Successful Treatment of Herpes Zoster Ophthalmicus Complicated by Intense Orbital Inflammation Using Laser Irradiation over the Stellate Ganglion

Abstract

A 56-year-old man presented with right-sided headache and ptosis accompanied by a facial skin rash. He was diagnosed with herpes zoster ophthalmicus (HZO). Despite acyclovir and steroid therapy, the ocular symptoms worsened. Magnetic resonance imaging (MRI) revealed severe orbital inflammation and abnormal lesions in the right trigeminal nucleus and tract. The effects of re-administration of intravenous acyclovir and steroid pulse therapy were limited. Laser irradiation of the stellate ganglion (SGL) and high-dose oral prednisolone therapy were effective. Our experience suggests the efficacy of early multimodal treatment, including SGL, in treating ocular symptoms associated with HZO.

Introduction

Herpes zoster ophthalmicus (HZO) is caused by reactivation of the varicella-zoster virus (VZV) in the trigeminal ganglia. It accounts for 10-25% of all herpes zoster cases and causes external ophthalmoplegia in approximately 10% of cases (1). It can also cause cranial neuropathies. In order of frequency, the oculomotor, abducens, and trochlear nerves may be affected. Several cranial nerves can be affected simultaneously (1). Treatment of HZO includes acyclovir, oral steroids, and steroid pulse therapy. Although it has been previously reported that stellate ganglion block (SGB) is effective in relieving pain in herpes zoster, there is no evidence of its effect on oculomotor dysfunction.

We herein report a patient with severe orbital inflammation secondary to HZO, who showed a good clinical response to laser irradiation of the stellate ganglion (SGL). SGL is performed in the supine position by placing the probe in contact with the skin of the neck and irradiating the stellate ganglion region. SGL is less invasive than SGB and has clinical efficacy similar to that of SGB therapy (2,3).

We also reviewed the literature concerning the effects of SGB on oculomotor dysfunction in HZO and discussed the effects of SGL in the current patient.

Case Report

The patient was a 56-year-old man with chief concerns of difficulty opening his right eye and headache on his right side. Three weeks before admission, he experienced pain in his right eye and drooping of the right upper eyelid. One week later, he consulted with a dermatologist at our hospital as a result of erythema, which appeared in the region of the skin innervated by the first branches of the right trigeminal nerve, including the dorsum nasi. He presented with a swollen eyelid with vesicles and right ocular pain, as well as difficulty opening his right eye. The patient was thus diagnosed with herpes zoster in the first branch of the right trigeminal nerve.

Acyclovir was administered intravenously at 250 mg/day for 1 week and oral prednisolone at 15 mg/day for 3 days. During treatment, he developed keratitis and iritis in his right eye and was started on topical acyclovir ointment. His skin rash improved, and he was discharged from the hospital. However, his difficulty opening his right eye and his right ocular pain did not improve after discharge, so he was admitted to the Department of Neurology. His medical history included gallbladder polyps, and he was not taking any regular medication.

Upon admission, the patient had no fever and was conscious and coherent. He had mild erythema on the right forehead and around the right eye, crusted vesicles on the right eyelid, and hyperemia of the right palpebral and bulbar conjunctiva.

His neurological findings included decreased right visual acuity, inability to open the right eye, and ocular motility disorder in all directions, characterized by severe abduction deficiency and limitation of adduction, elevation, and depression (Fig. 1a). The patient also had hypoesthesia in the region of the first branch of the right trigeminal nerve. No meningeal irritation was observed. A cerebrospinal fluid examination revealed the following: cell count, 28 /μL; predominance of small lymphocytes; protein level, 44 mg/dL; IgG index, 0.71; negative for VZV IgM antibodies; and positive for VZV IgG antibodies. A visual evoked potential test revealed a prolonged latency of P100. Magnetic resonance imaging (MRI) showed severe inflammation throughout the orbit with involvement of the extraocular muscles and retrobulbar soft tissues as well as abnormal contrast enhancement (Fig. 2a-f) and a high signal intensity on the right side of the lower medulla oblongata on diffusion-weighted imaging (DWI) (Fig. 3a-d, arrowhead).

Figure 1.

Eye movement examination findings. (a) At hospital admission. (b) After intravenous acyclovir therapy, steroid pulse therapy, and stellate ganglion laser irradiation.

Figure 2.

Orbital MRI. (a-c, g) Axial MRI. (d-f, h) Coronal MRI. (a-f) MRI on admission showing enlargement of the right external ocular muscles and irregular enhancement effects on the right internal and external orbital ocular muscles, perioptical nerve, and part of the intrafoveal lipid tissue. (g, h) MRI just before discharge revealed that the swelling of the right external ocular muscle had improved, and the abnormal signal in the right trigeminal nerve tract nucleus had become obscured. MRI: magnetic resonance imaging, STIR: short T1 inversion recovery imaging, T2WI: T2-weighted imaging, T1WI: T1-weighted imaging

Figure 3.

Axial brainstem MRI. (a-d) DWI on admission. (e-l) DWI and FLAIR images obtained 10 days after admission. (m-p) FLAIR images obtained at discharge. DWI: diffusion-weighted imaging, FLAIR: fluid-attenuated inversion recovery, STNT: spinal trigeminal nucleus and tract

Intravenous acyclovir (1,500 mg/day for 14 days) and a 5-day course of methylprednisolone pulse therapy (1,000 mg on days 1 to 3, followed by 250 mg on days 4 and 5) were administered. Following the initiation of treatment, his keratitis and iritis disappeared, and his right visual acuity improved. However, there was limited improvement in his ocular motility, and ptosis and ocular pain persisted. Oral prednisolone therapy (50 mg/day) was initiated 6 days after admission, and SGL using SUPER LIZER HA2200™ (Tokyo Iken, Tokyo, Japan) and supraorbital nerve block were performed. After the second SGL, the limitations in adduction, elevation, and depression in his right eye significantly improved.

Ten days after admission, fluid-attenuated inversion recovery (FLAIR) imaging and DWI revealed hyperintense lesions extending from the right side of the lower medulla oblongata to the upper medulla oblongata. These lesions represent the anatomical location of the right spinal trigeminal nucleus and tract (STNT) (Fig. 3e-l, arrowhead). There were no new symptoms or worsening of neurological findings, and oral prednisolone and SGL were continued. Follow-up MRI performed nine days later revealed that the STNT lesions had not improved. After the third SGL, abduction of the right eye gradually returned. After 49 days of hospitalization, MRI showed that the swelling of the right external ocular muscle had improved, and the abnormal signal in the right STNT had become obscured (Fig. 3m-p, arrowhead). The diplopia in his right gaze disappeared (Fig. 1b), and the patient was discharged after 56 days of hospitalization.

The clinical course of the patient is shown in Fig. 4. Outpatient follow-up was performed regularly, and the oral prednisolone dose was gradually decreased. Three months after discharge, his diplopia persisted only in the left gaze. Follow-up MRI performed one year later revealed that the STNT lesion had disappeared.

Figure 4.

Clinical course. ACV: aciclovir, IVMP: intravenous methylprednisolone pulse, PSL: prednisolone

Discussion

The therapeutic course of the patient suggests that SGL is effective not only for pain management due to herpes zoster but also for external ophthalmoplegia. Several papers have reported that SGB can improve facial pain following herpes zoster infection (4). However, to our knowledge, there have been only three reports of improved oculomotor dysfunction after treatment of herpes zoster by SGB (5-7). We summarized the findings of the five cases in which SGB was effective for treating eye movement disorders caused by herpes zoster (Table). In these reports, there was no improvement with steroid pulse or oral prednisolone therapies; however, after SGB was performed three to eight times, improvements in oculomotor disturbance were observed. After further SGB, diplopia disappeared. Several patients in previous reports showed improvements in oculomotor disorders during SGB, using only pain control medications without steroid therapy (5-7).

Table.

　Summary of Cases Treated with SGB/SGL for Oculomotor Disorder Due to Herpes Zoster.

References	Age/ sex	SGB or SGL	Steroid therapy before SGB/SGL	Number of SGB/SGL before improvement of oculomotor disorders	Other treatments in combination with SGB/SGL	Total number of SGB/SGL
SGB: stellate ganglion block, SGL: stellate ganglion laser irradiation, PSL: prednisolone, IVMP: intravenous methylprednisolone
(5)	81/F	SGB	PSL	3	Pain control	15
	72/F	SGB	PSL+IVMP	3	Pain control	13
(6)	61/M	SGB	No	8	PSL+pain control	16
	73/F	SGB	No	Not mentioned	Pain control	12
(7)	52/M	SGB	PSL	7	Pain control	16
The present patient	56/M	SGL	PSL+IVMP	2	PSL+pain control	5

How SGL contributed to the improvement of ocular symptoms in our patient is unclear. Movement disorders due to herpes zoster can occasionally improve spontaneously. However, this patient showed intense orbital inflammation, and if the treatment had not been initiated, he would have had severe visual sequelae. There is also a possibility that only steroid therapy was effective. However, the patient showed significant improvement after starting SGL. In a report of 18 cases of unilateral rather than bilateral ophthalmoplegia with ocular motor deficits in all 4 directions due to herpes zoster, ophthalmoplegia took an average of 4.4 months to disappear. Several patients had residual ophthalmoplegia despite antiviral drugs, or steroids, or a combination therapy with antiviral drugs and steroids (8). In our case, SGL was started four weeks after the onset, and the patient showed significant improvement in his ocular motility disorder five to six weeks after the onset. Based on the clinical course of the patient and previous reports, we propose that SGL itself was effective in improving ocular symptoms.

Previous papers have suggested that the therapeutic mechanisms involved in SGB and SGL are related to increased cerebral blood flow, which improves tissue ischemia (9,10). SGB has been reported to increase the blood flow of the optic nerve head and the peripapillary retina (9), and SGL has been reported to increase the blood flow to the ophthalmic and central retinal arteries (10). SGL is less invasive than SGB and has been reported to have clinical efficacy similar to that of SGB (2,3).

Several mechanisms underlying the oculomotor disorders in this patient have been proposed. The oculomotor nerve may first have been damaged by VZV, which is known to incubate in the trigeminal ganglion via the cavernous sinus, superior orbital fissure, and orbital apex. The trochlear and abducens nerves may have been affected by the invasion of the VZV or the spread of inflammation. Inflammation and swelling of extraocular muscles and retrobulbar soft tissues can also cause oculomotor disorders. The effect of SGL on oculomotor disorders suggests ischemia caused by occlusive vasculitis.

In the present patient, abnormal signals were observed along the STNT. It was previously reported that 9 of 16 patients with herpes zoster in the trigeminal and cervical nerve regions had abnormal signals in the brainstem or cervical spinal cord on MRI (11). However, there have been only five case reports in which the entire STNT has been delineated. In these patients with herpes zoster, the STNT showed a high signal on T2-weighted images, and in several patients, the STNT also showed a high signal intensity on FLAIR or DWI (12-16). In the present patient, DWI at the time of admission showed a hyperintense lesion in the right lower medulla oblongata, possibly involving the STNT. Ten days later, the lesion had extended to the superior medulla oblongata. The first branch of the trigeminal nerve terminates in the caudal part of the spinal trigeminal nucleus, and it is speculated that the abnormal lesion spread from the caudal part of the STNT in a cephalad direction during the clinical course.

In summary, we encountered a patient with severe orbital inflammation secondary to herpes zoster ophthalmicus with high-intensity signals in the STNT on DWI and FLAIR MRI who demonstrated a good clinical response to SGL. Early multimodal treatment with SGL may be required in patients with HZO with severe orbital inflammation.

The authors state that they have no Conflict of Interest (COI).