The Eye

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Chapter 4 The Eye

A. Generalities

The eye is often bypassed or cursorily examined. Yet from measurement of visual acuity to funduscopy, all components of the exam can unlock important secrets, not only of the eye but also of the body. Some findings are so important that they should be recognized by all practicing physicians.

C. Visual Fields

21 Describe the normal anatomy of the visual pathways.

This is quite complex and yet fundamental for the understanding of visual field defects (Fig. 4-1). Our visual world (i.e., visual field) is divided into right and left hemifields. Each eye gets information from both.

image

Figure 4-1 Neurologic visual pathways, and diseases originating from their interruption.

(From Mihailoff G: Crash Course Nervous System. St. Louis, Mosby, 2005.)

After originating in the photoreceptors of the retina, vision is transmitted via the optic nerve axons. These partially cross at the optic chiasm and then emerge as optic tracts, wrapping around the midbrain to finally reach the lateral geniculate nucleus (LGN), where they stop for synapsis. From the LGN, axons fan out through the deep white matter of the brain (parietal and temporal lobe) as optic radiations, ultimately reaching the primary visual cortex in the occipital lobes. The crucial aspect of this entire pathway is its inversion of images, insofar as the nasal retina of the right eye sees the right half of the world (i.e., the temporal half of the visual field), whereas the temporal retina of the right eye sees the left half of the world (i.e., the nasal half of the visual field). As a result, the right nasal retina and left temporal retina see very much the same aspect of the outside world: the right hemifield (i.e., if you drew a line through the world at your nose, they would see everything to the right of that line).

Because of all these crossings, a prechiasmal lesion will be very much akin to losing one eye (i.e., it will affect only one eye but both hemifields). Conversely, chiasmal lesions will affect parts of both eyes and both hemifields (i.e., inputs from the nasal retinas will be lost, thus causing loss of peripheral vision on both sides). Finally, postchiasmal lesions will affect parts of both eyes, but only one hemifield.

The anatomic distribution of the optic radiations follows a wide three-dimensional arc, which first dives into the temporal lobe (Meyer’s loop), then heads back though the parietal lobe, and finally terminates into the occipital lobe. Lesions involving Meyer’s loop (i.e., temporal lobe) cause loss of vision in the upper visual world, but only in the left hemifield. Lesions involving the parietal portion of the optic radiations cause loss of vision in the lower visual world, but only on one side (the left hemifield in this case). Finally, lesions affecting the occipital (visual) cortex cause loss of vision in one hemifield, but with macular sparing (i.e., notched hemifield). This sparing results from either overlapping blood supply or large cortical representation of the fovea.

D. Pupils

37 Why is examination of the pupils important?

Because attention to pupillary shape, size, and response to external stimuli provides extremely valuable clinical information. Figures 4-2 and 4-3 summarize the most common pupil abnormalities.

image

Figure 4-2 Pupil abnormalities.

(From Liporace J: Crash Course Neurology. St. Louis, Mosby, 2006, Fig. 6.3.)

image

Figure 4-3 Additional pupil abnormalities.

(From Mihailoff G: Crash Course Nervous System. St. Louis, Mosby, 2005.)

47 What are the most common causes of anisocoria?

image Simple (physiologic) anisocoria: A normal variant characterized by a physiologic difference of at least 0.4   mm between the two pupils, due, in turn, to an imbalance in muscular tone of the right and left sphincters. It is the most common anisocoria, present at all times in 3% of the population and at some times in up to 20%, with presence or absence depending on day of observation. In contrast to pathologic anisocoria, the physiologic form is characterized by a pupillary difference that does not change with various levels of illumination. Moreover, physiologic anisocoria is chronic, rarely >1   mm and always isolated (i.e., never associated with ptosis double vision or light-near dissociation see later). Hence, presence of concomitant findings makes anisocoria a much more ominous condition.

image Pharmacologic dilation: Another common and benign cause. This can be due to conscious or inadvertent instillation of mydriatic drops (like in Italian Renaissance women) or even to improper nebulization of anticholinergic agents. The latter may create a diagnostic dilemma in intensive care unit patients, whose mental status often waxes and wanes. A response to cholinergic eye drops (such as pilocarpine) may help separating pharmacologic paralysis (which will remain unresponsive) from either Adie’s pupil or a third nerve palsy (which, instead, will constrict in response to topical cholinergics—previously discussed).

image Third cranial nerve palsy (i.e., parasympathetic denervation): This is characterized by (1) ipsilateral mydriasis plus; (2) ptosis (from paralysis of the levator palpebrae); and (3) weakness of all extraocular muscles, with the exception of the lateral rectus and superior oblique (which are the only ones not controlled by the third cranial nerve). Hence, the affected eye will be deviated outward and downward, thus resulting in diplopia. Note that the dilated pupil will still constrict if a cholinergic drop is instilled in the eye. Moreover, due to defective constriction, the anisocoria of third-nerve palsy is greater in bright illumination.

image Horner’s syndrome (Fig. 4-4): First described in 1860 by the Swiss ophthalmologist Johann Friedrich Horner, this is characterized by miosis of the affected pupil (from paralysis of the pupillodilator muscle) plus dysautonomic findings, including (1) ipsilateral ptosis (from paralysis of the superior tarsal muscle), and (2) anhidrosis (from damage to sudomotor fibers). In contrast to physiologic anisocoria, the difference between pupils in Horner’s varies with illumination: greater in the dark (revealing defective dilation) and smaller in bright light (demonstrating intact constriction). Response to cocaine drops is also different: Horner’s worsens, whereas simple anisocoria improves. This has strong predictive value, with sensitivity and specificity > 95%, a positive likelihood ratio (LR) of 96.8, and a negative LR of 0.1. Horner’s should always prompt a search for lesions of (1) the first-order neuron (such as a brainstem stroke, the most common cause of Horner’s on a neurology service; hence, the need for a thorough neurologic exam, with special attention to a lateral medullary syndrome); (2) the second-order neuron (usually a tumor of lung or thyroid, the most common cause of Horner’s on a medical service; hence, the need for a thorough neck/supraclavicular/respiratory exam); or, finally (3) the third-order neurons. These are less common causes of Horner’s, usually due to vascular headache (migraine), trauma or inflammation of the orbit, and cavernous sinus syndrome. Lesions of third-order neurons may preserve facial sweating.

image Miscellaneous: These include (1) inflammatory processes (e.g., unilateral iritis), (2) old trauma, (3) acute angle closure glaucoma, (4) various neurologic disorders, and (5) previous intraocular surgery (i.e., cataract extraction). In case of the red eye (see later), presence of anisocoria argues in favor of a more serious disease.

50 Who was Hutchinson?

Sir Jonathan Hutchinson was an English surgeon and pathologist (1828–1913) who described his homonymous pupil in 1865. A devout Quaker, Hutchinson became involved with many philanthropic missions, and in fact even planned a career as a medical missionary. Instead, he gained the friendship of Sir James Paget and became one of the most versatile clinicians of 19th-century medicine. Besides being an ophthalmologist, he was also a venereologist, a clinician to the City of London Chest Hospital, and a general surgeon to the London and Metropolitan hospitals. He developed a special interest in congenital syphilis and was said to have seen more than 1 million patients. He published 1200 medical articles, with contributions in congenital syphilis and skin diseases (he also was among the first to describe sarcoidosis in 1877). Although his intellectual attributes were unchallenged, he had his critics, too. One commented: “He was totally devoid of any sense of humour, and like most humourless men, incredibly obstinate in clinging to his opinions long after they had been demonstrated to be untenable.” Another added: “There was nothing scintillating about it, but nonetheless you felt he was speaking out of immense knowledge.” In his private life, Hutchinson had 31 years of happy marriage and many children but kept his family in a country home while spending most of his week in London. He died at 85, choosing as an epitaph: “A Man of Hope and Forward-Looking Mind.”