| Brent Hanson - LasikFraud.com 2005-04-28, 8:54 am |
| Neural Basis of Sensation in Intact and Injured Corneas
Experimental Eye Research 78 (2004) 513-525
Carlos Belmonte, M. Carmen Acosta, Juana Gallar
Instituto de Neurociencias de Alicante, Universidad Miguel HernaŽndez-CSIC,
Apdo correos 18, 03550 San Juan de Alicante, Spain
Abstract
A renewed interest in the characteristics and neural basis of corneal and
conjunctival sensations is developing in recent years due to the high
incidence of discomfort and altered sensitivity of the cornea following
refractive surgery, use of contact lenses and dry eyes. Corneal nerves are
functionally heterogeneous: about 20% respond exclusively to noxious
mechanical forces (mechano-nociceptors); 70% are additionally excited by
extreme temperatures, exogenous irritant chemicals and endogenous
inflammatory mediators (polymodal nociceptors), and 10% are cold-sensitive
and increase their discharge with moderate cooling of the cornea (cold
receptors). Each of these types of sensory fibres contributes distinctly to
corneal sensations. Mechano-nociceptors mediate, sharp acute pain produced
by touching of the cornea. Polymodal nociceptors elicit the sustained
irritation and pain that accompany corneal wounding; cold receptors evoke
cooling sensations. Depending on the relative activation by the stimulus of
each subpopulation of corneal sensory fibres, different subqualities of
irritation and pain sensations are evoked. Corneal sensations can be
explored experimentally in humans with a gas esthesiometer that applies
controlled mechanical, chemical and thermal stimuli to the corneal surface.
When the cornea is wounded, corneal nerves are excited and eventually
severed in a variable degree and local inflammation is produced. Activated
corneal nerves release neuropeptides (SP, CGRP) that contribute to the
inflammatory reaction (neurogenic inflammation). They also become sensitized
by local inflammatory mediators, such as prostaglandins or bradykinin and
thus exhibit spontaneous activity, lowered threshold and enhanced responses
to new stimuli. This leads to spontaneous pain and hyperalgesia. Nerves
destroyed by injury soon start to regenerate and form microneuromas that
exhibit abnormal responsiveness and spontaneous discharges, due to an
altered expression of ion channel proteins in the soma and in regenerating
nerve terminals. Presumably, this altered excitability is the origin of the
lowered sensitivity and the spontaneous pain, dry eye sensations and other
disaesthesias reported in patients following refractive surgery.
Author Keywords: pain; corneal nerves; ocular surface; sensitivity;
conjunctiva; dry eye; corneal inflammation; photorefractive keratectomy;
laser-assisted in situ keratomileusis; nerve injury
The complete article in Adobe PDF Format may be downloaded here:
http://journals.ohiolink.edu/local-...55336425362.pdf
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