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separated, sclerosed fracture margins of orbital roof.

Two of our cases had plain skiagram showing sclerosed

fracture margins of orbital roofs (Fig. 2A). Both the

other two cases required diagnostic CT scans. Recon-

structed images of CT scan may help further in

delineating the extent of bony defect (Figs. 1D and2B). MRI may differentiate intra-orbital fluid collec-

tion (pseudomeningocoele) from herniated neural

tissue. Delineation of bony architecture is better

defined on coronal sections of CT scan, whereas

MRI (T2 weighted, coronal section) is better for intra-

cranial neural tissue, which herniates into orbit.2,5,7

Only four of the reported cases were repaired

without cranioplasty.1,7,9 Three of these cases had

good follow-up.7,9 All except one of our cases were

operated without cranial repair. All the cases have

been followed up to check for bony healing (Fig.

1D). Previous reports have questioned the role of

bony repair in treating growing skull fractures.10

Natural bony healing seems to be superior (Fig. 1D)

than cranioplasty, which is not always required,

especially in a cosmetic region like supraorbital ridge

(Fig. 1D). We feel that larger bony defects may be

supported with calvarial grafts (Case 4), but smaller

defects do not require cranioplasty.

Conclusion

Occasionally, paediatric head injuries may not be as

minor as considered and are left unattended or

neglected. It is the pliability of paediatric skull whichmakes it more prone to develop growing skull

fractures. These pathologies should be diagnosed

and managed early so as to prevent irreversible

neurological deficits. Plain radiographs may not help

in diagnosing orbital roof growing fractures. Coronal

sections of CT scan and MRI are the investigations

of choice, if such a diagnosis is suspected. It is the

dural repair, which is mandatory for a successful

outcome. The bony reconstruction of orbital roof or

supra-orbital ridge may not be attempted at all, asthe long-term outcome after isolated dural repair is

sufficient and satisfactory.

References

1 Bayar MA, Iplikcioglu AC, Kokes F, Gokcek C. Growing skull

fracture of the orbital roof. Surg Neurol 1994;41:80 2.

2 Caffo M, Germano A, Caruso G, et al. Growing skull fracture

of the posterior cranial fossa and of the orbital roof. Acta

Neurochir (Wien) 2003;145:201 8.

3 Ramamurthi B, Kalyanaraman S. Rationale for surgery in

growing fractures of the skull. J Neurosurg 1970;32:427 30.

4 Koltai PJ, Amjad I, Meyer D, Feustel PJ. Orbital fractures

in children. Arch Otolaryngol Head Neck Surg 1995;121:

1375 9.

5 Jamjoom ZA. Growing fracture of the orbital roof. Surg Neurol

1997;48:184 8.

6 Naim-Ur-Rahman, Jamjoom Z, Jamjoom A, Murshid WR.

Growing skull fractures: classification and management. Br J

Neurosurg1994;8:667 79.

7 Suri A, Mahapatra AK. Growing fractures of the orbital roof.

A report of two cases and a review. Pediatr Neurosurg 2002;36:

96100.

8 Ziyal IM, Aydin Y, Turkmen CS, et al. The natural history of

late diagnosed or untreated growing skull fractures: report on

two cases. Acta Neurochir (Wien) 1998;140:651 4.

9 Colak A, Akbasak A, Biliciler B, Erten SF, Kocak A. Anunusual variant of a growing skull fracture in an adolescent.

Pediatr Neurosurg 1998;29:36 9.

10 Gupta SK, Reddy NM, Khosla VK, et al. Growing skull frac-

tures: a clinical study of 41 patients. Acta Neurochir (Wien)

1997;139:928 32.

Herpes zoster of the trigeminal nerve following microvascular

decompression

H. N. SIMMS & L. T. DUNN

Department of Neurosurgery, Institute of Neurological Science, Southern General Hospital, Glasgow, UK

Abstract

A patient developed herpes zoster of the maxillary division of the trigeminal nerve after microvascular decompression.Varicella zoster virus lies dormant in the Gasserian ganglion until reactivation and can cause herpes zoster ophthalmicus.This can result in serious ocular complications including blindness. Antiviral agents are effective if commenced promptly.

Key words: Herpes zoster, microvascular decompression, trigeminal neuralgia.

Correspondence: Mr L. T. Dunn, Consultant Neurosurgeon, Institute of Neurological Science, Southern General Hospital, Glasgow, G51 4TT.

Fax: 01412012995 E mail: hnsimms@doctors org uk

Herpes zoster of the trigeminal nerve 423


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Case history

A 68-year-old gentleman presented with an acute

exacerbation of right-sided 3rd division facial pain.

He had suffered from trigeminal neuralgia for 3 years.

The pain was exacerbated by chewing and facialmovement and uncontrolled by maximal medical

therapy.

A right retromastoid craniectomy and microvas-

cular decompression of the trigeminal nerve was

performed. There was marked distortion and com-

pression of the nerve root entry zone by a loop of the

superior cerebellar artery, which was dislocated from

in front of the nerve and separated from the nerve

with Ivalon sponge.

Postoperatively he had complete relief of the facial

pain, but 3 days later a vesicular erythematous rash

developed in the distribution of the second division

of the trigeminal nerve on the right, consistent withherpes zoster infection (Fig. 1). The eye was red from

conjunctivitis, but the upper lid and nose were not

involved. This responded rapidly to topical acyclovir

and oral famciclovir. He had no long-term visual

sequelae.

Pathophysiology

Varicella zoster virus (VZV) infection initially pro-

duces chickenpox. Following resolution, the virus

lies dormant in the dorsal root ganglia or, specifically

in this case, the neurons of the Gasserian ganglion.This occurs because of VZV specific cell-mediated

immunity acquired during the primary infection. It

can remain latent for decades until focal reactivation

along a ganglions distribution results in character-

istic herpes zoster (shingles).1

The thoracic dermatomes are most commonly

affected (56%), followed by the cranial nerves

(13%). The trigeminal nerve is the usual location

and the 1st division is most commonly involved.

2

Themajority of trigeminal ganglia are latently infected

with alpha-herpes viruses, herpes simplex virus type-1

and VZV. Whereas HSV-1 periodically reactivates in

the trigeminal ganglia, VZV reactivates very rarely.3

At autopsy, VZV DNA was found in 50% trigeminal

ganglia samples.1

Clinical features

Herpes zoster manifests as an acute, localized vesi-

cular eruption, which causes a painful, blistering rash,

which is usually limited to a single dermatome.

Diagnosis is based on the appearance of the skinlesions, and strengthened by a prior history of

chickenpox or shingles. It can be confused with

herpes simplex.

Ocular involvement occurs in approximately one

half of patients who have zoster affecting the

ophthalmic division of the trigeminal nerve. Herpes

zoster ophthalmicus (HZO) represents reactivated

varicella zoster virus that travels down the ophthalmic

nerve from the trigeminal ganglion, taking 3 4 days

to reach the nerve endings. Cutaneous involvement

in the distribution of the nasociliary nerve heralds

ocular involvement. Eye lesions are rare without noselesions. Lower eyelid involvement alone is favour-

able, as regards eye complications, since it comes

from the superior maxillary nerve. Maxillary zoster

with corneal involvement has been reported, but it is

rare.4

However, severe ocular complications can occur

with a vesicular rash anywhere on the forehead and

usually develop within 3 weeks of the rash. They

either resolve rapidly and completely, or lead to a

chronic course. Symptoms include eye pain, red eye,

decreased vision, eyelid rash, pain, malaise, tearing

and fever. Long-term complications can be inflam-

matory, such as keratitis, episcleritis/scleritis, iritis,

ischaemic papillitis or orbital vasculitis. Nerve

damage may be associated with some ocular motor

palsies and neuralgia. Tissue scarring may result in

lid deformities, neuralgia and lipid keratopathy.

Potentially sight-threatening complications such as

conjunctivitis, keratitis, corneal ulceration, iridocy-

clitis and glaucoma occur in 50% HZO patients

without antiviral treatment.5

Herpes zoster may affect any age group, but it is

much more common in adults over 60 years old. The

progressive loss of regulatory control of T lympho-

cytes that accompanies aging is thought to play a rolein reactivation of the virus. It is also more frequent in

children who have had chickenpox before the age of

424 H. N. Simms & L. T. Dunn


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HIV-infected patients than in uninfected persons.6

Reduction of T lymphocytes is an explanation for the

high rate of occurrence of herpes zoster in HIV-

infected individuals. Chronic corticosteroid use,

malignancies such as Hodgkins lymphoma, chemo-

therapy and radiation therapy may increase the risk ofdeveloping herpes zoster.

Treatment

Acyclovir, a DNA polymerase inhibitor can shorten

the course, reduce pain and complications, or protect

an immunocompromised individual. For greatest

effect, acyclovir should be started within 24 h of

the appearance of pain or burning sensation, and

preferably before the appearance of the characteristic

blisters. Benefits have only been demonstrated in

patients who received antiviral agents within 72 h

after the onset of rash. Corticosteroids in combina-tion with antiviral treatment may help prevent post

herpetic neuralgia.

Discussion

Trigeminal nerve surgery has the potential to

stimulate reactivation of VZV. Herpes simplex virus

reactivation with manifestations in the sensory

distribution of the trigeminal nerve has been de-

scribed in 38 94% of trigeminal nerve procedures.

Prevention of this reactivation has been demon-

strated in placebo-controlled trials by using prophy-lactic acyclovir.7 There are no such studies

documenting the incidence of herpes zoster after

trigeminal nerve surgery, although anecdotal reports

do exist.8

The increased reporting of herpes simplex may be

due to greater levels of herpes simplex virus in

autopsy studies of trigeminal ganglia and they have a

greater tendency to reactivate than VZV.

Postoperative Ramsay Hunt syndrome from re-

activation of VZV of the geniculate ganglion after

acoustic neuroma resection has been reported. One

study details eight patients with delayed facial palsy

from 348 who had surgery for acoustic neuroma. The

mean time to onset was 8.75 days.9

A prospective study in which 20 consecutive

patients, who underwent acoustic neuroma surgery

showed that VZV IgM titres rose, on average, 495%

postoperatively among patients with delayed facial

palsy compared with a decline of 14% in those

without delayed facial palsy. This implies that

recrudescence of the virus has occurred playing a

role in the cause of delayed facial palsy. Antiviral

prophylaxis has been advocated based on this.10

There is also a report of a 56-year-old man suffering

from delayed facial palsy 7 days after microvasculardecompression of the trigeminal nerve. Serum anti-

body of varicella-zoster virus (VZV) was increased

suggesting that the delayed facial palsy after MVD

was caused by a re-activation of VZV.11

VZV reactivation seems more common after acous-

tic neuroma surgery, causing a delayed facial nerve

palsy. The incidence of herpes zoster of the trigeminal

nerve after microvascular decompression may beunder-diagnosed and not recognized by patients or

medical staff.

If there is any doubt in the diagnosis, it can be

confirmed by a serum antibody elevation. This was

not performed in this case, as we were satisfied with

the diagnosis based on the clinical features.

Conclusion

Herpes zoster and particularly herpes zoster ophthal-

micus is a potentially serious, possibly under-

reported complication from manipulation of the

trigeminal nerve at surgery. Prompt recognition andtreatment should avoid any of the serious ocular

complications, as well as the potential for developing

postherpetic neuralgia. Prophylactic antiviral therapy

should be considered for those at increased risk of

reactivation, such as immunocompromised patients

and the elderly. In the future, there may be a

decreased incidence of herpes zoster due to child-

hood vaccination, which is now common in the

USA.

However, in the meantime this potentially sight-

threatening complication should be considered and

patients warned, as often the onset could be delayedand appear after discharge from hospital.

References

1 Kennedy PG. Key issues in varicella-zoster virus latency.

J Neurovirol 2002;8(Suppl. 2):80 4.

2 Carbone V, Leonardi A, Pavese M, Raviola E, Giordano M.

Herpes zoster of the trigeminal nerve: a case report and review

of the literature. Minerva Stomatol 2004;54(1 2):49 59.

3 Theil D, Derfuss T, Paripovic I, et al. Latent herpesvirus

infection in human trigeminal ganglia causes chronic immune

response. Am J Pathol 2003;163:2179 84.4 Jain S, Rathore MK. Maxillary zoster with corneal involve-

ment. Ind J Ophthalmol 2004;52(4):323 4.

5 deLuise VP. Herpes zoster ophthalmicus; current diagnostic

and management issues. Res Staff Physician 1991;37:65 71.

6 Gulick RM, Heath-Chiozzi M, Crumpacker CS. Varicella-

zoster virus disease in patients with human immunodeficiency

virus infection. Arch Dermatol 1990;126:1086 8.

7 Gianoli GJ, Kartush JM. Delayed facial palsy after acoustic

neuroma resection: the role of viral reactivation. Am J Otol

1996;17:625 9.

8 Boucherat RJ. Herpes zoster ophthalmicus with trochlear nerve

involvement after alcohol injection into the Gasserian ganglion.

Br J Ophthalmol 1971;55(11):761 5.

9 Franco-Vidal V, Nguyen DQ, Guerin J, Darrouzet V. Delayed

facial paralysis after vestibular schwannoma surgery: role ofherpes viruses reactivationour experience in eight cases. Otol

Neurotol 2004;25:805 10.

10 Gianoli GJ Viral titres and delayed facial palsy after acoustic

Herpes zoster of the trigeminal nerve 425


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11 Furukawa K, Sakoh M, Kumon Y, et al. Delayed facial palsy

after microvascular decompression for hemifacial spasm due to

reactivation of varicella-zoster virus. No Shinkei Geka 2003;31:

899 902.

12 Gnann JW, Whitley RJ. Herpes zoster. N Engl J Med 2002;

347:340 6.

Remodelling potential of paediatric cervical spine after

type II odontoid peg fracture

S. BHAGAT, J. BROWN & R. JOHNSTON

Institute of Neurological Sciences, Department Of Neurosurgery, Southern General Hospital, Glasgow, UK

Abstract

We describe a case of odontoid process fracture below the synchondrosis associated with delayed diagnosis and anteriorsubluxation of C1 over C2. This was treated with an in situ posterior occipitocervical fusion. Long-term follow-up of 7 yearsshowed excellent remodelling of the deformity.

Key words: Occipitocervical fusion, odontoid peg fracture, paediatric cervical spine, remodelling.

Case description

A 2-year-old girl was involved in a motor vehicle

accident, was admitted at the referring hospital

and was subsequently discharged in the morning.

A lateral c-spine plain film was read as normal.

(Fig. 1). However, she continued to have pain in theneck during the weeks following accident. She did

not have any neurological deficit or sensory loss, but

neck pain was increasing in severity and restricting

her neck movements. Supporting the chin on her

hand relieved the pain. C-spine films were repeated

in 6 weeks, which showed a displaced type II

odontoid fracture with subluxation of C1 over C2

(Fig. 2). She was then transferred to the Institute of

Neurological Sciences, where flexion/extension films

were carried out, which did not reveal any movement

at C1/2 and it was not possible to reduce fracture

with gentle manual traction. A decision was taken to

fuse C0 C2 in situ to stop any further pain or

progressive deformity. She underwent an operation

through a posterior approach to carry out C0 C2

fusion using transosseous skull wires and autogenous

bone grafting from left side ribs (Fig. 3). Surgery was

carried out without any complications and post-

operatively she was maintained in a halo vest for a

period of 8 weeks. She was discharged with a plan to

closely follow her up initially and up to skeletal

maturity. At 7 months follow-up she was found to be

free from pain and resumed all normal activities for

her age. There was slight limitation in her neck

movements but this did not appear to be disabling in

any way. X-rays were satisfactory and did not show

any changes in alignment at this stage. A further

follow-up at 30 months showed a significant remo-

delling of her neck. Chest X-ray confirmed regenera-

tion of ribs used for bone grafting at this stage. At the

time of final follow-up (84 months), she has onlyslight limitation in lateral rotations on sides, no

neurological deficit and a greatly improved surgical

alignment on the lateral c-spine films (Fig. 4).

Discussion

The behaviour of the cervical spine in sagittal plane

after posterior atlantoaxial fusion in growing patients

is still a controversial issue.1 Risks of postoperative

cervical malalignment2,3 and the importance of the

position of C1 C2 fusion to avoid compensatory

subaxial changes for hyperextended fusion are well

known. The same authors3 have demonstrated that

the onset of sagittal postoperative malalignment in

growing patients is associated with the progressive

onset of spontaneous compensatory changes that

develop during the following months and can restore

the straight or even lordotic position of the cervical

spine. This phenomenon, known as Toyama remo-

delling is well known and so far has been described for

fusions carried out at C1 2 level for indications like

odontoid malformations (hypoplasia or os odontoi-

deum), instability secondary to juvenile rheumatoid

arthritis and traumatic rotary subluxation.

Correspondence: Mr Shaishav Bhagat, 31 Uplands Court, Upton Road, Norwich NR4 7PH, UK. Tel: 01603456750, 07866105026. Fax: 01603456750.

E mail: shaishav bhagat@rediffmail com

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