Persistent idiopathic facial pain

Maarbjerg, Stine; Wolfram, Frauke; Heinskou, Tone Bruvik; Rochat, Per; Gozalov, Aydin; Brennum, Jannick; Olesen, Jes; Bendtsen, Lars

doi:10.1177/0333102416675618

Cited by 39 publications

(32 citation statements)

References 38 publications

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“…On the other hand a simple contact was a very prevalent finding in cadavers without a history of TN, in healthy subjects and on the asymptomatic side in TN patients (25,(29)(30)(31). In patients with persistent idiopathic facial pain, an important differential diagnosis to TN, the prevalence of neurovascular conflict is similar to that found in asymptomatic nerves (32). Thus, a neurovascular conflict should be considered a normal neuroanatomic variant in patients with facial pain not fulfilling the TN diagnostic criteria.…”

Section: Etiology and Pathophysiologymentioning

confidence: 81%

Trigeminal neuralgia – diagnosis and treatment

et al. 2017

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Introduction Trigeminal neuralgia (TN) is characterized by touch-evoked unilateral brief shock-like paroxysmal pain in one or more divisions of the trigeminal nerve. In addition to the paroxysmal pain, some patients also have continuous pain. TN is divided into classical TN (CTN) and secondary TN (STN). Etiology and pathophysiology Demyelination of primary sensory trigeminal afferents in the root entry zone is the predominant pathophysiological mechanism. Most likely, demyelination paves the way for generation of ectopic impulses and ephaptic crosstalk. In a significant proportion of the patients, the demyelination is caused by a neurovascular conflict with morphological changes such as compression of the trigeminal root. However, there are also other unknown etiological factors, as only half of the CTN patients have morphological changes. STN is caused by multiple sclerosis or a space-occupying lesion affecting the trigeminal nerve. Differential diagnosis and treatment Important differential diagnoses include trigeminal autonomic cephalalgias, posttraumatic or postherpetic pain and other facial pains. First line treatment is prophylactic medication with sodium channel blockers, and second line treatment is neurosurgical intervention. Future perspectives Future studies should focus on genetics, unexplored etiological factors, sensory function, the neurosurgical outcome and complications, combination and neuromodulation treatment as well as development of new drugs with better tolerability.

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Section: Etiology and Pathophysiologymentioning

confidence: 81%

Trigeminal neuralgia – diagnosis and treatment

et al. 2017

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“…Patients with a neuropathic type pain following surgery or other trauma with neurosensory changes should be diagnosed as painful traumatic trigeminal neuropathy (PTTN), as defined by the IHS (1,19). These changes in inclusion criteria, both in classification systems and in published cases and case series, must be taken into account when interpreting the data on the clinical profile and indeed management protocols, see for example (16)(17)(18)20,21).…”

Section: Symptomatologymentioning

confidence: 99%

“…Typically, pain characteristics, location and associated features change over time. Rarely, some PIFP patients report pain free or remission periods (20). Often PIFP may coexist with other chronic orofacial pain or headache syndromes (20).…”

Section: Symptomatologymentioning

confidence: 99%

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Benoliel

Gaul

2017

Cephalalgia

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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.

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“…The cause(s) of PIFP is (are) elusive. Neurovascular contact with displacement of the trigeminal nerve is associated with TN, but not with PIFP [ 83 ]. Quantitative sensory testing of PIFP and of traumatic TN compared to healthy controls showed no significant differences among the groups for warm or cold thermal stimulation, or for tactile stimulation.…”

Section: Discussionmentioning

confidence: 99%

Chronic Facial Pain: Trigeminal Neuralgia, Persistent Idiopathic Facial Pain, and Myofascial Pain Syndrome—An Evidence-Based Narrative Review and Etiological Hypothesis

Gerwin

2020

IJERPH

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Trigeminal neuralgia (TN), the most common form of severe facial pain, may be confused with an ill-defined persistent idiopathic facial pain (PIFP). Facial pain is reviewed and a detailed discussion of TN and PIFP is presented. A possible cause for PIFP is proposed. (1) Methods: Databases were searched for articles related to facial pain, TN, and PIFP. Relevant articles were selected, and all systematic reviews and meta-analyses were included. (2) Discussion: The lifetime prevalence for TN is approximately 0.3% and for PIFP approximately 0.03%. TN is 15–20 times more common in persons with multiple sclerosis. Most cases of TN are caused by neurovascular compression, but a significant number are secondary to inflammation, tumor or trauma. The cause of PIFP remains unknown. Well-established TN treatment protocols include pharmacotherapy, neurotoxin denervation, peripheral nerve ablation, focused radiation, and microvascular decompression, with high rates of relief and varying degrees of adverse outcomes. No such protocols exist for PIFP. (3) Conclusion: PIFP may be confused with TN, but treatment possibilities differ greatly. Head and neck muscle myofascial pain syndrome is suggested as a possible cause of PIFP, a consideration that could open new approaches to treatment.

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Persistent idiopathic facial pain – a prospective systematic study of clinical characteristics and neuroanatomical findings at 3.0 Tesla MRI

Cited by 39 publications

References 38 publications

Trigeminal neuralgia – diagnosis and treatment

Trigeminal neuralgia – diagnosis and treatment

Persistent idiopathic facial pain

Chronic Facial Pain: Trigeminal Neuralgia, Persistent Idiopathic Facial Pain, and Myofascial Pain Syndrome—An Evidence-Based Narrative Review and Etiological Hypothesis

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