Post-Traumatic Injuries of the Trigeminal

and Facial Nerve

Alaaaldin M. Radwan, DDS, MD a,*, Charles Boxx, DDS a, John Zuniga, DMD, MS, PhD b

KEYWORDS
 Facial nerve injury  Trigeminal nerve injury  Post-traumatic injury  Anatomy

KEY POINTS
 An adequate understanding of the pertinent anatomy of the head and neck is necessary to successfully diagnose and treat
injuries of the facial and trigeminal nerves.
 There is a constantly evolving and improving collection of diagnostic tools that one must be familiar with and use to
advantage to provide the best care for patients.
 There is a wide range of therapeutic modalities when it comes to managing nerve injuries, anywhere from simple obser-
vation to complex grafting. No two nerve injuries are the same; it is the responsibility of clinicians to be familiar with the
treatment options and present them to patients.

Introduction
Despite the wide range of scope of practice of oral and
maxillofacial surgeons, one pertinent aspect of our training
that we must stay up to date on is an adequate knowledge of
the pertinent anatomy of the head and neck, and management
of these vital structures, especially in the setting of trauma.
This article provides a better understanding of the anatomy of
the facial and trigeminal (specifically mandibular branch)
nerves, and a method of diagnosis and management in the
setting of trauma.1
Anatomy
There are three main components of the pertinent neural
anatomy, composed of multiple layers that surround the cen-
tral axonal fibers (endoneurium, perineurium, and epineu-
rium), a knowledge of which is crucial in understanding the
varying degrees of inferior alveolar nerve (IAN) and facial nerve
injury.1
injury to the IAN are the Seddon and Sunderland systems. The
Seddon system, first described in 1943, consists of neurapraxia,
axonotmesis, and neurotmesis (Table 1). The Sunderland sys-
tem (1951) includes first through fifth degrees of peripheral
nerve injury, which are based on anatomic continuity defects
(Fig. 1).1
Facial nerve
When describing injury to the facial nerve, the Sunderland
classification and the House-Brackmann system are used. The
Sunderland system describes nerve injury by degree of injury
(total of 5 ), starting with neuropraxia and ending with neu-
rotmesis as the most severe. The House-Brackmann system
grades facial nerve injury on a scale of one through six based
on functional limitation, with one being normal symmetric
function and six being total facial paralysis (see Table 1 for
details).1,2
Diagnostic algorithms, tools

Nerve injury classification Trigeminal nerve

Inferior alveolar nerve
Despite multiple peripheral injury classification systems in
existence, the most widely used and accepted in describing
Disclosure Statement: The authors have nothing to disclose.
a
Oral and Maxillofacial Surgery, Virginia Commonwealth University,
Richmond, VA 23298, USA
b
Oral and Maxillofacial Surgery, University of Texas Southwestern,
Dallas, TX 75235, USA
* Corresponding author. VCU Medical Center and MCV Hospitals, 520
North 11th Street, PO Box 980566, Richmond, VA 23298-0566, USA.
E-mail address: dr.aradwan@gmail.com
Although there have been significant advances in the objective
assessment of peripheral nerve injury (including MRI, discussed
later), they are not required to conduct a reproducible and
accurate clinical examination.
The first step involves obtaining a detailed history from the
patient in their own words, and whether they describe symp-
toms of paraesthesia, dysesthesia, anesthesia, or a combina-
tion. Because sometimes neuropathic symptoms are difficult to
describe for some patients, it is helpful to have the patient
complete a preprinted questionnaire that breaks down in
detail exactly what the patient has been experiencing. It is
important to differentiate frequency, spontaneity, and dura-
tion, because these can all be helpful diagnostic factors in

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128
Table 1 House-Brackmann facial nerve classification
Grade Description Characteristics
I Normal Normal facial function in all areas
II Mild Slight weakness noticeable on close
dysfunction inspection, may have slight synkinesis
III Moderate Obvious, but not disfiguring, difference
dysfunction between 2 sides, noticeable but not
severe synkinesis, contracture, or
hemifacial spasm, complete eye
closure with effort
IV Moderately Obvious weakness or disfiguring
severe asymmetry; normal symmetry and
dysfunction tone at rest; incomplete eye closure
V Severe Only barely perceptible motion,
dysfunction asymmetry at rest
VI Total paralysis No movement
determining the time frame and severity of the nerve injury.
Often there is an obvious cause for the patient’s symptoms (eg,
trauma, iatrogenic); however, practitioners must be wary of
spontaneous symptoms because these are associated with
some form of pathology and/or malignancy. The time/onset of
injury is also critical because the success of nerve repair is
directly proportional to the time from injury (after 3 months
the chances of full recovery begin to decrease because of
Wallerian degeneration).3
There are many instruments/methods described in the
literature that are used for neurosensory testing. Some
commonly used methods involve a caliper, vitalometer (pulp
tester), algometer, thermal disks, Semmes-Weinstein mono-
filaments, or as simple as a cotton swab. The examination
should start with a typical head and neck examination, ruling
out any evidence of trauma (acute vs chronic), evidence of
previous surgery, or possible underlying pathology. Palpation of
the regions of typical nerve anatomy (below the infraorbital
rim, retromolar pad, and mental foramen) may illicit an
atypical response in the setting of nerve injury (pain, tingling,
itching). A painful response, or a nonpainful response that ra-
diates, is known as Tinel sign (an indication of nerve regener-
ation or possible neuroma).3
Fig. 1 (A) SEM image: epineurium (red circle), perineurium (yellow circle), and endoneurium (green circle). (B) Seddon and Sunderland
classification. ROS, Return of sensation; SEM, Scanning electron microscopy. ([A] Image courtesy of Axogen, Alacua, FL.)
Radwan et al.
Table 2 Level A testing distances
Scheme of discrimination sensation
Ending of tongue 1.1 mm
Tips of tongue 2.2 mm
Red part of the lips 4.5 mm
Back of tongue 9.0 mm
Skin of cheek 11.2 mm
Back of neck 67.5 mm
When completing neurosensory testing, it is recommended
that the evaluation be completed in a quiet room with the
patient in a seated position. Have the patient close their eyes,
with their lips slightly apart so that any stimulus/vibration is
not transferred to the opposite side. If simply wanting to assess
for altered sensation, the marching needle technique is
completed using a 27-gauge needle to contact the skin lightly
until the patient indicates sensation by raising their hand. This
technique is used to map areas of normal sensation, hypo-
esthesia, or complete anesthesia.3
The three main levels of neurosensory testing include levels
A, B, C, which is used to assess the degree of impairment. Level
A (testing myelinated A-alpha sensory fibers) is tested using
two-point discrimination, directional (brush stroke), or stim-
ulus localization. For two-point discrimination (using either a
caliper or Boley gauge), start by contacting the skin in the
region of interest with the caliper tips together (zero dis-
tance). Gradually increase the distance by 1 mm, until the
patient is able to detect two separate points. Normal values
vary based on the region (Table 2). Stimulus localization is
done by contacting the skin with the wooden end of a cotton
tip applicator, then asking the patient to touch the exact same
location with a separate applicator. Normal response is within
1 to 3 mm of the initial point of contact. Two-directional
response (brush stroke) is completed using a camel hair brush,
Semmes-Weinstein fibers, or cotton wisp to lightly contact the
skin in a series of directional movements, then asking the pa-
tient to verify the direction. If a patient passes level A testing
this correlates with a Sunderland first-degree injury, if a pa-
tient fails level A but passes level B this correlates with a
Post-Traumatic Injuries
Sunderland second-degree injury, if a patient fails levels A and
B that leaves level C. Level C testing includes a positive normal
response, abnormal response, and no response correlating with
Sunderland third, fourth, and fifth degree, respectively.
For all of these tests, start with the normal side first to
establish a control. Level B (testing myelinated A-beta sensory
fibers) measures static touch, and is completed using the
wooden end of a cotton tip applicator and lightly contact the
patient’s skin without indentation. On perception of the con-
tact, the patient is to raise their hand. Another technique in-
volves using either von Frey or Semmes-Weinstein fibers, which
are monofilaments that are labeled according to the amount of
force in grams of applied pressure required for them to bend.
Both the normal side and site of interest are tested using the
fibers, looking to rule out any significant difference between
the two required levels of force needed for touch perception.
Lastly, level C (testing poorly myelinate A-delta of unmyelin-
ated C fibers) is evaluated using a 27-gauge needle to test for
detection of painful stimuli. Have the patient raise their hand
once they are able to feel the needle as you lightly contact the
skin/region of interest (without indentation). It is under anal-
ysis of level C where some practitioners may also use algo-
meters, thermal disks, and vitalometers to further clarify
magnitude of stimulus required for sensation.3
Imaging
When assessing for possible nerve injury, at minimum some
form of two-dimensional imaging should be completed (pan-
orex, PAs) to look for obvious cause for patient’s symptoms (eg,
retained root tip, poorly placed dental implant, pathology). If
available, it is recommended to also obtain computed tomog-
raphy (CT; either cone beam or medical grade), to further
assess the pertinent anatomy. Ideally magnetic resonance
neurography is used, which is a modification of MRI that uses
specific water properties of neural tissue to optimize visuali-
zation of the nerve itself (rather than adjacent soft tissue).
Because the source of the image is the nerve itself, diagnoses,
such as compression, irritation, or nerve edema, are made
using magnetic resonance neurography. Other resources
include magnetic source imaging, which measures electric
brain activity using magnetic fields to evaluate nerve response;
high-resolution MRI; and ultrasound.4
Facial nerve
Assessment of nerve injury
Similar to the initial evaluation of an IAN injury, the first step of
facial nerve injury evaluation involves an extensive history and
physical. This includes not only any pertinent medical history
(CN VII palsy is seen in multiple medical conditions including
multiple sclerosis, myasthenia gravis, opercular syndrome, and
many others), but also surgical history (recent mastoid or pa-
rotid), or even recent travel (scuba diving) or trauma (skull
base fracture, penetrating injury).
Once an adequate history of present illness has been ob-
tained, there are multiple topognostic studies available (can
help determine the site of injury). These include salivary flow
test, stapedial reflex, lacrimal flow (Schirmer), and taste
sensation (specifically anterior two-thirds of the tongue). The
next set of diagnostic tools includes electrodiagnostic testing,
orthodromic conduction (nerve stimulated proximally and
distal muscle response recorded), and antidromic conduction
129
(nerve stimulated in a retrograde manner). These tests can be
used as facial nerve recovery prognostic indicators. Electro-
myography is used to detect subclinical early evidence of
neural regeneration by measuring electrical response during
needle insertion at rest and elective movements. Nerve con-
duction time uses electromyography technology to stimulate
the facial nerve at the stylomastoid foramen and then record
the latency between the stimulus and nerve response at a
specific muscle group (eg, frontalis, mentalis). Nerve excit-
ability test compares the amount of electrical current needed
to illicit a response when stimulating the nerve at the stylo-
mastoid foramen (using the unaffected side as a control).
Maximal stimulation testing involves similar technique as nerve
excitability test; however, it uses maximal stimulation rather
than minimal when stimulating the nerve. Magnetic stimulation
works by using magnetic fields to stimulate the motor cortex at
the nerve’s root entry zone, the response of which is measured
by surface electrodes on specific muscle groups. Electro-
neurography (ENoG), which has been shown to be the most
accurate prognostic indicator, uses bipolar electrodes to
deliver an electrical stimulus at the stylomastoid foramen. The
degree of response is compared between the normal and
injured side, a decrease in response amplitude correlating with
axonal injury.1,2
Imaging
Similar to radiologic assessment of the IAN, CT and MRI are the
modalities of choice for evaluation of the facial nerve. High-
resolution CT is most effective for intratemporal evaluation of
the nerve, which is important because 90% of facial nerve
disorders originate within the temporal bone. Gadolinium
(intravenous administration)-enhanced MRIs are frequently
used for their soft tissue detail, which typically allows easier
detection of pathology, such as neuromas.4
Nonsurgical management of nerve injury
Trigeminal nerve
Postinjury management varies significantly based on the mech-
anism of injury. A known transection, for example, would
best be treated with immediate exploration and repair. How-
ever, for many other forms of injury (implant compression,
endodontic material, displaced root, local anesthetic), there
are multiple nonsurgical modalities that can initially be applied.
Although nonsteroidal anti-inflammatory drugs and high-
dose corticosteroids are thought to reduce inflammation and in
theory minimize nerve injury, there is no profound evidence
that they have any significant effect on duration/extent of IAN
injury. Much of the management of IAN injury is dependent on
the time frame and mechanism. Table 3 depicts recommended
treatment of most common etiologies, based on their timing.
Therapeutic treatment involves either psychological, pharma-
cologic, or a combination of both. Pharmacologic agents
include topical agents for analgesia, and systemic agents.
Frequently used systemic agents are either low-dose antide-
pressants (nortriptyline, amitriptyline) or antiepileptic agents
(gabapentin, pregabalin). The two main treatment groups for
psychological management are acceptance and commitment
therapy and cognitive behavioral therapy. Both of these
methods are not used to decrease patients’ perception of pain,
more to aid with coping of their symptoms.5
130
Table 3 Management of iatrogenic IAN injury
Iatrogenic IAN injury management
Observed or highly suspected Immediate surgical
transection exploration, repair
Retained roots following Immediate surgical exploration
extraction
Endosseous implant If <30 h remove implant, >30 h
treat patient therapeutically
Endodontic material <30 h remove tooth/overfill,
>30 h treat therapeutically
Third molar surgeryerelated <3 mo consider exploration,
IAN injury (pain, disability) >6 mo treat therapeutically
Adapted from Renton T, Yilmaz Z. Managing iatrogenic trigeminal
nerve injury: a case series and review of the literature. Int J Oral
Maxillofac Surg 2012;41(5):636; with permission.
Facial nerve
Facial nerve injury management ranges depending on the
mechanism, cause, timing, and presentation of symptoms. As
with IAN if nerve transection is known/visualized, the best
management is immediate exploration and repair. However, in
cases of delayed onset of paralysis, incomplete paralysis, blunt
trauma, or injury medial to the lateral canthus (line of arbor-
ization), medical management and/or observation may be
appropriate. In most of these cases, however, if acceptable
recovery has not occurred by 6 months postinjury then surgical
intervention is often indicated to prevent further atrophy of
the facial musculature.
In cases of incomplete paralysis or blunt trauma, it is rec-
ommended to use a course of steroids to minimize edema. For
injuries medial to the line of arborization, there is such a high
degree of cross-innervation that spontaneous recovery typi-
cally occurs. Incomplete paralysis or delayed onset typically
means that the anatomic structure of the nerve is grossly intact
(however, unknown degree of injury). One method of man-
agement in these cases describes serial ENoG testing from
postinjury Day 3 through 14, with possible surgical decom-
pression if greater than 95% loss of axonal function. Facial
nerve injury from traumatic birth (typically involves forceps)
has been found to typically resolve spontaneously with obser-
vation only (>90%).2,5
Surgical management
Trigeminal nerve
Indications for surgical IAN repair include known/observed
transection, lack of clinical improvement of numbness/sensa-
tion for a period of greater than 3 months, foreign body
(endodontic material, dental implant), or dysesthesia second-
ary to neuroma formation. Contraindications or cases with
poor surgical prognosis include central nervous system symp-
toms, passage of greater than 1 year since the time of injury,
nerve injury related to local anesthesia, medically compro-
mised patients, or patients with evidence of neurosensory
improvement.6,7
Multiple surgical approaches exist to access the IAN
(including intraoral and extraoral), a decision that varies based
Radwan et al.
on surgeon experience/preference, mouth opening, location of
injury, and patient preference. The extraoral approach tends
to provide improved access/visualization; however, it comes
with the disadvantage of an external scar in the neck and
possible facial nerve injury. Intraorally is typically more
commonly used for IAN repair for cosmetic reasons; however, it
provides some degree of difficulty to the operating surgeon
because of microscope positioning (must often place the mi-
croscope at oblique angles because of visualization, unlike
extraoral where the microscope is placed at ideal 90 angles
from the area of interest). In the future, three-dimensional
microscopy (ORBEYE, Olympus America, Center Valley, PA) and
robotic navigation microscopy (SYNAPTIVE, Synaptive Medical,
Toronto, Canada) may solve problems of angulation while
preserving and/or enhancing magnified visualization using
surgical microscopy. The lingual nerve is accessed via a tradi-
tional third molar incision or Bilateral Sagittal Split Osteotomy-
style incision with lingual retraction and dissection of the
lingual nerve. Care must be taken to avoid injury to chorda
tympani if encountered.6,7
An alternative to the microscope is the use of surgical loupe
magnification (typically 4 or 5), again depending on surgeon
experience/preference. Once access to the mandible has been
achieved, the decision of method of corticotomy/direct nerve
access must be made. One of the most commonly used ap-
proaches involves a lateral block decortication using a combi-
nation of ultrasonic or reciprocating saws and chisels to
fracture off a sufficient block of cortical bone to expose the
area of injured nerve (taking care not to puncture too far
medially). This block is temporarily stored in saline during the
repair, and then secured back into its original location using
some sort of screw fixation at the end of the case. A traditional
sagittal split osteotomy can also be used to access the IAN;
however, this poses the risk of some form of malunion/
malocclusion at the end of the case.6,7
Another approach involves drilling directly through the
lateral aspect of the mandible to the region of interest with
the aid/use of cone-beam CT imaging; however, this typically
provides limited exposure. For IAN injuries that are immedi-
ately adjacent to the mental foramen, a “donut technique” is
completed whereby approximately 3 mm of cortical bone is
removed circumferentially around the mental foramen,
allowing access to the nerve in this region (Fig. 2). Another
described technique involves accessing the nerve through an
existing extraction site; however, this provides limited visual-
ization/access.6,7
Once access to the nerve has been achieved, the degree/type
of injury must be established (crush injury, transection [com-
plete or partial], presence of foreign body). The main categories
of nerve repair include primary repair, external neurolysis
(where the nerve is released from its tissue bed and all com-
pressions/restrictions removed to allow normal conduction),
internal neurolysis (involves opening of the epineurium to
evaluate/repair because of concern for fibrosis or compression),
or neuroma excision (with subsequent reanastamosis).
For clean transection injuries, primary end-to-end anasto-
mosis has been shown to work well when completed within 6 to
8 weeks of the initial injury. Typically 8e0 or 9e0 nylon or
prolene suture are used, with at least three (sometimes four)
sutures placed through epineurium only at the 3-, 6-, 9-, and
12-o’clock positions. Tension-less approximation at the cut
nerve endings is paramount to successful regenerating nerve
fibers from proximal to distal ends. The connector-assisted
repair is a recently described method that avoids epineurial
Post-Traumatic Injuries 131

Fig. 2 Postintraoral lateral corticotomy combined with donut technique to obtain adequate access to IAN.

suturing at the cut margins so that tension-less repairs are
accomplished. The method takes advantage of nerve connec-
tors (ie, AXOGUARD PROTECTOR, 4  10 mm, AxoGen, Alachua,
FL) that allow proximal and distal nerve endings, or allograft/
autograft endings to be aligned within the connector passively
by suturing the mesoneurium of the nerves to the connector
and approximating the cut ends within the connector when the
sutures are tied (Fig. 3).6,7
For partial transections, it is often recommended to excise
the proximal/distal stumps until healthy nerve tissue is noted,
at which time either primary anastomosis is completed if
adequate mobility or a graft/conduit is placed (Fig. 4). If a
crush injury or neuroma is identified, attempts to mobilize the
nerve as much as possible should be completed so that primary
anastomosis is obtained after resection of the injured
segment. If unable to obtain tension-free repair, it is better to
use a graft and/or conduit. For implant-related injuries, it
must be determined whether it is compression related
(impingement from the implant itself) or laceration from the
osteotomy drills. Excision of the compressed region with pri-
mary reanastamosis is typically achievable; however, injury
from a drill is often too extensive and requires grafting/
conduit after excision of the injured nerve structure. When
IAN injury is related to root canal sealant material, the

Fig. 3 (A) Connector-assisted gap repair. (B) Direct repair with suture versus connector-assisted repair with AxoGuard. (C) Direct versus
connector-assisted repair. It is recommended to attach the connector to proximal stump first, followed by the distal end. (D) Avance nerve
grafts and connectors size and dimension. * Epineurium and connective tissue have been removed for illustration purposes. ([A] Courtesy
of Walid Radwan, MD, MS (West Virginia University, Morgantown, WV); [BeD] Image courtesy of Axogen, Alacua, FL.)
132
Fig. 4 A conduit being used to repair a partially excised IAN
during ORN resection. ORN, osteoradionecrosis.
epineurium must be opened longitudinally and the fascicles
copiously irrigated to remove all sealant. The adjacent canal
must also be copiously irrigated. If completed within 48 to
72 hours of the initial injury, this method has been shown to
have a favorable prognosis.6,7
Often either because of avulsion injury or size of required
nerve resection, primary tension-free anastomosis is unob-
tainable and a graft and/or conduit are needed. Autogenous
grafts have previously been the gold standard for recon-
struction of nerve continuity defects; however, improve-
ments in allografts (eg, AVANCE, Axogen) have been shown
to provide similar results with the avoidance of a second
surgical donor site. The greater auricular, sural, and medial
antebrachial cutaneous nerves have all been described as
options for reconstruction of the IAN; however, the sural is
most ideal to its similar diameter to the IAN and minimal
donor site morbidity. Autogenous vein grafts (eg, facial or
saphenous vein) have also been described to serve as a
conduit for two proximal/distal nerve ends to regenerate new
nerve tissue. Allografts and xenografts (eg, Axogen porcine
extracellular matrix nerve wrap) are significantly increasing
in popularity/use because of findings of similar results as
autografts without the need for a second surgical/donor
site.6,7
Facial nerve
Similar to management of IAN injury, the treatment of facial
nerve trauma varies significantly depending on the mecha-
nism, cause, and time passed since the suspected injury. Not
all facial nerve injuries require surgical intervention. For
example, Bell palsy typically responds well to steroids and
antivirals alone. Blunt trauma often resolves with the com-
bination of high-dose steroids and time (allowing regenera-
tion); however, the use of ENoG has been described to
determine prognosis and aid in operative planning (if >90%
degeneration at 72 hours postinjury, recommend exploration).
However, for the purpose of this article, the authors discuss
management of acute facial nerve injury and chronic nerve
damage.2,8
For known transection lateral to the lateral canthus (in-
juries distal to this point are difficult to repair because of
nerve size, and also tend to self-recover well because of rich
cross-innervation of the area), it is recommended for imme-
diate exploration and primary reanastamosis if possible.
Radwan et al.
Beyond 3 days postinjury, often it is difficult to stimulate the
distal stumps, which makes locating them more challenging.
Ideally, tension-free primary repair is completed using three
or four 8e0 or 9e0 nylon sutures through the epineurium.
However, if tension-free closure is not possible, it is recom-
mended to use some form of autograft to reconstruct the
defect. Branches from the cervical plexus are most commonly
used; however, other options include greater auricular, sural,
and medial/lateral antebrachial cutaneous nerves. If grafting
is completed, nerve regeneration occurs at approximately
1 mm per day. If attempting a delayed injury, after about
2 weeks scar tissue and collagen replace the myelin and axons
at the severed ends and require excision before direct
repair.2,8
Often in the setting of trauma patients can incur
compression injury to the intratemporal aspect of the facial
nerve caused by neural edema. Timing of decompression is
debated; advocates for early decompression state that prog-
nosis worsens 12 to 14 days after injuries, opponents argue
favorable results with decompression as far as 3 months
out.2,8
In cases of significant trauma or pathology/resections
where the proximal aspect of the facial nerve is no longer
available, the surgeon has multiple options for repairing the
distal aspect and restoring facial animation. If possible, one
of the most popular methods involves using a combination of
nerve grafts (often sural) and the contralateral facial nerve
to innervate the affected facial muscles. Fascicular repair is
used and the nerve graft required is typically 6 to 8 cm. One
disadvantage of this method is the length of time until rein-
nervation occurs because of the length of the graft, and also
because typically only the buccal branch of the unaffected
side is used as a source of innervation, the muscle response
on the affected side is not as robust as in other techniques. If
the contralateral facial nerve is unavailable, a nerve cross-
over method may be applied. Most commonly used is the
hypoglossal nerve (however, also described are glossophar-
yngeal, spinal accessory, and phrenic); this technique in-
volves direct anastomosis of the hypoglossal nerve to distal
facial nerve.2,8
In cases of prolonged denervation (injury was >1e2 years
ago), such techniques as muscle transfer (either regional or
free functional) or static methods (gold weights, suspension
slings, selective neurectomies), are attempted to recreate
some degree of facial reanimation.2,8
Postoperative management
It is the authors’ preference that the patient be placed on
postoperative vitamin B complex to reduce incidence of
neuropathic pain; dexamethasone, 4 to 8 mg three times a day
for 1 week; and ibuprofen, 800 mg three times a day. Cognitive
neurosensory re-education is shown to be beneficial in
regaining sensory recovery. Frequent follow-up visits doc-
umenting recovery should be followed until acceptable re-
covery is achieved and accepted by the patient.
Acknowledgments
The authors credit Walid Radwan, MD, MS (Chief Resident,
Department of Neurosurgery, West Virginia University, Mor-
gantown, WV) as scientific artist for this article.
Post-Traumatic Injuries
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