Trigeminal Neuralgia Differential Diagnoses

  • Author: Manish K Singh, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: Apr 5, 2012
 
 

Diagnostic Considerations

Other causes of facial pain than trigeminal neuralgia (TN) are excluded by history, physical examination, and special investigations (when necessary). In symptomatic cases, a persistence of aching can occur between paroxysms, as well as signs of sensory impairment in the trigeminal division. Then, a cause is demonstrated by appropriate investigation.

Migraine, cluster headaches, and atypical face pain

Migraine and cluster headaches may produce severe unilateral pain, but unlike trigeminal neuralgia, these conditions are not triggered by movement or contact with the face nor do they respond promptly to carbamazepine. See Table 1, below.

Table 1. Characteristic Features of 3 Common Craniofacial Pains (Open Table in a new window)

ConditionMale:Female RatioAge of onset, yLocalizationAccompanying SymptomsAttack DurationCyclesProvocation
Trigeminal neuralgia1:2>50UnilateralNoneSecondsMonth intervalsTrigger zones
Cluster headache31:130-40Always unilateralHorner syndrome, conjunctival infection, epiphora15-180 minutesClusters with weeks to months intervalsNocturnal attacks
Migraine1:110-20VariablePhotophobia, phonophobia, gastrointestinal symptoms4-72 hoursDays to weeks intervalsVariable

According to Turp and Gobetti, atypical face pain usually extends beyond the distribution of the fifth cranial nerve, is rarely triggered, and presents with a steady unrelenting discomfort lasting hours to days.[18] See Table 2, below.

In persistent idiopathic facial pain, psychiatric disturbances are associated with pain that is of vague localization and long duration (usually chronic and daily). In Raeder syndrome (paratrigeminal neuralgia), ophthalmoparesis is present. In current practice, Raeder syndrome is believed to essentially be carotid dissection. Tolosa-Hunt syndrome (ophthalmoplegia) presents with pain of longer duration but that is not triggerable; cranial nerve deficits are observed. Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) present with pain of longer duration (2-3 min) and associated prominent autonomic symptoms (eg, lacrimation, rhinorrhea).[19]

Temporomandibular joint pain and dental problems in the evaluation of trigeminal neuralgia.

Table 2. Distinguishing Features Between Trigeminal Neuralgia and Atypical Facial Pain (Open Table in a new window)

FeatureTrigeminal NeuralgiaAtypical Facial Pain
PrevalenceRareCommon
Main locationTrigeminal areaFace, neck, ear
Pain durationSeconds to 2 minutesHours to days
CharacterElectric jerks, stabbingThrobbing, dull
Pain intensitySevereMild to moderate
Provoking factorsLight touch, washing, shaving, eating, talkingStress, cold
Associated symptomsNoneSensory abnormalities

Glossopharyngeal neuralgia and occipital neuralgia syndromes

Other syndromes with paroxysmal lancinating head pain include the less common glossopharyngeal neuralgia and occipital neuralgia syndromes.

Glossopharyngeal neuralgia causes pain in the tonsillar fossa, posterior pharynx, and ear and may be initiated by coughing, yawning, or swallowing cold liquids. During acute attacks of this condition, which is frequently associated with an underlying pathology, the patient may be unable to speak and tries to avoid moving the lips or tongue. An involuntary startle during an attempt to touch the affected side of the face is diagnostic.

Occipital neuralgia causes pain in the posterior head region. Thus, the distribution easily distinguishes it from trigeminal neuralgia. Confusion arises only if the patient cannot provide a clear history.

Paroxysmal hemicrania syndromes

According to Goadsby and Lipton, similar to trigeminal neuralgia, paroxysmal hemicrania syndromes typically last only seconds, however, the latter syndromes occur in and around 1 eye.[20] Intense unilateral conjunctival injection and lacrimation signal an autonomic component, which further distinguishes paroxysmal hemicrania syndromes. Another feature is that paroxysmal hemicrania syndromes do not respond to carbamazepine.

Secondary vs idiopathic trigeminal neuralgia

Symptomatic or secondary trigeminal neuralgia is a more likely consideration than the idiopathic form when pain is associated with hyperesthesia along the course of the fifth nerve or is observed with other cranial neuropathies. Further, consider secondary trigeminal neuralgia in patients with bilateral sensory loss or weakness of the facial muscles or jaw.

Additional investigation may reveal multiple sclerosis (MS), a tumor in the posterior fossa, or a tumor on the trigeminal nerve.

Acoustic neuromas, cerebral aneurysms, trigeminal neuromas, and meningiomas can produce syndromes similar to idiopathic trigeminal neuralgia. Consider these conditions in patients with onset of pain when younger than 40 years, those with predominant forehead and/or orbit pain (ie, first division of the trigeminal nerve), or those with bilateral facial pain. Also consider granulomatous inflammation (eg, tuberculosis, sarcoidosis, Behçet syndrome, collagen vascular diseases) and other vasculitides, as these may affect the trigeminal nerve and simulate trigeminal neuralgia.

Patients with prominent hemifacial spasm, especially if it is continuous, may have tic convulsif, a condition associated with a dilated and ectatic basilar artery or other vascular malformation compressing the trigeminal nerve.

Brain magnetic resonance imaging (MRI) with and without contrast is critical in diagnosing the secondary causes of trigeminal neuralgia.

Failure to properly assess for secondary trigeminal neuralgia is a major potential pitfall. A careful examination of the cranial nerves and an MRI of the brain, especially in an individual who develops the disorder when younger than 60 years, should protect against missing structural lesions (eg, tumor, cerebral aneurysm, acoustic neuroma).

Trigeminal neuropathy and atypical trigeminal neuralgia

Trigeminal neuropathy is also a consideration in the evaluation of trigeminal neuralgia. This condition presents as a constant, unilateral, often mild facial pain with prominent sensory loss. It is nontriggerable and unremitting, and it may be either symptomatic or idiopathic. By contrast, as previously discussed, idiopathic trigeminal neuralgia presents as episodic, unilateral, lancinating, triggerable, often shocklike facial pain with pain-free intervals.

To further complicate diagnostic matters, the clinician may encounter atypical trigeminal neuralgia, a syndrome that overlaps trigeminal neuralgia and trigeminal neuropathy. This syndrome consists of constant pain that episodically intensifies. According to Burcheil, these patients experience both lancinating triggered pain and a baseline, constant, dull, and throbbing discomfort.[21] The atypical form may occur in up to 5% of people after facial surgery or significant trauma and in 1-5% after the removal of impacted teeth. In the experience of many neurosurgeons, atypical trigeminal neuralgic pain results from lesions or injuries of the trigeminal nerve root distal to the route entry zone but with even greater compression than found in the idiopathic form of trigeminal neuralgia.

In contrast to trigeminal neuropathy, whether typical or atypical, atypical facial pain is distinguished by the extension of discomfort beyond the distribution of the fifth cranial nerve and by the frequent lack of lancinating pain and triggers.

Multiple sclerosis

As discussed in the Clinical section, rarely, multiple sclerosis (MS) presents with trigeminal neuralgia. Consider multiple sclerosis in the diagnostic evaluation of individuals who display other features of this demyelinating disorder.

Herpetic and postherpetic neuralgia

Herpetic and postherpetic neuralgia (PHN) usually affects the first branch of the trigeminal nerve. The diagnosis of postherpetic neuralgia usually requires the outbreak of shingles (herpes zoster) in the forehead or eye. Acute herpetic neuralgia is the norm in shingles, but pain that persists after the lesions have healed is postherpetic neuralgia. The risk of development of postherpetic neuralgia is directly related to patient age.

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
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 Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and 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, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

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.

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Illustration depicting the trigeminal nerve with its 3 main branches
Microscopic demonstration of demyelination in primary trigeminal neuralgia. A tortuous axon is surrounded by abnormally discontinuous myelin. (Electron microscope; 3300×).
Magnetic resonance image (MRI) with high resolution on the pons demonstrating the trigeminal nerve root. In this case, the patient with trigeminal neuralgia has undergone gamma-knife therapy, and the left-sided treated nerve (arrow) is enhanced by gadolinium.
Microvascular decompression (Jannetta procedure) used to treat trigeminal neuralgia. The anteroinferior cerebellar artery and the trigeminal nerve are in direct contact. Courtesy of PT Dang, CH Luxembourg
Table 1. Characteristic Features of 3 Common Craniofacial Pains
ConditionMale:Female RatioAge of onset, yLocalizationAccompanying SymptomsAttack DurationCyclesProvocation
Trigeminal neuralgia1:2>50UnilateralNoneSecondsMonth intervalsTrigger zones
Cluster headache31:130-40Always unilateralHorner syndrome, conjunctival infection, epiphora15-180 minutesClusters with weeks to months intervalsNocturnal attacks
Migraine1:110-20VariablePhotophobia, phonophobia, gastrointestinal symptoms4-72 hoursDays to weeks intervalsVariable
Table 2. Distinguishing Features Between Trigeminal Neuralgia and Atypical Facial Pain
FeatureTrigeminal NeuralgiaAtypical Facial Pain
PrevalenceRareCommon
Main locationTrigeminal areaFace, neck, ear
Pain durationSeconds to 2 minutesHours to days
CharacterElectric jerks, stabbingThrobbing, dull
Pain intensitySevereMild to moderate
Provoking factorsLight touch, washing, shaving, eating, talkingStress, cold
Associated symptomsNoneSensory abnormalities
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