Optic Nerve; Orbit, Eyeball, Vision
The orbit lies beneath the anterior cranial fossa. It is covered anteriorly by the eyelids and contains the eyeball, embedded in fat. Each eyelid has a firm, fibrous tarsal plate, and the upper and lower tarsal plates are joined by the medial and lateral palpebral ligaments: only the medial palpebral ligament is attached to bone. The posterior surface of the eyelids is covered with conjunctiva and this passes onto the front of the eyeball. When closed, the eyelids form a sealed conjunctival sac; tear fluid produced by the lacrimal gland (in the superolateral aspect of the orbit) passes through its ducts into the conjunctival sac and lubricates the front of the eyeball.
The fluid is drained medially through lacrimal canaliculi (figure 5), opening onto the medial end of each lid margin; it passes to the lacrimal sac and duct to drain into the nose. Because of the medial bony tarsal attachment, when the eyes blink or are screwed up, tears are massaged medially towards the lacrimal apparatus.
The eyeball is surrounded by orbital fascia and medial and lateral (check) ligaments attach it to the lacrimal and zygomatic bones respectively, suspending it within the orbital cavity and allowing it to be moved by the extraocular muscles.
The optic nerve passes back from the posteromedial aspect of the eyeball, and through the optic canal into the middle cranial fossa. The medial fibres from each side cross (decussate) to the opposite side in the optic chiasm. Beyond this level, each visual pathway receives impulses from the contralateral field of both eyes.
Diseases of the orbit encompass a large number of conditions, including those of the surrounding skin, the eyelids and the orbital contents. Internal and external angular dermoid cysts represent developmental abnormalities. The skin around the eyelids is a common site for congenital vascular malformations (capillary hemangiomas/ strawberry nevi) and skin tumours, particularly basal cell carcinomas. Facial edema, from myxedema and other general and local causes, usually affects the lax periorbital skin.
The edges of the eyelids and their eyelashes may be turned inwards (entropion), causing corneal abrasion, or outwards (ectropion), preventing adequate closure of the conjunctival sac and corneal protection. Retention cysts occur along the lid margin from the glands of Moll and sebaceous glands (meibomian cysts/chalazion). These cysts may become infected, and there may be infection of a hair follicle (stye), and infection of the conjunctiva (conjunctivitis) or lacrimal apparatus (dacrocystitis).
Conjunctivitis may be due to an allergy, foreign bodies, chemicals, trauma, and a number of viral and bacteriological agents. Infection from Chlamydia trachomatis is common across the tropics and trachoma is one of the commonest causes of blindness in the world. A red eye is a common differential diagnosis. It usually is related to inflammatory conditions but an important differential diagnosis is glaucoma.
Eye injuries include orbital fractures. A blow-out fracture of the orbit (as from the impact of a squash ball) may force the orbital contents through its thin walls into the nose, the anterior cranial fossa or the maxillary air sinus. Hemorrhage from the orbit may extend visibly underneath the conjunctiva (an important differential diagnosis is from a spontaneous subconjuntival hemorrhage, where the staining does not go beyond the cornea, and is usually of no clinical significance, although the blood pressure should be checked). Temporomaxillary fractures may alter the suspension of the eye and produce diplopia; these fractures may also damage the infraorbital nerve (giving anesthesia of the lower eyelid and upper lip) and affect movement of the temporomandibular joint.
Expansion of the orbital contents can produce proptosis, this may just affect the eyeball, as with the exophthalmus of thyrotoxicosis, but also includes severe infection, cavernous sinus thrombosis, and tumors of the orbit and its contents.
Visual disorders may be related to corneal disease, opacity of the lens (figure 6). Disorders of the eyeball (including retinal detachment, central retinal artery occlusion, diabetic retinopathy, and tumors such as retinoblastoma and malignant melanoma) and disease of the visual pathway. Raised intracranial pressure produces papilledema, this swelling of the optic disc is an important physical sign.
Damage to the optic nerve produces unilateral visual problem. Multiple sclerosis is the commonest cause of optic nerve disease, but it may also occur with trauma and tumors of the orbit. Pressure on the optic chiasm is usually due to pituitary tumors, and it produces a bitemporal hemianopia, damage beyond this level produces an homonymous hemianopia. Damage to the optic tract, optic radiation and the visual cortex are usually due to primary or secondary malignancy: cortical lesions, are usually congruous (affect the two eyes equally).
When examining the eye, first observe the surrounding skin, the eyelids and their edges (figure 7a,b). Small foreign bodies may be detected beneath the lids and the upper may need to be everted for their removal. Corneal abrasions and ulcers may need outlining by means of a drop of fluorescein.
Observe the retina from a distance through an ophthalmoscope (figure 8) to see a red central disc (red reflex). This is disturbed by opacities within the lens, or of the aqueous or vitreous humor. Observation of the retina using an ophthalmoscope begins with the subject looking straight ahead and then to each position of gaze (figure 9a-c).
In the normal retina, seen through an ophthalmoscope, the pale optic disc is the site of entry of the optic nerve and vessels that radiate from this point, branching dichotomously (figure10a,b). The arteries are brighter red and slightly narrower than the veins. The disc is insensitive to light and is termed the ‘blind spot’. The macula is the central part of the back of the retina; it is lateral to the disc and is largely devoid of vessels, but has a rich capillary network. The central depression beneath the macula is the fovea centralis, where visual resolution is highest.
Retinal changes accompany many vascular and neurological abnormalities, these include alteration of the arteriovenous diameter ratio, appearance of hemorrhages and exudates (figure 10c) and swelling of the optic disc in papilledema (10d).
Optic nerve tests encompass visual acuity, colour and visual fields, together with the visual component of pupillary reflexes.
Distant vision is assessed with a Snellen chart (figure 11a). Two numbers are reported. The first is the distance of the subject from the chart in meters (usually 6). The chart has 8 rows of letters, which can be seen with the normal eye at respectively 60, 36, 24, 18, 12, 8, 6 and 5 meters away. The second number reported is the distance of the smallest line that can be seen. At 6 meters, this is usually the seventh line and the reported vision is 6/6 for the tested eye. If the acuity is less than 6/60, the subject is moved towards the chart (e.g. 3/60).
If the top line cannot be read at one meter (i.e. worse than 1/60) visual acuity is reported as counting fingers (CF), seeing hand movements (HM) or perception of light (PL). Near vision is assessed with J Charts of different size prints, each with an assigned code. Color vision is assessed with an Ishihara Chart (figure 11b). This has the pattern outlined in colors in an otherwise uniform format.
Clinical assessment of the visual field is by confrontation; the observer sits or stands in front of the subject and both cover one opposing eye with a palm (figure 12a-d). The subject fixates on the bridge of the examiner’s nose. The examiner then brings a moving finger, or more sensitively a red headed pin (figure 12e), from outside his/her visual field radially inwards from each quadrant in turn.
A central target is used to identify a scotoma (loss of part of the visual field). The subject is asked to say as soon as the finger is noted, or in the case of the pin, the red colour is identified. The examiner compares this with his/her own observation (assuming he/she has normal vision).
Visual inattention defects are assessed by the examiner moving fingers of both hands, separately or together, the subject is asked to identify which finger(s) move (figure 13a,b).
A more precise mapping of the peripheral fields, and of the blind spot, are obtained using perimetry. The subject’s head is placed, by a chin rest, in the centre of the apparatus. This allows a light to be brought in from all directions. Alternatively, the Bjerrum screen is used, white and red discs are moved radially inwards against a black background. Loss of parts of the visual field and loss of nasal or temporal fields, such as damage to the optic radiation or pituitary tumors pressing on the optic chiasm, can be accurately mapped.
Direct light reflexes are tested with a pen torch, examining each eye in turn (figure 14). Pupillary contraction is noted in the stimulated and the contralateral eye (consensual response).
The accommodation reflex is assessed by asking the patient to fixate on a distant object and then on a finger placed close to the bridge of the nose – the pupil constricting on near vision (figure 15a,b). It may be necessary to retract the upper eyelid to better visualize the pupil. The shape of the pupils may be altered by adhesions from local disease, and the pupillary response by neurological disorders.