Professional Documents
Culture Documents
D
ental implants are used to replace missing teeth for restoration of function and esthetics.
Implant dentistry is practiced around the world. In the United States, the prevalence of
dental implants has increased from 0.7% in 1999 through 2000 to over 5% in 2015 through
2016, with the predicted increase in implant placement approaching 23% in 2026.1 As the place-
ment of dental implants increases, it is imperative to consider the possible complications. Surgical
complications such as hemorrhage (z24%) and neurosensory disturbances (z7%) are possible, with
a combined incidence of 30%.2 Chronic pain, such as posttraumatic trigeminal neuropathic pain
(PTNP) secondary to implant placement, has been reported; however, the prevalence is unclear.3
The patients have variable clinical manifestations, routinely reporting symptoms of persistent pain
secondary to implant therapy. This is accompanied with positive or negative sensory abnormalities,
which interfere with routine activities like mastication, eating, and speaking. These complications
can jeopardize the success of the implant and potentially impact the patient’s life.
According to the International Association for the Study of Pain, pain lasting more than 3
months is classified as chronic. Chronic pain is defined as pain occurring for more than 15 days per
month and lasting over 2 hours daily for at least 3 months.4 Chronic pain serves no biological
purpose. It affects the patient’s quality of life, and up through 85% of patients with chronic pain are
affected by severe depression.5,6 Dental treatments, including dental implants, may result in PTNP;
therefore, an awareness of these complications among dental clinicians is critical. In addition, the
role of informed consent is crucial, as patients must be provided with adequate information
regarding potential complications. Early recognition, accurate diagnosis, and adequate management
are imperative in preventing the development of PTNP.
EPIDEMIOLOGY
The exact epidemiology of PTNP secondary to implant placement is not clear. The prevalence of
neuronal injury secondary to implant placement has been reported as ranging from 0.5% to as
high as 37%.2,7-9 This wide range in prevalence can be owing to the fact that both transient and
permanent neurosensory disturbances secondary to implant placement have been included in the
data over a wide range of time, not accounting for clinician expertise and techniques. The re-
ported prevalence of permanent neurosensory disturbances as a result of trigeminal nerve (TN)
injury associated with implant placement is reported at approximately 8%.10 TN neurosensory
disturbance secondary to an injury can manifest as pain, numbness, tingling, or altered sensa-
tion.11 There is a lack of epidemiologic data, particularly in relation to chronic pain secondary to
implants. Some studies suggest an incidence of 8%.3,12 One of the reasons for the lack of
agreement on the prevalence of chronic pain secondary to implants is a lack of common
nomenclature and universally accepted diagnostic criteria. Chronic pain after dental treatments
Copyright ª 2021
has been classified in numerous terms including atypical odontalgia, atypical facial pain,
American Dental
phantom tooth pain, anesthesia dolorosa, painful posttraumatic trigeminal neuropathy, and Association. All rights
PTNP.13-16 reserved.
DIAGNOSIS
According to the 2020 International Classification of Orofacial Pain, the diagnostic criteria for
PTNP require the following characteristics: the presence of persisting or recurring pain within
trigeminal nerve distribution for more than 3 months duration with onset within 6 months of injury
and associated with somatosensory symptoms and, signs, or both. The injury to the trigeminal
nerve’s peripheral branches can be mechanical, thermal, radiation, or chemical with a confirmatory
diagnostic test for a lesion to the nerve.16 The International Classification of Orofacial Pain states
that the severity of nerve injury can vary, ranging from mild to severe, with dental implants as 1 of
the many possible dental treatmenteinduced iatrogenic injuries.
ETIOLOGY
Iatrogenic nerve injuries due to dental implants may result from direct or indirect trauma. The
preparation or osteotomy is more commonly associated with injury than placement. The prepara-
tion bur (during osteotomy) or the placement of the implant can cause direct trauma to the
nerve.17-19 Indirect trauma is secondary to mechanical or chemical causes including extrusion of
debris into the inferior alveolar canal, hemorrhage, and inflammation.17,18 The prevalence of
hemorrhage-induced nerve injury is approximately 24%, in which persistent ischemia of the nerve
occurs owing to hemorrhage caused during placement.2,20 Iron or hemoglobin from the blood can result
in a chemical injury, and hemorrhage can result in direct mechanical damage to the nerve.21-23 Nerve
injury is also possible while administering a local anesthetic (LA).24 Pain can also occur during the
restoration of the implant, rendering the implant nonrestorable.25 The innervation of peri-implant
tissue reportedly increases with postimplant loading, possibly explaining pain associated with placement
of a restoration in some patients.26 In a minority of patients, pain may develop in a well-placed implant
in the absence of complications even with adequate postoperative care. Figure 1 depicts potential nerve
injuries secondary to implant placement.
CLINICAL FEATURES
A combination of environmental, genetic, and psychosocial factors are implicated in the high
variability in the clinical manifestations after identical injuries.12 The type of nerve fibers involved
also determines the clinical phenotype exhibited. An injury to A beta nerve fibers, normally
responsible for light touch sensation, may result in positive (allodynia) and negative (numbness)
changes to light touch, whereas an injury to A delta and C type fibers, normally responsible for the
transmission of noxious stimuli, may manifest as an exaggerated response to painful stimuli
(hyperalgesia).12 The clinical features of pain are variable and mostly described as continuous,
unilateral pain (occurring most of the day and on most days) in the dermatome of the affected
nerve.27 Involvement of both intraoral and extraoral trigeminal dermatomes has been reported.28
Radiation of pain or spreading beyond the dermatome has also been reported,27,29 as have parox-
ysms of pain, which can be spontaneous or evoked by function or touch.30 The onset of pain
typically is reported immediately after implant placement but can occur on the loading of the
implant as well.25 The intensity is moderate to severe, with a quality most often described as
ASSESSMENT
A detailed history with specific emphasis on characteristics of pain and other symptoms is impor-
tant. The diagnosis of PTNP is accomplished via a thorough history and clinical examination. The
sensory examination plays a critical role in the evaluation and quantification of the sensory changes
associated with PTNP. Sensory symptoms must be recorded in acceptable terms such as allodynia,
dysesthesia, and paresthesia, as we have described previously.42 Patients with PTNP report thermal
and mechanical allodynia.43,44 Some of the methods used to detect somatosensory changes include
patient self-reports, questionnaires, nerve conduction studies, clinical neurosensory tests, and
thermal and electrical quantitative sensory testing (QST).45 Diminished perception of thermal
stimuli, in particular warm stimuli, has been associated with increased risk of developing chronic
pain and more severe sensory symptoms.46 Abnormality in thermal QST has been reported to persist
years after the injury, which represents long-standing sensory alterations.47
Sensory assessment tests (QST and neurosensory tests) may be considered impractical and
difficult to perform in a routine dental practice owing to their complexity and time and financial
constraints. These testing modalities are, therefore, limited to a research setting. Modifications of
these tests suitable for a dental setting have been suggested.12 Chairside neurosensory testing in-
cludes the use of commonly available instruments in a dental practice such as a cotton swab or
monofilament (von Frey, if available) to test for changes in light touch sensation (allodynia), a
dental probe to test for pinprick sensation (hypersensitivity to a noxious stimulus), and warm and
cool instruments for thermal sensation.12,45 It is suggested that clinicians perform the tests bilat-
erally, noting sensation as normal, increased, or reduced on affected and unaffected sides on the
basis of patients response. Regions of abnormal sensations must be mapped, marked, and photo-
graphed for maintaining proper records.12 These data can be used during follow-up visits to evaluate
the progress and patient motivation. The role of imaging is variable. Imaging can provide access to
the extent of nerve damage but can be historic if the offending implant has been removed.45
PREVENTION
Implant-related nerve injuries are avoidable, and hence PTNP is preventable. Dentists must give
adequate importance to preventive measures, which can be divided on the basis of the sequence of
events for the operative or causative procedure into preoperative, intraoperative, and postoperative
procedures. Prevention is of utmost importance as the available management modalities typically do
not offer complete pain relief and may have unpleasant adverse effects.
Preoperative
Recognition of Risk Factors
Age, sex, anxiety, depression, pain catastrophizing, preexisting chronic pain conditions, systemic
illness, and presence of preoperative pain in the site are some of the known factors associated with
Intraoperative
Clinicians must pay specific attention to guidelines for an adequate safety zone (2-4 millimeters) and
the use of shorter implants is recommended to minimize the risk of experiencing injury.28,57,58 The
extent of the required safety zone is determined individually on the basis of the operator’s skill and
radiographic interpretation.28 However, it is imperative to emphasize that even a 4-mm safety zone
is not always preventive, and in the presence of significant inflammation, the onset of symptoms
might be slow and eventually result in PTNP. In addition, perineural inflammation secondary to a
well-placed implant may result in PTNP. Intraoperative radiographs are suggested during implant
bed preparation.59 It is important for clinicians to remember that certain preparation drills are
longer than the implant. If a sudden give is encountered during preparation, this may indicate
penetration of the buccal or lingual cortical plate or inferior alveolar nerve canal roof fracture.60
The procedure must be stopped, and prompt action must be taken when bleeding, severe pain,
or sudden drop is encountered. In such cases, the patient should be informed about the possibility of
nerve damage. Immediate referral to an appropriate specialist in TN injuries is recommended in
cases in which nerve injury is suspected. It is recommended not to place the implant in the presence
of intraoperative bleeding. Some reports suggest that the placement should be delayed for 3 days
when intraoperative bleeding occurs.60 Severe pain during preparation is another factor to be
considered. The use of LA infiltrations over nerve blocks has been suggested, so that the patient can
feel pain symptoms if damage to a nerve occurs.28,61 Adequate analgesia is important, particularly
when performing high-risk procedures in susceptible patients; therefore, adequate preventive pre-
and postoperative analgesia is indicated.62,63
Postoperative
Early follow-up is critical in the prevention of chronic pain development. The dental practitioner
must contact the patient routinely within 6 through 12 hours postoperatively to detect any
symptoms of potential nerve damage. In case nerve damage is suspected, this home check is crucial
to ensure LA effect has been reversed and no symptoms have developed. In the event that the
patient reports symptoms of neuropathy, immediate appropriate referral and implant removal is
indicated.64 If numbness persists after LA has worn off, the implant must be removed within a 24-
through 36-hour window to facilitate recovery and prevent development of chronic pain.60,65,66
Delayed removal of implant, wait and watch, and conservative modalities are futile in alleviating
neuropathy and pain.30 If severe pain occurred on administration of LA, then implant removal is
Systemic drugs:
• Tricyclic antidepressants and • Cognitive-behavioral therapy
• Limited evidence
Serotonin norepinephrine • Psychosocial interventions
reuptake inhibitors • Some cases
• Massage therapy
• Pregabalin microneurosurgey
• Gabapentin • Intergrative and physical therapy
• Topical medications
Figure 2. Summary of modalities indicated in the management of posttraumatic trigeminal neuropathic pain secondary
to implant therapy.
not indicated, and the diagnosis of the cause of injury is LA.67 Steroids and nonsteroidal antiin-
flammatory drugs must be considered in such cases.64,68 Immediate steroid therapy has been shown
to aid in recovery by reducing perineural inflammation and swelling around the nerve.69 When the
nerve injury is confirmed, it is important to inform the patient and describe management options
and prognosis.
MANAGEMENT
The treatment of PTNP remains challenging, and the evidence of the efficacy of available in-
terventions is inconclusive; therefore, an interdisciplinary approach is indicated.70,71 Several mo-
dalities, summarized in Figure 2, with variable evidence have been indicated in the management of
PTNP. These include pharmacotherapy, surgical interventions, and complimentary therapies.72
The first step in management is patient education. Communication with the patient, clarification
regarding the condition, and support are part of initial psychological treatment, which begins with
the dental practitioner.19 The patient expectation is critical for successful management of PTNP;
therefore, patients should be educated regarding prognosis and treatment and should understand
that partial pain relief is a good and expected outcome. Many times, the dentist does not
communicate with the patient, and this increases the uncertainty of the disease in the patient’s
mind, adding to anxiety and stress. The number of required analgesics has been shown to decrease
when the patient education program was integrated with pharmacotherapy.73 Combination ther-
apies are recommended to lower pain, enhance the patient’s coping skills, restore function, and
potentially reduce adverse effects.74 A paradigm for prevention and management of PTNP is
summarized in the Figure 3 flowchart.
Pharmacologic interventions
Pharmacologic interventions are the most frequently used modalities in the management of PTNP
and include a wide variety of drug categories. Antiepileptic drugs and antidepressants, including
tricyclic antidepressants and selective serotonin norepinephrine reuptake inhibitors, are 2
commonly used drug classes.75,76 The first-line drug therapy includes tricyclic antidepressants and
serotonin norepinephrine reuptake inhibitors or gabapentinoids.77 To improve efficacy and reduce
adverse effects, a combination of 2 different drugs is suggested.78 The choice of drug depends on
patient factors, such as presence of systemic comorbidities, age, and drug adverse effect profile.79
The use of pharmacologic therapy in PTNP due to implants has been shown to reduce the pain
level better when early intervention is initiated.80 Overall, these drugs have limited efficacy and
often provide only partial pain relief. It has been reported that only 10% of patients report over 50%
reduction in pain, pointing to poor response of PTNP to pharmacotherapy.81 Topical medication
for PTNP is another possibility to avoid systemic adverse effects.82 The use of compounded topical
medications with various drug combinations, including ketamine, carbamazepine, gabapentin,
pregabalin, clonidine, lidocaine, capsaicin, and ketoprofen in variable concentrations, is also
available.83,84 In intraoral PTNP, the use of a neurostent for delivering topical medication specific
to the site of injury to increase the delivery to the site has been also reported.15
YES
Figure 3. Summary of the decision-making process in the prevention and management of posttraumatic trigeminal neuropathy (PTNP) secondary to
implant therapy.
Surgical interventions
Evidence supporting the efficacy of surgical interventions in the management of PTNP is limited.
When neuropathy occurs without pain, surgery to improve sensations may be considered.86,87 As
discussed previously, timing for intervention is important because early removal of the offending
implant is suggested to reduce incidence of pain and neuropathy.68 When the implant has
osteointegrated, the evidence for implant removal to alleviate pain and prevent PTNP is limited
because permanent damage is unavoidable. Microneurosurgery has been recommended for total
resection of nerves, but no consensus on timing or a type of surgery is available to date.88 A referral
to a microneurosurgeon is recommended when no obvious pathology is seen on imaging and the
symptoms of anesthesia and hypoesthesia persist for over 3 months with no improvement or dys-
esthesia persists for over 3 months with resolution as a response to peripheral nerve blocks.87
CONCLUSIONS
Implant therapy can cause injury to branches of the TN; therefore, it is important to consider
possible complications. The dental practitioner must be aware of the risks of such injuries, discuss
them with the patient during treatment planning, and have the patient sign an informed consent
form. Fortunately, most injuries are preventable via preoperative assessment, including careful pa-
tient and implant site selection. Avoidance of nerve injuries by means of implementing appropriate
preoperative and intraoperative strategies is critical. The clinician must be aware of the signs and
symptoms of nerve injury during and immediately after a procedure and must contact the patient
the following day to ensure there are no complications. Prompt recognition is key in preventing the
transition to a chronic, irreversible neuropathy. Persistent pain and sensory distortions can be
debilitating to the patient and can negatively affect the quality of life, causing a significant
Dr. Kohli is an orofacial pain resident, Center for Orofacial Pain and Rutgers School of Dental Medicine, Rutgers, the State University of New
Temporomandibular Disorders, Rutgers School of Dental Medicine, Rutg- Jersey, Room D-830, 110 Bergen St, Newark, NJ 07101, e-mail olga.
ers, the State University of New Jersey, Newark, NJ. korczeniewska@rutgers.edu. Address correspondence to
Dr. Katzmann is an orofacial pain resident, Center for Orofacial Pain and Dr. Korczeniewska.
Temporomandibular Disorders, Rutgers School of Dental Medicine, Rutg- Disclosure. Dr. Benoliel was remunerated as editor-in-chief of Journal of
ers, the State University of New Jersey, Newark, NJ. Oral & Facial Pain and Headache. None of the other authors reported any
Dr. Benoliel is a professor, Department of Diagnostic Sciences, Rutgers disclosures.
School of Dental Medicine, Rutgers, the State University of New Jersey,
Newark, NJ. Pain Update is published in collaboration with the Neuroscience Group of
Dr. Korczeniewska is an assistant professor, Department of Diagnostic the International Association for Dental Research.
Sciences, Center for Orofacial Pain and Temporomandibular Disorders,
1. Elani HW, Starr JR, Da Silva JD, Gallucci GO. 17. Nazarian Y, Eliav E, Nahlieli O. Nerve injury 31. Pigg M, Svensson P, Drangsholt M, List T. Seven-
Trends in dental implant use in the U.S., 1999-2016, and following implant placement: prevention, diagnosis and year follow-up of patients diagnosed with atypical odon-
projections to 2026. J Dent Res. 2018;97(13):1424-1430. treatment modalities [in Hebrew]. Refuat Hapeh Veha- talgia: a prospective study. J Orofac Pain. 2013;27(2):151-
2. Goodacre CJ, Bernal G, Rungcharassaeng K, Kan JY. shinayim (1993). 2003;20(3):44-50, 101. 164.
Clinical complications with implants and implant pros- 18. Renton T. Prevention of iatrogenic inferior alveolar 32. Siqueira SR, Siviero M, Alvarez FK, Teixeira MJ,
theses. J Prosthet Dent. 2003;90(2):121-132. nerve injuries in relation to dental procedures. SADJ. Siqueira JT. Quantitative sensory testing in trigeminal
3. Korczeniewska OA, Eliav E, Benoliel R. Neuropathic 2010;65(8):342-344, 346-348, 350-351. traumatic neuropathic pain and persistent idiopathic
rofacial pain. In: Farah CS, Balasubramaniam R, 19. Juodzbalys G, Wang HL, Sabalys G. Injury of the facial pain. Arq Neuropsiquiatr. 2013;71(3):174-179.
McCullough MJ, eds. Contemporary Oral Medicine: A inferior alveolar nerve during implant placement: a liter- 33. List T, Leijon G, Svensson P. Somatosensory ab-
Comprehensive Approach to Clinical Practice. New York NY: ature review. J Oral Maxillofac Res. 2011;2(1):e1. normalities in atypical odontalgia: a case-control study.
Springer International Publishing; 2018:1-75. 20. Yilmaz Z, Ucer C, Scher E, Suzuki J, Renton T. Pain. 2008;139(2):333-341.
4. Treede RD, Rief W, Barke A, et al. Chronic pain as a A survey of the opinion and experience of UK dentists, 34. Baad-Hansen L, Pigg M, Ivanovic SE, et al. Intraoral
symptom or a disease: the IASP Classification of Chronic part 1: the incidence and cause of iatrogenic trigeminal somatosensory abnormalities in patients with atypical
Pain for the International Classification of Diseases (ICD- nerve injuries related to dental implant surgery. Implant odontalgia: a controlled multicenter quantitative sensory
11). Pain. 2019;160(1):19-27. Dent. 2016;25(5):638-645. testing study. Pain. 2013;154(8):1287-1294.
5. Bair MJ, Robinson RL, Katon W, Kroenke K. 21. Mahon N, Stassen LF. Post-extraction inferior alve- 35. Smith JG, Elias LA, Yilmaz Z, et al. The psychoso-
Depression and pain comorbidity: a literature review. Arch olar nerve neurosensory disturbances: a guide to their cial and affective burden of posttraumatic neuropathy
Intern Med. 2003;163(20):2433-2445. evaluation and practical management. J Ir Dent Assoc. following injuries to the trigeminal nerve. J Orofac Pain.
6. Williams LS, Jones WJ, Shen J, Robinson RL, 2014;60(5):241-250. 2013;27(4):293-303.
Weinberger M, Kroenke K. Prevalence and impact of 22. Renton T, Janjua H, Gallagher JE, Dalgleish M, 36. Melek LN, Smith JG, Karamat A, Renton T.
depression and pain in neurology outpatients. J Neurol Yilmaz Z. UK dentists’ experience of iatrogenic trigeminal Comparison of the neuropathic pain symptoms and psy-
Neurosurg Psychiatry. 2003;74(11):1587-1589. nerve injuries in relation to routine dental procedures: why, chosocial impacts of trigeminal neuralgia and painful
7. Tay AB, Zuniga JR. Clinical characteristics of tri- when and how often? Br Dent J. 2013;214(12):633-642. posttraumatic trigeminal neuropathy. J Oral Facial Pain
geminal nerve injury referrals to a university centre. Int J 23. Pogrel MA, Thamby S. Permanent nerve involve- Headache. 2019;33(1):77-88.
Oral Maxillofac Surg. 2007;36(10):922-927. ment resulting from inferior alveolar nerve blocks. JADA. 37. Pogrel MA, Jergensen R, Burgon E, Hulme D. Long-
8. Ellies LG, Hawker PB. The prevalence of altered 2000;131(7):901-907. term outcome of trigeminal nerve injuries related to dental
sensation associated with implant surgery. Int J Oral 24. Hillerup S, Jensen RH, Ersboll BK. Trigeminal nerve treatment. J Oral Maxillofac Surg. 2011;69(9):2284-2288.
Maxillofac Implants. 1993;8(6):674-679. injury associated with injection of local anesthetics: needle 38. Freeman R, Baron R, Bouhassira D, Cabrera J,
9. Allen PF, McMillan AS, Smith DG. Complications lesion or neurotoxicity? JADA. 2011;142(5):531-539. Emir B. Sensory profiles of patients with neuropathic pain
and maintenance requirements of implant-supported 25. Devine M, Taylor S, Renton T. Chronic post- based on the neuropathic pain symptoms and signs. Pain.
prostheses provided in a UK dental hospital. Br Dent J. surgical pain following the placement of dental implants 2014;155(2):367-376.
1997;182(8):298-302. in the maxilla: a case series. Eur J Oral Implantol. 2016;9(2 39. Maier C, Baron R, Tölle TR, et al. Quantitative
10. Gregg JM. Neuropathic complications of mandibular suppl 1):179-186. sensory testing in the German Research Network on
implant surgery: review and case presentations. Ann R 26. Huang Y, Jacobs R, Van Dessel J, Bornstein MM, Neuropathic Pain (DFNS): somatosensory abnormalities
Australas Coll Dent Surg. 2000;15:176-180. Lambrichts I, Politis C. A systematic review on the in 1236 patients with different neuropathic pain syn-
11. Penarrocha M, Cervello MA, Marti E, Bagan JV. innervation of peri-implant tissues with special emphasis dromes. Pain. 2010;150(3):439-450.
Trigeminal neuropathy. Oral Dis. 2007;13(2):141-150. on the influence of implant placement and loading pro- 40. Kim HK, Kim ME. Quantitative and qualitative
12. Benoliel R, Teich S, Eliav E. Painful traumatic tri- tocols. Clin Oral Implants Res. 2015;26(7):737-746. sensory testing results are associated with numbness rather
geminal neuropathy. Oral Maxillofac Surg Clin North Am. 27. Benoliel R, Zadik Y, Eliav E, Sharav Y. Peripheral than neuropathic pain in patients with post-implant tri-
2016;28(3):371-380. painful traumatic trigeminal neuropathy: clinical features geminal neuropathy: a cross-sectional pilot study.
13. Headache Classification Committee of the Interna- in 91 cases and proposal of novel diagnostic criteria. Somatosens Mot Res. 2019;36(3):202-211.
tional Headache Society (IHS) The International Classi- J Orofac Pain. 2012;26(1):49-58. 41. Hegedus F, Diecidue RJ. Trigeminal nerve injuries
fication of Headache Disorders, 3rd edition. Cephalalgia. 28. Renton T, Dawood A, Shah A, Searson L, Yilmaz Z. after mandibular implant placement: practical knowledge
2018;38(1):1-211. Post-implant neuropathy of the trigeminal nerve. a case for clinicians. Int J Oral Maxillofac Implants. 2006;21(1):
14. Scholz J, Finnerup NB, Attal N, et al.; Classification series. Br Dent J. 2012;212(11):E17. 111-116.
Committee of the Neuropathic Pain Special Interest Group 29. Politis C, Agbaje J, Van Hevele J, et al. Report of 42. International Association for the Study of Pain.
(NeuPSIG). The IASP classification of chronic pain for neuropathic pain after dental implant placement: a case IASP Terminology. Available at: https://www.iasp-pain.
ICD-11: chronic neuropathic pain. Pain. 2019;160(1):53-59. series. Int J Oral Maxillofac Implants. 2017;32(2):439- org/Education/Content.aspx?ItemNumber¼1698.
15. Baad-Hansen L, Benoliel R. Neuropathic orofacial 444. Accessed June 21, 2020.
pain: facts and fiction. Cephalalgia. 2017;37(7):670-679. 30. Renton T, Yilmaz Z. Profiling of patients presenting 43. Rasmussen PV, Sindrup SH, Jensen TS, Bach FW.
16. International Classification of Orofacial Pain, 1st with posttraumatic neuropathy of the trigeminal nerve. Symptoms and signs in patients with suspected neuro-
edition (ICOP). Cephalalgia. 2020;40(2):129-221. J Orofac Pain. 2011;25(4):333-344. pathic pain. Pain. 2004;110(1-2):461-469.