Elias WJ, Burchiel KJ.
Trigeminal neuralgia and other neuropathic pain syndromes of the head and face.
Curr Pain Headache Rep. 2002 Apr;6(2):115-24. doi: 10.1007/s11916-002-0007-8.
Abstract/Text
Trigeminal neuralgia is the most common craniofacial pain syndrome of neuropathic origin. Although the diagnosis remains based exclusively on history and symptomatology, modern diagnostic techniques, particularly high-resolution magnetic resonance imaging, provides valuable new insight into the pathophysiology of these cases with additional implications for therapeutic strategies. Other neuropathic syndromes affect the trigeminal nerve and warrant different treatments with varied rates of success. Rarely, neuralgias of other cranial nerves mimic trigeminal neuralgia. Finally, it is imperative to distinguish atypical facial pains from these neuropathic syndromes to avoid unsuccessful therapies.
福井次矢, 黒川清. ハリソン内科学 第5版（原著第19版）. メディカル・サイエンス・インターナショナル，2017; 2707-12.
Stavropoulou E, Argyra E, Zis P, Vadalouca A, Siafaka I.
The Effect of Intravenous Lidocaine on Trigeminal Neuralgia: A Randomized Double Blind Placebo Controlled Trial.
ISRN Pain. 2014;2014:853826. doi: 10.1155/2014/853826. Epub 2014 Mar 10.
Abstract/Text
Trigeminal neuralgia is the most common neuralgia. Its therapeutic approach is challenging as the first line treatment often does not help, or even causes intolerable side effects. The aim of our randomized double blind, placebo controlled, crossover study was to investigate in a prospective way the effect of lidocaine in patients with trigeminal neuralgia. Twenty patients met our inclusion criteria and completed the study. Each patient underwent four weekly sessions, two of which were with lidocaine (5 mgs/kg) and two with placebo infusions administered over 60 minutes. Intravenous lidocaine was superior regarding the reduction of the intensity of pain, the allodynia, and the hyperalgesia compared to placebo. Moreover, contrary to placebo, lidocaine managed to maintain its therapeutic results for the first 24 hours after intravenous infusion. Although, intravenous lidocaine is not a first line treatment, when first line medications fail to help, pain specialists may try it as an add-on treatment. This trial is registered with NCT01955967.
Gronseth G, Cruccu G, Alksne J, Argoff C, Brainin M, Burchiel K, Nurmikko T, Zakrzewska JM.
Practice parameter: the diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies.
Neurology. 2008 Oct 7;71(15):1183-90. doi: 10.1212/01.wnl.0000326598.83183.04. Epub 2008 Aug 20.
Abstract/Text
BACKGROUND: Trigeminal neuralgia (TN) is a common cause of facial pain.
PURPOSE: To answer the following questions: 1) In patients with TN, how often does routine neuroimaging (CT, MRI) identify a cause? 2) Which features identify patients at increased risk for symptomatic TN (STN; i.e., a structural cause such as a tumor)? 3) Does high-resolution MRI accurately identify patients with neurovascular compression? 4) Which drugs effectively treat classic and symptomatic trigeminal neuralgia? 5) When should surgery be offered? 6) Which surgical technique gives the longest pain-free period with the fewest complications and good quality of life?
METHODS: Systematic review of the literature by a panel of experts.
CONCLUSIONS: In patients with trigeminal neuralgia (TN), routine head imaging identifies structural causes in up to 15% of patients and may be considered useful (Level C). Trigeminal sensory deficits, bilateral involvement of the trigeminal nerve, and abnormal trigeminal reflexes are associated with an increased risk of symptomatic TN (STN) and should be considered useful in distinguishing STN from classic trigeminal neuralgia (Level B). There is insufficient evidence to support or refute the usefulness of MRI to identify neurovascular compression of the trigeminal nerve (Level U). Carbamazepine (Level A) or oxcarbazepine (Level B) should be offered for pain control while baclofen and lamotrigine (Level C) may be considered useful. For patients with TN refractory to medical therapy, Gasserian ganglion percutaneous techniques, gamma knife, and microvascular decompression may be considered (Level C). The role of surgery vs pharmacotherapy in the management of TN in patients with MS remains uncertain.
Lambru G, Zakrzewska J, Matharu M.
Trigeminal neuralgia: a practical guide.
Pract Neurol. 2021 Oct;21(5):392-402. doi: 10.1136/practneurol-2020-002782. Epub 2021 Jun 9.
Abstract/Text
Trigeminal neuralgia (TN) is a highly disabling disorder characterised by very severe, brief and electric shock like recurrent episodes of facial pain. New diagnostic criteria, which subclassify TN on the basis of presence of trigeminal neurovascular conflict or an underlying neurological disorder, should be used as they allow better characterisation of patients and help in decision-making regarding medical and surgical treatments. MR imaging, including high-resolution trigeminal sequences, should be performed as part of the diagnostic work-up. Carbamazepine and oxcarbazepine are drugs of first choice. Lamotrigine, gabapentin, pregabalin, botulinum toxin type A and baclofen can be used either alone or as add-on therapy. Surgery should be considered if the pain is poorly controlled or the medical treatments are poorly tolerated. Trigeminal microvascular decompression is the first-line surgery in patients with trigeminal neurovascular conflict while neuroablative surgical treatments can be offered if MR imaging does not show any neurovascular contact or where patients are considered too frail for microvascular decompression or do not wish to take the risk.
© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.
日本頭痛学会・国際頭痛分類委員会訳. 国際頭痛分類 第3版. 2018.
Krafft RM.
Trigeminal neuralgia.
Am Fam Physician. 2008 May 1;77(9):1291-6.
Abstract/Text
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.
Peng KP, Oppermann T. Orofacial pain disorders: An overview and diagnostic approach. Cephalalgia Reports, 2022; 5: 1-8. doi:10.1177/25158163221097349.
Duvall JR, Robertson CE.
Clinical Reasoning: A misdiagnosis of atypical trigeminal neuralgia.
Neurology. 2019 Jul 16;93(3):124-131. doi: 10.1212/WNL.0000000000007790.
Abstract/Text
Lambru G, Elias LA, Yakkaphan P, Renton T.
Migraine presenting as isolated facial pain: A prospective clinical analysis of 58 cases.
Cephalalgia. 2020 Oct;40(11):1250-1254. doi: 10.1177/0333102420933277. Epub 2020 Jun 17.
Abstract/Text
BACKGROUND: Sparse evidence has detailed the clinical phenotype of migraine presenting as isolated facial pain.Objective and methods: This was a prospective audit, part of our multidisciplinary facial pain service evaluation, aiming to phenotype patients with migraine presenting as isolated facial pain who attended our service between 2013 and 2018.
RESULTS: Fifty-eight patients were diagnosed with migraine with isolated facial pain (F = 46, 79.3%; mean age: 49.0 years, ± 9.85). Sixty-six percent of patients met the criteria for episodic migraine. The pain was strictly unilateral in 79% and located over the maxillary region in 85% of patients. Associated cranial autonomic signs/symptoms were reported by 45% of our cohort. A percentage of 77% of patients was triptan responders.
CONCLUSIONS: Migraine presenting as isolated facial pain is a rare but treatable condition with some distinct demographic and clinical characteristics. It is a diagnosis of exclusion that should be evaluated in specialised multidisciplinary facial pain clinics.
Benoliel R, Gaul C.
Persistent idiopathic facial pain.
Cephalalgia. 2017 Jun;37(7):680-691. doi: 10.1177/0333102417706349. Epub 2017 Apr 20.
Abstract/Text
Background Persistent idiopathic facial pain (PIFP) is a chronic disorder recurring daily for more than two hours per day over more than three months, in the absence of clinical neurological deficit. PIFP is the current terminology for Atypical Facial Pain and is characterized by daily or near daily pain that is initially confined but may subsequently spread. Pain cannot be attributed to any pathological process, although traumatic neuropathic mechanisms are suspected. When present intraorally, PIFP has been termed 'Atypical Odontalgia', and this entity is discussed in a separate article in this special issue. PIFP is often a difficult but important differential diagnosis among chronic facial pain syndromes. Aim To summarize current knowledge on diagnostic criteria, differential diagnosis, pathophysiology and management of PIFP. Methods We present a narrative review reporting current literature and personal experience. Additionally, we discuss and differentiate the common differential diagnoses associated with PIFP including traumatic trigeminal neuropathies, regional myofascial pain, atypical neurovascular pains and atypical trigeminal neuropathic pains. Results and conclusion The underlying pathophysiology in PIFP is still enigmatic, however neuropathic mechanisms may be relevant. PIFP needs interdisciplinary collaboration to rule out and manage secondary causes, psychiatric comorbidities and other facial pain syndromes, particularly trigeminal neuralgia. Burden of disease and psychiatric comorbidity screening is recommended at an early stage of disease, and should be addressed in the management plan. Future research is needed to establish clear diagnostic criteria and treatment strategies based on clinical findings and individual pathophysiology.
