POST-TRAUMATIC HERPES ZOSTER

DONALD WINSTOCK, M.B., F.D.S.

Departments of Oral Surgery, the Middlesex and the Royal Dental Hospitals, London

THE condition of herpes zoster as it affects those territories encountered by the

oral sugeon is not very common. For this reason it is perhaps forgotten as a
possible cause of facial pain, especially in its pre-eruptive phase, and, less com-
monly, as a possible effect of oral trauma. It may be described as an acute disease
of the skin or mucous membranes characterised by an eruption of grouped vesicles
on a reddened base, preceded by pain and associated with inflammatory changes
in the corresponding spinal root or cranial ganglia.
Suggested predisposing causes are legion and include tuberculosis, tabes
dorsalis and G.P.I., the lymphomas, injury, exposure, infectious diseases, drugs
such as arsenic, bismuth and gold, and malignancy. However, Hope-Simpson
(z965) in his series of nearly 2oo cases found possible precipitating factors in
z per cent. only. A generalised form of the disease--herpes zoster generalizatus--
is particularly prone to occur in leukaemia and Hodgkin's disease (Wethered,
I964). The sexes are affected about equally but the disease is undoubtedly more
common after the fifth decade.
For a long time an association between the virus of chicken pox and Zoster
was suspected and in z958, Weller et al. and again in I963, Tyrrell, presented
proof that the two viruses were identical, causing identical pathological changes
in tissue culture and seeming to bear identical antigens. However, subjects with
zoster do have more antibody than those with chicken pox and this may be the
host factor which accounts for the clinical difference between the two diseases.
The incidence in a given population was found by Hope-Simpson (I964) to be
3"4 per thousand persons. Its infectiousness is slight and no cases were seen
amongst contacts so that it is probably not caught from other cases. There was
no correlation with epidemics of chicken pox, but zoster cases may cause chicken
pox in contacts. The most heavily attacked nerves were the fifth cranial and the
third dorsal to the second lumbar. However, Spillane (I954) stated that the
seventh nerve was the most vulnerable of t h e cranial nerves in zoster of the head
and neck, whilst Berggreen and Schuler (I938) found that the first division of the
fifth nerve was the most frequently affected branch of this nerve.
In the typical clinical picture, the onset is usually sudden, with pain felt
along the distribution of the affected nerve. It is in this pre-eruptive stage that the
diagnosis may remain unsuspected and the pain has been quoted as leading to a
wrong diagnosis of appendicitis, gall stones or renal colic (Mackey, z962). A few
days later, grouped vesicles appear accompanied by fever and regional lymph
node enlargement. The vesicles have usually crusted over within a week or two
and the pain begins to abate. In older stibjects, the disease is notorious for
producing longer periods of pain and this may be intractable for several years,
despite the fact that the residual scars are invariably anaesthetic. In the head
region special senses may be affected, particularly taste, smell and hearing.
Lacrimation may be impaired and in the eye, corneal ulcers may occur.
The pathology of zoster, like varicella and herpes simplex, is characterised by
c 29
30 B R I T I S H J O U R N A L OF ORAL SURGERY

multilocular vesicles lined b y baUoon cells. T h e vesicles are within the epidermis
or between the epidermis and corium. T h e condition used to be regarded as a
d~sease o f the posterior root ganglia but the work of Kendall (I957) showed that
it is essentially an affection of the central nervous system rather than the dorsal
root ganglia, hence the not infrequent appearance of motor symptoms. D e n n y -
Brown et aL (I944) felt that zoster may be primarily a unilateral segmental polio-
myelitis in which most of the damage falls upon the dorsal part of the cord.
T h e only constant laboratory finding is a small rise in the C.S.F. pressure,
and a mild lymphocytosis during the acute phase. T h e part played by trauma
in the aetiology has not been very well documented as far as the head is concerned.
Spinal trauma has been reported by Roith (I956) as a predisposing cause of herpes
of the trunk. In the mouth, we have a region which is commonly subjected to
surgical trauma and where nerve trunks may be directly affected by hypodermic
needles or instrumentation and it is mainly with this aspect of the disease that I
would like to present some illustrative cases.
Case I. A student nurse, aged 22 years, who had had varicella as a child, complained
of pain in the left lower second molar of one day's duration, radiating to the ear. This
tooth proved to be non-vital and was removed with a local nerve block. There was no
pain the following day, but by the fourth post-extraction day she was complaining of
severe pain. The socket was found to be infected and local remedies were used in

A B
FIG. IA
Case I. Eruption of zoster vesicles along the left lower lip.
FIG. IB
Case I. Herpes simplex lesions on the left lower lip.

treatment. The next day the pain was worse and there was malaise and fever of 99'4 .
She was admitted as an in-patient. One day later the pain was throbbing and radiated
to the head, and only mild relief was gained from codeine compound tablets. Next day
the pain was worse and there was bleeding from the socket, which was sutured and
pethidine given for the pain. The left ear seemed clear. The following day, pain was
 P O S T - T R A U M A T I C HERPES ZOSTER 31

present over the left antrum, the fever continuing. An X-ray of the jaw showed no
sequestra and the antrum was clear, One day later the pain was unchanged, but there
was marginal gingivitis developing on the left side. Two days later, i.e. I I days after
the extraction, an eruption of ulcers was noted along the lower lip mucosa on the left
side (Fig. IA). There was tingling of the lip radiating to the ear and infra-orbital region.
Pain was very severe. The next day, herpes zoster of the left inferior dental and long
buccal nerves was diagnosed, i.e. IX days after the extraction. The pain was intractable.
She was seen by a neurologist and a dermatologist, who noted the absence of lesions on
the skin of the lip, but there were some on the side of the neck and erythema of the
anterior wall of the left auditory canal. She was prescribed pethidine injections, injections

A B
FIG. 2A
Case 2. Right facial lesions over the maxillary and mandibular nerve distribution areas.
FIG. 2B
Case ~. Intra-oral and lip lesions.
of vitamin B12 daily, Neo-cortef for the lip and Corlan tablets for the mouth. The
following day she complained of pins and needles in the legs, but no neurological signs
were present. One dose of deep X-ray therapy was given to the face. Over the next
five days gradual improvement took place, with only a few residual lip ulcers. Two
weeks later, after a spell of convalescence, she was well. Two weeks later, i.e. about
6~ weeks after the extraction, she developed throbbing pain in the lower right second
molar. This was removed under local anaesthetic. Perhaps this was tempting Fate, but
apart from yet another dry socket which followed a difficult extraction and some simple
mouth ulcers, no zoster ensued. Three months after the initial illness, she developed a
crop of ulcers in the mouth, including the site of the zosteric lesions (Fig. IB). These
ulcers were subjected to virological tests but the results were inconclusive. It should be
noted that, whereas the ulcers have a similar appearance, the pain was not comparable,
32 BRITISH JOURNAL OF ORAL SURGERY
the zosteric lesions being accompanied by intense neuralgic pain, the simplex ulcers
being painful locally only. Over the next nine months this unfortunate girl had a lumbar
disc lesion, appendicectomy and a urinary infection. She left hospital for good soon after.
Case 2. A man, aged 75 years, a head waiter, attended complaining of sores on the
right lip which started three days before, followed a day later by an increase in the area
of involvement and the following day by involvement of the whole of the right side of
the face. The right hearing was impaired. A right second molar tooth had been removed
under local anaesthesia by his own dentist two weeks previously. An X-ray taken of the
jaw suggested that the tooth had been severely affected by periodontal disease but no other
abnormality was detected. On examination there were vesicles and pustules on a
generalised erythematous base on the right side of the face (Fig. 2A), lips, external
auditory meatus, temple, right palate and cheek (Fig. 2B). No lesions were present on
the upper eyelid but this was oedematous. The temperature was 99'4 . A blood count
was normal.
He was given Neomycin cream for the face and codeine tablets for the pain. Two
days later there was no pain, the skin lesions were crusting and the periorbital oedema
decreasing.
Four days later the improvement continued. By the fifteenth day after the initial
symptoms, the palate and fauces were clear and only a few healing lesions remained on
the left side of the face. He now complained of noises in the ear. Four days later there
was pain in the right ear, of a neuralgic type. Four days later the rash had faded but
the ear pain was still troublesome, especially at night. One week later, he was sleeping
satisfactorily, i.e. one month after the onset. One month later the left lower second molar
was extracted under local anaesthesia, with no complications. His only residual symptom
of the herpes was slight pain over the right side of the chin on shaving, and by one year
after the onset, only a small area of anaesthesia persisted on the chin. The scars were
anaesthetic.
C a s e 3. A man, aged 62 years, a bus driver, who had had varicella as a child and
had no recent contact with chicken pox. About three months before this patient was
first seen, he had complained of crackling noises in his left ear, especially on swallowing.
There was no pain. He was seen by an E.N.T. surgeon and had eustachian catheterisation
five times, the last occasion being about one week before an eruption appeared on his left
face. When I saw him, he was complaining of pain and swelling on the left side of the
face and mouth of two weeks duration. The pain extended from the temple to the angle
of the jaw. The left side of the tongue was painful and swollen. The left lower gums
began to pain one week after the initial onset and he was unable to wear his dentures.
The left ear became painful one day before presentation at Hospital. His doctor had
prescribed ear drops and analgesic tablets, both without effect. When seen his tempera-
ture was 99 . Vesicles were present under the left lower lip, side of temple, inside the
lip and left side of the tongue (Figs. 3A, B and c). The left ear was oedematous, with
a purulent discharge and granulations on the meatal walls. There was generalised
swelling of the left face, and palpable lymph nodes in the left submandibular region.
The tongue was heavily coated, swollen and sore, and the oral foetor intense. He was
tender in the labial sulcus and there was a discharge about the left teeth.
The mouth was cleaned with hydrogen peroxide, painted with gentian violet, and a
course of tetracycline, codeine and Soneryl tablets prescribed. X-ray examination of
the jaws showed nothing abnormal. Four days after his first visit, he felt generally better
but the left lower teeth and gums felt numb. More skill vesicles were present, some
crusted with blood clot. The mouth was much cleaner, the left ear drying up, but deaf.
Treatment was repeated as before.
Eight days later, i.e. 26 days after the initial symptoms, he complained of severe
pain in the left ear and side of face. The left ear was discharging and ulcers were present
on the left tongue, and he was unable to close the left eye.
 POST-TRAUMATIC HERPES ZOSTER 33
He was referred for an E.N.T. opinion. His sense o f smell was normal, the corneal
reflex on the left was reduced and there was sensory impairment over the areas supplied
by the mandibular and maxillary nerves. Fifth nerve motor function was normal, but
there was facial weakness o f the lower motor
neurone type. Tongue taste sensation was absent,
plus bilateral deafness of the conduction type.
There was left ofitis externa with discharge. The
rest of the nervous system was normal. He was
sent to Moorfields where a lateral tarsorrhaphy
was performed. By thirteen days later there was
complete left facial palsy. Most of the pain was
confined to the ear, but the inside of the mouth
was still sore.
Twenty-one days later he was still complain-
ing of pain in the cheek and temple. Numbness
was present over an area of the left chin and lower
lip. He described his left cheek as if it 'were in
an oven, being roasted'. Shaving was very pain-
ful. The tip of the tongue was burning. He now
could close his left eye and blow his lips. T h e eye FI~. 3 A
stitches had been removed four days previously.
One week later, with pain continuing in the Case 3. Left facial lesions. Seventh
ear, there was anaesthesia of the inferior[dental nerve palsy not yet marked.

B C

FIG. 3B
Case 3. Eruption on left lower lip and gingiva.
FIG. 3c
Case 3. Lesions on side and under surface of tongue.

nerve, and the tongue tingled at the tip. The feeling in the left face was described as if
'thousands of needles were sticking in the face', plus a burning sensation. Noises in
the left ear were 'like a train puffing'. No giddiness was present and there was no
difficulty in swallowing. Codeine gave little relief.
Four months after the onset of pain, he was still experiencing slight pain over the
temple, but the general picture was one of gradual resolution.
34 B R I T I S H J O U R N A L OF ORAL S U R G E R Y

DISCUSSION
Herpes Zoster, usually a simple diagnostic entity with well-defined obiective
and subjective features, would seem to occur in most cases spontaneously, the
basis for its causation being a reactivation of the varicella virus which has become
established as a latent infection in sensory ganglia during the stage of viraemia
in the attack of chicken pox. It is suggested (Hope-Simpson, I964) that if, at a
later date, antibody has declined below the critical value for neutralisafion, at the
next reactivation infectious virus will be able to multiply and be transported
antidromically down the sensory nerve causing neuritis and neuralgia, before it is
released around the sensory nerve endings in the skin to produce clusters of
zoster vesicles.
In coniecturing the association between trauma and the onset of the disease,
one can assume that the trauma is the reactivating factor, the low antibody level
thus facilitating the multiplication of the virus with the production of the disease.
However, reports have been published suggesting non-traumatic dental cause of
zoster. Sternlicht (I954) reported a case in which an impacted third lower molar
was noted on the side of the pain, to be followed by skin lesions. This would
postulate irritation from the unerupted tooth as the cause of the disease but the
author does not press this point too strongly. Weinberger (I933) reported three
cases of zoster said to have been caused by decayed teeth, and Prinz and Greenbaum
(z939) quote Zilz's (I9zI) case with lesions in the mental region believed to be
due to a misplaced supernumerary canine--the pain and vesicles disappearing
on the removal of the tooth. Even if this latter case were of dental origin, the
disappearance of the signs and symptoms so promptly after the extraction does
not quite fit in with the observed natural history of zoster, since a virus disease
will tend to run its natural course unless some specific therapy which is known
to counteract the virus is administered, and the extraction of a tooth hardly
constitutes such therapy. The most that one would expect would be some
alleviation of symptoms without immediate cure. Sweeney (I96o) reported a
case of a man with right ear pain, believed to be due to an unerupted wisdom tooth
and operation which was planned was only iust averted by the timely occurrence
of a discharging ear and facial palsy plus an eruption on the palate and buccal
mucosa. This illustrates very well how severe pain which would seem to be in
excess of what one would expect from the pathology present, may well be due to
an early zoster and not to an unerupted tooth.
I am inclined to believe that the iniection of a substance or other instrumental
trauma in the vicinity of a nerve trunk or into that trunk itself is the principal
premise that we can accept for a cause and effect hypothesis of zoster in the
mouth.
In i932, Chalier and Martin formulated two circumstances in order to associate
trauma with the presence of zoster:
I. Herpes zoster should appear in the region or within the range of iniury.
2. The disease should appear within one day to one month after the iniury.
On this basis, Cases I and 2 would fit in with the criteria laid down. Case 3,
I believe, could well be the sequel to trauma from the eustachian catheterisation.
This manoeuvre involves the passage of a metal catheter along the nasal floor until
it reaches the region of the eustachian tube, when it is rotated so as to lie at the
 P O S T - T R A U M A T I C HERPES ZOSTER 35

entrance of this tube in the naso-pharynx. Branches from the fifth and ninth
nerves supply this area and it seems not unlikely that the forceful blowing of air
into the tube could constitute some degree of irritation to these nerves.
The timing of the operation here is in accord with the criteria mentioned
above whereas the initial ear symptoms, i.e. crackling noises, occurred some three
months before the onset of the herpetic symptoms and are therefore unlikely to
have been in themselves early manifestations of zoster.
The treatment of zoster is far less satisfactory than the diagnosis. A review
of the literature indicates that very many remedies have been tried at some time
or another, especially in cases of post-herpetic neuralgia. It has often been stated
that when a multiplicity of remedies are used for treatment of a disease, the one
thing of which we can be certain is that none are of much use. Amongst the
remedies that have been and are used are: Aspirin, Nepenthe, Opium, Pethidine,
Levorphenol tartrate, local injections of procaine, ultra-violet light, liver extract
injections, posterior pituitary injections, Ergotamine, Dexedrine, Chlorpromazine,
antibiotics, deep X-ray therapy (Barford, I946), sympathetic nervous system
blocks (Moore, I954), intravenous sodium iodide, Autohaemotherapy, Vitamin B1,
Diathermy (Mackey, I962), Steroids (Elliott, I964) , and tranquillisers.
In one case which I have encountered, a case of ophthalmic zoster, post-
herpetic neuralgia was still present eighteen months after the onset and the supra-
orbital nerves were pulled out of the tipper eyelid to afford relief. Six months
later, with pain still present, a hemi-tarsorrhaphy was performed and ten months
later a leucotomy carried out. The pain persisted. Thus the solution remains
somewhat elusive. Nevertheless, in most cases, herpetic pain does not persist
and the pain of the active condition tends to burn itself out within a few weeks
to a few months, perhaps in spite of and not because of the treatment.
From the oral surgeon's interest in this condition, there are three factors to
be considered:
I. The possibility of oral surgical trauma as a predisposing cause.
2. The diagnosis of the condition as a cause of post-traumatic pain.
3. The significance of post-herpetic lesions in and about the mouth.
I think we can accept that herpes zoster is a possible, albeit uncommon, cause of
post-extraction pain and I would suggest that in those cases where the clinical
symptom of pain is out of all proportion to the lesion, for example post-extraction
dry-socket, alveolar fragmentation or exposure, or close proximity of the apices
of the tooth in question to the main nerve canal, or the onset of complications
such as osteomyelitis (which I have never known to produce pain of the severity
of zoster), the possibility of zoster should be borne in mind. This is all the more
relevant when we remember that a lower posterior tooth pathology will often
cause referred pain to the ear and it is in and around the ear that some of the most
severe pain of facial zoster occurs. Vigorous surgical intervention should therefore
not lightly be resorted to until the clinical picture has had time to crystallise
more dearly.
Zoster will ultimately make itself known by the appearance of vesicles, although
cases have been recorded where the condition has been diagnosed in the absence
of vesicles and some cases labelled as Bell's Palsy are thought to be the manifesta-
tions of such zosteric attacks (Salas, I957), and a period of judicious waiting may
sometimes yield clinical rewards, if only to save the patient unnecessary surgical
36 BRITISH J O U R N A L OF ORAL S U R G ER Y

intervention or being branded as a neurotic and perhaps being denied the relief
that the more potent analgesics may offer. If the condition is suspected early
enough and with sufficient conviction, the early administration of steroids may
hold out some hope for positive relief. Elliott (1964) reported his success with
the use of large doses of prednisone (60 mg. per day for the first week, thereafter
in diminishing doses), with an average duration of pain of 31 days compared with
3 weeks in untreated cases, with no persistent neuralgia in the treated cases.
This regimen seems worthy of further trials, especially when the facial nerve is
involved.
Finally, the significance of post-herpetic scars is important to us since
Wyburn-Mason (1955) recorded, after investigations carried out at the Royal
Marsden Hospital, numerous lesions developing at the site of old zoster scars--
these included lichen planus, leukoplakia, rodent ulcers and squamous cell
carcinomata. Moynihan in 1964 drew attention to the same phenomenon with a
small series of cases. He pointed out that the work of Stoker (in 1962) and Burkitt
(in 1962) added weight to the association of viral infection and cancer. Thus, a
history of zoster in the mouth should alert one to the potentiality that this may
have far more sinister changes.

SUMMARY
Three cases have been presented as tentative illustrations of the possible
connection between trauma and the onset of herpes zoster. This connection may
provide a basis for a broader clinical outlook in the face of severe post-traumatic
pain; the recognition of'the established condition and its management; and finally
the significance of post-herpetic lesions in the evolution of oral pre- and frank
malignancy.

ACKNOWLED GEMENTS
I wish to express my thanks to Mr. G. T. Hankes and Mr. J. H. Hovell for permission
to study patients under their care and to Dr. Hugh Wallace for allowing me to review cases
under his care. I am grateful to the photographic departments of St. Thomas's, St. Bartholo-
mew's and the Royal Dental Hospital of London for the illustrations.
 POST-TRAUMATIC HERPES ZOSTER 37
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