Clinical Ophthalmology Dovepress

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Bilateral vision loss associated

with radiofrequency exposure

This article was published in the following Dove Press journal:

Clinical Ophthalmology
11 December 2012
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Dianna Liu Abstract: A 57-year-old otherwise healthy woman presented with painless binocular vision
Franz Marie Cruz loss 1 week after direct application of radiofrequency energy to her orbits. She had no light
Prem S Subramanian perception bilaterally. Pupils were dilated and not reactive to light. Fundoscopic exam initially
showed optic disc swelling in the right eye and a normal-appearing disc in the left eye. Magnetic
Wilmer Eye Institute, The Johns
Hopkins School of Medicine, resonance imaging of the brain and orbits showed gadolinium enhancement of both intraorbital
Baltimore, Maryland, USA optic nerves. She underwent a course of high-dose steroid treatment without recovery of vision.
Optic discs were pale 11 weeks after injury. With exclusion of other possible causes, this rep-
resents a unique case of irreversible binocular optic nerve damage and blindness secondary to
radiofrequency exposure.
Keywords: optic neuropathy, blindness, radiofrequency, vision loss

Radiofrequency radiation (RFR) is a form of electromagnetic radiation at frequencies

ranging from 3 kHz to 300 GHz. Several household appliances emit RFR, including
the television, radio, microwave oven, and cellular phones. In medicine, RFR is emit-
ted by diathermy equipment, electrocautery devices, magnetic resonance imaging
(MRI) scanners, and hyperthermia devices for cancer treatment. RFR causes damage
by heating body tissues, producing protein denaturation, cell membrane disruption,
and cell death.1
Few papers report optic nerve damage as the result of RFR.2–5 Monocular blindness
resulted as an immediate complication of trigeminal RF rhizotomy for the treatment
of trigeminal neuralgia. Visual loss has also been reported following the use of elec-
trocautery probes to achieve hemostasis in orbital and sinus surgeries. 4,5 Conflicting
data exist on the induction of cataract in humans (primarily radar operators) by low-
level chronic RFR exposure.6 We report on a case of binocular blindness from RFR
exposure for alternative medical therapy.

Case report
A 57-year-old Asian female with no significant past medical history presented to the
neuro-ophthalmology clinic with visual loss in both eyes. Family medical history
Correspondence: Prem S Subramanian was unremarkable. She was a moderate (6.00 D OU) myope. About 18 months
Wilmer Eye Institute, Johns Hopkins
Hospital, 600 North Wolfe Street, before presentation, the patient was collecting rocks in stagnant water and soon
Baltimore, Maryland 21287, USA thereafter developed a sensation of tapeworms in her scalp. She was seen by mul-
Tel 1 410 955 8679
Fax 1 410 614 9240
tiple local dermatologists; no parasites were ever identified. She was diagnosed
Email [email protected] with delusional parasitosis and was advised psychiatric evaluation. She reported

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Liu et al Dovepress

seeing white spaghetti strands of worms across her face

and hearing the movement of the worms in her ears. She
had acquired mebendazole tablets from Hong Kong and had
been self-administering the drug on an intermittent basis.
She had also tried topical treatments with chemicals, such
as turpentine.
When none of these alleviated her symptoms, she
acquired a ProGen II 4050 frequency generator (Resonant
Light Technology Inc, Courtenay, British Columbia, Can-
ada) for bioelectronic therapy, which claims to kill microor-
ganisms. She applied the contact pads on her scalp several
times. Feeling that immature worms were in her eyelids and
lashes, she applied the contact pads (38  88 mm) directly
over her eyelids for a single treatment of each eyelid, during
which the generator output ranged between 90 to 580 kHz
for about 30 seconds at 14 volts. She did not recall the pulse
frequency. She had the contact pads in place for 10 minutes
on her left and 15 minutes on her right eye. During that time
she reported no pain or heat. She felt only the pulsations
“beating her eyelids.” No pressure was applied to the eyelids
to hold the patches in place.
The following day she noted blurred vision in both eyes,
which she described as “snowy.” She had no pain with eye
movement, redness, photosensitivity, or transient visual
obscurations. She denied any headache, fever, numbness,
weakness, or paresthesia. Over the next week, her vision
slowly worsened to complete blindness. She was admit-
ted to a local hospital where computed tomography (CT)
of the head showed moderate atrophic changes in both
frontal lobes. Orbital CT demonstrated myopic globes
without any mass. Magnetic resonance imaging (MRI) of
the brain and orbits with gadolinium contrast showed T2
hyperintensity in the right optic nerve (Figure 1). Cranial
magnetic resonance (MR) venography was unremarkable.
Erythrocyte sedimentation rate (ESR) was 7 mm/hour and
C-reactive protein (CRP) , 0.1 mg/L. Additional work-up to Figure 1 Orbital MRI T2-weighted sequences demonstrating hyperintensity in the
posterior aspect of the right optic nerve (arrows). Hyperintensity is seen in both
exclude autoimmune, nutritional, and inflammatory causes axial (A) and coronal (B) images.
of bilateral vision loss, including complete blood count Abbreviation: MRI, magnetic resonance imaging.
with platelet count, antinuclear antibody (ANA), antibody
markers for neuromyelitis optica, Lyme disease and syphilis, perception in each eye. The pupils were 6 millimeters and
serum levels of vitamin B12 and folic acid, and chest CT nonreactive to light. They constricted on convergence effort.
were normal or negative. She was diagnosed with bilateral Extraocular muscle movements were full. Anterior chambers
retrobulbar optic neuritis and treated with 5 days of 1 gram were deep and quiet. She had mild nuclear sclerotic cataracts
IV methylprednisolone with a tapering dose of oral predni- in both eyes; intraocular pressures were normal. The right
sone starting at 60 mg/day. optic nerve was swollen, while the left optic nerve was tilted
She presented to our clinic 3 weeks after onset of visual with peripapillary atrophy (Figure 2). Both optic nerve heads
loss. On ophthalmic examination, visual acuity was no light were hyperemic. The retinal vasculature, especially the

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Dovepress Bilateral vision loss associated with radiofrequency exposure

Figure 2 Fundus photos at presentation. (A) optic disc swelling in the right eye and Figure 3 Optic disc appearance about 3 months after radiofrequency radiation
(B) a tilted optic disc with peripapillary atrophy in the left eye. injury. Diffuse optic disc pallor is shown in both eyes with (A) resolving right optic
disc swelling and (B) marked arteriolar attenuation.

arterioles, was markedly attenuated in both eyes. There was the left (Figure 3). The retina exhibited marked arteriolar
an inactive chorioretinal scar anterior to the inferior arcade narrowing. On 3 month follow-up, the patient’s vision loss
in the right eye. No retinal hemorrhages, exudates, or cotton was unchanged and there were no significant changes to her
wool spots were appreciated. health. She continued to deny any systemic symptoms.
Fluorescein angiogram of the right fundus showed delayed
filling of the choroid and retina and late dye leakage from the Discussion
optic disc. Late images of the left fundus did not show any We present a patient with subacute, painless, binocular,
abnormal leakage, staining, or capillary nonperfusion. No complete vision loss after orbital RFR exposure. Disc
further treatment was recommended aside from psychiatric swelling with dye leakage on fluorescein angiography
consultation, which the patient refused. was present in the right eye, while the left eye had a
She returned after 8 weeks. Repeat examination normal-appearing disc. Gadolinium-enhancement and T2
revealed vision remained to be no light perception. There hyperintensity of the optic nerves were appreciated on
was diffuse optic nerve pallor of the right eye more than the MRI.

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Liu et al Dovepress

Sudden monocular blindness has been reported as a result fiber layer, circumpapillary telangiectatic microangiopathy,
of trigeminal RF rhizotomy in the treatment of trigeminal and absence of disc leakage on fluorescein angiography. True
neuralgia.2,3 In these cases optic nerve damage resulted from optic disc edema with documentation of optic disc leakage on
misdirection of the stylet to the inferior orbital fissure and fluorescein angiography in our patient points against LHON
into the optic canal where it was in contact with the optic as the diagnosis.
nerve. In three of four reported cases wherein immediate Although arteritic ischemic optic neuropathy (AION)
ophthalmologic referral and assessment were made, fundos- from giant cell arteritis (GCA) has been reported to be
copy revealed normal-appearing optic discs. Pathology of associated with optic nerve enhancement with gadolinium
the optic nerve from one of these cases revealed edematous on MRI,9 vision loss from bilateral simultaneous AION was
axonal fibers and coagulation necrosis with focal areas of unlikely due to absence of other systemic symptoms of GCA.
acute hemorrhage compatible with thermal injury to the optic The optic discs did not exhibit the typical pallid swelling of
nerve 2–3 cm behind the globe.3 AION. ESR, CRP, and platelet count were not elevated, and
Irreversibility of vision loss in our patient suggests that the patient’s age also makes GCA less likely.
there was axonal injury rather than pure demyelination, just Neuromyelitis optica (NMO) may cause bilateral, simulta-
as was seen in the rhizotomy cases. A purely demyelinating neous, severe optic neuritis with poor visual recovery. While
process may be reversible. Electrocautery can cause variable a negative NMO immunoglobulin G (IgG) test does not rule
degrees of demyelination.5 In a case report, it was shown that out NMO, our patient fails to meet the diagnostic criteria for
blindness from electrocautery use during orbital surgery was NMO, which requires not only optic neuritis but also transverse
reversible, with the patient regaining 20/40 vision from no myelitis plus two of three of the following: NMO IgG seroposi-
light perception 10 weeks after surgery. tivity, longitudinally extensive transverse myelitis on imaging,
While the case reports we have mentioned involved and a brain MRI not suggestive of multiple sclerosis.10
direct contact of the optic nerve with the RF-generating Nutritional optic neuropathy is usually characterized
instrument, RF energy can penetrate deeper into the body by slowly progressive, bilateral visual decline. Total vision
and cause heating of remote tissues or organs.1 For example, loss is also unusual in nutritional optic neuropathy.11 Normal
monocular blindness has been reported following electroco- vitamin B12 and folate levels further exclude nutritional
agulation during sinus surgery,4 although even in this case optic neuropathy as the cause of our patient’s vision loss.
the instrument was directly adjacent to the optic canal. In Other causes of bilateral optic neuritis, including sarcoidosis,
our case, the RF source was between 5 and 25 mm from the syphilis, and Lyme disease, were excluded by negative labo-
injured tissue (retinal ganglion cell layer), which is quite ratory test results. Optic neuropathy in these cases is typically
different from previously reported cases. We thus postulate associated with pain and may show a dramatic response to
that thermal injury can occur without direct contact with steroids. Infiltrative optic neuropathy, particularly meningeal
the instrument, which is likely what happened to the patient carcinomatosis, may cause subacute, profound, bilateral
we have reported as the RF application occurred on the vision loss. However, this seems unlikely due to the absence
eyelids. Thermal injury to the retinal ganglion cells might of other neurological signs or MRI findings.
occur though disruption of axonal ultrastructure, including Visual loss by thermal injury following RF exposure is
microtubules,7 which would result in the subacute vision loss rare. Without tissue analysis, the diagnosis of RFR-induced
noted by this patient. Direct thermal injury and occlusion of optic neuropathy is made by exclusion of other entities. We
the retinal and/or optic nerve vasculature is much less likely encourage physicians to inquire about RFR-generating device
to have occurred because immediate severe vision loss would use in patients with optic neuropathy in whom the cause of
be expected in that case. the vision loss may be elusive.
Other possible causes of this patient’s vision loss include
Leber’s hereditary optic neuropathy (LHON), which can Acknowledgments
cause subacute, simultaneous, painless, bilateral, profound This research was supported in part by an unrestricted
vision loss but rarely gives no light perception. Although grant to the Wilmer Eye Institute from Research to Prevent
LHON is more common in men, the rate of vision loss Blindness, Inc, New York, NY, USA.
among women at risk ranges from 8% to 32%.8 LHON in
the acute stage is also characterized by the triad of fundus Disclosure
findings, including pseudoedema of the peripapillary nerve The authors report no conflict of interest in this work.

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Clinical Ophthalmology 2012:6
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Dovepress Bilateral vision loss associated with radiofrequency exposure

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4. Vanden Abeele D, Clemens, A, Tassignon MJ, van de Heyning PH. 10. Thornton IL, Rizzo JF, Cestari DM. Neuromyelitis optica: a review.
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sinus surgery. J Laryngol Otol. 1996;110:261–264. 11. Phillips PH. Toxic and deficiency optic neuropathies. In: Miller NR,
5. Schietroma JJ, Tenzel RR. The effects of cautery on the optic nerve. Newan NJ, Biousse V, Kerrison JB, editors. Walsh and Hoyt’s Clinical
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