Trigeminal Pain During and After Herpes Zoster Ophthalmicus

Herpes zoster, a viral inflammation, commonly affects the ophthalmic division of the trigeminal nerve. In fact, the trigeminal nerve is the cranial nerve most commonly affected by herpes zoster and postherpetic neuralgia, being involved in about 16% of cases (Schott, 1980). The inflammation affects arteries, peripheral branches of the trigeminal nerve, and the Gasserian ganglion. It is usually unilateral and affects males more commonly than females. There is an increasing incidence with advancing age. Although a complete discussion of the ocular complications from herpes zoster is presented in Volume 3, we are concerned here with the pain that results from this severe, chronic neuritis. The pain may begin 2---3 days before the onset of the diagnostically characteristic vesicular rash. Recognition of the prodromal pain of herpes in the prevesicular stage would be highly desirable, but, in most cases, the cause of the patient's complaints is not suspected until the skin changes appear. The patient may consult an ophthalmologist during the prevesicular stage, convinced that he has glaucoma or an ocular inflammation, only to be told that there is no ocular explanation for his pain.

The quality and duration of the pain associated with acute herpetic neuritis is variable. In contrast with the pain of trigeminal neuralgia, the pain of herpes zoster is steady and sustained. It is both burning and aching, nonthrobbing, and usually diminishes gradually in intensity. It may be experienced in any part of the distribution of the trigeminal nerve, although involvement of the forehead is most common. Examination soon after onset reveals erythema and the typical herpetiform lesions of the skin associated with hyperalgesia, hypalgesia, and/or paresthesia . The pain often spontaneously regresses within 2 or 3 weeks but it may also merge imperceptibly into the postherpetic stage of pain. There may even be a pain-free interval of days or weeks.

The pain of postherpetic neuralgia is often severe and may be lancinating, burning, or aching. There may be persistent dysesthesia, hyperalgesia, and/or hypalgesia. At times, this is so severe that the lightest touches provoke pain even though firm pressure may be bearable. There is a tendency for the pain to improve slowly over several months; however, when it occurs in persons past 70, as it frequently does, it may last for a year or more (Doggart, 1933). Even after resolution of pain, there may be areas of hypesthesia and hyperalgesia as well as scarring and pigmentation of the skin (Figure 36.6B). There may be weakness of the masseter and pterygoid muscles on the ipsilateral side.

The treatment of both the acute phase of herpes zoster and the persistent, postherpetic neuralgia must be considered one of the most vexing and discouraging therapeutic problems confronting any physician. There is no treatment that can be relied upon to give either partial or complete relief in all cases. Acute herpes zoster has been treated with autohemotherapy (Beesom, 1928; Barksdale, 1937), vitamins (Vorhaus, 1937; Borgoon el al., 1957), radiotherapy (Borgoon et al., 1957), Protamide (Vorhaus, 1937), diphtheria antitoxin (Walker and Walker, 1938), hyperimmune serum (Gunderson, 1940), smallpox vaccine (Lillie, 1943), systemic corticosteroids and/or adrenocorticotropic hormone (ACTH) (Scheie and McLellan, 1959; Elliot, 1964; Eaglstein et al., 1970; Epstein, 1973), 5-iodo-2-dioxuridine (Juel-Jensen et al., 1970; Marsh, 1977), cytabarine (Pierce and Jenkins, 1973), interferon (Groth et al., 1978), and acyclovir (Weller, 1983, a and b). Of these agents, only interferon and acyclovir appear to hold significant therapeutic promise.

Kernbaum and Hauchecorne (1981) treated 47 patients with acute herpes zoster with either oral levodopa and benserazide or placebo in a double-blind controlled study. They analyzed both the total patient group and a ``high-risk'' group of patients older than 65 years. In both groups, those patients who received levodopa had a significant decrease in pain intensity, more frequent complete cessation of pain, and less frequent occurrence of postherpetic neuralgia. This regimen would also appear to be of benefit.
As a general rule, surgical treatment of acute herpetic pain has been unsuccessful; however, Olson and Ivy (1981) performed stellate ganglion blocks in 27 patients with herpes zoster ophthalmicus and achieved dramatic reduction in pain. Because of the retrospective nature of this investigation, the lack of adequate patient numbers, and the absence of controls, no conclusion on the efficacy of this treatment can be made; however, Olson and Ivy believe that their results justify the establishment of a double-blind controlled trial of local stellate ganglion block in patients with acute herpes zoster.

Treatment of postherpetic neuralgia has also proved disappointing. Taub (1973) reported relief with psycho-therapeutic drugs, and both intravenous Procaine (Shanbrom, 1961) and sensory nerve block with Bupivacaine (Hannington-Kiff, 1971) have been reported as being effective. As noted above, in a double-blind, controlled study, Kernbaum and Hauchecorne (1981) found that herpes zoster patients treated acutely with levodopa and benserazide had less frequent postherpetic neuralgia than did patients receiving placebo. Dr. Melvin Epstein, Associate Professor of Neurosurgery at The Johns Hopkins Hospital, has used a combination of amitriptyline hydrochloride (Elavil) and fluphenazine hydrochloride (Prolixin) with some success in patients with both acute and chronic herpes zoster. Rowbotham et al (1995) found that topical lidocaine gel may relieve postherpetic neuralgia by direct drug action on painful skin. I have found that the combination of baclofen (Lioresol) and carbamazepine (Tegretol) which appear to act synergistically may be quite helpful.
 

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