Overview Show
Practice EssentialsTrigeminal neuralgia (TN), also known as tic douloureux, is a distinctive facial pain syndrome that may become recurrent and chronic. It is characterized by unilateral pain following the sensory distribution of cranial nerve V (typically radiating to the maxillary or mandibular area in 35% of affected patients) and is often accompanied by a brief facial spasm or tic. See the image below.  Signs and symptomsTN presents as attacks of stabbing unilateral facial pain, most often on the right side of the face. The number of attacks may vary from less than 1 per day to 12 or more per hour and up to hundreds per day. Triggers of pain attacks include the following:
Pain localization is as follows:
The pain has the following qualities:
Other diagnostic clues are as follows:
See Clinical Presentation for more detail. DiagnosisNo laboratory, electrophysiologic, or radiologic testing is routinely indicated for the diagnosis of TN, as patients with a characteristic history and normal neurologic examination may be treated without further workup. Strict criteria for TN as defined by the International Headache Society (IHS) are as follows [1] :
IHS criteria for symptomatic TN vary slightly from the strict criteria and include the following [1] :
A blood count and liver function tests are required if therapy with carbamazepine is contemplated. Oxcarbazepine can cause hyponatremia, so the serum sodium level should be measured after institution of therapy. See Workup for more detail. ManagementTreatment of TN comprises the following:
Features of pharmacologic therapy are as follows:
Features of surgical treatment include the following:
See Treatment and Medication for more detail. BackgroundTrigeminal neuralgia (TN), also known as tic douloureux, is a common and potentially disabling pain syndrome, the precise pathophysiology of which remains obscure. This condition has been known to drive patients with trigeminal neuralgia to the brink of suicide. Although neurologic examination findings are normal in patients with the idiopathic variety, the most common type of facial pain neuralgia, the clinical history is distinctive. Trigeminal neuralgia is characterized by unilateral pain following the sensory distribution of cranial nerve V—typically radiating to the maxillary (V2) or mandibular (V3) area in 35% of affected patients (see the image below)—often accompanied by a brief facial spasm or tic. Isolated involvement of the ophthalmic division is much less common (2.8%). Typically, the initial response to carbamazepine therapy is diagnostic and successful. Despite obtaining this satisfying early relief with medication, patients may experience breakthrough pain that requires additional drugs and, in some patients, one or more of a variety of surgical interventions. Historical informationThe clinical description of trigeminal neuralgia can be traced back more than 300 years. Aretaeus of Cappadocia, known for one of the earliest descriptions of migraine, is credited with the first indication of trigeminal neuralgia when he described a headache in which "spasms and distortions of the countenance took place." Nicholaus Andre coined the term tic douloureux in 1756. John Fothergill was the first to give a full and accurate description of this condition in a paper titled "On a Painful Affliction of the Face," which he presented to the medical society of London in 1773. Osler also described trigeminal neuralgia in great and accurate detail in his 1912 book The Principles and Practice of Medicine. [3] In 1900, in a landmark article, Cushing reported a method of total ablation of the gasserian ganglion to treat trigeminal neuralgia. See also Trigeminal Neuralgia Surgery. AnatomyThe trigeminal nerve is the largest of all the cranial nerves. It exits laterally at the mid-pons level and has 2 divisions—a smaller motor root (portion minor) and a larger sensory root (portion major). The motor root supplies the temporalis, pterygoid, tensor tympani, tensor palati, mylohyoid, and anterior belly of the digastric. The motor root also contains sensory nerve fibers that particularly mediate pain sensation. The gasserian ganglion is located in the trigeminal fossa (Meckel cave) of the petrous bone in the middle cranial fossa. It contains the first-order general somatic sensory fibers that carry pain, temperature, and touch. The peripheral processes of neurons in the ganglion form the 3 divisions of the trigeminal nerve (ie, ophthalmic, maxillary, and mandibular). The ophthalmic division exits the cranium via the superior orbital fissure; the maxillary and mandibular divisions exit via the foramen rotundum and foramen ovale, respectively. The proprioceptive afferent fibers travel with the efferent and afferent roots. They are peripheral processes of unipolar neurons located centrally in the mesencephalic nucleus of the trigeminal nerve. The image below depicts the anatomy of the trigeminal nerve. PathophysiologyBecause the exact pathophysiology remains controversial, the etiology of trigeminal neuralgia (TN) may be central, peripheral, or both. The trigeminal nerve (cranial nerve V) can cause pain, because its major function is sensory. Usually, no structural lesion is present (85%), although many investigators agree that vascular compression, typically venous or arterial loops at the trigeminal nerve entry into the pons, is critical to the pathogenesis of the idiopathic variety. This compression results in focal trigeminal nerve demyelination. The etiology is labeled idiopathic by default and is then categorized as classic trigeminal neuralgia. Neuropathic pain is the cardinal sign of injury to the small unmyelinated and thinly myelinated primary afferent fibers that subserve nociception. The pain mechanisms themselves are altered. Microanatomic small and large fiber damage in the nerve, essentially demyelination, [4] commonly observed at its root entry zone (REZ), leads to ephaptic transmission, in which action potentials jump from one fiber to another. [5] A lack of inhibitory inputs from large myelinated nerve fibers plays a role. Additionally, a reentry mechanism causes an amplification of sensory inputs. A clinical correlate, for instance, is the potential for vibration to trigger an attack. However, features also suggest an additional central mechanism (eg, delay between stimulation and pain, refractory period). EtiologyAlthough a questionable family clustering exists, trigeminal neuralgia (TN) is most likely multifactorial. Most cases of trigeminal neuralgia are idiopathic, but compression of the trigeminal roots by tumors or vascular anomalies may cause similar pain, as discussed in Pathophysiology. In one study, 64% of the compressing vessels were identified as an artery, most commonly the superior cerebellar (81%). [6] Venous compression was identified in 36% of cases. [6] Trigeminal neuralgia is divided into 2 categories, classic and symptomatic. The classic form, considered idiopathic, actually includes the cases that are due to a normal artery present in contact with the nerve, such as the superior cerebellar artery or even a primitive trigeminal artery. Symptomatic forms can have multiple origins. Aneurysms, tumors, chronic meningeal inflammation, or other lesions may irritate trigeminal nerve roots along the pons causing symptomatic trigeminal neuralgia. An abnormal vascular course of the superior cerebellar artery is often cited as the cause. Uncommonly, an area of demyelination from multiple sclerosis may be the precipitant (see the following image); lesions in the pons at the root entry zone of the trigeminal fibers have been demonstrated. These lesions may cause a similar pain syndrome as in trigeminal neuralgia. Tumor-related causes of trigeminal neuralgia (most commonly in the cerebello-pontine angle) include acoustic neurinoma, chordoma at the level of the clivus, pontine glioma or glioblastoma, [7] epidermoid, metastases, and lymphoma. Trigeminal neuralgia may result from paraneoplastic etiologies. Vascular causes include a pontine infarct and arteriovenous malformation or aneurysm in the vicinity. Inflammatory causes include multiple sclerosis (common), sarcoidosis, and Lyme disease neuropathy. Infrequently, adjacent dental fillings composed of dissimilar metals may trigger attacks, [8] and one atypical case followed tongue piercing. Another case report of trigeminal neuralgia was reported in a patient with spontaneous intracranial hypotension; both conditions resolved following surgical treatment of a cervical root sleeve dural defect. [9] EpidemiologyIn 1968, Penman reported the US prevalence of trigeminal neuralgia (TN) as approximately 107 men and 200 women per 1 million people. [10] By 1993, Mauskop noted approximately 40,000 patients have this condition at any particular time, [11] with an incidence of 4-5 cases per 100,000. More recent estimates suggest the prevalence is approximately 1.5 cases per 10,000 population, with an incidence of approximately 15,000 cases per year. Rushton and Olafson reported that approximately 1% of patients with multiple sclerosis (MS) develop trigeminal neuralgia, [12] whereas Jensen et al noted that 2% of patients with trigeminal neuralgia have multiple sclerosis. [13] Patients with both conditions often have bilateral trigeminal neuralgia. No geographic tendency or racial differences have been found for trigeminal neuralgia. However, females are affected up to twice as often as males (range, 3:2 to 2:1). In addition, in 90% of patients, the disease begins after age 40 years, with a typical onset of 60-70 years (middle and later life). Patients who present with the disease when aged 20-40 years are more likely to suffer from a demyelinating lesion in the pons secondary to multiple sclerosis; younger patients also tend to have symptomatic or secondary trigeminal neuralgia . There have also been occasional reports of pediatric cases of trigeminal neuralgia. Another risk factor for this syndrome is hypertension. PrognosisAfter an initial attack, trigeminal neuralgia (TN) may remit for months or even years. Thereafter the attacks may become more frequent, more easily triggered, disabling, and may require long-term medication. Thus, the disease course is typically one of clusters of attacks that wax and wane in frequency. Exacerbations most commonly occur in the fall and spring. Among the best clinical predictors of a symptomatic form are sensory deficits upon examination and a bilateral distribution of symptoms (but the absence thereof is not a negative predictor). Young age is a moderate predictor, but a fair degree of overlap exists. Lack of therapeutic response and V1 distribution are poor predictors. Although trigeminal neuralgia is not associated with a shortened life, the morbidity associated with the chronic and recurrent facial pain can be considerable if the condition is not controlled adequately. This condition may evolve into a chronic pain syndrome, and patients may suffer from depression and related loss of daily functioning. Individuals may choose to limit activities that precipitate pain, such as chewing, possibly losing weight in extreme circumstances. In addition, the severity of the pain may lead to suicide. ComplicationsThe chief complication in trigeminal neuralgia is the adverse effects and toxicity experienced routinely with long-term use of anticonvulsant agents. Another complication is the waning efficacy over several years of these drugs in controlling neuralgia, necessitating the addition of a second anticonvulsant, which may cause more drug-related adverse reactions. Failure to diagnose a brainstem tumor and bone marrow aplasia as an idiosyncratic adverse effect of carbamazepine are common pitfalls to avoid. Standard care must be applied to invasive procedures, which are most subject to potential claims. Percutaneous neurosurgical procedures and microvascular decompression procedures pose risks of long-term complications. Perioperative risks also exist. See Trigeminal Neuralgia Surgery. Moreover, patients may have to wait for weeks or months after the operation for relief, and some find relief only for 1-2 years and then must weigh the option of a second operation. Some patients permanently lose sensation over a portion of the face or mouth. Occasionally, patients may suffer jaw weakness and/or corneal anesthesia. Corneal ulceration can result because of trophic disturbances from nerve deafferentation. After any invasive treatments, reactivation of a herpes simplex infection is not uncommon. The worst complication is anesthesia dolorosa, an intractable facial dysesthesia, which may be more disabling than the original trigeminal neuralgia. This dysesthesia may be caused by procedures and, sometimes, surgery. Patient EducationPatients benefit from an explanation of the natural history of the disorder, including the possibility that the syndrome may remit spontaneously for months or even years before they need to consider long-term anticonvulsant medications. For this reason, some may elect to taper off their medication after the initial attack subsides; thus, they should be educated about the importance of being compliant with their medication regimen. Patients also must be educated about the potential risks of anticonvulsant medications, such as sedation and ataxia, particularly in elderly patients, which may make driving or operating machinery hazardous. These drugs may also pose risks to the liver and the hematologic system. Document the discussion with the patient about these potential risks. No specific preventative therapy exists. Patients may have a premonitory atypical pain for months; therefore, appropriate recognition of this pre–trigeminal neuralgia syndrome may lead to earlier and more efficient treatment. Patients should avoid maneuvers that trigger pain. Once the diagnosis is established, advise them that dental extractions do not afford relief, even if pain radiates into the gums. In patients wishing to undergo a procedure, they should be aware of potential adverse effects, as well as report any altered sensation in the face, especially after a procedure. They should be informed about the potential for anesthesia dolorosa. Other resourcesSome patients may wish to consult the resources below. NINDS Trigeminal Neuralgia Information Page (updated: February 18, 2011) NIH Neurological Institute PO Box 5801 Bethesda, MD 20824 Phone: (800) 352-9424 or (301) 496-5751 TTY (for people using adaptive equipment): (301) 468-5981 E-mail: http://www.ninds.nih.gov/contact_us.htm Web site: http://www.ninds.nih.gov/disorders/trigeminal_neuralgia/trigeminal_neuralgia.htm TNA Facial Pain Association (formerly: Trigeminal Neuralgia Association) 408 W University Ave Suite 602 Gainesville, FL 32601 Phone: (800) 923-3608 or (352) 384-3600 E-mail: Website: http://www.endthepain.org An interactive questionnaire developed by the Oregon Health & Science University Department of Neurological Surgery allows patients to self-diagnose facial pain based on a brief series of questions. The "Trigeminal Neuralgia - Diagnostic Questionnaire" may be found at: https://neurosurgery.ohsu.edu/tgn.php (accessed April 7, 2011). An artificial intelligence method (neural network modeling) provides immediate feedback to the patient regarding the diagnosis and patient education resources. [14] For patient education information, see Brain & Nervous System Center, as well Trigeminal Neuralgia (Facial Nerve Pain), Tic Douloureux, and Pain Medications.
Author Manish K Singh, MD Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Headache Society, American Association of Physicians of Indian Origin, American Medical Association, American Society of Regional Anesthesia and Pain Medicine Disclosure: Nothing to disclose. Coauthor(s) Gordon H Campbell, MSN, FNP-BC Neuroscience Nurse Practitioner, Neurology Service, Portland Veterans Affairs Medical Center; Primary Faculty, Clinical Instructor, and Guest Lecturer, Family Nursing Department, Oregon Health Sciences University School of Nursing Gordon H Campbell, MSN, FNP-BC is a member of the following medical societies: American Academy of Neurology Disclosure: Nothing to disclose. Siddharth Gautam, MBBS Resident Physician, Jersey Neuroscience Institute Disclosure: Nothing to disclose. Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Abbott Laboratories, advisory group. Chief Editor Acknowledgements Jane W Chan, MD Professor of Neurology/Neuro-ophthalmology, Department of Medicine, Division of Neurology, University of Nevada School of Medicine Jane W Chan, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Ophthalmology, American Medical Association, North American Neuro-Ophthalmology Society, and Phi Beta Kappa Disclosure: Nothing to disclose. James R Couch, MD, PhD, FACP Professor of Neurology, University of Oklahoma Health Sciences Center Disclosure: Nothing to disclose. Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology Disclosure: Nothing to disclose. Andrew W Lawton, MD Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association Disclosure: Nothing to disclose. Marc E Lenaerts, MD, FAHS Staff Neurologist, Mercy Medical Group; Associate Clinical Professor of Neurology, Department of Neurology, University of California, Davis, School of Medicine Marc E Lenaerts, MD, FAHS is a member of the following medical societies: American Academy of Neurology, American Headache Society, and International Headache Society Disclosure: Nothing to disclose. Jorge E Mendizabal, MD Consulting Staff, Corpus Christi Neurology Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association Disclosure: Nothing to disclose. Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology Disclosure: Nothing to disclose. Tom Scaletta, MD Chair, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society Disclosure: Nothing to disclose. What are the symptoms of a patient with trigeminal neuralgia?Symptoms. Episodes of severe, shooting or jabbing pain that may feel like an electric shock.. Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth.. Attacks of pain lasting from a few seconds to several minutes.. Pain that occurs with facial spasms.. Which description of symptoms is characteristic of a client with diagnosed with trigeminal neuralgia tic douloureux )?Tic Douloureux Symptoms
The main symptom of tic douloureux is a sudden, severe, stabbing, sharp, shooting, electric-shock-like pain on one side of the face. Because the second and third divisions of the trigeminal nerve are the most commonly affected, the pain is usually felt in the lower half of the face.
What is the diagnosis of trigeminal neuralgia?There's no specific test for trigeminal neuralgia, so a diagnosis is usually based on your symptoms and description of the pain. If you've experienced attacks of facial pain, the GP will ask you questions about your symptoms, such as: how often do the pain attacks happen. how long do the pain attacks last.
What is the most common cause of trigeminal neuralgia?Evidence suggests that in up to 95% of cases, trigeminal neuralgia is caused by pressure on the trigeminal nerve close to where it enters the brain stem, the lowest part of the brain that merges with the spinal cord. This type of trigeminal neuralgia is known as primary trigeminal neuralgia.
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Which description of symptoms is characteristic of a client diagnosed with trigeminal neuralgia?
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