March 23, 2015

Trigeminal neuralgia: diagnosis and management

By Daniel Cabrera

Author: Daniel Cabrera, MD

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Trigeminal neuralgia (TN) is a common reason for presentation to the Emergency Department (ED) and although not life threatening, the pain can be quite severe creating distress for both patient and health care providers.

TN is common, with an incidence of about 5 per 100000 people. It is more frequent in women than men (1:1.7) and far more usual in patients 50 years and older. The pathophysiology is unclear but most experts agree that likely is caused by microvascular compression of the nerve on its trajectory leading to demyelinazation and abnormal propioception. Secondary to the mechanism, TN is classified as Classic (or classical) when is idiopathic or believed to be secondary to microvascular compression or Painful Trigeminal Neuropathy when is caused by others conditions.

Some causes of Painful Trigeminal Neuropathy (Secondary):

  • Painful trigeminal neuropathy attributed to acute herpes zoster
  • Postherpetic trigeminal neuropathy
  • Painful posttraumatic trigeminal neuropathy
  • Painful trigeminal neuropathy attributed to multiple sclerosis plaque
  • Painful trigeminal neuropathy attributed to space-occupying lesion

 

Diagnosis

Typically patients will present with sudden onset unilateral face pain, often triggered by stimulation of the trigeminal branches such as brushing teeth, cold air, chewing, contact with face or vibration. The pain is electric in type, characterized for trains or waves of pain alternating with pain-free (refractory) periods; the pain usually goes in-crescendo.  Frequently affects all three branches of the Trigminal nerve but sometimes can affect one one or two.

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The key for the diagnosis is a good history and physical exam. Often TN is confused with dental pain or even eye pain, delaying the diagnosis and potentially leading to unnecessary procedures such as dental blocks or root canals. The pain is described in the face and is almost always unilateral (97%), general and neurologic exam is otherwise normal.

Unusual traits at presentation that should rise red flags and make you consider secondary causes:

  • Onset younger than 40 years old
  • Sensory changes in face
  • Concomitant neurological findings
  • Difficulty hearing
  • Rashes (vesicles) in face
  • Family history of multiple sclerosis
  • Ophthalmic branch only

Typically neuroimaging is not necessary in the ED if the clinical diagnosis is consistent. MRI is the diagnostic modality of choice and is usually indicated for patients with early onset, family history of multiple sclerosis or other red flags; often MRIs are not readily available in the ED and CT can be considered if there are concerns for life threatening secondary causes such as space occupying lesions or trauma.

 

Treatment

Analgesia can be quite difficult in the ED as most medications will require several days to weeks to show improvement. The medication with the best level of evidence is Carbamazepine with up to 70% of complete pain relief in some series.

Medical treatment of TN includes

  • Carbamazepine
  • Oxcarbamazepine
  • Baclofen
  • Lamotrigine
  • Gabapentin
  • Pregablin

For patients with secondary causes of refractory classic TN, surgical decompression is an option and they can be referred to the appropriate specialist.

 

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The main issue in the ED is the management of a TN crisis. In general, initiating oral mediocations such carbamazepine or adjusting its dose will take time and it is unlikely to see any acute evidence of improvement. There is a significant lack of good quality evidence on the treatment of TN crisis and most of the recommendations are based on anecdotes, case reports and very small series. In general opiates are of marginal benefit, but anxyolisis can be a significant adjuvant for the overall analgesia strategy.

Some options for severe TN crisis are

  • Intravenous phenytoin
  • Local trigeminal block (by experienced anesthesiologist)
  • Intranasal lidocaine

 

References

  • Zakrzewska JM, Linskey ME. Trigeminal neuralgia. BMJ. 2014 Feb 17;348(feb17 9):g474–g474.
  • Cox, GM. Mucormycosis (zygomycosis). In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on March 10, 2015.)
  • Cruccu G, Gronseth G, Alksne J, Argoff C, Brainin M, Burchiel K, et al. AAN-EFNS guidelines on trigeminal neuralgia management. Eur J Neurol. 2008 Oct;15(10):1013–28.
  • Lemos L, Flores S, Oliveira P, Almeida A. Gabapentin supplemented with ropivacain block of trigger points improves pain control and quality of life in trigeminal neuralgia patients when compared with gabapentin alone. Clin J Pain. 2008 Jan;24(1):64–75.
  • McCleane GJ. Intravenous infusion of phenytoin relieves neuropathic pain: a randomized, double-blinded, placebo-controlled, crossover study. Anesth Analg. 1999 Oct;89(4):985–8.
  • Kanai A, Suzuki A, Kobayashi M, Hoka S. Intranasal lidocaine 8% spray for second-division trigeminal neuralgia. Br J Anaesth. 2006 Oct 1;97(4):559–63.

Image

  1. Ryan Weisgerber from Flickr used under Creative Commons License Attribution 2.0.
  2. Google Image Search Labeled for reuse.
  3. Jason Eppink from Flickr used under Creative Commons License Attribution 2.0.

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