Syncope and the eye

W Wieling*, R.K. Khurana #
Department of Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam (The Netherlands); # Division of Neurology, Union Memorial Hospital, Baltimore, Maryland (U.S.A).

Case Reports

A 52-year-old male physician was referred to our syncope unit for evaluation of unexplained loss of consciousness. He had no history of cardiovascular or other medical problems. He was physically active and used no medication. The patient was playing a tennis match when he was hit hard by the tennis ball on the left eye. Immediately after the impact, he dropped to the floor and lost consciousness for a few seconds. On regaining consciousness he felt well and continued playing at his normal capacity.

The next day he visited his general practitioner. His general physical and somatic neurological examination including functions of trigeminal nerves were normal. He was referred to a cardiologist. The electrocardiogram, echocardiogram, 24-hour holter monitor study, and exercise stress test were normal. He was referred to our unit for analysis of unexplained syncope.

The patient declined further laboratory assessment. His only interest was an explanation of the event in order to reassure his concerned spouse. Based on a typical history, syncope due to eyeball pressure was diagnosed. The underlying mechanism was explained to the patient, and he felt reassured.


Editor's Comments

An unexplained attack of syncope in an otherwise healthy individual is an alarming event for the patient. In order to explain the occurrence of transient loss of consciousness to the patient, knowledge of the involved mechanism is required [1]. In our patient, syncope due to sudden pressure on the eyeball (oculocardiac reflex, OCR) was diagnosed. The OCR was first described in 1908 by Bernard Aschner of Vienna and Guiseppe Dagnini of Bologna in almost simultaneous independent reports [2][3]. The OCR is a physiological response of the heart to physical pressure on the eyeball and orbital contents, including extraocular muscles. It is characterized by bradycardia or cardiac arrhythmia, which may lead to cardiac asystole. This is a trigiminal-brainstem-vagal reflex. Aschner demonstrated that the reflex was abolished by cutting the trigeminal nerve [2]. Gandevia and colleagues showed that vagotomy or atropinization almost abolished bradycardia, and a slight residual bradycardia still evoked by eyeball pressure was eliminated after administration of propranolol. This suggests that vagus (predominantly) and sympathetic nerves constitute efferent limbs of the OCR [4].

Besides the usefulness of OCR as a technique in the unarmed combat to produce syncope or death [5], it has been used for several diagnostic and therapeutic purposes. Gastaut found enhanced OCR in patients prone to vasovagal syncope [6]. Lambroso and Lerman demonstrated a sixty-one percent incidence of asystole exceeding two seconds induced by eyeball pressure in infants with pallid breath-holding spells, while twenty-five percent of the infants in the cyanotic group and seven percent of the control group had such a period of asystole [7]. Stephenson employed the OCR to differentiate between syncopal and epileptic seizures in infants syncopal group demonstrating hypersensitive OCR with asystole ≥ 4 seconds [8]. The OCR has been reported to be beneficial in aborting or attenuating attacks of paroxysmal atrial tachycardia. This reflex is routinely elicited by ophthalmologists during strabismus surgery when traction is applied to the extraocular muscles [9]. This can serve as a surgical aid in identifying a slipped or lost extraocular muscle during surgery. More often, however, the OCR can occur as an intraoperative complication of the procedure and may be potentially fatal [10].

Although stimulation of the trigeminal nerve at diverse sites, peripheral and central to the trigeminal ganglion, including the trigeminal tract and nucleus, can produce bradycardia, this discussion is confined to ocular stimulation Besides pressure on the globe or traction on the extraocular muscles, OCR can be induced by several other ocular manipulations, including blepharoplasty, laser in situ keratomileusis (lasik), subconjuctival injection, cataract extraction, contact lens insertion, acute glaucoma, removal of a foreign body from the cornea, and insertion of Schirmer’s lacrimation strips [9][11][12][13][14][15]. It is easy to presume that stimulation of the trigeminal afferents induces the OCR in all such patients. In a patient, in whom application of Schirmer’s lacrimation strips in each conjuctival sac caused vasodepression and cardioinhibition, chemical deafferentation with topical administration of proparacaine hydrochloride did not influence vasodepression or cardioinhibition. This indicates lack of contribution from trigeminal afferents and raises the possibility that some of the reported cases of bradycardia in response to ocular stimulation belong to vasovagal type of situational syncope [15].


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