PubMed · 14807434
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N K WESLEY, G N JESSEN, D PATTIS. 1950-11-09. Corneal vascularization.. https://pubmed.ncbi.nlm.nih.gov/14807434/
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This paper explores the seminal contributions of David Maurice to the field of ophthalmic instrumentation. His development of the specular microscope, the scanning slit optical confocal microscope, and the corneal microfluorometer resulted in advances in our understanding of corneal morphology, physiology, and pathology. The development of the scanning slit, clinical confocal microscope is not a new paradigm or a paradigm shift, but a continuous series of interlinked technical advances from the early work of Vogt to Thaer's development of a clinical confocal microscope. For each instrument both the connection to the prior work of others and the unique advances are discussed and contrasted. This paper develops the connections and parallel developments in the instrument developments of Goldmann, Maurice, Svishchev, Baer, Koester, Masters, and Thaer. The evidence in support of the thesis consists of published papers, patents, personal communication, and study of Goldmann's book collection in Bern. A second theme is that knowledge of physics is a prerequisite for optical instrument development in ophthalmology. David Maurice had a university degree in physics and Hans Goldmann learned physics from his books. The contributions of David Maurice to optical instrumentation follow the major contributions of Goldmann and facilitated and stimulated other scientists who acknowledged their important intellectual debt to David Maurice.
The thickness of the cornea was reported in more than 100-year-old textbooks on physiological optics (Helmholtz, Gullstrand). Physiological interest was revived in the 1950s by David Maurice, and over the next 50 years, this 'simple' biological parameter has been studied extensively. Several techniques for its measurement have been described and physiological and clinical significance have been studied. In this review, the different methods and techniques of measurement are briefly presented (optical, ultrasound). While the corneal thickness of many animals are the same over a considerable part of the surface, in the human cornea anterior and posterior curvature are not concentric giving rise to a problem of definition. Based on this the precision and accuracy of determining the central corneal thickness are discussed. Changes in corneal thickness reflects changes in function of the boundary layers, in particular the endothelial barrier. The absolute value of thickness is of importance for the estimation of IOP but also in diagnosis of corneal and systemic disorders. Finally it is discussed to what extent the thickness is a biometric parameter of significance, e.g. in the progression of myopia or in the development of retinal detachment.
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.