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Expert Opinion
Section Editor: Steven Mandel, MD
Iatrogenic Hypoglossal
Nerve Palsy
Mark A. Fritz, MD, Bryan J. Kang, MD, Timothy P. Fox, MD, Nicky Bhatia, MD,
and Steven M. Mandel, MD
T
he hypoglossal nerve or twelfth cranial nerve
(CNXII) innervates all of the intrinsic and extrinsic muscles of the ipsilateral tongue, except
palatoglossus. Therefore, injuries to this nerve
have the potential to affect a patient’s articulation and
swallow substantially. The nerve can be transected during trauma or surgery but there are also several reports in
the otolaryngology, anesthesia, and neurology literature
concerning iatrogenic hypoglossal nerve palsy without
direct nerve injury following tonsillectomy,1,2 laryngoscopy,3 transoral intubation,4 use of the laryngeal mask
airway (LMA)5 tooth extraction,6 or poor body position.7
A full listing of cases is listed in Table 1.
Case Report
A 32-year-old man with a past medical history of diastolic
congestive heart failure, morbid obesity (BMI 66), obesity
hypoventilation syndrome and obstructive sleep apnea,
hypertension, and diabetes mellitus type 2 presented with
respiratory distress secondary to an acute CHF exacerbation. During his hospital stay, the patient was found to be
unresponsive and a secure airway was placed emergently.
Multiple intubation attempts failed, due to the patient’s
body habitus and extremely short neck. Following intubation attempts, blood was found to be in the pharynx, likely
secondary to trauma. Finally, an LMA #5 was secured with
cuff inflated with 20mL of air, however position was noted
to be poor, and the patient was subsequently taken to the
OR for an emergent tracheotomy. Anesthesia premedicated
the patient with Versed 5mg and Rocuronium 50mg x2.
Anesthesia was maintained with oxygen and MAC (conscious sedation). A size 8 endotracheal tube was used to
fashion an extra long tracheotomy tube, due to the large
amount of subcutaneous fat on the patient’s neck. The duration of the procedure was 133 minutes. After the procedure,
the patient was transferred to the ICU with a Shiley #8 tracheotomy tube.
The patient was maintained with the tracheotomy tube
for the next 16 days. Prior to removal of the tracheotomy
tube, he received a consultation from speech language
pathology. The therapist noted that the patient was
unable to protrude, elevate, or lateralize his tongue. The
patient was able to trigger a swallow with a small piece
of ice, however the swallow effort was noted to be weak.
Speech was also noted to be dysarthric, due to inability to
move his tongue. The patient tolerated a Passy-Muir valve
and was able to produce a weak voice.
Neurology was consulted and determined that the
patient had absent tongue movement; the tongue was
flaccid. There was a question of mild atrophy; no fasciculations were observed. Sensation of the tongue to light pin
and touch stimulus was intact. The remainder of the cranial nerves as well as general neurological examination was
unremarkable. Needle EMG testing of the tongue revealed
grade 3+ fibrillations with positive sharp waves of the right
and left hyoglossus. There was no acute denervation seen
at the cricothyroid and thyroarytenoid muscles. These
findings confirmed a bilateral hypoglossal nerve palsy.
Clinically, the patient fully recovered function within three
months with no residual weakness and essentially normal
speech and swallow function.
Pathophysiology
The hypoglossal nerve originates from the hypoglossal
nuclei in the medulla at the inferior aspect of the fourth
ventricle.8,9 It then exits the skull base from the hypoglossal canal in close association with CN IX, X, and XI and
medial to the internal jugular vein and lateral to the internal carotid artery.10 It then descends vertically between
the vessels and anterior to the vagus until the angle of the
mandible. The nerve then crosses the lingual artery a little
above the greater cornu of the hyoid. It then curves anteriorly and inclines upwards on hyoglossus, passing deep
to the stylohyoid, tendon of the digastric, submandibular
january/february 2014 Practical Neurology 13
Expert Opinion
Table 1 - Literature review of iatrogenic hypoglossal nerve palsies with relation to their site
of surgery, length of surgery, side of injury, and recovery.
1st Author
YEAR
Age
Type of Surgery
Lopes19
2009
64
Breast reconstruction
36
Breast reduction, abdominoplasty
Hong22
2008
37
Laparoscopic Cholecystectomy
Una23
2009
28
Mediastinotomy for tumor
Hung20
2009
57
Rotator Cuff Repair
Yelken24
2008
22
Septoplasty
Tesei25
2006
30
Rhinoplasty
Sharp1
2002
25
Tonsillectomy
Stewart26
2002
54
Knee Arthroscopy
Nalladaru27
2012
49
Coronary artery bypass
Rubio-Nazabal4
2002
63
Repair of abdominal aortic aneurysm
Boisseau28
2002
42
Shoulder Surgery
Yavuzer16
2004
42
Septorhinoplasty
Bruce29
2004
21
Correction of ear deformity
Cinar30
2005
20
Open rhinoplasty
Nagai5
1994
62
Shoulder Joint Replacement’
King14
1994
55
Removal of Rush Pins
Evers13
1999
56
Transsphenoidal hypophysectomy
Streppel31
1997
35
Sinus Surgery
gland, lingual nerve, and the posterior border of the mylohyoid. It finally passes onto the lateral aspect of genioglossus where it continues as far as the tip of the tongue. A
stylized illustration of this anatomy is presented in Figure
1 depicting where the tip of the laryngoscope blade can
exert maximal force on the hypoglossal nerve as it enters
the base of tongue laterally.
Hypoglossal nerve injuries occurring from intubation
are often neuropraxic in nature, though they may also be
due to axonotmesis. Neuropraxic injuries are mild and may
result from ischemia or mechanical compression; these
injuries should resolve within three months. With axonotmesis, the axon is irreversibly damaged as a result of crush
injuries or nerve stretch injuries, necessitating a slower
recovery due to distal axon sprouting.11 Winfree and Kline
wrote about peripheral nerve injury associated with intraoperative positioning.12 They noted that severe stretching
may tear the intraneural connective tissue, resulting in
intraneural hemorrhage and possible necrosis. Severe compression may elevate the intraneural venous pressures and
14 Practical Neurology january/february 2014
Surgery (min) Unilateral/ Recovery Time to
Bilateral
Recovery
(months)
330
Uni
Full
6
270
Uni
Full
6
60
Uni
Full
3
NA
Bi
Full
4
108
Uni
Full
0.75
120
Uni
Full
2
100
Uni
Full
4
45
Uni
Partial
15
45
Bi
Full
1.5
1080
Uni
Full
2.5
240
Bi
Full
3
130
Uni
Full
6
65
Uni
Partial
6
75
Uni
Full
5
180
Bi
Full
1
180
Uni
Full
0.25
25
Uni
Full
0.25
180
Uni
Full
4
85
Uni
Full
1
produce endoneurial edema, resulting in impaired axoplasmic flow resulting in nerve dysfunction for hours to weeks.
Continued compression may lead to Schwann cell damage and demyelination or even axonal loss and Wallerian
degeneration. Michel and Brusis published a cadaver study
showing that the hypoglossal nerve was stretched by up
to 1.3cm due to insertion of a laryngoscope on the lateral
tongue base.2 They additionally found more nerve distension with more extension of the neck, more lateral placement of the laryngoscope on the tongue, and more force
placed on the tip of the blade.
Multiple different etiologies have been proposed for the
development of hypoglossal nerve palsy associated with
anesthesia. These etiologies include forceful laryngoscopy,
hyperextension of the head, cricoid pressure, tight throat
packs in the oropharynx, overinflation of the LMA, and the
effect of nitrous oxide on the LMA cuff.5,13,14 Lumb, et al.
published a study that found a consistent, linear increase
in LMA cuff pressure during anesthesia with nitrous oxide
due to its ability to diffuse much more rapidly through the
Expert Opinion
tion, but due to the crossed innervation
from corticobulbar fibers the effects
become minimal with time. Bilateral
upper motor neuron involvement can
occur, again without evidence of atrophy or fasciculations. Swallowing can be
inhibited due to inability to manipulate
food for mastication as well as due to
trouble initiating the oral phase of swallowing. Electromyogram (EMG) will
show a spastic paralysis of the tongue
musculature that will distinguish it from
lower lesions. Nuclear lesions will cause a
paresis and atrophy of the tongue, ipsilateral to the site of the lesion. Because
of the close proximity of hypoglossal
nuclei bilateral lesions can occur. Patients
Figure 1 - Illustration of the hypoglossal nerve course in relation to the tongue base
will usually only have transient dysarand a laryngoscope used for airway visualization. The tip of the laryngoscope shows
thria as well as trouble initiating swalwhere pressure can be exerted on the hypoglossal nerve when placed laterally
lowing. Fasciculations can be seen later
(Timothy P. Fox, MD).
in the course. Nuclear lesions are best
differentiated from peripheral lesions
cuff walls.15 This pressure increase in some patients was as
due to presence of other brain stem findings relating to
high as 50 percent more after a 30 minute procedure. No
involvement of motor and sensory long-tracts, resulting for
further difference in etiology has been postulated in those
example in contralateral hemiplegia and/or loss of vibrapatients that have developed bilateral hypoglossal nerve
tion sense. Peripheral lesions will cause ipsilateral paresis,
palsy as opposed to unilateral.
atrophy and a flaccid paralysis with deviation towards the
In addition to hypoglossal injury, there are multiple
side of the lesion. Because of proximity to other lower crareports of concomitant injuries to other nerves in the
nial nerve (IX, X, XI) in posterior cranial fossa one or more
vicinity that can be affected by anesthesia or oropharynthese nerves can be involved depending on the anatomical
geal manipulation. Tapia’s syndrome is a hypoglossal nerve site of pathology. The lingual nerve (branch of V) can be
injury with ipsilateral vagal nerve injury of the recurrent
co-involved with deep tongue lesions. Needle EMG can be
laryngeal nerve with associated vocal fold paralysis. This
performed of the tongue to ascertain presence of acute
has been attributed to pressure neuropathy of both nerves denervation (fibrillations and fasciculations), which typidue to inflation of the endotracheal tube cuff within the
cally have onset three weeks after axonal injury. Needle
larynx.16 The lingual nerve, which supplies taste and sensaEMG can also be performed of vocal cord musculature
tion to the anterior two-thirds of the tongue, can also be
to determine associated recurrent laryngeal nerve/vagal
damaged along with the hypoglossal nerve due to its siminerve involvement. Flexible endoscopic imaging by speech
lar course along the hyoglossus muscle and subsequent
language pathology or otolaryngology will also be able to
ability to be stretched in the same manner.13
determine a vagal nerve palsy by the presence of vocal fold
paralysis.
Diagnosis
After the clinical exam and EMG are utilized, an MRI is
The diagnosis of peripheral hypoglossal nerve injury can
probably the most useful imaging tool to help localize the
be made through a combination of history, physical, and
lesion or rule out associated pathologies, due to its ability
ancillary tests. The key differentiation should be made
to follow the nerve in its entirety.18 Computed tomogra17 A
phy (CT) is best at imaging the skull base foramina if there
between a supranuclear, nuclear, or peripheral lesion.
supranuclear lesion will most often be in the motor strip
is suspicion of skull base pathology.
of the precentral gyrus but can also involve the internal
capsule and pons. The lesion will typically be unilateral,
Prevention / Treatment
and the tongue will have an initial deviation away from the
Many of the reported cases of hypoglossal nerve injury
cerebral lesion without evidence of atrophy or fasciculafollowing intubation were due to improper cuff usage.
january/february 2014 Practical Neurology 15
Expert Opinion
Steps to reduce this risk include monitoring cuff pressure, inflating the cuff with the least amount of volume
required to seal the airway, and deflating the cuff in all
patients undergoing anesthesia with nitrous oxide for
more than 30 minutes.5,7,15 It has also been suggested that
malpositioning of the patient’s body during surgery, particularly hyperextension of the neck, may result in nerve
stretching and injury.19 Similarly, previous case reports
have suggested using a shorter blade on the laryngoscope
or intermittently releasing and repositioning the mouth
gag or laryngoscope during longer cases.1 In addition, two
predisposing factors have been identified: calcification of
the ligamentum stylohyoideum and deformities of the
skull base.4,16
From cases reported in the literature, complete recovery of hypoglossal nerve function is expected within
the first six months.20 Due to this progressive pattern of
recovery, it has been postulated that the nerve experiences a neuropraxic injury and would therefore not benefit
from intervention.21 Most case reports describe the use of
steroids for several days in the immediate postoperative
period following identification of hypoglossal nerve palsy,
but there is no support within the literature. Patients will
benefit from the inclusion of a speech language pathologist to help them with their loss of function, especially
for swallow. Patients can be counseled to only chew and
manipulate food on their non-involved side.
The treatment of bilateral hypoglossal nerve paralysis,
on the other hand, is more involved. These patients will
have total loss of tongue movement, making speech and
the voluntary initiation of swallow extremely difficult.17
Therefore, alternative feeding methods should be utilized,
such as a nasogastric tube or gastrostomy tube to maintain nutrition. Additionally, if patients are unable to initiate a swallow, they may develop difficulty handling their
secretions. Tympanic neurectomy, botulinum toxin injection to the submandibular glands, and salivary diversion
procedures can be utilized to decrease the flow of saliva
depending on the clinical scenario. If the patient still
has intractable aspiration, a tracheotomy can be placed
along with closure of the larynx if no return of function is
expected.
Conclusion
Hypoglossal nerve palsy represents a not uncommon
finding in patients after surgery or anesthesia intervention even when no direct transection has occurred. Many
proposed etiologies are preventable with careful attention to reducing compression of the lateral tongue base
during prolonged surgery or intubation. However, the
patients that have unilateral palsy have a good prog-
16 Practical Neurology january/february 2014
nosis and most will recover full function in weeks to
months. n
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