia between patients aged 65 or younger and patients older than 65 years, and to clarify the efficacy and safety of the MVD in elderly patients. Methods: In 40 patients MVD was used for treatment of typical TN. The pain relief immediately and 2 years after MVD for TN in 22 patients aged more than 65 years and in 18 patients younger than 65 years was evaluated and compared between the groups. Other parameters were also compared, such as duration of pain before surgery, operative fitness status, type of vessel (artery or vein) compressing the nerve, length of hospital stay, and complications after the surgery. Results: There was no significant difference in immediate pain relief and pain relief 2 years after MVD between the older and younger patients (P = 0.381, P = 0.185). 2 years after MVD, more pain free patients were found in cases of arterial compression in both groups (P < 0.001). The patients in the younger group showed better operative fitness status (P = 0.027). Length of hospital stay was shorter in younger patients (P < 0.001). There were no fatal outcomes, cranial nerve deficits, or any other permanent neurological deficits in either of the groups. Conclusions: Microvascular decompression is a safe and effective treatment for typical trigeminal neuralgia in elderly patients. This surgical technique is more successful in cases of trigeminal nerve compression by an artery. Physical fitness and not patient age should be a limiting factor for microvascular decompression as the treatment of choice for trigeminal neuralgia.

SUNCT Syndrome Associated with Compression of Trigeminal Nerve

SUNCT Syndrome Associated with Compression of Trigeminal Nerve

Gamma knife surgery for trigeminal neuralgia: Outcome, imaging, and brainstem correlates

Purpose To review our results with gamma knife surgery (GKS) in the treatment of trigeminal neuralgia (TN), and to determine whether pain relief, medication usage, and the development of facial numbness are affected by trigeminal nerve compression, MRI imaging quality, or brainstem radiation dose. Methods and materials One hundred twelve patients with TN refractory to medical or surgical management were treated at the University of Maryland Gamma Knife Center between June 1996 and July 2001. Patients were treated using a 4-mm shot to the trigeminal nerve, at a point 2–4 mm anterior to the root entry zone of the nerve into the pons. The median dose prescribed was 75 Gy (range, 60–80 Gy). T1- and T2-weighted, axial, 1.5-mm-thick MRI images were obtained using three-dimensional gradient echo acquisition after contrast injection for treatment planning. MRI images were evaluated for imaging quality (i.e., the adequacy of visualization of the affected prepontine trigeminal nerve), the presence of trigeminal nerve compression, and the brainstem dose. Follow-up data were obtained via telephone interviews, and patients were asked to rate their pre-GKS and post-GKS pain using the Barrow Neurological Institute (BNI) Pain Intensity Scale. Patients were also asked about side effects from GKS and were asked to rate any facial numbness on the BNI Facial Numbness Scale. Medication use, time to pain response, and duration of relief were also evaluated. Results Ninety-six patients who had follow-up data were included in the analysis. Eighty-six patients (89.6%) responded to GKS with an improvement in BNI pain class. Ten patients (10.4%) were found to have an MRI of poor quality, 30 (31.3%) fair quality, and 56 (58.3%) good quality. Forty-two (43.8%) received 10% of the maximal dose to the brainstem edge, whereas 54 (56.2%) received 20%. Eleven (11.5%) patients were found to have obvious nerve compression by MRI. Imaging quality ( p = 0.1863), presence of compression ( p = 0.1147), and brainstem dose ( p = 0.3168) did not correlate with treatment response. There was also no correlation between these variables (MRI quality, compression, and brainstem dose) and medication use ( p = 0.5372, p = 0.0913, p = 0.6832, respectively). Facial numbness was the only side effect experienced. Thirteen patients reported varying degrees of facial numbness, but there was no correlation between imaging quality ( p = 0.0600), brainstem dose ( p = 0.6773), and presence of compression ( p = 0.5785) with the development of facial numbness. Conclusions Gamma knife surgery is effective in the treatment of TN and has a favorable side effect profile. Treatment response and the development of facial numbness do not correlate with MRI imaging quality, presence of nerve compression, or radiation dose to the brainstem.

Case Report: Meningioma with Granulofilamentous Inclusions

The authors report a case of intracranial meningioma with granulofilamentous inclusions. A 50-year-old man had right trigeminal neuralgia due to trigeminal nerve compression by a petroclival tumor and received tumor resection. Microscopically, tumor cells containing eccentric nuclei and intracytoplasmic hyaline inclusions were arranged in sheets and whorls. The inclusions were negative for periodic acid-Schiff reaction. No histological anaplasia was seen. Immunohistochemistry showed epithelial membrane antigen reactivity on the cytoplasmic membrane. Immunoreactivity for vimentin was recognized in cytoplasm adjacent to inclusions. However, confocal laser microscopic study revealed immunoreactivity for vimentin even inside some inclusions. Ultrastructurally, interdigitation of cytoplasmic processes and desmosomes connecting adjacent cells were noted. Inclusions were composed of numerous fine osmiophilic granules attached by intermediates filaments. These findings were consistent with a meningioma with the granulofilamentous inclusions described earlier. The findings demonstrated by confocal laser microscopy and electron microscopy suggest that these granular materials may be the metabolic products of vimentin filaments.

Percutaneous Trigeminal Nerve Compression for Treatment of Trigeminal Neuralgia

The purpose of this study was to review the results of the treatment of trigeminal neuralgia by percutaneous trigeminal nerve compression in 50 patients during a period of 7.5 years and to review the factors associated with pain recurrence. Mean patient age was 61 years (range, 35-86). Among the patients, 52% had previous destructive peripheral procedures; 24% had first division pain; and 10% had multiple sclerosis. The mean follow-up was 3 years (range, 9 mo to 7.5 yr). Eighty-six percent of the patients were satisfied or very satisfied with their pain relief. Mild numbness persisted in 74%, and one patient thought it was severe. Minor masseter weakness resolved in all patients in a maximum of 1 year. Aseptic meningitis occurred in 3 patients. Minor dysesthesia was seen in 20%. Transient 6th nerve palsy was present in one patient. Anesthesia dolorosa or absence of the corneal reflex did not happen. The recurrence rate was 26% (13/50). The mean time until recurrence was 1.5 years (range, 14 d to 3.5 yr). Sixty-two percent (8/13) of patients with recurrence required a subsequent compression. When another compression was done, four of eight had recurrent pain once again. Three of these four patients had undergone two to eight previous destructive procedures. Overall, 8 of 13 patients with recurrence had undergone previous destructive procedures. Early recurrence (in < 1 week) or failure to relieve pain occurred in 8% (4/50) of patients. Half of those with early failure had a subsequent compression. After compression, 70% of patients with recurrence did have numbness.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical correlates of acoustic neuroma morphology.

Thirty-eight patients with vestibular schwannomas were reviewed. A correlation was found between tumour morphology and clinical presentation. Based on our knowledge of the variability in the neurilemmal-neurologlial junction and therefore the site of origin of these tumours in relation to the internal auditory canal, a classification into three different appearances on magnetic resonance imaging was possible. Dumbbell shaped tumours (21 per cent) represented laterally arising schwannomas, lollipop shaped tumours (18 per cent) were medially arising and cone shaped tumours (61 per cent) were the more common intermediate form. Patients with laterally arising dumb-bell shaped tumours were more likely to present early with hearing loss and had smaller tumours than patients with medially arising lollipop shaped ones. The relatively well preserved hearing in patients with medially arising tumours made them more likely to present at a later stage with signs of trigeminal compression, cerebellar dysfunction and raised intracranial pressure.

Unilateral reduction of head pain and facial vasodilatation after gasserian ganglion lesion.

The features of histamine-induced headache and its associated vascular responses were studied in 52 patients with different surgical lesions of the gasserian ganglion and in 12 control subjects. Certain features of headache (eg, intensity, type, and duration) were similar in patients and control subjects. However, the pain was absent on the side of the trigeminal lesion in 26 (50%) of the patients. This unilateral absence of pain was not related to the hypoesthesia that was caused by the operation, and it was associated with a decrease in vascular responses (histamine-induced facial flushing and increase in temperature) on the side operated on. These abnormalities were more prevalent in patients who had undergone thermocoagulation and presented with more severe damage of the trigeminal ganglion than in those who were subjected to trigeminal compression or glycerolization. The trigemino-vascular system seems to control headache of a vascular type and associated craniofacial vasodilatation in human subjects.

Subarachnoid hemorrhage and ???normal pressure hydrocephalus???

A 62-year-old man underwent percutaneous balloon catheter compression of the gasserian ganglion for typical trigeminal neuralgia. After this, a subarachnoid hemorrhage was discovered and normal pressure hydrocephalus developed, which required shunting. Although the neurological function recovered, the patient died 8 months later because of supervening hepatic insufficiency, probably caused by protracted antibiotic therapy. Such a fatal complication, the first one associated with the technique of percutaneous trigeminal compression, was perhaps predisposed by preexistent cerebral atrophy with enlargement of the subarachnoid spaces; the unforeseen piercing of the dilated trigeminal cistern probably permitted the intracranial subarachnoid diffusion of an otherwise trivial hemorrhage. The safety of the procedure may be greatly reduced in such instances.

Subarachnoid hemorrhage and “normal pressure hydrocephalus”

A 62-year-old man underwent percutaneous balloon catheter compression of the gasserian ganglion for typical trigeminal neuralgia. After this, a subarachnoid hemorrhage was discovered and normal pressure hydrocephalus developed, which required shunting. Although the neurological function recovered, the patient died 8 months later because of supervening hepatic insufficiency, probably caused by protracted antibiotic therapy. Such a fatal complication, the first one associated with the technique of percutaneous trigeminal compression, was perhaps predisposed by preexistent cerebral atrophy with enlargement of the subarachnoid spaces; the unforeseen piercing of the dilated trigeminal cistern probably permitted the intracranial subarachnoid diffusion of an otherwise trivial hemorrhage. The safety of the procedure may be greatly reduced in such instances.

Loss of substance P immunoreactivity in the nucleus of the spinal trigeminal tract after intradural tumour compression of the trigeminal nerve

The peptide, substance P (SP), is suspected of being a mediator of nociception. Immunoreactive SP is conspicuously present in areas of the mammalian central nervous system which receive nociceptive input. We have observed that compression of the trigeminal nerve by an intradural tumour deposit results in the ipsilateral depletion of SP immunoreactivity in human spinal trigeminal nucleus. These results expand previous experimental animal studies which associate this peptide with a subpopulation of primary sensory neurones and, in addition, demonstrate a correlation between the levels of SP immunoreactivity and premortem clinical sensory alterations.