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Transcript
■Case Report■
Anesth Pain Med 2012; 7: 16~21
Auriculotemporal and greater auricular nerve blocks have roles
in patients with Ramsay Hunt syndrome with trigeminal nerve
involvement
-A report of two casesDepartment of Anesthesiology and Pain Medicine, Samsung Medical Center, Sungkyunkwan University
School of Medicine, Seoul, Korea
Hyun Seung Jin, Woo-Seok Sim, and Hee-Jin Roe
Ramsay Hunt syndrome (RHS) refers to herpes zoster infection of
the geniculate ganglion of the facial nerve. Cases complicated by
multicranial nerve involvement in the process of reactivation of the
virus, which are known to show virulent clinical course and worse
prognosis, are not common in literature as in practice, and there
has been only one reported case of suspected co-involvement of
the trigeminal nerve in Korean literature. Therefore, in cases of
RHS with severe rash over the face and neck, it is pertinent to give
consideration to such multiple involvement in their early presentation. Facial nerve palsy and herpes related pain are the two
worrisome complication, which could be alleviated by early treatment
with neural blockade in addition to oral medication. Especially,
nerve blocks are known to decrease the extent of nerve inflammation or damage, thereby facilitating recovery and probably
preventing postherpetic neuralgia. We report two rare cases of
Ramsay Hunt syndrome with trigeminal nerve involvement, where
early implementation of blockade of somatic peripheral nerve
branches, in addition to the conventional treatment, promoted early
recovery. (Anesth Pain Med 2012; 7: 16∼21)
CN VIII or cervical spinal nerves are also involved in the
disease process, in which symptoms and the clinical course are
heavier and the prognosis worse, emphasizing the greater need
for appropriate and earlier treatment. Although pain physicians
may actually encounter cases with multicranial nerve involvement in RHS once in a while in practice, there has been
only one such case report in Korean literature, where the
authors finally concluded RHS was mistaken for a trigeminal
herpes zoster, rather than co-involement [1]. In search for
foreign literature related to Koreans, one article reported of a
Korean patient with concurrent involvement of trigeminal and
facial nerve, and another report by Korean authors evaluated
the clinical characteristics and prognosis of over 300 patients
with RHS and multicranial nerve involvement [2], but none of
the articles discussed about the optimal treatment in such
cases, especially related to somatic peripheral nerve blocks.
Key Words: Herpes zoster, Polyneuropathy, Ramsay Hunt
The goals of all treatment modalities of acute herpes zoster
syndrome, Somatic peripheral nerve branch block.
infection including RHS, are to reduce edema and inflammation of the involved nerves and associated pain, thus
Ramsay Hunt syndrome (RHS) is herpes zoster infection of
reducing central sensitization and thereby preventing posther-
the geniculate ganglion, characterized by vesicular skin lesions
petic neuralgia (PHN) or nerve palsy. Especially, the usefulness
in the auricle of ear, external ear, palatal and tongue mucosa
of neural blockade with local anesthetics with or without
and associated pain, usually accompanied by facial nerve palsy.
steroids, has been proven in numerous studies [3,4].
The authors are presenting, with review of literature, two
Cranial nerve (CN) VIII, and rarely cranial nerves other than
rare cases of RHS with co-involvement of the trigeminal
nerve, where early suspicion and diagnosis of multicranial
Received: October 20, 2011.
Revised: October 24, 2011.
Accepted: November 18, 2011.
Corresponding author: Woo-Seok Sim, M.D., Ph.D., Department of
Anesthesiology and Pain Medicine, Samsung Medical Center,
Sungkyunkwan University School of Medicine, 50, Irwon-dong,
Gangnam-gu, Seoul 135-710, Korea. Tel: 82-2-3410-0356, Fax:
82-2-3410-0361, E-mail: [email protected]
nerve involvement, and early institution of blockade of specific
somatic peripheral nerve branches in the involved dermatome
combined with conventional treatments, were associated with
good prognosis.
16
Hyun Seung Jin, et al:Somatic peripheral nerve block in Ramsay Hunt syndrome 17
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examination
CASE REPORTS
Case 1
revealed
no
specific
abnormalities,
and
was
prescribed with oral valacyclovir 1 g daily for 1 week under
the impression of recurrent herpes zoster virus infection of the
trigeminal nerve. The skin lesion seemed to improve after the
A 64-year-old man presented with a 3-day history of
initiation of such treatment, but the pain did not subside, and
right-sided headache and earache accompanied by vesicular
starting from the 5th day of oral medication, the patient newly
skin lesions. The pain was stinging in nature, and started from
developed difficulty in mouth opening and lip movement on
the right ear and surrounding temporal area that spread through
the right side and blinking of the right eye (Fig. 1). He also
the inner ear toward the mandible, and multiple papules and
complained of tingling and numbness on the right side of the
vesicles developed in the face along the mandibular nerve
gingiva and tongue, and visited the neurology department,
dermatome. The patient immediately visited otolaryngology and
where Bell’s palsy due to herpes zoster virus, RHS was
dermatology outpatient clinic, but the otolaryngological physical
diagnosed. He was admitted to the neurology department, and
the laboratory examination on admission showed slightly
increase in neutrophil count and ESR, and right facial nerve
lesion was observed in both nerve conduction and corneal
reflex test. The aggravation of pain and development of new
clinical symptoms such as facial nerve palsy seemed to be a
sign of progression of the inflammation even after the previous
7-day oral valacyclovir treatment. This raised the possibility of
zoster
meningitis,
encephalitis
or
multiple
cranial
nerve
involvement including the trigeminal nerve, and a 7-day
intravenous treatment with 650 mg of acyclovir every 8 hr
was initiated. The cranial nerve magnetic resonance imaging
(MRI) showed multiple enhancement around the fundus of
internal auditory canal, labyrinth segment of the facial nerve,
geniculate fossa, which were all compatible with his clinical
RHS with right facial nerve involvement (Fig. 2). Steroid
therapy was commenced with oral prednisolone 60 mg daily
Fig. 1. This picture shows the skin lesion and facial paralysis on
admission in the first patient.
for 3 days and maintained on 50 mg daily for another 3 days.
On hospital day 5, the movement of the right eyelid began to
Fig. 2. This picture shows the two
sections of cranial nerve MRI of the first
patient, showing enhancement around
the fundus of right internal auditory
canal, the labyrinthine segment of facial
nerve, and geniculate fossa. Arrows
indicate the lesion.
18 Anesth Pain Med Vol. 7, No. 1, 2012
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pain
his admission. However, he had a history of hearing loss
necessitated supplementation with carbamazepine 200 mg/d and
immediately after admission, and the otolaryngologic exami-
gabapentin 300 mg/d. After his discharge on hospital day 8,
nation revealed a mild unilateral sensorineural hearing loss,
prednisolone was tapered off, while oral carbamazepine and
which improved quickly and returned to normal within 5 days
gabapentin was maintained. However, the patient came to our
of admission. Although the possibility of RHS could not be
outpatient clinic due to unrelenting pain. At his first visit,
totally ruled out, no further radiologic examination was taken,
facial muscle movement and skin sensation had both improved
and the treatment was focused on reducing the skin lesions
to grade 4/5 by Medical Research Council (MRC) scale,
and accompanying pain with antivirals and analgesics, since
whereas his pain intensity was describe as 70−80/100 mm by
apparent facial nerve palsy was absent throughout the course
visual analogue scale (VAS). The most painful area was
and the cochlear symptoms resolved. He was discharged after
around the right side cheek and chin, which included
intravenous injection treatment for 7 days with improvement of
electric-shock like pain spreading from the auricle forward
acute skin lesions, and was maintained thereafter on ibuprofen,
accompanied by dull ache with pruritis of the same area,
acetaminophen and codein (Mypol capⓇ, Sungwon Adcock
stabbing pain of the tongue, dull ache of the teeth and
Pharm., Korea) every 8 h. He visited our clinic due to
gingiva. Spontaneous pain and hyperalgesia was observed in all
remaining pain, and at his first visit, his pain score on
areas. He was taking carbamazepine 600 mg/d, amitriptylin 10
aggravation reached VAS 80−90/100 mm, and its relief of
mg/day,
show
improvement,
pregabalin
whereas
150
the
mg/d,
persisting
without
severe
significant
about 50% after the medication, was only transient. There was
improvement in his pain. A stellate ganglion block (SGB) was
a
no observable facial nerve palsy, while skin pigmentation
given using 8 ml of 1% lidocaine, which resulted in a relief
without vesicles were diffusely scattered around the ear auricle
of pain to VAS 50/100 mm at 1-week follow up. Pain
and right mandibular nerve dermatome, and crusted skin lesion
persisting around the area ahead of the auricle, and below the
remained in the external auditory canal. The most severe pain
lower lip, raised suspicion of the involvement of the trigeminal
was the earache, and all the above mentioned skin areas were
nerve, and the cranial nerve MRI findings were reassessed, to
accompanied by spontaneous pain and hyperalgesia. Concu-
reveal an ill-defined signal change along the spinal nucleus of
rrence of the trigeminal nerve lesion with RHS was suspected,
trigeminal nerve suggesting a change following viral infection.
and
During the following month, he was given 4 times of SGBs,
alternatively, including a right SGB, a right greater auricular
twice each of auriculotemporal nerve block (ATNB) and
nerve block (GANB) using a mixture of 20 mg of triam-
mental nerve block (MNB), to report a decreased pain score of
cinolone in 5 ml of 0.375% ropivacaine, and a right mental
VAS 30/100 mm. The somatic blocks and sympathetic blocks
nerve block with 10 mg of triamcinolone in 2 ml of 0.375%
were given alternatively. Thereafter, 3 more SGBs, and another
ropivacaine, and oral gabapentin was commenced. Brain MRI
each of ATNB and MNB was given alternatively, in the
was carried out to discern the possibility of progressive cranial
following 3 month, which was associated with a stepwise
neuropathies, which detected an enhancement of the origin of
decrease of pain, and the oral medication was tapered off
trigeminal nerve and an indefinite signal change in the
accordingly. Thereafter, he is on observation at a 3-month
geniculate ganglion, suggestive of polyneuropathy of both
interval, with his pain nearly subsided and only complaining of
trigeminal and facial nerves (Fig. 3). For the following month,
a decreased sensory of grade 4/5 in his right lower lip.
4 times of SGB, twice each of ATNB, GANB and MNB were
Case 2
somatic
and
sympathetic
nerve
blocks
were
given
given. The somatic and sympathetic nerve blocks were given
alternatively during the first half of the follow up period, and
An 89-year-old male was hospitalized in a dermatology
simultaneously thereafter. In addition, gabapentin was increased
department, due to a 4 days onset of vesicular eruptions
to 1,200 mg/d, with supplementary tramadol 150 mg/d. His
followed by throbbing pain in the right ear, root of nose,
pain score around the ear has decreased to VAS 20−30/100
mandible and tongue with a pain scale of VAS 80−90/100
mm with almost no hyperalgesia, and has no complaint other
mm. He was diagnosed as herpes zoster infection of trigeminal
than the intermittent mild tingling sense in right side of the
nerve, and treated for 7 days. He did not complain of
tongue. He is under regular follow up for stepwise tapering off
apparent facial nerve symptoms except for a slightly heavy
of the oral medications.
tongue and lips on the right side during the first few days of
Hyun Seung Jin, et al:Somatic peripheral nerve block in Ramsay Hunt syndrome 19
󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏
Fig. 3. This picture shows the four
sections of brain MRI of the second
patient, showing the clearest image of
enhancement around the origin of the
trigeminal nerve, and geniculate fossa of
the facial nerve. Arrows indicate the
lesion.
associated pain, and facial nerve paralysis. The 8th nerve
features such as tinnitus, hearing loss, nausea, vomiting are
DISCUSSION
regularly present.
We would like to make two points; First, all pain
Although Ramsay Hunt, who first reported RHS, had already
physicians should be familiar with the atypical presentation of
mentioned the co-involvement [6], concurrent involvement of
RHS, which might mimic trigeminal neuralgia, or show dual
one or more cranial or cervical nerves other than the 8th
involvement of both facial and trigeminal nerve. Second, in
nerve in RHS is rare [1,2,7]. They include various cranial
such cases, severe presentation should be expected, and early
nerves V, IX, X, XI, and XII, and even the spinal nerves C2
implementation of the nerve blockade of the specific peripheral
and C3, leading to a complex form of neurologic disturbance
somatic branches in the involved dermatome, together with
with symptoms such as trigeminal neuralgia, hoarseness, and
SGBs, should be considered to minimize the complications.
swallowing
Herpes zoster oticus occurs when the latent varicella-zoster
difficulty
or
rash
typical
to
herpes
zoster
cephalicus.
virus is reactivated along the distribution of the sensory nerves
The suggested explanation of such multiple involvements
innervating the ear, which usually includes the geniculate
refers to their embryologic and anatomical correlation. The
ganglion.
the
vestibulocochlear nerve is in close proximity to the geniculate
infection is called RHS. The annual incidence of RHS has
ganglion within the bony facial canal, and the gasserian,
been reported as 5 per 10,000 [5]. The syndrome presents as a
geniculate and other cranial and 2nd−3rd cervical ganglia
triad of vesicular lesion around the ear, palate and tongue,
comprise a chain in which inflammation of a single ganglion
When
associated
with
facial
nerve
palsy,
20 Anesth Pain Med Vol. 7, No. 1, 2012
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could extend to nearby ganglia [6]. In addition, contiguous
sympathetic stimulation, and deafferentation causing synaptic
cranial neuropathies may be partly due to the selective
reorganization
vulnerability of blood vessels to varicella-zoster virus and the
management
common blood supply [6].
inflammation and damage of the nervous system, is critical in
in
of
the
the
central
acute
nervous
pain,
system.
which
Therefore,
represents
the
In our cases, the first patient presented with a trigeminal
improving the outcome. In fact, acute pain, along with
rash in addition to the typical clinical symptoms of RHS, in
patient’s age, severity of rash and many other factors, were
which the diagnosis of polyneuropathy was confirmed by
shown to be a reliable risk factor or predictor of PHN [11].
radiologic studies, whereas the second patient, concluding
Neural blockades minimize this inflammatory process [12,13],
clinically and radiologically, seemed to have had a mild RHS
reduce the abnormal activation of the sympathetic nervous
without facial nerve palsy upon trigeminal herpes zoster with a
system, and steroids used in the blockade are known to further
possible involvement of the vestibulocochlear nerve.
reduce inflammation and control C-fiber conduction through
Cases with multiple nerve involvement are known to show
membrane stabilization. As a matter of fact, articles reporting
more severe symptoms and relate to worse prognosis compared
that the early implementation of nerve blocks in AHZ lead to
to simple cases with only 7th, or 7th and 8th nerve involve-
complete recovery of pain and prevention of PHN after AHZ,
ment, which calls upon the need for early accurate diagnosis
have been published [12,13]. In addition, according to the
and more aggressive treatments. However, since the ear has
articles which reviewed the effect of neuraxial and sympathetic
complex innervations as to be commented later, and the facial
blockade on herpes zoster related pain [3,4], although yet
nerve symptoms might be a late manifestations [1], or even
controversial, it has been a general opinion that, neural
absent [8] in RHS, such multicranial involvement may be a
blockades, both epidural analgesia and sympathetic blocks, are
diagnostic challenge to a naive physician in the early stages of
effective in the relief of acute pain in AHZ, and prevention of
the disease.
PHN in patients with AHZ. Unfortunately, there were no
Another main concern of such cases of complicated RHS, is
how to minimize the two dreaded complications, namely facial
articles that studied the role of peripheral somatic nerve
blockade separately.
The
nerve palsy and herpes zoster related pain. The mechanism of
majority
of
the
literature
on
the
subject
had
facial nerve paralysis in RHS, is known to be the infla-
methodologic shortcomings reducing the reliability and clinical
mmation and demyelination of the facial nerve from the virus,
applicability of the results, and the effect of nerve block in
which cause edema and compression of the nerve within the
the treatment of acute pain in AHZ, although apparent, is
facial canal. Spontaneous and complete recovery from facial
known to be transient, lasting for no longer than 1 month,
nerve paralysis occurs only in the minority of cases. Therefore,
questioning its role in the development of PHN [14]. However,
correct diagnosis and subsequent proper treatment, including a
as
combination therapy of steroids and antivirals, and neural
implementation, since a neural block performed by a skilled
blockade, are essential in improving the outcome. Consideration
medical personnel is safe without serious complication, and is
of early treatment of all Ramsay Hunt syndrome patients with
generally accepted in evidence-based practice. A concern may
a course of acyclovir (800 mg, five times daily for 7−10
be raised regarding the risk of spread of infection or
days) and oral prednisone (60 mg daily for 3−5 days) was
secondary bacterial infection induced by injecting into the skin
recommended, which have been shown to be both safe and
lesion, but the possibility has been reported to be very low
effective [6,7]. The earlier initiation of treatment resulted in
[13].
of
now,
it
would
be
wise
to
consider
its
early
better outcome [9,10]. In addition, sympathetic nerve blocks
One more important issue is to become familiar with the
are known to reduce edema within the facial canal by
complicated somatic innervations of the skin around the ear.
improving the blood flow [4], and repetitive SGBs could
External ear and the anterior part of the auricle is supplied
promote recovery of the facial nerve paralysis [1].
mainly by the auriculotemporal nerve, derived from the third
Another serious complication, is pain, both acute pain due to
branch of trigeminal nerve, the mandibular nerve, with minor
acute herpes zoster (AHZ), and postherpetic neuralgia (PHN).
contribution from cranial nerves VII, IX, X. On the other
This herpes related pain, is mediated by the inflammation and
hand, the posterior part of the auricle, cervical area below the
damage of the nerves by the virus that induces peripheral and
ear and the lower part of the mandible opposing the
central
mandibular nerve dermatome, are innervated by the greater
sensitization,
abnormal
activation
of
C-fibers
by
Hyun Seung Jin, et al:Somatic peripheral nerve block in Ramsay Hunt syndrome 21
󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏󰠏
auricular nerve (GAN) which originates from the cervical
plexus and is composed of branches of C2−3. Therefore, the
ATN and GAN, are the main branches innervating the ear.
Especially, the GAN is divided into two branches that each
communicates with the facial nerve. This complicated dual
innervation and communication with the facial nerve, suggests
their concurrent involvement, and the role of their blockade in
disease management.
Since the role of SGB in the treatment of RHS and herpes
zoster infection is well known [15], and mental nerve block is
commonly given in patients with trigeminal neuralgia, the
authors combined ATNB, GANB with the conventional MNB
and SGBs, the somatic blocks with steroids mixed in local
anesthetics. SGB was for its known effect in improving both
the facial nerve palsy and zoster pain, whereas somatic branch
blocks were mainly to alleviate pain, which were both
effective. The patients showed satisfactory improvement both of
facial nerve palsy and pain in relatively short time periods.
The superiority between a somatic versus sympathetic block,
or the optimal frequency of each block, has not yet been
evaluated in any literature. In our experience, when given
alternatively, somatic peripheral branches block seemed slightly
superior to SGB in subjective satisfaction in regard to relieving
pain. However, the objective findings in the improvement of
the VAS scores after each treatment, did not show a
significant difference. Therefore, it is not enough to derive a
conclusion
whether
somatic
or
sympathetic
block
has
superiority over one another.
In conclusion, whenever patients show severe RHS with
extensive
facial
and
cervical
vesicular
lesions,
vigilant
suspicion of co-involvement of the trigeminal nerve should be
given, and a comprehensive, early management with antiviral
agents, steroids, analgesics and adjuvants, together with early
implementation
of
neural
blockade
should
be
attempted.
Especially, repetitive blocks of the somatic peripheral nerve
branches,
specifically,
ATN,
GAN,
together
with
the
conventional methods, such as MNB, if apparently involved,
and SGB, either alternatively or simultaneously, might shorten
the time course, thus improve the outcome.
REFERENCES
1. Park JM, Yu SJ, Park AR, Lee SM. Treatment of Ramsay Hunt
syndrome that is mistaken for trigeminal herpes zoster. Korean J
Pain 2008; 21: 237-40.
2. Shim HJ, Jung H, Park DC, Lee JH, Yeo SG. Ramsay Hunt
syndrome with multicranial nerve involvement. Acta Otolaryngol
2011; 131: 210-5.
3. Kumar V, Krone K, Mathieu A. Neuraxial and sympathetic bocks
in herpes zoster and postherpetic neuralgia: an appraisal of current
evidence. Reg Anesth Pain Med 2004; 29: 454-61.
4. Wu CL, Marsh A, Dworkin RH. The role of sympathetic nerve
blocks in herpes zoster and postherpetic neuralgia. Pain 2000; 87:
121-9.
5. Furuta Y, Aizawa H, Ohtani F, Sawa H, Fukuda S.
Varicella-Zoster virus DNA level and facial paralysis in Ramsay
Hunt syndrome. Ann Otol Rhinol Laryngol 2004; 113: 700-5.
6. Sweeney CJ, Gilden DH. Ramsay Hunt syndrome. J Neurol
Neurosurg Psychiatry 2001; 71: 149-54.
7. Coleman C, Fozo M, Rubin A. Ramsay Hunt syndrome with
severe dysphagia. J Voice 2011; ahead of print.
8. Leong SC, Karkanevatos A. Unusual presentation of Ramsay Hunt
syndrome without facial nerve palsy. Br J Hosp Med (Lond) 2005;
66: 542-3.
9. de Ru JA, van Benthem PP. Combination therapy is preferable for
patients with Ramsay Hunt syndrome. Otol Neurotol 2011; 32:
852-5.
10. Murakami S, Hato N, Horiuchi J, Honda N, Gyo K, Yanagihara
N. Treatment of Ramsay Hunt syndrome with acyclovir-prednisone: significance of early diagnosis and treatment. Ann Neurol
1997; 41: 353-7.
11. Opstelten W, Zuithoff NP, van Essen GA, van Loon AM, van
Wijck AJ, Kalkman CJ, et al. Predicting postherpetic neuralgia in
elderly primary care patients with herpes zoster: prospective
prognostic study. Pain 2007; 132: S52-9.
12. Ji G, Niu J, Shi Y, Hou L, Lu Y, Xiong L. The effectiveness of
repetitive paravertebral injections with local anesthetics and
steroids for the prevention of postherpetic neuralgia in patients
with acute herpes zoster. Anesth Analg 2009; 109: 1651-5.
13. Hardy D. Relief of pain in acute herpes zoster by nerve blocks
and possible prevention of post-herpetic neuralgia. Can J Anaesth
2005; 52: 186-90.
14. van Wijck AJ, Opstelten W, Moons KG, van Essen GA, Stolker
RJ, Kalkman CJ, et al. The PINE study of epidural steroids and
local anaesthetics to prevent postherpetic neuralgia: a randomized
controlled trial. Lancet 2006; 367: 219-24.
15. Shim KS, Kim EJ, Min BW, Ban JS, Lee SG, Lee JH. Treatment
& experience of stellate ganglion block for child herpes zoster
ophthalmicus -A case report-. Anesth Pain Med 2011; 6: 169-72.