The orbicularis oculi response can be evoked both by mechanical stimulation of the cornea (corneal reflex) and by electrical stimulation of the skin overlying the supraorbital nerve (blink reflex). Mechanical stimuli to the cornea activate A delta and C free nerve endings of the corneal mucosa. Electrical stimuli to the supraorbital nerve activate A beta, A delta and C fibers of the nerve trunk. Both reflexes present a bilateral late response, but the blink reflex shows in addition an early ipsilateral component (R1), which has never been observed with the corneal stimulation in man. We have developed a simple technique of electrical stimulation of the cornea which provides stable responses and allows precise measurements of threshold and latency of the reflex. In normal subjects, the threshold ranged from 50 to 350 μA, and the maximal stimulus that the subject could bear (tolerance level) ranged from 1000 to 2500 μA. The minimal latency to tolerance level stimuli was 39 ± 3 msec. The latency difference between the direct responses evoked from the two opposite corneas never exceeded 8 msec and the difference between the direct and consensual responses elicited from the same cornea exceeded 5 msec. An early ipsilateral component similar to the R1 response of the blink reflex was not observed, even with supramaximal stimulation. The electrically evoked corneal reflex was normal in 10 cases of essential trigeminal neuralgia, while the responses showed significant abnormalities in 18 subjects submitted to thermocoagulation of the Gasserian ganglion as a treatment of neuralgic pain, as well as in 2 cases of symptomatic neuralgia. The most frequent change was an elevation of the threshold of the reflex. Among 46 patients with definite multiple sclerosis, the corneal reflex was abnormal in 19 cases while the blink reflex was abnormal in 23. The blink reflex therefore appears to be a more significant test of brain stem pathology than the corneal reflex, mainly because it involves, besides the R2 component, the short latency circuit mediating the R1 component. In fact, among the 23 cases of blink reflex abnormalities, the R2 component was defective only in 14 patients. However, the corneal reflex was abnormal in 2 cases showing normal blink responses. Among 30 patients with hemispheral vascular lesions, the corneal reflex was depressed in 24 and the blink reflex in 15 cases. The defect of the corneal reflex was generally of afferent type, and the most frequent change was an increase of the latency. The blink reflex was less frequently affected, probably because its central pathways are not exactly similar to the circuit mediating the corneal response and have a larger security factor. The defect of the corneal reflex was proportional to the severity of the motor impairment and to the extent of the lesion, but could not be related to any particular site of lesions. It is concluded that the electrical stimulation of the cornea seems to be more reliable than the mechanical stimulation. Besides, some differences exist between the corneal reflex and the blink reflex. First, supraorbital nerve stimulation activates concomitantly large myelinated fibers. Second, the corneal reflex and the R2 component of the blind reflex share only in part the same brain stem circuit, the corneal reflex possessing a larger number of synapses.
|Translated title of the contribution||The corneal reflex in normal subjects and in some nervous diseases|
|Number of pages||6|
|Publication status||Published - 1985|
ASJC Scopus subject areas
- Clinical Neurology