Trigeminal Neuralgia (TN) is a facial disorder described as one-sided, spasmodic stabbing, and recurrent pain found in the one or more of the sensory branches located near the fifth cranial nerve. This is one of the most common diseases associated with cranial nerves and one of the most often diagnosed facial pain complications (Sabalys, Juodzbalys, & Wang, 2012).
TN can be a very debilitating disorder as the painful experience can last anywhere from a few seconds to many minutes, and the episodic pain may occur a few times a day or can manifest hundreds of times in a 24-hour time frame (Zakrzewska & Linskey, 2014). The pain associated with trigeminal neuralgia may not always be constant due to this disease process is known for having periods of remission that can last for several months or even a year (Sabalys, Juodzbalys, & Wang, 2012). However, the pain does return after some time without treatment.
TN occurs at the incidence of four in 100,000 individuals and is most commonly diagnosed in persons over the age of 40. The rate of occurrence elevated with age and a peak age of 67 is when the disorder is frequently manifested (Ferri, 2018). The prevalence of trigeminal neuralgia is about 155 people in one million, and the disease is found in both the male and female populations respectively. Risk factors associated with this condition include multiple sclerosis, diabetes mellitus, rheumatism, and vascular disorders (Ferri, 2018; Sabalys et al., 2012).
There are three widespread etiologies surrounding TN in the medical community. The disease is thought to develop from allergic, compression, and or neurovascular compression syndromes. The allergic theory denotes an etiology of odontogenic inflammatory and otolaryngological pathology found within the facial structures (Sabalys et al., 2012). The compression hypothesis suggests the etiology surrounds the constricting of the osseous canals, while the neurovascular compression theory proposes the cause of TN to be associated with compression around the “root entry zone due to arteriovenous malformation, vestibular schwannomas, meningiomas, epidermoid cysts, tuberculomas, various other cysts and tumours, aneurysm, vessels aggregation and occlusion due to arachnoiditis and others” (Sabalys et al., 2012, p. 2). The cusp of the pathophysiology surrounding TN has been highly speculated with no clear indication as to how the severe attacks develop (Xia et al., 2014). The most unifying concept is that some form of compression, hyperexcitability, or irritation of the trigeminal nerve occurs and subsequently, sharp stabbing pain pursues from the fifth cranial nerve disturbance (Xia et al., 2014).
Diagnosing TN come directly from an extensive health history and physical examination. A comprehensive health history will reveal a past medical history associated with vascular intrusion and or advanced patient age (Sabalys et al., 2012). Patients will complain of sharp, stabbing discomfort in the mouth/ear or nasal orbit areas that radiates backward or upward (Ferri, 2018). No sensory disturbances will be noted on the physical examination of the patient; this diagnosis is made primarily by subjective symptom criteria inclusion (Zakrzewska & Linskey, 2014).
The first line treatment for TN is medical management using anticonvulsants. Carbamazepine 400-800 mg two to three times a day is the recommended standard treatment option; Oxycarbazepine may also be utilized if the patient cannot tolerate Carbamazepine well (Ferri, 2018; Xia et al., 2014). These medication regimens should be explored for a minimum of three weeks to allocate enough time for the medications to show efficacy (Ferri, 2018).
Initial treatment should be evaluated and followed up on a weekly basis to determine if symptom alleviation is being acquired. A magnet resonance image (MRI) of the face may be necessary for those who do not respond to therapy to locate areas of possible compression found within the skull (Ferri, 2018). Patients who do not get any relief from medical management may then be referred to a neurologist/neurosurgeon for microvascular decompression which has been shown to be up to 83.5% effective in relieving TN pain symptoms (Xia et al., 2014).
Pertinent patient education includes a thorough explanation of the disease process of trigeminal neuralgia and how pain can be induced. Patients also need to be aware that touching of the face, cold air, strong winds or any facial movements can provoke the condition’s onset; clients need to be informed about nonpharmacological interventions that can be utilized to ease discomfort such as ice packs and maintaining a healthy balanced diet with plenty of exercise as well (Trigeminal neuralgia, 2016).
Ferri, F. F. (2018). 2018 Ferri’s Clinical Advisor. Philadelphia, PA: Elsevier.
Sabalys, G., Juodzbalys, G., & Wang, H. (2012). Aetiology and pathogenesis of trigeminal neuralgia: A comprehensive review. Journal of Oral Maxillofacial Research, 3 (4), 1-12. https://doi.org/10.5037/jomr.2012.3402
Trigeminal neuralgia (TN) [Educational standards]. (2016). Retrieved from The Ohio State University Wexner Medical Center: https://patienteducation.osumc.edu/documents/tn.pdf
Xia, L., Zhong, J., Zhu, J., Wong, Y., Dou, N., Liu, M., … Li, S. (2014). Effectiveness and safety of microvascular decompression surgery for treatment of trigeminal neuralgia: A systematic review. The Journal of Craniofacial Surgery, 25 (4), 1-5. Retrieved from http://lushenjing.com/files/papers/1426658693-3.Effectiveness-and-Safety-of-Microvascular-Deco.pdf
Zakrzewska, J. M., & Linskey, M. E. (2014). Trigeminal neuralgia. BMJ Clinical Evidence, 1207, 1-18. Retrieved from http://europepmc.org/articles/pmc4191151