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British Journal of Anaesthesia Jul 2013The diagnosis and management of facial pain below the eye can be very different dependant on whether the patient visits a dentist or medical practitioner. A structure... (Review)
Review
The diagnosis and management of facial pain below the eye can be very different dependant on whether the patient visits a dentist or medical practitioner. A structure for accurate diagnosis is proposed beginning with a very careful history. The commonest acute causes of pain are dental and these are well managed by dentists. Chronic facial pain can be unilateral or bilateral and continuous or episodic. The commonest non-dental pains are temporomandibular disorders (TMDs), especially musculoskeletal involving the muscles of mastication either unilaterally or bilaterally; they may be associated with other chronic pains. A very wide range of treatments are used but early diagnosis, reassurance and some simple physiotherapy is often effective in those with good coping strategies. Dentists will often make splints to wear at night. Neuropathic pain is usually unilateral and of the episodic type; the most easily recognized is trigeminal neuralgia. This severe electric shock like pain, provoked by light touch, responds best to carbamazepine, and neurosurgery in poorly controlled patients. Trauma, either major or because of dental procedures, results in neuropathic pain and these are then managed as for any other neuropathic pain. Red flags include giant cell arteritis which much be distinguished from temporomandibular disorders (TMD), especially in >50 yr olds, and cancer which can present as a progressive neuropathic pain. Burning mouth syndrome is rarely recognized as a neuropathic pain as it occurs principally in peri-menopausal women and is thought to be psychological. Chronic facial pain patients are best managed by a multidisciplinary team.
Topics: Diagnosis, Differential; Facial Pain; Humans; Neuralgia; Pain Management; Pain Measurement; Temporomandibular Joint Disorders; Trigeminal Neuralgia
PubMed: 23794651
DOI: 10.1093/bja/aet125 -
Diagnostic and Interventional Imaging Oct 2013Two different clinical entities, essential or secondary neuralgia, are associated with different pathologies. The pathways of CN V comprise the cervical spine, the... (Review)
Review
Two different clinical entities, essential or secondary neuralgia, are associated with different pathologies. The pathways of CN V comprise the cervical spine, the brainstem, the root of the nerve and the three peripheral branches: V1, V2 and V3. The lesions responsible for neuralgia are neoplastic, vascular, inflammatory, malformative or post-traumatic. The examination protocol should explore the set of CN V pathways. Neurovascular compression is the main cause of essential neuralgia. It is investigated by T2-weighted inframillimetric volume. Two conditions are necessary to diagnose a neurovascular compression: localised on the root entry zone [(REZ), 2-6mm from the emergence of the pons] and perpendicularly. In the absence of neurovascular compression, thin slices and a gadolinium injection are necessary.
Topics: Cranial Nerve Neoplasms; Diagnosis, Differential; Humans; Image Enhancement; Image Interpretation, Computer-Assisted; Magnetic Resonance Imaging; Nerve Compression Syndromes; Neural Pathways; Neurologic Examination; Sensitivity and Specificity; Trigeminal Nerve; Trigeminal Nerve Diseases; Trigeminal Nerve Injuries; Trigeminal Neuralgia; Trigeminal Nuclei
PubMed: 24007773
DOI: 10.1016/j.diii.2013.08.002 -
BMJ Clinical Evidence Oct 2014Trigeminal neuralgia is a sudden, unilateral, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. Pain occurs in... (Review)
Review
INTRODUCTION
Trigeminal neuralgia is a sudden, unilateral, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. Pain occurs in paroxysms, which can last from a few seconds to several minutes. The frequency of the paroxysms ranges from a few to hundreds of attacks a day. Periods of remission can last for months to years, but tend to shorten over time. The condition can impair activities of daily living and lead to depression.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical question: What are the effects of ongoing treatments in people with trigeminal neuralgia? We searched: Medline, Embase, The Cochrane Library, and other important databases up to September 2013 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found seven studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review, we present information relating to the effectiveness and safety of the following interventions: baclofen; carbamazepine; gabapentin; lamotrigine; oxcarbazepine; microvascular decompression; and destructive neurosurgical techniques (radiofrequency thermocoagulation, glycerol rhizolysis, balloon compression, and stereotactic radiosurgery).
Topics: Anticonvulsants; Humans; Neurosurgery; Trigeminal Neuralgia
PubMed: 25299564
DOI: No ID Found -
Molecular Pain 2020Schwann cells are components of the peripheral nerve myelin sheath, which supports and nourishes axons. Upon injury of the trigeminal nerve, Schwann cells are activated... (Review)
Review
Schwann cells are components of the peripheral nerve myelin sheath, which supports and nourishes axons. Upon injury of the trigeminal nerve, Schwann cells are activated and cause trigeminal neuralgia by engulfing the myelin sheath and secreting various neurotrophic factors. Further, Schwann cells can repair the damaged nerve and thus alleviate trigeminal neuralgia. Here, we briefly describe the development and activation of Schwann cells after nerve injury. Moreover, we expound on the occurrence, regulation, and treatment of trigeminal neuralgia; further, we point out the current research deficiencies and future research directions.
Topics: Animals; Humans; Schwann Cells; Trigeminal Neuralgia
PubMed: 33054604
DOI: 10.1177/1744806920963809 -
American Family Physician Jul 2016
Review
Topics: Analgesics, Non-Narcotic; Carbamazepine; Electrocoagulation; Humans; Microvascular Decompression Surgery; Radiosurgery; Trigeminal Neuralgia
PubMed: 27419329
DOI: No ID Found -
American Family Physician May 2008Trigeminal neuralgia is an uncommon disorder characterized by recurrent attacks of lancinating pain in the trigeminal nerve distribution. Typically, brief attacks are... (Review)
Review
Trigeminal neuralgia is an uncommon disorder characterized by recurrent attacks of lancinating pain in the trigeminal nerve distribution. Typically, brief attacks are triggered by talking, chewing, teeth brushing, shaving, a light touch, or even a cool breeze. The pain is nearly always unilateral, and it may occur repeatedly throughout the day. The diagnosis is typically determined clinically, although imaging studies or referral for specialized testing may be necessary to rule out other diseases. Accurate and prompt diagnosis is important because the pain of trigeminal neuralgia can be severe. Carbamazepine is the drug of choice for the initial treatment of trigeminal neuralgia; however, baclofen, gabapentin, and other drugs may provide relief in refractory cases. Neurosurgical treatments may help patients in whom medical therapy is unsuccessful or poorly tolerated.
Topics: Analgesics, Non-Narcotic; Carbamazepine; Diagnosis, Differential; Humans; Physical Examination; Trigeminal Neuralgia
PubMed: 18540495
DOI: No ID Found -
Science Advances Jan 2024Anxiety and depression are frequently observed in patients suffering from trigeminal neuralgia (TN), but neural circuits and mechanisms underlying this association are...
Anxiety and depression are frequently observed in patients suffering from trigeminal neuralgia (TN), but neural circuits and mechanisms underlying this association are poorly understood. Here, we identified a dedicated neural circuit from the ventral hippocampus (vHPC) to the medial prefrontal cortex (mPFC) that mediates TN-related anxiodepression. We found that TN caused an increase in excitatory synaptic transmission from vHPC neurons to mPFC inhibitory neurons marked by the expression of corticotropin-releasing hormone (CRH). Activation of CRH neurons subsequently led to feed-forward inhibition of layer V pyramidal neurons in the mPFC via activation of the CRH receptor 1 (CRHR1). Inhibition of the vHPC-mPFC circuit ameliorated TN-induced anxiodepression, whereas activating this pathway sufficiently produced anxiodepressive-like behaviors. Thus, our studies identified a neural pathway driving pain-related anxiodepression and a molecular target for treating pain-related psychiatric disorders.
Topics: Humans; Corticotropin-Releasing Hormone; Trigeminal Neuralgia; Neurons; Hippocampus; Pain
PubMed: 38241377
DOI: 10.1126/sciadv.adj4196 -
Journal of Neurosurgery Oct 2013
Topics: Decompression, Surgical; Female; Humans; Male; Nerve Compression Syndromes; Trigeminal Neuralgia
PubMed: 23952974
DOI: 10.3171/2012.12.JNS11965 -
Molecular Pain 2021Trigeminal neuralgia (TN) is a severe facial pain disease of unknown cause and unclear genetic background. To examine the existing knowledge about genetics in TN, we...
Trigeminal neuralgia (TN) is a severe facial pain disease of unknown cause and unclear genetic background. To examine the existing knowledge about genetics in TN, we performed a systematic study asking about the prevalence of familial trigeminal neuralgia, and which genes that have been identified in human TN studies and in animal models of trigeminal pain. MedLine, Embase, Cochrane Library and Web of Science were searched from inception to January 2021. 71 studies were included in the systematic review. Currently, few studies provide information about the prevalence of familial TN; the available evidence indicates that about 1-2% of TN cases have the familial form. The available human studies propose the following genes to be possible contributors to development of TN: CACNA1A, CACNA1H, CACNA1F, KCNK1, TRAK1, SCN9A, SCN8A, SCN3A, SCN10A, SCN5A, NTRK1, GABRG1, MPZ gene, MAOA gene and SLC6A4. Their role in familial TN still needs to be addressed. The experimental animal studies suggest an emerging role of genetics in trigeminal pain, though the animal models may be more relevant for trigeminal neuropathic pain than TN per se. In summary, this systematic review suggests a more important role of genetic factors in TN pathogenesis than previously assumed.
Topics: Animals; Facial Pain; Humans; NAV1.7 Voltage-Gated Sodium Channel; Serotonin Plasma Membrane Transport Proteins; Trigeminal Neuralgia
PubMed: 34000891
DOI: 10.1177/17448069211016139 -
Acta Medica Academica Aug 2021Trigeminal neuralgia is a long-term facial pain syndrome. Our aim was to review the anatomy of the trigeminal nerve and its anatomical relationship with the adjacent... (Review)
Review
OBJECTIVE
Trigeminal neuralgia is a long-term facial pain syndrome. Our aim was to review the anatomy of the trigeminal nerve and its anatomical relationship with the adjacent structures that may contribute to the pathogenesis of trigeminal neuralgia METHODS: Eligible articles were identified by a search of the Medline Embase, Pubmed Cinahl and Google Scholar bibliographical databases. We checked all the references of the relevant reviews and eligible articles that our search retrieved, in order to identify potentially eligible conference abstracts. Titles of interest were further reviewed by abstract. Case reports were excluded.
RESULTS
Trigeminal neuralgia syndrome seems to be caused by anatomical variations of the trigeminal nerve and its adjacent anatomical structures, mainly through compression. We depict the causes, the pathogenesis, and the clinical manifestations of the syndrome. The classification, diagnostic approach, differential diagnosis, and treatment modalities are also presented and they may be personalized according to the anatomical variations of the trigeminal nerve present, which may lead to trigeminal neuralgia syndrome.
CONCLUSION
It is very important to be very careful in cases of new emerging neuralgia and to avoid the term "idiopathic" until proven otherwise by validating the newer and more appropriate tests and diagnostic criteria. Current data are insufficient and future research is needed in order to discover innovative and more effective treatments of trigeminal neuralgia, considering the anatomy and the anatomical variations of the trigeminal nerve.
Topics: Humans; Treatment Outcome; Trigeminal Nerve; Trigeminal Neuralgia
PubMed: 34847681
DOI: 10.5644/ama2006-124.344