Journal of Neuro-Ophthalmology, March 1991, Volume 11, Issue 1

Bee sting optic neuritis. A case report with visual evoked potentials.

Simultaneous recordings of the pattern visual evoked potential and the pattern electroretinogram were recorded in a case of unilateral optic neuritis following a bee sting on the eye. The patient presented with severe eye pain, apoplectic visual loss, acute optic disc swelling and minimal signs of ocular inflammation and eyelid edema. The vision failed to recover. The electrophysiological recordings initially showed a delay in the P100 wave of the pattern visual evoked potential. On follow-up, a normal latency and amplitude of the P50 wave of the pattern electroretinogram was recorded with the flattening of the N95 component, but the pattern visual evoked potential was absent. The data suggests that the optic nerve was demyelinated acutely, and that subsequently axonal loss and degeneration of retinal ganglion cells occurred.

Journal of Clinical Neuro- ophthalmology 11( 1): 45-- 49, 1991. Bee Sting Optic Neuritis A Case Report with Visual Evoked Potentials Hu- Shien Song, M. D., and Shirley H. Wray, M. D., Ph. D., F. R. C. P. © 1991 Raven Press, Ltd., New York Simultaneous recordings of the pattern visual evoked potential and the pattern electroretinogram were re­corded in a case of unilateral optic neuritis following a bee sting on the eye. The patient presented with severe eye pain, apoplectic visual loss, acute optic disc swelling and minimal signs of ocular inflammation and eyelid edema. The vision failed to recover. The electrophysio­logical recordings initially showed a delay in the PIOO wave of the pattern visual evoked potential. On follow­up, a normal latency and amplitude of the PSO wave of the pattern electroretinogram was recorded with the flat­tening of the N9S component, but the pattern visual evoked potential was absent. The data suggests that the optic nerve was demyelinated acutely, and that subse­quently axonal loss and degeneration of retinal ganglion cells occurred. Key Words: Bee sting optic neuritis- Pattern visual evoked potential- Pattern electroretinogram. From the Unit for Neurovisual Disorders, Department of Neurology, Massachusetts General Hospital, Boston, Massa­chusetts, U. S. A. Address correspondence and reprint requests to Dr. Shirley H. Wray at Massachusetts General Hospital ACC 837, 15 Park­man Street, Boston, MA 02114, U. S. A. /.-.~~------~~, 45 Bee stings in the eye or on the adjacent areas of the head or face are a well- recognized cause of acute ocular inflammation. The inflammatory reac­tion is usually confined to the anterior segment of the eye, and acute mucopurulent keratoconjunc­tivitis with corneal infiltrates is the most common manifestation ( 1,2). Corneal perforation, iritis, hy­phema, an anterior or posterior lens capsular opac­ity, lens subluxation, mydriasis, and internal oph­thalmoplegia have also been reported ( 3- 6). Involvement of the retina or of the optic nerve is, however, extremely rare; only five cases of optic neuritis following an insect sting have been re­ported. The first case was published in 1960 by Goldstein et al. The patient, a 30- year- old man, lost vision in the left eye ( OS) 2 weeks after a bee sting on the left temple had caused left- sided facial swelling ( 7). The eye examination showed no ab­normality in the right eye ( 00). Vision was 6/ 7 ( 20/ 23) as with a full peripheral visual field and enlargement of the blind spot. The fundus showed swelling of the optic disc with capillary engorge­ment and a few peripapillary hemorrhages. A di­agnosis of optic neuritis was made. Over the next two months the disc edema resolved. No change in the vision was reported. Walsh and Hoyt examined a boy 7 years after he had lost vision in one eye following a bee sting on the upper lid ( 8). Fundoscopy revealed optic atro­phy, narrowing of the retinal arterioles and exten­sive sheathing of the retinal veins. These authors concluded that the optic neuropathy was the se­quel to an attack of papillitis caused by the bee sting. A third case of optic neuritis following an insect sting was reported by Konstas and Nikolinakos ( 9). Their patient was stung on the upper lid by a wasp and developed impaired visual acuity to 20/ 46 11- 5. SONG AND S. H. WRAY 40 00 within 1 week. Vision then recovered grad­ually over several weeks to near normal acuity, but a small paracentral scotoma persisted. In this case, the optic nerve lesion was presumed to be retro­bulbar, since the disc appeared normal acutely and on follow- up. Breen et al.' s patient was the most severely af­fected case ( 10). He was a 72- year- old man who sustained multiple bee stings to the hands, arms, and neck; within 24 hours he developed sudden painless loss of vision bilaterally. Visual acuity 00 was reduced to 20/ 60 and as was reduced to counting fingers at 2 feet, accompanied by marked swelling of the optic discs and peripapillary retinal hemorrhages. The patient was treated with pred­nisone 100 mg daily with the dose tapered over 1 month. Six months later, visual acuity was re­ported to be 20/ 20 00 and 20/ 20 as. Singh et al. published the case of another wasp sting victim, a 36- year- old woman agricultural la­borer who had multiple wasp stings on the head, neck, and hands, followed by severe local pain and swelling ( 11). The edema of the face and eyelids prevented her from opening her eyes for 2 days. When the swelling subsided, vision was found to be reduced to counting fingers at 1 foot in both eyes ( aU), with dense central scotoma. There was no inflammation of the anterior segments, but both optic discs were hyperemic and swollen. There were no systemic or neurological complica­tions. Steroid treatment was given, and she re­ceived a daily retrobulbar injection of dexametha­sone 0.5 ml and oral betamethasone 3 mg, together with chlorpheniramine maleate 12 mg for 1 week. In the second week, the retrobulbar injections were stopped and oral betamethasone was re­duced to 1.5 mg daily for several days and tapered to 0.5 mg daily for 2 more weeks. Within 5 days of starting the treatment, the visual acuity recovered promptly to 80% of the final visual acuity. 20/ 30 00,20/ 40 as, and the optic discs were observed to be almost normal. In all of these patients, the authors postulated that the neuritis was due to an allergic reaction to the insect venom, and they accepted that both the delay in onset and the minimal inflammatory re­action in the anterior segment were consistent with this etiology. The purpose of this paper is to report a case of unilateral optic neuritis following an insect sting on the eye in a patient in whom we had the unique opportunity to record simultaneously the pattern visual evoked potential ( pattern VEP) and the pat­tern electroretinogram ( pattern ERG). ''''.' " I'hihulmol, Vol. 11, No. 1, 1991 CASE REPORT In July 1985, a healthy 38- year- old man was hit in the left eye by a flying insect thought to have been a bee, while mowing the grass. He immedi­ately developed pain, irritation, redness, tearing, and blurred vision in that eye. Within hours, an ophthalmologist recorded a visual acuity of 20/ 20 00 and 20/ 200 as accompanied by a dense ceco­central scotoma in the left eye. There was also min­imal conjunctival injection and blurring of the op­tic disc margin nasally, superiorly and inferiorly without any abnormality of the macula or periph­eral retina. Later the same day, the acuity dropped to counting fingers but over the next 24 hours the acuity recovered to 20/ 200. The dense cecocentral scotoma and disc swelling remained unchanged, and the rest of the eye examination showed no abnormality. A diagnosis of optic neuritis was made and the patient was referred to a neurolo­gist. No abnormality was found on examination of the central nervous system. A noncontrast com­puterized tomogram ( CT) of the brain and orbit was normal. A lumbar puncture was performed 7 days after the sting and showed an opening pres­sure of 180 mmHg, 12 RBCs/ cmm, 1 WBClcmm, protein 55 mg/ dl ( normal 15- 45 mg/ dl), glucose 76 mg/ dl ( normal 50- 75 mg/ dl), myelin basic protein of < 2mg/ dl ( normal 0- 4 mg/ dl), and a nonreactive VORL. Cultures for bacteria and tubercle bacilli were negative. The patient was treated acutely, starting on the third day after the sting, with oral prednisone 60 mg daily for 10 days; the prednisone dose was then tapered over 2 weeks and stopped. There was no recovery of vision. He was then re­ferred to us for a second opinion. The neuro- ophthalmic examination performed 2 months after the ocular sting documented no ab­normality in the right eye. Signs in the left eye were an acuity of counting fingers at 3 feet; ab­sence of color vision; a dense cecocentral scotoma to the I4e and I2e isopters with a full peripheral field; an afferent pupil defect; no proptosis; full eye movement without nystagmus; and temporal pal­lor of the disc without retinal arterial or venous changes. A contrast CT of the brain with axial and coronal views showed no abnormality, apart from a retention cyst in the maxillary antrum and a small venous angioma on the medial surface of the left frontal lobe. Magnetic resonance imaging ( MRl) of the brain, without gadolinium, showed no focal white matter lesions. The pattern YEP and pattern ERG were recorded by one of us ( H- SS). The standard eIectrophysio- /------'" BEE STING OPTIC NEURITIS 47 logical methods used in our laboratory are re­ported elsewhere ( 12). We chose to use a Burian­Allen bipolar contact lens to record the pattern YEP and the pattern ERG simultaneously in the left eye to assure proper fixation. In the right eye, however, because of the discomfort from the con­tact lens, a gold foil electrode was used. Table 1 shows the serial measurements for latency and amplitude of the PI00, the major positive wave of the pattern YEP, and for the P50, the major posi­tive wave of the pattern ERG. The stimulus used was a reversing black and white checkerboard, check size of 50 minutes of arc. The results were compared with normative data for the pattern YEP and the pattern ERG for our laboratory ( 12,13). In 1985, the initial pattern YEP recording showed a prolonged latency of PI00 of 122 msec as and a normal latency of the PlOO of 97 msec 00 ( normal mean: 102.0 ± 5.5 msec for check size 50') ( Fig. 1). At follow- up two years after the sting, the simultaneous recording of the evoked potentials showed that the PI00 of the pattern YEP was ab­sent in the left eye in the presence of a normal latency ( 48 msec) and amplitude ( 3.3 Il- V) of the P50 of the pattern ERG ( normal mean 48.5 ± 2.5 msec: amplitude 2.1 ± 0.7Il- V). A similar recording 4 years after the sting is shown in Fig. 2. At that time, the visual acuity as was 20/ 200, the cecocen­tral scotoma was unchanged and temporal pallor of the optic disc was present ( Fig. 3). DISCUSSION Bees and other species of the family Hy­menoptera, i. e., wasps, hornets, and ants, are known to produce pain when they sting their vic­tim, and it is well recognized that the sting can be associated in some individuals with a severe aller­gic reaction or death. The sting, a modified ovipos­itor in the female, contains venom, which is a com­plex mixture of many biogenic amines, enzymes, and polypeptide toxins ( 14). Histamine, dopamine and norepinephrine are three amines found in bee venom. These amines cause immediate pain and swelling after release. The venom of all species of Hymenoptera also con­tains the enzymes hyaluronidase and phospholi­pase. Hyaluronidase potentiates the effects of the other venom factors. Phospholipase, on the other hand, attacks structural lipids in biologic mem­branes directly. This enzyme can cause failure of cell function and increased vascular permeability. Phospholipase also causes histamine release from mast cells ( 15). In addition, four polypeptide toxins, melittin, apamin, mast- cell degranulating peptide, and min­imine, have been discovered in bee venoms ( 16). Melittin, the major toxin, is highly basic and has strong surface activity that increases the perme­ability of red blood cells and other cells. This toxin causes a considerable degree of cellular damage as well as the release of cellular components, e. g., lysosomal enzymes from leukocytes, serotonin from thrombocytes, and histamine from mast cells. Melittin produces pain and increases capillary per­meability. Apamin, in contrast to melittin, has a highly specific mode of action causing central ner­vous system excitation. Mast- cell degranulating peptide also has a specific activity; it causes hista­mine release from mast cells immediately after a TABLE 1. Serial measurements of the latency and amplitude of the P100 wave of the pattern VEP and the P50 wave of the pattern ERG and the normal range of all parameters to check size 50' ( 13) PVEP PERG P100 P50 Latency ( msec) Amplitude ( fJ. V) Latency ( msec) Amplitude ( fJ. V) Date 00 OS OD- OS 00 OS OD- OS 11/ 85 97.0 122.0 25.0 4.0 3.0 11/ 87 95.0 A 3.5 0 5/ 88 98.0 A 3.0 0 8/ 89 97.5 A 3.0 0 10/ 89 A 0 P100 00 49.5 OS 48.0 50.0 48.0 50.0 OD- OS 1.5 P50 00 2.1 OS 3.3 1.9 2.6 1.9 OD- OS 0.5 Latency ( msec) Latency ( msec) Amplitude ( fJ. V) Normal range mean + SO OD- OS Amplitude ( fJ. V) mean ± SO OD- OS mean ± SO OD- OS mean ± SO OD- OS 102.0± 5.5 7.9 11.4± 3.5 6.4 48.5± 2.5 7.0 2.1 + 0.7 1.1 OO- OS, upper limit of the normal inter- eye difference established at 2 standard deviations above the mean; A, absent potential. JClin Neuro- ophthalmol, Vol. 11, No. 1, 1991 IfS. SONG AND S. H. WRAY as 4 ). l V FIG. 1. Two superimposed recordings of pattern VEP in the right eye ( A) and in the left eye ( 8) two months after a bee sting in the left eye, showing a delayed P100 in the left eye. The P100 00 had latency 97 msec, amplitude 4 fLV; the P100 as had latency 122 msec, ampli­tude 3 fLV. P100 100msec 2S6msec bee sting. Minimine, a minor constituent of bee venom, appears to have a toxic effect similar to melittin. Phospholipase, hyaluronidase, and some pep­tide toxins are potential allergens to humans, and exposure can result in various types of allergic re­actions, ranging from an acute local reaction to se­vere systemic anaphylaxis ( 17). Such reactions are not uncommon, but the delayed onset of remote manifestations, i. e., encephalitis ( 18,19), Guillain­Barre syndrome ( 20), and optic neuritis, are less common and not always readily recognized. Also, the precise nature of the acute pathological changes in central nervous tissue following such an allergic response is unknown. In our single case study, we believe the results of the simultaneous recording of the pattern YEP and pattern ERG permit us to propose a mechanism for the optic nerve lesion. The initial observation of the markedly prolonged latency of the PlOO wave of the pattern YEP, clearly suggests that the optic nerve was acutely demyelinated and that ische­mia, which characteristically produces only a mild delay in nerve conduction, did not playa major role ( 21,22). Two years later, the loss of the pattern YEP indicated a complete block of optic nerve con­duction and implied that the demyelination was irreversible and that there had been secondary de­generation of denuded axons and retinal ganglion cells. Coupled with this observation was the find­ing that both the latency and the amplitude of the P50 of the pattern ERG was normal ( Fig. 2), which indicates normal viability of the proximal retinal cells ( i. e. photoreceptors and Muller cells) in the macular area ( 23,24). Consistent with this is the flattening of the N95 component of the pattern ERG in the affected left eye compared to a normal amplitude N95 [ 1.3 fJ- V ( normal mean 1.7 ± 0.6 fJ- V)] OD ( A) os ( B) FIG. 2. Simultaneous recording of the follow- up pattern VEP ( A, 00; 8, OS) and pattern ERG ( A', 00; 8', OS), show­ing normal P50s of the pattern ERG in both eyes and an absent pattern VEP in the left eye and flattening of the N95 component of the pattern ERG as com­pared to a normal amplitUde [ 1.3 fLV 001 ( normal mean 1.7 ± 0.6 fLV)]. 4 flY [ 100msec 250msec /---------......... A BEE STING OPTIC NEURITIS B 49 FIG. 3. Fundus photography comparing normal disc OD ( A) with OS showing a sector of temporal pallor ( B). in the right eye ( Fig. 2) since the N95 component is selectively affected in diseases of the optic nerve ( 13,25,26). From these data, we concluded that demyelin­ation of the optic nerve had occurred as a result of an acute allergic response to a toxin and that this process had been confined to the optic nerve, since neither the cerebrospinal fluid nor the brain MRI revealed any evidence of disseminated demyeli­nating disease. In this case focal demyelination with ensuing axonal and ganglion cell loss thus appears to reflect the effect of the bee venom. REFERENCES 1. Young CA. Bee sting of the cornea. Am I Ophthalmol 1931; 14: 20~ 16. 2. Smolin G, Wong I. Bee sting of the cornea: case reports. Ann Ophthalmol 1982; 14: 342- 3. 3. Gilboa M, Gdal- on M, Zonis S. Bee and wasp stings of the eye. Retained intralenticular wasp sting: a case report. Br I OphthalmoI1977; 6l: 622- 4. 4. Knannig HD. Skleraverletzung durch Bienenstich und hin­tere sternformige katarakt ( Scleral injury by bee sting and posterior stellate cataract). Klin Monatsbl Augenheilkd 1955; 126: 250- 3. 5. Singh G. Bee sting of the cornea. 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Vol. 11, No. 1, 1991