ANESTHESIA/FACIAL PAIN

The Presence of Neuropathic Pain Predicts

Postoperative Neuropathic Pain Following
Trigeminal Nerve Repair
John R. Zuniga, DMD, MS, PhD,* David M. Yates, DMD, MD,y
and Ceib L. Phillips, MPH, PhDz
Purpose: The risk for the continuation or recurrence of neuropathic pain following trigeminal nerve
repair has never been examined. The objective of this study was to determine which risk factors might
be associated with the continuation or recurrence of neuropathic pain following trigeminal nerve micro-
neurosurgery.
Patients and Methods: An ambispective study design was used to assess subjects who underwent tri-
geminal nerve repair of the inferior alveolar nerve and lingual nerve between 2000 and 2010. The primary
outcome was the presence or absence of neuropathic pain at 3, 6, and 12 months after surgery. Explana-
tory variables, including age at surgery, gender, presence of neuropathic pain before surgery, site of nerve
injury, etiology of nerve injury, classification of nerve injury, duration of nerve injury, and type of repair
performed, were abstracted from patient charts. Fisher exact tests were used to compare the demographic
and injury characteristics of patients who presented with pain before surgery and those who did not. The
McNemar test was used to assess whether there was a significant change in neuropathic pain report from
before to after surgery. The level of significance was set at .50.
Results: Of the 65 patients analyzed, two-thirds were women; the average age was 36  16.1 years, and
the median time between the injury and surgery was 6.4 months (interquartile range, 6.7 months). Lingual
nerve injury type was the most frequent (62%). There was no statistically significant change in pain status
from before to after surgery (P = .104). Only 1 patient had pain after surgery who had not had pain before
surgery, while 67% of those with pain before surgery continued to have pain after surgery. Pain prior to
surgery as a predictor of pain after had sensitivity of 91%, specificity of 88%, positive predictive value of
67%, and negative predictive value 97%.
Conclusions: The presence of neuropathic pain prior to trigeminal microneurosurgery is the major risk
factor for the continuation or recurrence of postoperative neuropathic pain. These findings suggest that
trigeminal nerve surgery is not a risk factor for developing neuropathic pain in the absence of neuropathic
pain before surgery.
2014 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 72:2422-2427, 2014

Neuropathic pain is the painful condition that is charac- bution of an injured sensory nerve.1 The definition of
terized by a variety of positive and negative signs and neuropathic pain has recently been redefined as pain
symptoms (eg, allodynia, hyperpathia, hyperalgesia, arising as a direct consequence of a lesion or disease
painful numbness, painful paresthesia) within the distri- affecting the somatosensory system. 2 Lesions or

*Professor and Chairman, Division of Oral and Maxillofacial
Surgery, Department of Surgery, University of Texas Southwestern
Medical Center at Dallas, Dallas, TX.
yResident in Oral and Maxillofacial Surgery, Parkland Health
Services Hospital, Dallas, TX.
zProfessor, Department of Orthodontics, School of Dentistry,
University of North Carolina at Chapel Hill, Chapel Hill, NC.
Conflict of Interest Disclosures: Dr Zuniga is a consultant for
AxoGen (Alachua, FL).
Address correspondence and reprint requests to Dr Zuniga:
Department of Surgery, University of Texas Southwestern Medical
Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75390-9109;
e-mail: john.zuniga@utsouthwestern.edu
Received April 30 2014
Accepted August 3 2014
2014 American Association of Oral and Maxillofacial Surgeons
0278-2391/14/01309-3
http://dx.doi.org/10.1016/j.joms.2014.08.003

2422
ZUNIGA, YATES, AND PHILLIPS
diseases involving the peripheral trigeminal somatosen-
sory system occur most frequently by mechanical (eg,
compression, stretching, cutting) and chemical (eg,
local anesthetics, topical medications) insults and occur
primarily in the inferior alveolar/mental and lingual
nerve distributions.3,4 The exact cause of neuropathic
pain of the trigeminal system is still unknown, but
several risk factors have been suggested, including
changes in ion channels, putative neurotransmitter
excess or inhibition, endothelin receptor activity,
and glial cell dysfunction causing trigeminal
hyperexcitability following constriction and/or tran-
section injuries of different branches of the trigeminal
nerve.5-8 However, an injury or insult to the nerve is
the common clinically measureable etiology of the
onset of neuropathic pain of the trigeminal nerve.
The incidence of neuropathic pain in the population
of patients who have trigeminal nerve injuries is uncom-
mon. Marchiori et al9 reported an incidence of 0.42% in a
large cohort (1,671 patients between 2007 and 2012) of
patients who underwent sagittal osteotomy of the
mandible. Only 7 patients developed neuropathic pain
(within 30 days) in the distribution of the inferior alve-
olar nerve (IAN) (no lingual nerve [LN] involvement
was reported). The median age of the study subjects
was 48 years, and all were Caucasian women. Tay and
Zuniga4 reported that 9.7% of patients presenting to a
tertiary referral source with neurosensory symptoms
demonstrated neuropathic pain on presentation. They
found that in the group of patients with IAN injuries,
the incidence of neuropathic pain was 14.6%, and
they demonstrated mild or no sensory impairment on
neurosensory testing.10,11 When present, and in
contrast to pain-free patients, Gregg3,12 reported that
neuropathic pain was generally constant (80%) or
intermittent (20%). Sixty percent of patients with
neuropathic pain had allodynia (painful response to
normally nonpainful stimuli) and/or hyperalgesia
(lowered pain threshold to painful stimulus). Eighty-
five percent of patients had hyperpathia (complex pain-
ful response to repetitive nonpainful stimulus), while
29% demonstrated characteristics of anesthesia dolo-
rosa (pain in the zone of complete anesthesia), and
42% exhibited elements of sympathetic-mediated pain
(complex pain described as burning, nagging, or
agonizing). Thus, there exists a population of patients
who have injury as a common factor, but differ from
pain-free patients by characteristic findings on neuro-
sensory testing.10
The relationship between an intentional injury of a
peripheral trigeminal nerve and the onset of neuro-
pathic pain has not been explored. Microneurosurgery
of the trigeminal nerves has been an accepted treat-
ment sensory deficits and painful neuropathy of the tri-
geminal nerves.3,12,13 Microneurosurgery requires
mechanical manipulation (eg, stretching), intentional
2423
resection (ie, cutting), neurorrhaphy, and/or
neurolysis with or without direct repair and thus
should be considered an elective injury of the
peripheral trigeminal nerves.14 If injury (surgical
repair) is the major risk factor for the onset of neuro-
pathic pain, then the risk for developing neuropathic
pain following trigeminal nerve surgery would be a sig-
nificant finding in those patients who did not have
neuropathic pain before nerve repair. The hypothesis
that guided this study was that patients who have no
neuropathic pain before trigeminal nerve repair will
have neuropathic pain after nerve repair due to elec-
tive and intentional injury of the trigeminal nerve.
Patients and Methods
An ambispective study design was used. Approvals
from the institutional review boards at the University
of North Carolina School of Dentistry and the Univer-
sity of Texas Southwestern were obtained. One hun-
dred twenty-four charts of patients who underwent
elective trigeminal nerve repair of either the IAN or
LN between 2000 and 2006 were retrospectively as-
sessed. Thirty-eight patients who underwent surgery
between 2006 and 2010 were prospectively assessed.
Inclusion criteria were patients with neurosensory
symptoms in the distribution of the IAN or LN who
elected to undergo surgical intervention. The neuro-
sensory symptoms could be unacceptable altered
sensation with or without neuropathic pain. Patients
were excluded if they had acute infections at the
time of surgery, had histories of radiation therapy to
the head and neck, had current or past histories of ma-
lignancy, had osteonecrosis of the jaw (medication-
related osteonecrosis of the jaw), or did not undergo
postsurgery neurosensory testing. No subjects were
excluded on the basis of age or sex.
The following data were collected for each patient:
gender and age; type of procedure or event associated
with the injury, prompted by 7 options that included
third molar odontectomy, implantation, orthognathic,
periodontal, benign pathology surgery, endodontic, or
other; time from injury to repair; classification of
injury found at the time of surgery using the Sunder-
land classification15; and type of repair performed.
Each patient underwent microneurosurgery, and
the surgical specimen report or the surgeons opera-
tive report was used to determine the classification
of the injury. One of the 4 following categories of sur-
gical findings and classification was assigned: normal/
intact (class 2), compressed/intact (class 3), partial
transection (class 4), or complete transection (class 5).
Each patient had a surgical report, and the type of
repair was assigned to 1 of the 4 following categories:
neurolysis, direct neurorrhaphy without autograft or
allograft, neurorrhaphy with autograft, or neurorrhaphy
2424 NEUROPATHIC PAIN AFTER TRIGEMINAL NERVE REPAIR

with allograft. Allografts (AVANCE; AxoGen, Inc, Table 1. DESCRIPTIVE STATISTICS FOR PATIENT
Alachua, FL) were not used prior to 2008, but were GROUPS WITH AND WITHOUT PRESURGERY PAIN ON
included in the neurorrhaphy with graft group because THE BASIS OF GENDER, AGE, INJURY TYPE, REPAIR
TYPE, ETIOLOGY OF INJURY, AND TIME FROM INJURY
an interpositional graft material was required to estab- TO REPAIR
lish continuity in this group of patients.
The presence or absence of neuropathic pain was Pain No Pain
recorded as the primary end point value using a previ- All Before Before
ously described classification system.10 Neuropathic Variable Patients Surgery Surgery P
pain was defined as stimulus-induced or spontaneous
pain associated with 1) allodynia (painful response Gender
to normally nonpainful stimulus on level A testing); Male 22 (33.9%) 4 (23.5%) 18 (37.5%) .40
2) hyperpathia (painful response to repetitive non- Female 43 (66.1%) 13 (76.5%) 30 (62.5%)
Injury type
painful stimulus with aftersensation, overshoot, sum-
LN 40 (61.5%) 5 (29.4%) 35 (72.9%) .003
mation, or delayed onset on level B testing); 3) IAN 25 (38.5%) 12 (70.6%) 13 (27.1%)
hyperalgesia (lowered pain threshold to painful stim- Class
ulus on level C testing); or 4) anesthesia dolorosa or 3 8 (17.8%) 6 (42.9%) 2 (6.5%) .01
sympathetically mediated pain (anesthetic or auto- 4 17 (37.8%) 5 (35.7%) 12 (38.7%)
nomic blocks on level D testing). There was no 5 20 (44.4%) 3 (21.4%) 17 (54.8%)
attempt to subcategorize the neuropathic pain state Etiology
or determine the intensity level. The primary out- Third molar 30 (66.7%) 7 (50.0%) 23 (74.2%) .04
comes were the presence or absence of neuropathic Implant 5 (11.1%) 4 (28.6%) 1 (3.2%)
pain assessed before and after surgery (at 3, 6, and Other 10 (22.2%) 3 (21.4%) 7 (22.6%)
12 months). Repair type
Direct 17 (38.6%) 6 (42.9%) 11 (36.7%) .08
The demographic and injury characteristics of the
Neurolysis 6 (13.6%) 4 (28.6%) 2 (6.7%)
patients who presented with pain before surgery and Autograft 5 (11.4%) 2 (14.3%) 3 (10.0%)
those who did not were compared to assess if the 2 Allograft 16 (36.4%) 2 (14.3%) 14 (46.7%)
groups were similar (using Fisher exact tests). The
McNemar test was used to assess whether there was Zuniga, Yates, and Phillips. Neuropathic Pain After Trigeminal
a significant change in neuropathic pain report from Nerve Repair. J Oral Maxillofac Surg 2014.
before to after surgery.
ences for age (P = .02), trigeminal nerve type (P = .003),
and etiology (P = .04). Patients who had neuropathic
Results
pain before surgery were older, 44  13 versus 32 
Data were available for 65 of the 162 patients. Of the 16 years of age on average, but there was no statistically
124 retrospective patients, 97 were not available for significant difference in the average time since injury
adequate chart review, because of inaccessibility at the (P = .49). For those with pain, 71% had had IAN in-
study site. Of the 65 patients, two-thirds (n = 43) were juries, while only 27% of those without pain had had
women. The average age was 36  16.1 years, and the IAN injuries. Fifty percent of those with pain had had
median time between the injury and surgery was 6.4 third molars removed, and 29% experienced pain
months (interquartile range, 6.7 months). LN injury following implant placement. This is consistent with
type was the most frequent (62%). The most common the known literature.4 In those without pain, 74%
Sunderland injury classifications were classes 4 and 5 had undergone third molar removal, while only 3%
(38% and 44%, respectively), which reflects the inclu- had had implants placed. Analysis of the presence
sion criteria bias for patients needing surgery. Direct and absence of presurgical neuropathic pain by class
neurorrhaphy and neurorrhaphy with allograft were of nerve injury (Sunderland class 3, 4, and 5) demon-
the most common repair types (39% and 36%, respec- strated a statistically significant difference between
tively), reflecting the best surgical options for Sunder- the 2 groups (P = .01). The relationship between the
land class 4 and 5 injuries. Third molar removal was by distributions from class 3 to 5 were reversed in the 2
far the most common etiology (67%). Table 1 shows groups with higher class injuries present in the group
the descriptive statistical results described above. with no neuropathic pain than the group with neuro-
Table 1 shows the bivariate c2 and Fisher exact tests pathic pain. Of those with no pain prior to surgery,
of the presence and absence of neuropathic pain 55% had class 5 injuries, 39% had class 4 injuries, and
before surgery by age, gender, trigeminal nerve type, 6% had class 3 injuries, while for those with pain,
etiology, duration of injury, Sunderland classification, only 21% were class 5, 36% class 4, and 43% class 3.
and type of repair performed. There was no difference The type of repair performed was not significantly
by gender, but there were statistically significant differ- different for those with and without pain (P = .08).
ZUNIGA, YATES, AND PHILLIPS
Between those patients for whom postsurgery re-
sponses were obtained (n = 51) and those who did
not have recall data (n = 14), there was a statistically
significant difference in repair type (P = .01). Most
(67%) of those who did not return for follow-up had
undergone allograft procedures, while most (50%) of
those who did return had undergone direct repair.
However, those with and without recall data were
similar with respect to other presurgical characteris-
tics (P > .14) and report of presurgery pain (P = .32).
Figure 1 shows the association between the pres-
ence of neuropathic pain after surgery compared
with before surgery. There was no statistically signifi-
cant change in pain status from before to after surgery
(P = .10). Of those who reported pain prior to surgery,
67% reported pain following surgery. There was only 1
patient with no neuropathic pain prior to surgery who
had neuropathic pain after surgery. Neuropathic pain
prior to surgery as a predictor of pain after surgery
had sensitivity of 91% (pain present before surgery
would be present after surgery), specificity of 88%
(no pain before surgery, no pain after surgery), posi-
tive predictive value of 67% (pain before surgery was
a predictor of pain after surgery), and negative predic-
tive value of 97% (pain before surgery would not have
pain afterward, 3%).
Discussion
This study showed that elective microsurgery of the
IAN and LN is not a risk factor in the recurrence of tri-
geminal neuropathic pain after surgery. In fact, only 1
case of neuropathic pain was recorded in the group of
patients who did not have neuropathic pain before sur-
gery. Pogrel16 reported that none of the patients who
had no dysesthesia before surgery reported postoper-
ative dysesthesia when the outcomes of microneuro-
surgery of the IAN and LN in 51 patients were
analyzed. Bagheri et al17 reported similar findings in
FIGURE 1. The presence of neuropathic pain in the cohort group of patients before surgery (dark solid) versus the cohort group of patients with
no neuropathic pain before surgery (light solid) over time in months from surgery. The statistical difference between the groups over time was
P = .0078.
Zuniga, Yates, and Phillips. Neuropathic Pain After Trigeminal Nerve Repair. J Oral Maxillofac Surg 2014.
2425
62 patients with numbness only before microsur-
gical repair of the IAN. None of these patients devel-
oped chronic, intractable pain after microsurgery.
The presence of neuropathic pain prior to elective
microsurgery of the IAN and LN was the major risk fac-
tor for continued postoperative neuropathic pain. The
positive predictive value for neuropathic pain after
surgery when neuropathic pain was present before
surgery was 67%, indicating that the best predictor
of continued or recurrent pain after surgery for any pa-
tient who undergoes microsurgery of the IAN or LN is
the presence of neuropathic pain before surgery. The
negative predictive value was 97%, meaning that for
patients with neuropathic pain before surgery, the
likelihood that they will not have continued or recur-
rent neuropathic pain after surgery is quite small.
Our recovery data suggest that the recurrence rate
increased over time, but the likelihood of neuropathic
pain recurring was greatest in the first 6 months after
surgery. These results vary tremendously from previ-
ously reported success rates in the treatment of neuro-
pathic pain via IAN and LN microsurgery. Gregg12
reported 60% or more reductions in pain levels after
microsurgery of the IAN and LN in 84 patients,
49.2% at 3 to 6 months and 41.1% at 1 to 3 years. LaB-
anc and Gregg18 reported favorable pain reduction in
67.5% of patients to surgical exploration and repair.
Pogrel and Kaban19 reported elimination of dysesthe-
sia following microsurgical repair of the IAN. On the
contrary, Robinson et al20 reported no significant dif-
ference in the number of patients who reported neuro-
pathic pain before microsurgery in 53 LN repairs
compared with after surgery. Hillerup and Stoltze21 re-
ported that of 14 patients who had neuropathic pain
before microsurgery of the LN (from a total of 74 pa-
tients), the recurrence of neuropathic pain symptoms
was unchanged and unaffected by the repair.
Because the presence of neuropathic pain before
surgery was the most important risk factor for
2426
postoperative neuropathic pain after surgery, we
looked at secondary end points between the cohort
groups before and after surgery to determine whether
any significant differences existed that might predict
the onset of neuropathic pain in a nerve injury popu-
lation of patients requiring microneurosurgery. In
this small group of patients, age, trigeminal nerve
type, and class of nerve injury were significantly
different from those in patients without neuropathic
pain before surgery. Patients who elected to undergo
microsurgery of their trigeminal nerve and who had
neuropathic pain before surgery were older and had
IAN injuries of class 3 Sunderland variation compared
with the cohort of patients who did not have neuro-
pathic pain before surgery. There was no effect by
gender, etiology of injury, or duration of injury to
repair. However, it should be noted that duration of
the time from injury to surgical repair was nearly sig-
nificant and may be a significant variable in a larger
cohort of patients. Marchiori et al9 found that gender,
older age, surgical site infection or hematoma (in or-
thognathic surgery), and depression were risk factors
for developing neuropathic pain after orthognathic
surgery. Bagheri et al17 reported that compared with
patients with numbness only of the IAN who under- between studies. The reader is cautioned to distin-
went microsurgery, the patients who had pain as a
component of their chief reason for seeking surgery
were more likely to be women, were operated on later
(greater duration from injury to repair), and were
more likely to have compression injuries (equivalent
to Sunderland class 3) or to have lateral or exophytic
neuromas. Except for gender, our findings concur
with these authors finding that age is a predominant
factor for the presence of neuropathic pain or the
continuation of neuropathic pain, as well as class of
injury and duration of injury. We did not examine sur-
gery site complications or Axis II pathology (depres-
sion) in our study.
The results support those of Bagheri et al,17,22
Hillerup and Stoltze,21 and Robinson et al20 that sur-
gery has little effect on pain. Our findings concur
with those of Bagheri et al17 that, at least for the IAN,
the most common procedure was neurolysis rather
than neurorrhaphy, with or without auto- or allograft.
Together, these findings point out that at the current
time, there is no specific neuropathic-relieving mi-
croneurosurgical option. This means that for micro-
neurosurgeons, the options for treatment are based
on the class of injury found at the time of surgery, not
on the presence of neuropathic pain or adjusted to
the sole purpose of the neuropathic pain symptoms.
Future studies must be done to direct attention to
neuropathic pain in this difficult cohort of patients.
Our study suffered from an inherent bias for patients
who were seeking surgery for their neurosensory
symptoms, including neuropathic pain. Thus, we
NEUROPATHIC PAIN AFTER TRIGEMINAL NERVE REPAIR
preselected a small number of patients who had neuro-
pathic pain of different intensities, causations, and so
on, from a larger group of patients who did not seek
surgery or whose neuropathic pain resolved over
time, as shown by Marchiori et al.9 In their study, pa-
tients who developed neuropathic pain after mandib-
ular orthognathic surgery reported that their pain
resolved with nonsurgical modalities for a median
duration of 52 days (range, 22 to 72 days). In our study,
the mean time from injury to surgery in the neuro-
pathic pain cohort was 462 days, but ranged from 30
to 2,490 days. Thus, it is likely that our study excluded
those patients who would have spontaneously
resolved with nonsurgical treatment or by time alone.
Also, the primary end point in our study was the pres-
ence or absence of neuropathic pain. In our study, we
did not distinguish pain intensity levels before or after
surgery over time in the data analysis. Gregg12 and LaB-
anc and Gregg18 reported pain reduction compared
with presurgical pain levels as favorable outcomes in
nearly two-thirds of the patients with neuropathic
pain before surgery. We distinguished total relief of
pain as a dependent variable in our analysis, which
would account for the lowered success rate reported
guish the differences, because reduction of pain
should be considered a clinically important and posi-
tive outcome of any treatment for pain over time, espe-
cially chronic debilitating pain conditions such as
neuropathic trigeminal pain. On the other hand, we
and our patients should be aware that on the basis of
this analysis, permanent pain relief is uncommon
and approaches only 9% following surgery.
In conclusion, this study showed that trigeminal
nerve microsurgery of the IAN and LN is not a risk fac-
tor for postoperative trigeminal neuropathic pain in
the absence of neuropathic pain before surgery. The
presence of neuropathic pain prior to trigeminal nerve
microsurgery is the major risk factor for the continua-
tion or recurrence of neuropathic pain following
nerve surgery. These patients are likely to be older,
to have IAN injuries, and to have Sunderland class 3
injuries and likely will have had a long duration of
time from injury to repair.
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