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1990, Journal of Neurology, Neurosurgery & Psychiatry
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9 pages
1 file
The trigeminal reflexes (corneal reflex, blink reflex, masseter inhibitory periods, jaw-jerk) and far field scalp potentials (nerve, root, brainstem, subcortical) evoked by percutaneous infraorbital stimulation were recorded in 30 patients with "idiopathic" trigeminal neuralgia (ITN) and 20 with "symptomatic" trigeminal pain (STP): seven postherpetic neuralgia, five multiple sclerosis, four tumour, two vascular malformation, one Tolosa-Hunt syndrome, and one traumatic fracture. All the patients with STP and two of those with ITN had trigeminal reflex abnormalities; 80% of patients with STP and 30% of those with ITN had evoked potential abnormalities. The results indicate that 1) trigeminal reflexes and evoked potentials are both useful in the examination of patients with trigeminal pain, and in cases secondary to specific pathologies provide 100% sensitivity; 2) in "symptomatic" and "idiopathic" paroxysmal pain the primary lesion affects the afferent fibres in the proximal portion of the root or the intrinsic portion in the pons; 3) primary sensory neurons of the A-beta fibre group are involved in both paroxysmal and constant pain, but in the latter the damage is far more severe.
2005
Introduction: Trigeminal neuralgia (TN) is characterized by touch-evoked unilateral brief shock-like paroxysmal pain in one or more divisions of the trigeminal nerve. In addition to the paroxysmal pain, some patients also have continuous pain. TN is divided into classical TN (CTN) and secondary TN (STN). Etiology and pathophysiology: Demyelination of primary sensory trigeminal afferents in the root entry zone is the predominant pathophysiological mechanism. Most likely, demyelination paves the way for generation of ectopic impulses and ephaptic crosstalk. In a significant proportion of the patients, the demyelination is caused by a neurovascular conflict with morphological changes such as compression of the trigeminal root. However, there are also other unknown etiological factors, as only half of the CTN patients have morphological changes. STN is caused by multiple sclerosis or a space-occupying lesion affecting the trigeminal nerve. Differential diagnosis and treatment: Important differential diagnoses include trigeminal autonomic cephalalgias, posttraumatic or postherpetic pain and other facial pains. First line treatment is prophylactic medication with sodium channel blockers, and second line treatment is neurosurgical intervention. Future perspectives: Future studies should focus on genetics, unexplored etiological factors, sensory function, the neurosurgical outcome and complications, combination and neuromodulation treatment as well as development of new drugs with better tolerability.
The trigeminal nerve, fifth equal of cranial nerves, a mixed nerve is considered by possessing motor and sensitive components. The sensitive portion takes to the Nervous System Central somesthesics information from the skin and mucous membrane of great area of the face, being responsible also for a neural disease, known as the Trigeminal Neuralgia. The aim of this study was to review the literature on the main characteristics of Trigeminal Neuralgia, the relevant aspects for the diagnosis and treatment options for this pathology. This neuralgia is characterized by hard pains and sudden, similar to electric discharges, with duration between a few seconds to two minutes, in the trigeminal nerve sensorial distribution. The pain is unchained by light touches in specific points in the skin of the face or for movements of the facial muscles, it can be caused by traumatic sequels or physiologic processes degenerative associate the vascular compression. Prevails in the senior population, frequently in the woman. In a unilateral way it attacks more the maxillary and mandibular divisions, rarely happens in a simultaneous way in the three branches of trigeminal nerve three branches.
Journal of medicine and life, 2013
Trigeminal neuralgia (TN) is defined as sudden, usually unilateral, severe, brief, stabbing recurrent episodes of pain within the distribution of one or more branches of the trigeminal nerve. It is the most frequent cranial neuralgia, the incidence being 1 per 1,000,00 persons per year. Pain attacks start abruptly and last several seconds but may persist 1 to 2 minutes. The attacks are initiated by non painful physical stimulation of specific areas (trigger points or zones) that are located ipsilateral to the pain. After each episode, there is usually a refractive period during which stimulation of the trigger zone will not induce the pain. According to the European Federation of Neurological Societies (EFNS) guidelines on neuropathic pain assessment and the American Academy of Neurology (AAN)-EFNS guidelines on TN management the neurophysiological recording of trigeminal reflexes represents the most useful and reliable test for the neurophysiological diagnosis of trigeminal pains. ...
Southeast Asian Journal of Health Professional
Out of all the cranial nerves “Trigeminal Nerve” is the fifth cranial nerve. Trigeminal nerve possesses both the components i.e. mixed components as well as sensitive components that’s why trigeminal nerve is known as a mixed nerve. The sensitive component of the trigeminal nerve takes up the sensation from most of the part of the face and the mucous membrane to the central nervous system and that’s why it is responsible for the disease which is known as trigeminal neuralgia. The characteristic feature of the trigeminal neuralgia is the sudden onset of pain which is sharp and lacerating, and that may last from few of the seconds to few minutes. Trigeminal neuralgia more frequently affects the female as compared to the male.
Clinical Neurophysiology, 2005
The trigeminal nerve and nuclei (the trigeminal complex) are unique in the human body with regard to their anatomical and physiological characteristics. They are also special regarding the lesions in which they are involved, both at the peripheral level because of the susceptibility of some terminal branches, and at the nuclei because of their large size and the large amount of connections with other centers. Conventional magnetic resonance imaging studies are often not sufficiently informative to demonstrate very tiny lesions that could be responsible for an important damage in the brainstem. Therefore, clinical neurophysiology and specifically, the techniques used in the study of the trigeminal functions, remain as convenient diagnostic and research tools to document clinically evident lesions or uncover subclinical abnormalities. This review is focussed on the clinical applicability of the study of trigeminal reflexes, including methods employed in the documentation of focal lesions of peripheral branches, trigeminal involvement of peripheral neuropathies, specific lesions of the trigeminal ganglia, central nervous dysfunctions causing abnormalities in the excitability of trigeminal neurons, and the possible use of trigeminal nerve reflexes in the study of facial pain syndromes and headache.
The Clinical Journal of Pain, 2002
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-inflow 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.
WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES, 2021
Trigeminal neuralgia (TN) is a debilitating disorder that presents with a sudden onset of severe, unilateral, paroxysmal, and lancinating pain in one or more of the distributions of the trigeminal nerve. Trigeminal neuralgia affects the trigeminal nerve, fifth most developed and extensive cranial nerve, with a broad distribution territory. Its name - “trigeminal” - is derived from the fact that each nerve, one on each side of the pons, has three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2) and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory. The mandibular nerve has both sensory and motor functions.[1] It is a mixed nerve conducting sensitive and motor somatic fibers to the face, and is ideally responsible for all its sensitive innervation (touch, pain, temperature and propioception) together with the motor innervation of the mastication apparatus. Though it has been known by various names in the literature such as tic douloureux, trifacial neuralgia, fothergill’s disease (named after john fothergill), the currently accepted terminology is trigeminal neuralgia.[2]
2014
Trigeminal neuralgia (TN), the most common and the most serious of the facial neuralgias, is characterized by an extremely severe electric shock like or lancinating pain limited to one or more branches of the trigeminal nerve. Among the very many diagnostic and treatment options in the management of TN only very few have proven their efficacy to modern evidence-based medicine standards. For thorough and accurate management, a stepwise diagnostic and treatment approach is recommended. Surgical management should be recommended if sufficient and compliant medical therapy failed. The aim of this review article is to discuss the etiopathogenesis, diagnostic criteria, and treatment strategies for trigeminal neuralgia.
2008
ABSTRACT The diagnosis of Trigeminal Neuralgia (TN) has been a source of confusion for clinicians and remains a difficult condition to manage. The study was conducted on 50 patients to evaluate the area of pain distribution and involved nerve. The diagnosis was based on history, clinical examination and response of pain to carbamazepine. The branch of the nerve was identified and confirmed with 2% lignocain with adrenaline 1: 200,000 injection at the identified site and repeated three times on consecutive days.
Pain Physician, 2016
Background: Trigeminal neuralgia (TN) is characterized by paroxysmal pain attacks affecting the somatosensory distributions of the trigeminal nerve. It is thought to be associated with a neurovascular conflict most frequently, but pathomechanisms have not been fully elucidated. In general, no sensory deficit is found in routine clinical examination. There is limited data available, however, showing subtle subclinical sensory deficits upon extensive testing. Objective: We used quantitative sensory testing (QST) to detect abnormalities in sensory processing in patients with TN by comparing the affected and non-affected nerve branches with their contralateral counterparts and by comparing the results of the patients with those of controls. Study Design: Observational study. Setting: University Hospital, Departments of Neurosurgery, Institute for Cognitive and Clinical Neuroscience. Methods: QST was conducted on 48 patients with idiopathic TN and 27 controls matched for age and gender u...
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