The Visual System

Editor's Notes

• #2: Visual system extends from the eye anteriorly to the occipital cortex posteriorly. This pathway is vulnerable to many conditions: such as vascular events, space occupying lesions like tumours, etc.
• #3: In this presentation, I’m going to be talking about the basic anatomy of the visual system, including the structure of the eye, the vascular supply and innervation, the muscles of the eye. Then a little embryology of the retina to have an understanding about its function. After that, I will talk about the physiology of the eye. I will explain the visual pathways and then mention few common pathologies.
• #4: We can divide the anatomy of the eye into Anterior and Posterior structures.
• #5: Explain: Aqueous humour: A water like fluid, produced by the ciliary body, it provides the cornea and lens with oxygen and nutrients. It drains back into the blood stream through the canals of schlemmn. Anterior chamber is the space between cornea and lens. Posterior chamber: is the space between iris and lens. Choroid: a layer of blood vessels between the retina and sclera; it supplies blood to the retina. In the disease called Macular Degeneration, abnormal blood vessels grow into the space between the retina and choroid damaging the macula. The sclera is the white, tough wall of the eye. It along with internal fluid pressure keeps the eyes shape and protects its delicate internal parts.
• #6: Explain: Aqueous humour: A water like fluid, produced by the ciliary body, it provides the cornea and lens with oxygen and nutrients. It drains back into the blood stream through the canals of schlemmn. Anterior chamber is the space between cornea and lens. Posterior chamber: is the space between iris and lens. Choroid: a layer of blood vessels between the retina and sclera; it supplies blood to the retina. In the disease called Macular Degeneration, abnormal blood vessels grow into the space between the retina and choroid damaging the macula. The sclera is the white, tough wall of the eye. It along with internal fluid pressure keeps the eyes shape and protects its delicate internal parts.
• #7: The Optic nerve (Cranial II) is not a peripheral nerve. It behaves like a central tract. It’s myelinated (or covered) by oligodendrocytes (not schwann cells-responsible for peripheral n. myelination) It suffers from the diseases that affect the Central Nervous System, such as Multiple Sclerosis It does not regenerate (unlike peripheral nerves which regenerate after injury) Embryologically speaking, it is an out-pouching from diencephalon It’s covered by meningeal layers (dura, arachnoid and pia matter)- unlike peripheral n. which are covered by a collagenous layer called epineurium. Its function is receiving info. From retina via photoreceptors, which are the rods and cones. These photoreceptors convert light energy-electromagnetic waves- into chemical signals  generate a membrane potential
• #8: Retina Development: from neuroectoderm. It’s a derivative from diencephalon. It comes out as optic vesicle. Then lens invaginate it and then it becomes double layered. The outer layer forms the choroid, and the inner layer forms the retina.
• #9: The first important feature is the optic disc. Note it is not centrally placed. It’s slightly on the nasal side. About 3.5mm from centre of fundus medially. You must be able to appreciate a physiological cup, a clear cut optic disc margins, and retinal vessels. The Macula lutea- very rich in cones. The very centre of it is called fovea centralis which has maximum conc. of cones. So it’s concerned with max. visual acuity. Silver wiring – hypertension
• #10: The optic disc has no rods and cones. So images falling on this point cannot be seen  called physiological blind spot. During a physical examination, the optic nerve can be tested in many ways: Visual acuity is tested by using a snellens chart, counting fingers
• #11: This slide shows the cellular organisation of the retina. The photoreceptors being the deepest layer and the ganglion cells being the most superficial
• #12: There are also connecting cells which basically connect these cells together. For example Horizontal cells connect the terminal bundles of rods and cones. Amacrine cells connect ganglionic cells with each other and also with Bipolar cells Muller cells Oligodendroglial cells- for myelination
• #13: 2. Rods are present more on peripheral parts of retina, their conc becomes less centrally (pupil dilates to include peripheries in dim light) Cones are present more centrally and less on peripheries  pupil constricts to focus light on central parts of retina Rods and cones undergo hyperpolarisation (decreased Na influx) when stimulated. They do not produce an action potential. They produce local or gradient potentials.
• #14: Remember the pneumonic SO4 LR6 which stands for superior oblique supplied by cranial nerve 4 and Lateral rectus supplied by the 6th cranial nerve. muscle movements A given extraocular muscle moves the pupil, at the front of the eye, in a specific direction or directions, as follows: medial rectus (MR)— moves the eye inward, toward the nose (adduction) lateral rectus (LR)— moves the eye outward, away from the nose (abduction) superior rectus (SR)— primarily moves the eye upward (elevation) secondarily rotates the top of the eye toward the nose (intorsion) tertiarily moves the eye inward (adduction) inferior rectus (IR)— primarily moves the eye downward (depression) secondarily rotates the top of the eye away from the nose (extorsion) tertiarily moves the eye inward (adduction) superior oblique (SO)— primarily rotates the top of the eye toward the nose (intorsion) secondarily moves the eye downward (depression) tertiarily moves the eye outward (abduction) inferior oblique (IO)— primarily rotates the top of the eye away from the nose (extorsion) secondarily moves the eye upward (elevation) tertiarily moves the eye outward (abduction)
• #15: See anatomy booklet. How damage of muscle lead to deviation of eye….
• #16: Visual system extends from the eye anteriorly to the occipital cortex posteriorly. This pathway is vulnerable to many conditions: such as vascular events, space occupying lesions like tumours, etc.
• #18: Nasal fields: the half near nose Temporal fields: the half further away from the nose
• #19: So light falls on photoreceptors which are connected to bipolar cells to ganglion cells which have peripheral processes that converge in optic disc then move as Optic nerve. Optic nerve extends from optic disc to optic chiasma. In chaisma nasal fibres decussate (or cross). Fibres then diverge backward and laterally as Optic tracts. Optic tracts move backward and 10% diverge into midbrain and 90% terminate at lateral geniculate bodies. From LGB to calcarine area of brain, optic radiations start. Optic radiations are divided into upper fibres which pass through temporal lobe, and lower fibres which pass through parietal lobe and it’s called the loop of mayer. Disruptions anywhere along the pathway results in a characteristic loss of vision in a particular part of the visual field.
• #20: This diagram shows the common lesions in the visual pathway: -lesion at A (The Right Optic nerve) causes loss of vision in the same eye. This is called . And the cause is usually -lesion at B (Right Optic chiasm) causes loss of vision on both temporal sides of the visual field. The nasal fibers cross in the optic chias and as mentioned before, the nasal fibres carry images from the temporal visual fields. So when damages, vision is lost in the temporal part of the visual field. This is called Bi-temporal hemianopia. The cause is usually a pituitary adenoma pressing on the optic chiasm from below. -lesion at C (Right Optic tract) causes loss of vision on R. nasal field and L. temporal field. That’s because the R. Temporal fibres and L. nasal fibres are damaged. This is called Left homonymous hemianopia -lesion at D (Right Lower radiation fibers) causes loss of vision at the Left upper field. This is called Left homonymous qudrantanopia, or pie in the sky. -lesion at E (Right radiation fibers) causes loss of vision in R nasal and L temporal fields, but sparing the macula. It’s called Left homonymous hemianopia with macula sparing-this is because the occpital lobe has dual blood supply from posterior and middle cerebral arteries. Therefore, strokes affecting occipital lobe may not lead to total infarction of the occipital cortex so sparing the macula. Visual disturbance DOES NOT necessarily mean the problem is in the eyes Visual disturbance can arise from: A pathological process affecting the eye A pathological process affecting brain structures involved in visual processing
• #21: myopia, hyperopia, astigmatism If the incoming light from a far away object focuses before it gets to the back of the eye, that eye’s refractive error is called “myopia” (nearsightedness). Here the image if formed in front of the retina, rather than on the retina! Myopia is the most common refractive error seen in children and can be corrected with eyeglasses or contact lenses. If incoming light from something far away has not focused by the time it reaches the back of the eye, that eye’s refractive error is “hyperopia” (farsightedness). Hyperopia is a condition in which an image of a distant object becomes focused behind the retina, making objects up close appear out of focus. In the case of “astigmatism,” one or more surfaces of the cornea or lens (the eye structures which focus incoming light) are not spherical (shaped like the side of a basketball) but, instead, are cylindrical or toric (shaped a bit like the side of a football).  As a result, there is no distinct point of focus inside the eye but, rather, a smeared or spread-out focus.  Astigmatism is the most common refractive error. The abnormal curvature of the cornea can cause two focal points to fall in two different locations, making objects up close and at a distance appear blurry. 
• #22: A very useful way of dividing causes of visual disturbance is to put it into 3 categories: Eye causes, Brain causes and Systemic causes. This table only mentions few common diseases affecting the visual system. In the next two slides I’m going to mention 2 diseases that are mainly caused by an increased pressure in the skull or inside the eye…
• #23: The first is Papilloedema. Which is the swelling of the optic disc. The main causes are Increased intracranial pressure (ICP), a space-occupying lesion and optic neuritis At high ICP, the pressure increases in the subarachnoid space around the optic disc. This increase in ICP will compress the veins first (as this is a low pressure system compared with the arteries). Therefore the Drainage is impaired. This leads to oedema in the retina (mostly marked at area of optic disc) So we get a Blurred optic disc.
• #24: It is the Imbalance between production and absorption of aqueous humour, leading to accumulation of fluid and increased pressure in the eye Glaucoma is the second commones cause of blindness in the UK (Cataract being the first). Normal intraocular pressure is 11 - 21 mm Hg Raised intraocular pressure leads to a condition called ‘glaucoma’ Glaucoma usually results in: Optic neuropathy (loss of nerve fibres in the optic nerve leads to a cupped disc and sometimes pallor) Visual field defects due to loss of retinal nerve fibres Peripheral visual field affected first, so patients often do not notice any symptoms until disease is advanced Pathophysiology There are 2 types of Glaucoma: an open angle and a closed angle glaucoma. Aqueous humour is the clear fluid that circulates in the front portion of the eye Intraocular pressure is dependent on the rate at which aqueous humour is made in the eye and the rate at which it is absorbed Management Need to lower intraocular pressure We most commonly use drops in the first instance Prostaglandin analogues like latanoprost (‘xalatan) increase the rate of aqueous outflow (through the uveo-scleral pathway) Beta-blockers like timolol are a commonly used treatment for glaucoma If drops are unsuccessful, the patient will often require laser treatment or surgery
• #25: During a physical examination, the optic nerve can be tested in many ways: Visual acuity is tested by using a snellen chart, counting fingers or reading text. ‘Normal’ visual acuity is 6/6, although many people (especially younger people) can see 6/5 or 6/4. Colour vision is tested using Ishihara plates Visual fields are also tested. The examiner will ask the patient to cover one eye and stare at the examiner. The examiner will then move her hand out of the patient's visual field and then bring it back in. The patient signals the examiner when her hand comes back into view. Blind spot is checked by using an ophthalmoscope. Light reflexes (direct and indirect/consensual)- the examiner flashes light on the Left eye and observe the Right eye for pupillary constriction (This is the direct reflex of the left eye). The indirect reflex for the Left eye is elicited by flashing the light in the Left eye but looking for pupillary constriction in the Right eye! Swinging light reflex Ophthalmoscopy (or fundoscopy) is also carried out
• #26: The motor nerves innerveting the extraocular muscles of the eye are tested as follows: The accommodation reflex is a reflex action of the eye, in response to focusing on a near object, then looking at distant object (and vice versa). Usually the pupil constricts when looking at a near object and dilates when looking at a further object. It is dependent on the optic nerve and occulmotor nerve. Eye movements: this is done by moving a pen or the examiner's finger in a ‘H’ shape, so that the superior, inferior, lateral, medial and oblique movements of the eye are tested. While doing this, ask the patient if they experience any double vision (whether it’s horizontal or vertical!), and also don’t forget to look for nystagmus which has multiple causes.
• #27: Now you know anatomy of the eye, and where the visual system lies in the Brain. You also know some embryolgy of the retina and the Physiology of the eye. This is important to understand the pathology affecting the visual pathway and the extraocular muscles