[Trigeminal neuralgia - trigeminal neuritis; therapy of trigeminal neuritis with hydrogen peroxide injections at the nerve exits].
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Evoked potentials in trigeminal neuralgia.
Trigeminal evoked potentials and sensory thresholds in response to maxillary gum stimulation were obtained in patients with a complaint of unilateral face pain. The patients and the volunteer, normal control groups had undergone no prior surgical or other procedures involving cranial or cervical structures. For statistical purposes, patient data were analyzed with respect to the diagnostic classification of classical trigeminal neuralgia, atypical trigeminal neuralgia, or other face pain states in which the pain extended beyond the trigeminal nerve distribution. Latencies of trigeminal evoked potentials on the affected side were significantly increased (compared to normal control group responses) in patients with classical but not in those with atypical trigeminal neuralgia nor other face pain syndromes. All three patient groups had statistically significant threshold elevations on the affected side compared to the unaffected side. A high level of significance for this test was obtained for the classical trigeminal neuralgia group. Ratings for patients based upon the preoperative electrophysiological findings were highly correlated with long term results of microvascular decompression of the 5th nerve root for classical, but not for atypical trigeminal neuralgia patients. These results support the view that atypical and classical trigeminal neuralgia symptom complexes are caused by different types of physiological dysfunction and that classical trigeminal neuralgia is associated with compression of the trigeminal nerve root. It was suggested that the rating system may be a useful, objective, clinical adjunct in evaluating patients with classical trigeminal neuralgia.
Afferent Pathways↗
Evaluation of surgical procedures for trigeminal neuralgia.
Trigeminal neuralgia is a type of facial pain that is difficult to treat. The pain can be excruciating and debilitating. The wide range of treatments currently used for trigeminal neuralgia is ample evidence that there is no simple answer to how it should be managed. This review will evaluate the current surgical procedures used for the treatment of trigeminal neuralgia. A critical analysis of the evidence-based studies to date was done to evaluate and compare the efficacy of the different surgical procedures. Arguments for and against the use of surgery for trigeminal neuralgia are presented. In addition, the surgical procedures were compared with other treatments for trigeminal neuralgia.
Catheterization↗
Therapeutic potential of cannabinoids in trigeminal neuralgia.
Trigeminal neuralgia is a disorder of paroxysmal and severely disabling facial pain and continues to be a real therapeutic challenge to the clinicians. While the exact cause and pathology of this disorder is uncertain, it is thought that trigeminal neuralgia caused by irritation of the trigeminal nerve. This irritation results from damage due to the change in the blood vessels, the presence of a tumor or other lesions that cause the compression of the trigeminal root. The pain of trigeminal neuralgia is characterized by unilateral pain attacks that start abruptly and last for varying periods of time from minutes to hours. The quality of pain is usually sharp, stabbing, lancinating, and burning. The attacks are initiated by mild stimuli such as light touch of the skin, eating, chewing, washing the face, brushing the teeth, and exposure to wind. Although antiepileptic drug therapy may be beneficial in the treatment of trigeminal neuralgia, up to one-half of the patients become refractory or intolerant to these medications. At present there are few other effective drugs. In cases of lacking effect after pharmacotherapy, surgical options may be considered. Currently there is growing amount of evidence to suggest that the psychoactive ingredient in cannabis and individual cannabinoids may be effective in alleviating neuropathic pain and hyperalgesia. Evidence suggests that cannabinoids may prove useful in pain modulation by inhibiting neuronal transmission in pain pathways. Considering the pronounced antinociceptive effects produced by cannabinoids, they may be a promising therapeutic approach for the clinical management of trigeminal neuralgia.
Afferent Pathways↗
Review article: the medical management of trigeminal neuralgia.
Trigeminal neuralgia results from disturbances in the trigeminal root entry zone which generate repetitive action potentials. Drugs which relieve the pain of trigeminal neuralgia depressed these potentials. Anticonvulsants which exert this or related effects, and which have been demonstrated to be efficacious in trigeminal neuralgia, include carbamazepine, phenytoin, clonazepam, and valproic acid. Baclofen may act by facilitating segmental inhibition of the trigeminal complex. The mechanism of action of pimozide for treating trigeminal neuralgia is not known. Carbamazepine is suggested as the drug of first choice; baclofen or clonazepam could be added if carbamazepine monotherapy is ineffective. When these fail, monotherapy with phenytoin, pimozide, or valproic acid would be a reasonable next step.
Anticonvulsants↗
[Diagnosis and treatment of trigeminal neuralgia].
Trigeminal neuralgia is a disease affecting older individuals. The clinical hallmark of trigeminal neuralgia is a sudden, excruciating paroxysm of pain in the area of the trigeminal nerve. Drug therapy is considered the first line of treatment for trigeminal neuralgia. Anticonvulsant carbamazepine has been used. If relevant pharmacotherapy has been tried without any effect, other procedures are selected. These procedures are microvascular decompression(a radical technique), glycerol trigeminal rhizotomy, percutaneous trigeminal nerve decompression and nerve block. Nerve block with neurolytic solutions and radiofrequency thermocoagulation is a simple, less invasive therapy. In order to avoid hypesthesia and dysesthesia, nerve block using a high concentration of local anesthetics is recommended. In recent years, stereotactic radiosurgery for trigeminal neuralgia has emerged as a new therapeutic modality.
Anticonvulsants↗
Surgical treatment of trigeminal neuralgia.
TRIGEMINAL NEURALGIA, which is unilateral electric shock or knifelike pain occurring in one or more branches of the trigeminal nerve, is evoked by stimulation of the face, lips, or gums caused by activities such as shaving, brushing the teeth, or moving trigger zones. IT GENERALLY IS ACCEPTED that classic trigeminal neuralgia is a consequence of vascular compression and demyelination of the trigeminal nerve. Although medical therapy is available, it gradually becomes less effective because of the progressive nature of trigeminal neuralgia. MICROVASCULAR DECOMPRESSION of the trigeminal nerve to treat trigeminal neuralgia is discussed in this article. Perioperative care, expected course of recovery, and potential complications are described.
Aged↗
Diagnosis and differential diagnosis of trigeminal neuralgia.
Trigeminal neuralgia is a chronic facial pain classified as a neuropathic pain. There is widespread agreement regarding the International Association for the Study of Pain definition of classical idiopathic trigeminal neuralgia as "a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve." However, there are variations in presentation that are less easy to diagnose and an erroneous diagnosis of trigeminal neuralgia is occasionally made. In patients with tumors or multiple sclerosis, trigeminal neuralgia is termed secondary. Currently, clinical manifestations are the mainstay for diagnosis because there are no objective tests to validate the diagnosis. The sensitivity and specificity of these clinical manifestations is reviewed. Magnetic resonance imaging (MRI) and three-dimensional fast-in-flow with steady-state precession MRI are performed to determine the presence of tumors or plaques of multiple sclerosis and to assess possible compressions and deformations of the trigeminal nerve. Their specificity and sensitivity regarding compressions found at the time of surgery is reviewed. Other differential diagnoses for chronic unilateral orofacial pain are discussed.
Diagnosis, Differential↗
[Odontologic and other etiologic factors in trigeminal neuralgia].
Trigeminal neuralgia may be due to many causes, being in this respect secondary. To a certain degree trigeminal neuralgia may be facilitated by an individual increase of reactivity in the trigeminal system to noxious factors. For this reason, in treating trigeminal neuralgia, it is necessary first of all to take into consideration the possible etiological factors including different diseases of the teeth, in the innervation of which an important role is played by the fibers of the trigeminal nerve.
Adult↗
New insight into trigeminal neuralgia.
Trigeminal neuralgia is universally considered the neuropathic facial pain most and best known in medical practice. We propose a short review on trigeminal neuralgia reporting its main clinical aspects, unsolved problems and highlighting differential diagnosis between classical and symptomatic trigeminal neuralgia.
Diagnosis, Differential↗
Subclinical sensory abnormalities in trigeminal neuralgia.
Trigeminal neuralgia is considered as a paroxysmal single nerve phenomenon. Abnormal sensory perception has been previously described in 15-25% of patients with clinical examination. Quantitative sensory testing (QST) was used to evaluate sensory perception in patients with idiopathic trigeminal neuralgia (ITN). Nine patients and 10 normal control subjects were evaluated in all six trigeminal branches. QST abnormalities were found in the symptomatic division and in the other two branches on the same side. Minor contralateral changes were also found. Differences consisted of cold and warm hypoaesthesia and higher cold and heat pain thresholds in patients. All differences proved statistically significant. Our findings suggest that trigeminal neuralgia is not only a paroxysmal single nerve disorder, but also that other higher structures may be involved.
Adult↗
Long-term cohort study comparing medical (oxcarbazepine) and surgical management of intractable trigeminal neuralgia.
Trigeminal neuralgia is a recurrent severe shooting neuropathic pain which can be managed both pharmacologically and surgically. However, there are no prospective data that compare these two therapeutic strategies. This study therefore aimed to assess long-term outcome in patients with intractable trigeminal neuralgia treated with oxcarbazepine and later with surgery. Fifteen patients (11 females) with trigeminal neuralgia intractable to available drugs (carbamazepine, phenytoin and baclofen), were prospectively followed for 13 years (1986-1999) with a total follow up time from onset of disease of 16 +/- 6 years (mean +/- SD), range 8-30 years. All patients were contacted in 1999 and 12 replied, two had died and one had last replied in 1996. Patients were first treated with oxcarbazepine 1200 +/- 600 mg daily dosage (mean +/- SD) and subsequently with surgery of their choice. The outcome measures used were: McGill Pain Questionnaire, Hospital Anxiety and Depression Scale, patient satisfaction questionnaire and clinicians' global evaluation. Pain control was initially achieved in all patients and oxcarbazepine was used continuously or intermittently for 4.0 +/- 3 years (mean +/- SD). Thirteen patients experienced some mild side effects and a dose-dependent hyponatraemia was noted. Subsequently, 12 patients required surgery (five microvascular decompressions and seven surgery at the level of the Gasserian ganglion) to control their pain and were followed up for 4.3 +/- 1.7 years post surgery (mean +/- SD). Three patients required repeat surgery to control their pain, which was successful in two. A further two patients continued with low dose medication post initially successful surgery. Three patients reported numbness and one hearing loss after surgery. Kaplan Meier analysis 3 years after oxcarbazepine use and then 3 years after surgery showed that the mean time for recurrence of pain after oxcarbazepine treatment was 10 months whilst for surgery it was 28 months (P<0.0001). Pain free periods and types of complications post surgery varied and depended on the type of surgery performed. Due to the small numbers, it was not possible to analyse the different types of surgical procedures individually. Outcomes after any type of surgery were better on all evaluations and eight patients felt that they should have had surgery earlier. Oxcarbazepine is a potent antineuralgic drug with very good acceptability and tolerability. However, its effectiveness was rather short term necessitating surgical intervention. As surgery was associated with better outcome, patients may therefore benefit from having surgery earlier rather than later in the disease process in order to improve quality of life, freedom from medication and the need for regular follow up. Surgery does not provide pain relief for all patients. This is the first study that has compared outcome in a group of patients who have had both pharmacological and surgical treatments. As these data cannot be extrapolated to other antineuralgic drugs, similar comparative studies would be appropriate.
Adult↗
[Acupuncture and ganglionic local opioid analgesia in trigeminal neuralgia].
Trigeminal neuralgia (TN) is defined as a chronic, severe, electrifying and burning pain in one side of the face. The attacks are initiated by tactile irritations in a so-called trigger area of the trigeminal nerve and are perceived within the borders of this nerve's innervation. TN is a chronic condition which initially goes into spontaneous remission but these become fewer as the condition progresses. TN is classified as symptomatic when the etiology is known and as idiopathic when the etiology is unknown. There are various forms of treatment: drugs such as anticonvulsants, local ganglionic opioid analgesia (GLOA) at the superior cervical ganglion or sphenopalatine ganglion, percutaneous intervention at the trigeminal ganglion as well as neurosurgery. None of these various procedures has been found to be the most suited and best method. A retrospective analysis of the data of 39 patients who had sought treatment for TN at our pain and acupuncture outpatients' department from 1993 to 1994 was undertaken. Group A (n = 17) had received carbamazepine and acupuncture therapy, group B (n = 11) carbamazepine and GLOA + acupuncture, whereas group C (n = 11) had received carbamazepine and GLOA without acupuncture. All subjects had taken carbamazepine for at least 4 weeks and their plasma levels were within the therapeutic range. Acupuncture therapy was carried out once a week and the number recorded. GLOA was carried out with 0.045 mg buprenorphine at the superior cervical ganglion or the sphenopalatine ganglion as a series of at least 5 injections. The number of attacks of pain and the degree of pain (visual analogue scale [VAS]) were documented. The reduction in pain was categorized in 4 groups: I = pain free, II = reduction of at least 50% on the VAS, III = reduction of less than 50% on the VAS, and IV = no improvement. The statistical analysis was carried out using the chi 2-text, p < 0.05 was considered as significant. Of the groups who received acupuncture as an additive, 8 of the 17 subjects of group A, and 5 of the 11 subjects of group B were pain free, but only 2 of the 11 subjects of group C (no acupuncture). The results of the patients with marked pain reduction (category II) were similar. The most patients with no improvement were from the group which did not receive acupuncture (C). The statistical analysis showed significant differences in the categories I, II, and IV between groups A and C. These results show that the combined use of acupuncture and carbamazepine with/without GLOA achieves an additional therapeutic effect in the treatment of trigeminal neuralgia. The addition of acupuncture seems to have a superior effect to the addition of GLOA. These results support the use of acupuncture as an additional form of therapy for the treatment of trigeminal neuralgia.
Acupuncture Therapy↗
Gamma knife radiosurgery as a primary treatment for prolactinomas.
OBJECT: The purpose of this study was to estimate the efficacy of gamma knife radiosurgery (GKS) in controlling tumor growth and endocrinopathy associated with prolactinomas. METHODS: Between 1993 and 1997, 164 of 469 patients with pituitary adenomas treated by GKS harbored prolactinomas. The dose to the tumor margin ranged from 9 to 35 Gy (mean 31.2 Gy), and the visual pathways were exposed to a dose of less than 10 Gy. The mean tumor diameter was 13.4 mm. The mean follow-up time for 128 cases was 33.2 months (range 6-72 months). Tumor control was observed in all but two patients who underwent surgery 18 and 36 months, respectively, after GKS. Clinical cure was achieved in 67 cases. Clinical improvement was noted with a decrease in the hyperprolactinemia after GKS. Nonetheless, in 31 (29%) of 108 patients who were followed for more than 2 years no improvement in serum prolactin levels was demonstrated, although this could be normalized by bromocriptine administration after treatment. Nine infertile women became pregnant 2 to 13 months after GKS and all gave birth to normal children. There was no visual deterioration related to GKS. Five women experienced premature menopause. In these patients there was subtotal disappearance of the tumor and an empty sella developed. CONCLUSIONS: Gamma knife radiosurgery as a primary treatment for prolactinomas can be safe and effective both for controlling tumor growth and for normalization of prolactin hypersecretion. A higher margin dose (> or = 30 Gy) seemed to be associated with a better clinical outcome. Gamma knife radiosurgery may make prolactinomas more sensitive to the bromocriptine.
Humans↗
Magnetic resonance imaging in the diagnosis of trigeminal neuralgia.
Trigeminal neuralgia is not a specific disease, but a symptom elicited by pathology involving the fifth cranial nerve. Advances in the field of magnetic resonance imaging (MRI) have made this the premier imaging modality in the diagnostic workup of trigeminal neuralgia. This article reviews the pertinent anatomy of the trigeminal nerve as well as the structural lesions that produce the symptoms of the condition. The advantages of MRI over other imaging methods are outlined, and the indications for obtaining this study are discussed.
Female↗
Fatal paranasal sinusitis presenting as trigeminal neuralgia.
Trigeminal neuralgia is rare in patients with paranasal sinusitis. The authors describe a case of paranasal sinusitis that appeared as an insidious onset of trigeminal neuralgia along the distribution of ophthalmic and maxillary branches, followed by rapid intracranial invasion with temporal meningoencephalitis and subdural empyema, and finally a fatal outcome.
Aged↗
[Etiology and therapy of trigeminal neuralgia].
Trigeminal neuralgia is an exactly defined syndrome with a non-uniform aetiology but an obviously uniform pathogenesis. 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.
Humans↗
Medical management of trigeminal neuralgia.
Trigeminal neuralgia is a sudden, severe, brief, recurrent stabbing pain in the distribution of the trigeminal nerve whose aetiology remains unknown. Medical management is the first line of treatment and when this fails, surgical treatment needs to be undertaken. Carbamazepine is the best anti-neuralgic drug available at present, but may cause unacceptable side-effects. Phenytoin, baclofen and clonazepam are other drugs used, either as monotherapy or together with carbamazepine, but they are not as effective. Oxcarbazepine, a new drug, similar to carbamazepine but with fewer side-effects, may prove to be the drug of the future. Once diagnosed, these patients should be managed by specialists who can offer a range of treatments.
Carbamazepine↗