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https://doi.org/10.1007/s11916-022-01018-w
Abstract
Purpose of Review Traumatic neuromas in general, and trigeminal traumatic neuromas in particular, are relatively rare
entities originating from a damage to a corresponding nerve or its branches. This manuscript is a comprehensive review of
the literature on trigeminal traumatic neuromas based on an interesting and challenging case of bilateral intraoral lesions.
Recent Findings The diagnosis for this patient was bilateral trigeminal traumatic neuromas. It is possible that these patients
have a genetic predisposition to the development of these lesions. It is a neuropathic pain condition and may mimic dental
and other trigeminal pain entities. Topical treatment with lidocaine gel, utilizing a custom-made neurosensory stent, rendered
the patient significant and sustained pain relief.
Summary Trigeminal traumatic neuromas present a diagnostic challenge even to a seasoned clinician, due to the complex
clinical features that may mimic other entities. Topical medications such as local anesthetics may be a good viable alternative
to systemic medications to manage the pain associated with the condition. Early identification of the lesion and the associ-
ated pain helps in the succinct management of symptomatic trigeminal traumatic neuromas.
Keywords Traumatic neuroma · Oral · Neuropathic pain · Tinel’s sign · Neurosensory stent · Topical medication ·
Trigeminal nerve
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Case Report With regards to the mandibular pain, she described bursts
of pain intensity of seven on the same scale.
History of Presenting Illness
Quality
A 56-year-old Indian female patient presented with chief
complaints of chronic pain in the distribution of the second The background pain had a quality of “dull aching” in both
division (maxillary, V2) of the left trigeminal nerve and the arches, and the exacerbated pain had “pulsating” on the
the third division (mandibular, V3) of the right trigemi- maxillary site, and “shooting” on the mandibular site.
nal nerve. Her medical history was positive for diabetes
mellitus and hypercholesterolemia, both managed well Temporal Characteristics
with medications. The pain has been existing for the past
approximately 30 years. These two pains had started sub- Over a time period of approximately 30 years, the pain
sequent to different surgical procedures, separated by a few evolved to a slow chronic progressive type.
years. The quality of the pain had changed over the past 15
to 30 years; the intensity was variable, and she was una-
ble to achieve any meaningful pain relief, although going Aggravating Factors/Triggers
through multiple dental procedures in an attempt to do so.
The details of the characteristics of the pain appear below. The pain worsened upon chewing, “after a meal,” acid foods
(such as citrus fruits, cheese, tamarind), and left lateral
recumbent sleep position.
Onset
Relieving Factors
The pain was described as of slow onset.
None reported.
Location
Response to Past Treatment
The reported sites of pain were maxillary left buccal gin-
giva in relation to upper molar tooth (left V2), and man- Since the onset of the pain, the patient underwent several
dibular right buccal gingiva in relation to the molar tooth dental procedures without any pain relief. The patient also
(right V3). reported change in the pain characteristics, sometimes for
the worse, every time another dental procedure was done.
Medications that were “tried” included but were not limited
Frequency to (varying dosages of) non-steroidal anti-inflammatories
(NSAIDs), anti-epileptic medications, nortriptyline, benzo-
The patient reported continuous “background” pain on the diazepines, and vitamin supplementations. These medica-
left V2 division, and occasional exacerbations of approxi- tions were relatively ineffective.
mately twice a week on the same area, and continuous pain
on the right V3 division with nocturnal exacerbations. Associated Features
None reported.
Duration
Association with Sleep
Intensity
The patient reports a reduced quality of sleep in general. She
The intensity of the background pain on the maxillary site is tired during the day and takes sleep aid medications. The
was five to six on a visual analog scale (VAS) of zero to ten. pain does not wake her up from sleep. She does wake up at
Exacerbated pain was described as ten on the same scale. her routine waking time and realizes she has pain.
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Fig. 1 Trigeminal traumatic neuroma: etiology, appearance, and gross neuroanatomy of traumatic neuroma pain
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Table 1 Trigeminal traumatic neuroma: differential diagnoses and management
Management modalities Neuropathic pain in general Trigeminal neuropathic pain Traumatic neuroma in general Trigeminal traumatic neuroma
Evidence on prevention - Modification of surgical techniques - Avoidance of trigeminal nerve - Monopolar diathermy and electrical - Administration of systemic steroids
[68] injuries by: coagulation [6, 66, 71] [29]
1. Not using high concentrations - Capping of the cut nerve end [72, - Adequately stabilized wiring
of local anesthetics especially the 73] without rigidity [29, 59]
ones that can be neurotoxic [69] - Implantation of cut nerve into the - Absolute mobilization of proximal
2. Not employing multiple nerve adjacent muscle [72] fragments [29, 57, 59]
blocks at the same site [70••] - Local administration of chemicals - Use of external cortical plate wire
3. Appropriate imaging to prevent such as alcohol, phenol, steroids at osteosynthesis [29, 58]
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nerve injury [69] the site of surgical trauma - Use of thin spatula osteotome [29,
- Use of lasers [72] 58]
- Triamcinolone and 5-fluorouracil
[74]
Surgical management - Neuromodulation via motor cortex - Microvascular decompression, - Surgical excision [77–79] - Surgical resection [3•, 12, 14, 25,
stimulation (MCS) and deep brain Percutaneous rhizotomy, Gamma - Microsurgery, use of nerve grafts 29]
stimulation (DBS) [75] knife radiosurgery, Neuromodulation [80, 81]
via motor cortex stimulation (MCS) - Neuromodulatory or reconstructive
and deep brain stimulation (DBS) modalities [82]
[75] - Regenerative peripheral nerve
- Radiofrequency thermocoagulation, interface (RPNI) [83–86]
Subcutaneous peripheral nerve - Targeted muscle reinnervation
field stimulation [76] (TMR) [83, 87, 88]
- Cap assisted resection [89]
Pharmacological management: - Tricyclic antidepressants (TCA) / - Steroids [97] - Antidepressants [107] Antiepileptic drugs (carbamazepine
Systemic medications Serotonin- - TCA/SNRI antidepressants [10, - Anticonvulsants [108] and gabapentin) and pregabalin
Norepinephrine Reuptake Inhibitors 97] - Calcitonin [82, 108] [114]
(SNRI) [90–92] - Anticonvulsants (gabapentin and - Calcium channel blockers [82]
- Anticonvulsants (gabapentin and pregabalin) [10, 75] - Beta-blockers [82]
pregabalin) [90, 91, 93, 94] - Botulinum toxin type A [75, - Perineural/neuraxial analgesia with
- Botulinum toxin type A [93, 95] 98–106] local anesthetic and morphine
- Opioids [91, 93] [109–111]
- Anti-arrhythmics [96] - TNF-a blockers (etanercept) [112,
113]
Topical: - Oromucosal cannabinoids [93] - Local anesthetics or 8% capsaicin - Local injections of steroids [117, - Use of neurosensory stent [114, 119,
- Capsaicin [93] patch [97] 118••] 120]
- Topical lidocaine [90, 91, 93] - Topical lidocaine [70••, 116] - Local steroid infiltration [3•]
- Topical anesthetics and
combination cream [115]
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percussion, ultrasound [14] medications may help manage residual pain after surgical
- Stereotactic radiosurgery,
excision [28].
Pharmacological Management
Complications and Prognosis
ablation [126]
- Transcutaneous magnetic
mirror therapy [91, 121]
of the Literature
Clinical Presentation
[96]
133–135]. The fact that the patient had developed the lesion
after surgical procedures is consistent with the available lit-
erature [18, 25–28] The pain characteristics of the current
case, as they relate to the literature, are given below.
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Consistent with the literature, this case exemplifies TrN of Aggravating Factors/Triggers
the terminal branch of V2 and V3 divisions of the trigem-
inal nerve [6]. However, the occurrence of two anatomi- The triggering of the pain in the present case, by functions
cally independent lesions in the same patient (left and right such as chewing, talking, and jaw movements, is consistent
sides and differing branches of the trigeminal nerve) is a with the current literature [18, 19, 28, 29, 112, 138]. How-
unique feature of this case that is largely inconsistent with ever, the aggravation of pain by acidic foods, citrus fruits,
the established TrN literature. Considering the variability and sleep position is rather unusual.
of clinicians and procedures between the two sites/sides,
we the authors strongly feel that there might be a genetic
Relieving Factors
predisposition in this patient to TrN formation. Genetic pre-
disposition to neuropathic pain has been published in the
The lack of relieving factors for the background pain (as
literature [137].
was in this case), and relief achieved by complete rest to the
affected areas (thereby avoiding triggers), and by the use of
Frequency topical anesthetics are consistent with the current literature
on trigeminal TrN [120].
We could not find pertinent focused literature on the nature
of the background pain or frequency of pain associated with
trigeminal TrN. Response to Past Treatment
The fact that our current patient had no relief from pain
Duration
even after multiple dental procedures is consistent with the
published literature [14, 130]. The lack of response to mul-
The continuous nature (“hours”) of the background pain in
tiple drugs, although part of published literature, the specific
this particular case is in agreement with past literature on
absolute lack of pain relief upon trial of anti-seizure and
similar TrNs in other anatomic areas of the body [28, 107].
SNRI medications (gabapentin, carbamazepine, nortriptyl-
ine) seems consistent with the literature [117].
Intensity
Intensity of the pain varying from five to six (moderate) Associated Features
on a numerical pain scale of zero to ten is at par with the
literature for oral and extraoral sites of TrN [19]. The seven As different from this case, associated features of skin/
out of ten pain (severe) for the exacerbated episodes is also mucosal changes, paresthesias, dysesthesias, and auto-
consistent with much of the published literature for TrN in nomic features have been reported in the literature [14, 19,
trigeminal and other nerve distributions [28, 29, 107]. 29, 139–141].
Quality Radiation/Referral
The description of dull aching background pain goes along Referral pattern in this patient’s case goes along with the
with the published literature in the oral and extraoral sites of published literature of pain in the distribution of the affected
TrN [29]. However, the pulsating quality of exacerbated pain nerve [8, 29, 142, 143].
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Association with Sleep trigeminal TrN has been established, the clinician should opt
for conservative modalities such as topical pharmacotherapy,
The lack of association with sleep disturbances, as observed possible systemic pharmacotherapy, and adjunct modalities,
in this case, is not consistent with the current literature on thereby avoiding aggressive surgical treatments and possibil-
neuropathic pain [19]. ity of recurrence.
Investigations
Conclusion
The size of the TrN lesion in this case as elicited clinically is
consistent with the literature on trigeminal TrN [34]. Repro- Traumatic neuromas in general, and trigeminal TrNs in
duction of patient’s familiar pain from the local TrN lesion particular, present with varied clinical features, and may
is one of the clinical methods to confirm the location of pose a diagnostic challenge to the clinician. TrN is a neuro-
the lesion. Specifically, eliciting a Tinel sign is considered pathic pain condition that results from attempted repair by
one of the clinical diagnostic features of TrN in the other an injured nerve. When TrN occurs in the trigeminal nerve
anatomic areas of the body [44, 45, 121]. The pain relief distribution, they present as small, non-encapsulated, often
obtained in this case by both topical and infiltration of local non-palpable lesions making it difficult to palpate. The diag-
anesthetic goes along with the published literature [46, 52]. nosis of this neuropathic pain entity is often by exclusion of
other similarly behaving entities and eliciting classic features
Management such as Tinel’s sign. Surgical resection, although may be a
choice, may have limited value due to the relative inability
Specific guidelines for the management of TrN lesions in to locate the lesion and probably running the risk of a recur-
general, and trigeminal TrN lesions in particular, are lacking. rence of the entity. Systemic medications may help; how-
TrN is considered a neuropathic pain entity [2•, 107, 144]. ever, topical medications form the choice of management,
Conceivably, management modalities that work for neuro- due to reduced risk of side effects and better efficacy from
pathic pain in general may work very well for TrN lesions localized application. Further, the use of custom fabricated
as well. One of the medications used in management of neu- delivery methods, such as a stent, further increases the effi-
ropathic pain conditions similar to TrN is topical lidocaine cacy by successfully retaining the medication locally for a
[145, 146]. In an attempt to retain the topical medications longer time. There may be a genetic predilection for patients
such as lidocaine at the site of the lesion, a custom fabricated to form TrNs subsequent to incidental or surgical trauma.
dental stent may be utilized [114]. There is a necessity for consensus amongst the pioneer pain
management organizations as to diagnostic criteria, manage-
Clinical Pearls ment protocols, and classification of TrNs.
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