Central Retinal Artery Occlusion (CRAO) PDF

# Central Retinal Artery Occlusion (CRAO) ## Pathogenesis - Site of obstruction is usually at the lamina cribrosa (where the vessels normally become slightly narrowed) but occlusion may occur in any branch of the CRA. - CRAO (end artery) leads to: 1. Infarction of inner 2/3s of the retina, unl...

# Central Retinal Artery Occlusion (CRAO) ## Pathogenesis - Site of obstruction is usually at the lamina cribrosa (where the vessels normally become slightly narrowed) but occlusion may occur in any branch of the CRA. - CRAO (end artery) leads to: 1. Infarction of inner 2/3s of the retina, unlike retinal vein occlusion, No hemorrhage is seen 2. Reflex constriction of the retinal arterial tree. 3. Stasis in the retinal capillaries. - Retinal cells undergo necrosis and are phagocytized with macrophages. - With time, the edema and necrotic tissue are absorbed, leaving a thin retina with loss of bipolar cells, ganglion cells and nerve fibers. - Gliosis is minimal because the glial cells are destroyed along with the nerve cells. ## Etiology 1. **Embolization**: the most common cause - From the heart: Vegetations on the heart valves - From the ascending aorta or the carotid arteries: Atheromatous patch 2. **Vaso-obliteration**: - Atherosclerosis-related thrombus. - Arteritis (giant cell arteritis, systemic lupus erythematosus, polyarteritis nodosa) 3. **Circulatory collapse due to raised IOP**: - Acute angle closure glaucoma. - Excessive pressure on the globe during retinal detachment surgery. ## Clinical Features ### Symptoms 1. Sudden - severe - painless drop of vision in the affected eye. 2. Central tubular vision may be preserved if a cilio-retinal artery is present & patent. ### Signs 1. Vision: counting fingers to no light perception range. 2. Pupil: Poor relative afferent pupillary defect or absolute afferent pupillary defect 3. Fundus: 1. Retinal opacification occurs few hours after the occlusion. 2. Retina at the posterior pole becomes white and edematous except at the fovea: where a cherry-red spot is observed. 3. **Cherry-red spot**: - It is the bright red appearance of the fovea centralis surrounded by a white halo of the necrotic opaque retina. - Because the fovea is very thin and transparent, it allows the visibility of the underlying intact choroidal circulation that stands out in contrast to the surrounding opaque retina. 4. Retinal arterioles: Marked narrowing and in severe cases segmentation of the blood column can be seen in both retinal arteries and veins. 5. **After 4-6 weeks, there is...**: 1. Retinal opacification resolves and cherry-red spot disappears 2. Atrophy of the retina develops 3. Consecutive optic atrophy develops 4. Attenuated and sheathed arteries ## Causes of Cherry-red spot 1. Vascular: Central retinal artery occlusion. 2. Commotio Retinae: Central retinal edema due to blunt ocular trauma. 3. Cherry-red spot syndromes: Lipid storage metabolic disorders as Tay- Sachs disease. ## Treatment of acute CRAO - Treatment should be initiated _immediately_ upon presentation if it is less than < 24 hours of duration. - The time for irreversible retinal damage to occur with no visual recovery is _unknown_ but has been suggested to be 6 hours... 1. The patient should lie flat to increase retinal perfusion pressure. 2. Measures to lower intraocular pressure the perfusion pressure behind the obstruction will push an obstructing embolus further down the arterial tree. e.g. a. Intermittent firm ocular massage: Firm pressure is applied to the globe through the eyelid for 10 seconds & then suddenly released....This cycle is repeated for up to 5 min. b. Anterior chamber paracentesis. c. Drugs to lower intraocular pressure: Intravenous acetazolamide 500mg d. Retro bulbar injection of anesthesia or vasodilators such as papaverine. 3. Inhalation of carbogen (95% oxygen- 5% carbon dioxide mixture) or rebreathing into paper bag Hyper capnea → increase retinal blood flow 4. Sublingual Nitroglycerine. 5. Intravenous methylprednisolone 100mg, for possible arteritis. 6. Cardiovascular evaluation is essential subsequently. # Retinal Vein Occlusion ## Incidence - Retinal venous occlusion is the most common retinal vascular disorder after DR. - Branch retinal vein occlusion (BRVO) is 3 times as common as central retinal vein occlusion (CRVO). ## Pathogenesis - Central retinal artery & vein share a common adventitial sheath as they exit the optic nerve head and pass through a narrow opening in the lamina cribrosa. - This anatomical position predisposes to thrombus formation in the central retinal vein by various factors, including: 1. slowing of the blood stream 2. changes in the vessel wall 3. changes in the blood - Venous occlusion → Elevation of venous & capillary pressure with stagnation of blood flow → Hypoxia of the retina drained by the obstructed vein → Damage to the capillary endothelial cells & extravasation of blood constituents into the extracellular space → Tissue pressure is increased, causing further stagnation of the circulation & hypoxia, so that a vicious cycle is established. ## Classification ### According to Site of occlusion: 1. **In central retinal vein occlusion (CRVO)**: - Site of occlusion is behind the lamina cribrosa. 2. **In branch retinal vein occlusion (BRVO)**: - Site of occlusion is anterior to the lamina cribrosa at an arterio-venous crossing. ## Predisposing factors 1. **Blood dyscrasias**: 1. Hyper viscosity due to: a. Hyper cellularity: Chronic leukemia - Polycythemia b. Changes in the plasma proteins: Macroglobulinemia c. Sickle-cell disease. d. Oral contraceptive pills. e. DM. 2. Inherited hypercoagulable states. 2. **Changes in the wall of the vein**: a. Periphlebitis: Sarcoidosis - Bechet syndrome - Wegener granulomatosis. b. Congenital narrowing of central retinal vein. 3. **Changes outside the vein**: a. Rigid artery compresses the vein in: arteriosclerosis - diabetes - hypertension. b. Elevated intraocular pressure. c. Pressure on the vein as in: orbital cellulitis - orbital tumors. # Central Retinal Vein Occlusion (CRVO) There are 2 clinical forms of CRVO according to severity of obstruction of venous outflow ## Non-ischemic CRVO (most common type accounting for 75% of cases) - **Symptoms**: Sudden, painless, unilateral blurred vision. ## Ischemic CRVO (less common & accounts for the remaining 25% of cases) - **Symptoms**: Sudden, painless, unilateral, severe visual impairment. - Often noticed on waking up in the morning (during sleep circulation is slower). ### Signs **Non-ischemic CRVO**: 1. Visual acuity: Mild to moderate loss ≥ 6/60. 2. Relative afferent pupillary defect: mild or absent 3. Retina: - Retinal veins: Mild dilatation & tortuosity of all branches of the central retinal vein - Mild dot, blot & flame-shaped retinal hemorrhages distributed in all quadrants of the retina, especially at the periphery. - Cotton wool spots: few - Macular edema: mild or absent. 4. Optic disc: mild edema or absent. **Ischemic CRVO**: 1. Visual acuity: Severe loss < 6/60, usually counting fingers 2. Relative afferent pupillary defect: marked. 3. Retina: - Retinal veins: Marked dilatation and tortuosity of all branches of the central retinal vein - Extensive deep blot and flamed-shaped four-quadrant retinal hemorrhages affecting both the central and peripheral retina. - Cotton-wool spots: many - Macular edema: marked 4. Optic disc: edema ## Prognosis - 30% of cases: resolve with visual improvement. - 35% of cases: show partial resolution - 35% of the cases: progress to ischemic type with visual deterioration. - Visual prognosis is poor - 50% of eyes develop rubeosis iridis & neovascular glaucoma within 2 - 4 months after onset of venous occlusion (100 days glaucoma) ## Treatment of central retinal vein occlusion 1. Treatment of any systemic underlying disease. 2. Treatment of CRVO complications: - **Macular edema**: is treated by.... 1. Intravitreal injection of anti-vascular endothelial growth factor (VEGF) agents, or 2. Intravitreal injection of Triamcinolone. - **Rubeosis iridis** is treated by: - pan retinal laser photocoagulation to induce regression of the iris neovascularization. - **Neovascular glaucoma**: is treated by... 1. Pan retinal laser photocoagulation. 2. Intravitreal injection of anti-VEGF agents: is an adjunctive measure while waiting for the effect of PRP 3. **Medical treatment**: a. Topical atropine 1% and Beta Blockers. b. Carbonic anhydrase inhibitors topical and systemic. c. Topical corticosteroids. 4. **Surgical treatment**: Filtration surgery a. Trabeculectomy with 5-fluorouracil or mitomycin C. b. Glaucoma drainage implants. 5. Ciliary body ablation: by cyclodiode laser # Branch Retinal Vein Occlusion (BRVO) - BRVO occurs at an arterio-venous crossing site by arterial compression. - According to site of obstruction it may be: 1. Major branch vein occlusion. 2. Macular branch vein occlusion. 3. Peripheral branch vein occlusion. - **Clinical picture**: Depends on the anatomical location of the occlusion - **Symptoms**: Sudden painless monocular blurred vision. ### Signs 1. **Visual acuity**: - variable, depending on the involvement of the macula and the extent of its affection. 2. **Affected venous segment**: Dilated and tortuous. 3. **Sector of the retina drained by affected vein shows**: - Intra-retinal hemorrhages usually flame-shaped. - Cotton wool spots. - Retinal edema. ## Complications of BRVO 1. Chronic macular edema. 2. Retinal neovascularization. 3. Vitreous hemorrhage. ## Treatment 1. Treatment of risk factors & underlying diseases if present. 2. **Macular edema**: is treated by... - Intravitreal injection anti-vascular endothelial growth factor (VEGF) agents or Intravitreal triamcinolone. - Grid laser photocoagulation. 3. **Retinal neovascularization**: is treated by.... - Scatter laser photocoagulation covering entire sector of the involved retina # Retinal Dystrophies ## Retinitis Pigmentosa - It is the most common type of retinal dystrophy, - usually bilateral, symmetrical, progressive. - **Etiology**: 1. It may occur as an isolated disorder (sporadic cases) or 2. can be inherited as: - autosomal dominant - autosomal recessive - X-linked recessive trait ## Pathology - Degeneration first affects the rods. Later on, all photoreceptors are affected. - Degeneration starts at the equator and progresses peripherally and centrally towards the macula. - Macuia & optic nerve are affected in the late stages of the disease. ## Clinical Picture ### Symptoms 1. Night blindness: is the earliest & most common symptom. 2. Gradual progressive constriction of the visual field until tubular field of vision. 3. Marked diminution of vision is very late, due to: - Macular affection. - Consecutive optic atrophy. ### Signs 1. **Fundus examination**: - Optic disc: Waxy pallor. - Arteries: Markedly attenuated. - Retinal midperiphery: Bone-spicule pigmentation with spidery outline, black in color and clustered around the blood vessels. - With progression of the disease, these pigmentary changes extend both posteriorly and anteriorly. 2. **Other ocular findings include**: - Posterior sub capsular cataract. - Consecutive optic atrophy. - Cystoid macular edema. - Myopia. 3. **Visual field testing reveals**: - Multiple midperipheral scotomata that later coalesce to form complete ring scotoma. - Tubular field: Later on. ## Treatment - No effective treatment. - High doses of vitamin A, antioxidants and minerals may be of help. - Low vision aids. - Genetic counseling. # Retinal Detachment (RD) ## Definition - Separation of the neurosensory retina from the underlying retinal pigment epithelium (RPE) by sub-retinal fluid. ## Classification of retinal detachment 1. **Rhegmatogenous retinal detachment**: - The presence of a retinal break allows the passage of fluid resulting from vitreous liquefaction into the subretinal space. 2. **Tractional retinal detachment**: - The neurosensory retina is pulled away from the RPE by contracting vitreoretinal membranes. - Source of sub retinal fluid in such cases is unknown. 3. **Exudative retinal detachment**: - The subretinal fluid is derived from vessels of the retina and/or the choroid. ## Rhegmatogenous Retinal Detachment ### Risk factors 1. Pathologic myopia. 2. Previous intraocular surgery: cataract surgery 3. Trauma. ### Clinical picture ### Symptoms 1. **Photopsia**: - Subjective sensation perceived by the patient as flashing lights. - Caused by traction of the posterior hyaloid on areas of vitreoretinal Adhesions stimulating the rods and cones. 2. **Floaters**: - Moving vitreous opacities that cast variously sized and shaped dark shadows in the patient's visual field. - It can be due to fresh vitreous hemorrhage caused by tearing of a retinal blood vessel during vitreous contraction. 3. **Visual field defect**: - Caused by spread of the sub-retinal fluid posterior to the equator. - Perceived by the patient as a black curtain. - Occurs in area opposite to retinal detachment. 4. **Loss of central vision**: - when the macula is detached. - It is rapid and painless. ### Signs 1. **Pupil**: - Relative afferent pupillary defect if the detachment is old and extensive.. - Grayish red reflex corresponding to area of retinal detachment because the detached retina prevents light from reaching the choroid. 2. **Intraocular pressure**: Reduced as compared to the normal fellow eye. 3. **Posterior segment**: - **Retinal break**: - It is the hallmark of rhegmatogenous retinal detachment. - Red in color due to color contrast between grayish detached retina and underlying red choroid. - Shape may be horseshoe tears - round holes - retinal dialysis disinsertion at the ora serrata - **Detached retina**: - Appears grayish in color. - Retinal surface is convex, has corrugated appearance and undulates with eye movements. - Sub-retinal fluid extends to ora serrata rapidly. - Blood vessels appear wavy and darker in color than in the flat retina. - In cases of opaque media: Retinal detachment is detected by ultrasonography. ## Principles of surgery for retinal detachment are 1. To find all retinal breaks: By careful preoperative & intraoperative examination. 2. To create firm chorio-retinal adhesion surrounding each break by use of: - Cryo - therapy in cases of RD or - Laser photocoagulation in cases of retinal break without RD. 3. To support & close all retinal breaks with RD by use of: - Scleral buckle which indents the sclera beneath retinal break, or - Injecting intra vitreal gas bubble. ## Surgical options 1. **Laser photocoagulation**: - indicated in cases of retinal breaks without RD. 2. **Pneumatic retinopexy**: - Gas bubble is injected into the eye, it floats and tamponades the break. - Indicated in cases of upper RD with upper retinal breaks. 3. **Scleral buckling & cryo-therapy**: - Standard procedure for cases of fresh rhegmatogenous RD. 4. **Pars plana vitrectomy**: - is indicated in cases of: - Giant retinal tears, - Posterior retinal tears. - Proliferative vitreoretinopathy. # Diagnostic Features of Different Types of Retinal Detachment | Feature | Rhegmatogenous RD | Exudative RD | Tractional RD | |---|---|---|---| | History: | Aphakia, myopia, blunt trauma | Hypertension, malignancy, renal failure | Diabetes, prematurity, penetrating trauma | | Retinal break | Present | No | No | | Surface & height | Convex, Bulbous from superior breaks & shallow from inferior breaks but never touches the lens | Convex, Often high and can touch the lense | Concave, that peaks to traction point, Not high., | | Retinal mobility | Undulating bullae or folds. Extends to ora serrata early. | Shifting elevated bullae. May extend to ora. | Taut retina. Doesn't extend to ora | | SRF | Clear, no shift. | Turbid, shifts rapidly to dependent locations | Clear, no shift. | | IOP | Low. | Variable | Usually normal | | Causes | Retinal break | Uveitis | 1. PDR, 2. Retinopathy of prematurity, 3. Intra-ocular foreign body | # Retinopathy of Prematurity (ROP) - Normally, at full term of pregnancy: - the medial portion of the retina is fully vascularized, - while the lateral portion is only incompletely vascularized. - If premature infants of very low birth weight (1500g or less) is treated with oxygen, the oxygen may cause constriction of the retinal blood vessels → Ischemia in the retina → Neovascularization at retinal periphery → Retinal hemorrhage and fibroses. ## Screening for ROP 1. Infants weight: < 1500 g. 2. Gestational age: 31 weeks or less. 3. ROP Begins at: 6 weeks post-nataly, not immediately. 4. Follow up: Two-weekly intervals and Weekly if ROP develops until it regresses. 5. Indirect ophthalmoscope & sclera indenter are required to see the peripheral retina (Pupils should be dilated by mydriatic ). ## Stages - **Stage1 (Demarcation line)**: Flat, tortuous, grey-white line running roughly parallel with ora serrate. - **Stage 2**: Ridge arising in the region of the demarcation line. - **Stage 3**: Extra retinal fibro vascular proliferation from the ridge into the vitreous. - **Stage 4**: Partial retinal detachment. - **Stage 5**: Bilateral total retinal detachment. # Age Related Macular Degeneration (ARMD) - Degeneration of the macula affecting people aged 50 and older, causing damage to the central vision. ## Risk factors for ARMD include 1. Age is a major risk factor. 2. Smoking. 3. + ve Family history. ## Types of ARMD: 1. **Dry (Non - exudative) form**: - Drusens: Yellow deposits between the retina and choroid. - Pigmentary changes under the retina: pigmented cells break down and release their pigment, Dark clumps of pigment and, areas less pigmented. - Geographic atrophy: There is breakdown of the light sensitive cells in the macula that convey visual information to the brain. 2. **Wet (Exudative) form**: - New vessels grow underneath the retina( stimulated by vascular endothelial growth factor). - These vessels can leak fluid & blood in the macula. ## The following is essential 1. Visual acuity test. 2. Fundus examination after use of mydriatics. 3. Amsler grid. 4. Fluorescein angiogram. 5. Optical coherence tomography. ## Treatment 1. Eyes at risk: is examined regularly, at least once a year 2. **Dry (Non - exudative) form**: - Avoid smoking. - Exercise regularly. - Maintain normal blood pressure and cholesterol levels. - Eat a healthy diet rich in: green - leafy vegetables - fish. - Vitamin C - vitamin E - beta-carotene - zinc - copper lutein - omega-3 fatty acids - Beta-carotene has been linked to an increased risk of lung cancer in smokers. - Lutein and zeaxanthin appear to be safe regardless of smoking status 3. **Wet (Exudative) form**: - Anti-VEGF injection therapy blocks growth of new abnormal blood vessels. # Optic Nerve & Visual Pathway ## Anatomy of optic nerve - It is the sensitive and innermost layer of the eye. - It extends from the margins of the optic disc centrally to the ora serrata peripherally. - Ora serrata is the site of junction of the retina to the pars plana of the ciliary body. ### Gross Anatomy - The optic nerve is the 2nd cranial nerve, which carries the visual impulses from the retina to the brain. - It contains 1 million nerve fibers which are the axons of the ganglion cells of the retina. - The optic nerve starts at the optic disc and ends at the chiasma, divided anatomically into 4 portions: 1. Intra-ocular part (1.0 mm) 2. Intra-orbital part (2.5cm) 3. Intra-canalicular part (1.0cm) 4. Intra-cranial part (1.5 cm) - Myelin sheath starts to cover the nerve just behind lamina cribrosa. ### Minute Anatomy - The never is surrounded by dura, arachnoid, pia matter - The subarachnoid space is continuous with that of the brain. - The pia matter sends septa between the nerve fibers. ## Papilledema - It is a swelling of the optic nerve head that results from increased intra- cranial tension - It is nearly always bilateral but may be a symmetrical - All other causes of disc edema in the absence of raised intra-cranial tension are termed optic disc edema. ### Etiology **Causes of papilledema Intracranial**: (Increased intracranial tension) 1. Intracranial space occupying lesions: tumors, cysts or aneurysms 2. Benign intracranial hypertension: Psuedo-tumor cerebri 3. Subarachnoid hemorrhage. 4. Cavernous sinus thrombosis. 5. Meningitis. **Causes of disc edema**: 1. Orbital: Tumors or orbital cellulitis. 2. Ocular: Central retinal vein occlusion or hypotony 3. General systemic disorders: Malignant hypertension. ### Mechanism of papilledema - Increased CSF pressure around the optic nerve → block of axoplasmic flow → swollen axons compress the capillaries & veins → Congestion → disc edema. ### Clinical picture - Papilledema is not a disease, but a sign of serious diseases. ### Symptoms 1. General symptoms of increased ICT (headache, projectile vomiting, rarely diplopia) 2. Attacks of transient visual loss for few seconds (amaurosis fugax). 3. Vision is not affected in early cases. 4. Vision is affected late due to secondary optic atrophy. ### Signs - Vision, color vision, pupils are not affected early. - Visual field shows enlarged blind spot. - Fundus examination: 4 stages. - **First stage**: - Retinal vein engorgement. - Loss of venous pulsations. - Mild optic disc swelling with blurred edge. - **Second stage**: - The veins become more engorged. - Filling of the physiological cup. - The swelling increases and the margins become more ill-defined. - **Third stage**: - Elevation of the disc. - Hemorrhages on or near the disc. - Edema spreads to the retinal producing (retinal folds) - **Fourth stage**: Secondary optic atrophy. ### Treatment - Treatment of the cause. # Acute Optic Neuritis - It is acute inflammation of the optic nerve. ## Classification ### Aetiological classification: 1. Demyelinating: most common & occurs in multiple sclerosis 2. Para-infectious: follow viral infection or immunization 3. Infectious: - direct infection with Herpes Zoster - invading from surrounding orbit or brain 4. Non-infectious: as in sarcoidosis ### Clinical classification: 1. Papillitis: occurs either at the optic disc 2. Retrobulbar neuritis: affecting the nerve behind the eye. ## Clinical picture ### Symptoms 1. Acute painful diminution of vision 2. Pain: more with adduction and elevation of the eye. - Due to stretch on the optic nerve sheath as medial and superior recti take origin from the optic nerve sheath ### Signs 1. Visual loss: is mild (6/12) to severe (PL). 2. It is accompanied with impaired color vision. 3. Pupillary reaction: RAPD. 4. Visual field: Central and centrocecal scotoma, relative for red and green. 5. Fundus Picture: - Normal in retrobulbar neuritis. - In papillitis: - Blurring of disc margin with disc swelling. - Obliteration of physiological cup. - Disc hyperemia and splinter hemorrhage. - Vitreous cells. ## Differential diagnosis | Feature | Papilloedema | Papillitis | |---|---|---| | Laterality | Usually bilateral | Usually unilateral | | V/A | Good | Severe drop of vision | | Disc swelling | Severe | Moderate | | Field of vision | Enlargement of blind spot. | Central & centrocecal scotoma for red and green | | Vitreous | Normal vitreous | Vitreous opacities (cells) | | Pupil Reaction | Normal | RAPD | ## Treatment 1. Methyl prednisolone (250 mg - I.V - every 6 hours for three days) Then followed by Prednisone tablets (orally - 1mg/Kg daily for 11 days.) 2. Multi vitamins. 3. Interferone for resistant cases # Optic Atrophy - It is a damage of the optic nerve fibers at any point in their course from the ganglion cells in the retina to the lateral geniculate body leading to loss of its function. ## Types 1. Primary optic atrophy 2. Secondary optic atrophy 3. Consecutive optic atrophy 4. Post glaucomatous optic atrophy ## Primary optic atrophy - Damage occurs behind the eye - Pituitary tumors. - Retrobulbar neuritis. - Optic nerve trauma - Toxic amblyopia ## Secondary optic atrophy - Post neuritic or - post papilledemic optic atrophy ## Consecutive optic atrophy - Caused by a retinal disease - Retinitis pigmentosa - Neglected retinal detachment. - CRAO. ## Post glaucomatous optic atrophy - In cases of absolute glaucoma. | Feature | Primary optic atrophy | Secondary optic atrophy | Consecutive optic atrophy | Post glaucomatous optic atrophy | |---|---|---|---|---| | Causes | Pituitary tumors, Retrobulbar neuritis, Optic nerve trauma, Toxic amblyopia | Post neuritic or post papilledemic optic atrophy | Caused by a retinal disease, Retinitis pigmentosa, Neglected retinal detachment, CRAO | In cases of absolute glaucoma | | Color | pale white | Pale grey | Pale waxy yellow | Pale white | | Edges | well defined | Irregular | Slightly irregular | Well defined | | Cup | atrophic and enlarged | Filled | Obliterated atrophic. | Deep and undermined shifted nasally. | | Retinal Vessels | Normal | Sheathed | Attenuated and sheathed | | | Retinal background | Normal | - | - | - | | Notes | Foster Kennedy Syndrome:... | | | | ## Visual Pathway - Object in front of the eye → Inverted image on the retina (Photoreceptor) → Erect image - Visual pathway to the brain ### Visual pathway is formed of 1. Rods and cones: Photoreceptor & start the impulses. 2. Retinal ganglion cells. 3. Optic nerve: Formed by axons of the ganglion cells & extends to the optic chiasma 4. Optic chiasma: - Site of hemi-decussation where the fibers from the nasal part of the both retina pass to the opposite optic tract, so that the visual information from the right retina passes to the left visual cortex and that from the left retina passes to the right visual cortex. 5. Optic tracts: - Passes from the posterior aspect of the optic chiasma to the lateral geniculate body. - Contains ipsilateral temporal retinal fibers & contralateral nasal retinal fibers. 6. Lateral geniculate body (L.G.B ): - Site of termination of all afferent fibers of the anterior visual pathway. - Site of the synapse between fibers of the optic tract & that which will form the optic radiation 7. Optic radiation: - Pass from the L.G.B to the visual cortex. - **Superior fibers**: proceed directly to the visual cortex - **The inferior fibers**: loop around the ventricular system into the temporal lobe so small infarct or a tumor here will lead to contralateral superior hemianopic visual field defect (Pie on the sky). 8. Visual cortex: - Situated along the superior and inferior lips of the calcarine fissure. - Concerned mainly with macular vision which represented posteriorly and extends variably into the lateral aspect of the cerebral hemisphere where the peripheral fibers are represented more anteriorly along the medial aspect of the hemisphere. - Area 17: is concerned with perception of form and color. - Area 18 & 19: are concerned with the recognition of objects and recalling the visual memory related to objects. ## Visual field defects due to lesions of the visual pathway **I) Optic nerve lesions:** 1. Ipsilateral централ scotoma: Involves the fixation point 2. Centro caecal scotoma: - Extends from point of the fixation to the blind spot (in toxic neuropathy) 3. Arcuate defect: - typically seen in glaucoma, due to damage to the superior or inferior retinal nerve fibers. 4. Altitudinal field defect: - Involves superior or inferior visual field. - Occurs in: - Anterior Ischemic Optic Neuropathy - BRAO & BRVO 5. Complete loss of visual field: occurs in complete optic atrophy **II) Chiasmal lesions**: - Typically produce bitemporal hemianopia without loss of visual acuity. **III) Optic tract and lateral geniculate body lesions:** - Contralateral homonymous hemianopia. **V) Optic radiation lesions:** - Superior Homonymous Quadrantanopia if contralateral temporal lobe is affected (Pie on the sky). - Inferior Homonymous Quadrantanopia if contralateral parietal lobe is affected (Pie on the floor). **V) Occipital cortex lesions:** - Homonymous hemianopia with macular sparing... This is due to: - Macula is represented in a wide area. - Macula is bilaterally represented. - Occipital pole is supplied by double blood supply posterior & middle cerebral arteries. # Errors of Refraction ## Accommodation - It is the ability of the eye to change its refractive power in order to see objects clearly placed at different distances from the eye. ### Mechanism 1. The ciliary muscle: contracts and this makes the ring formed by the ciliary body smaller 2. The suspensory ligament: relaxes 3. The elastic lens capsule: will compress the lens and increase its curvature, so the lens power will increase. ### The range of accommodation - It is the distance between the far and the near point #### The far point (punctum remotum, PR ): - is the most far distant point from the eye where objects appear clear. - Accommodation is completely relaxed - In emmetropia: P.R. is at infinity. - In myopia: it is infront of the eye (nearer than infinity) - In hypermetropia: it is a virtual point behind the eye. #### The near point (punctum proximum, P.P. ): - the nearest point from the eye at which an object can be seen clear. - At this point the maximum accommodation is exerted. - It varies with age ### The amplitude of accommodation - It is the difference between the refractive power of the eye at rest and when fully accommodated. - It is equal = accommodation for near - accommodation for far ## The Lenses ### A. Spherical lens - It is a piece of glass bounded by 2 surfaces each is a portion of a sphere. - The lens produces the image in the form of point #### Convex (plus lenses ): - converge the rays - used for correction of hypermetropia & presbyopia. #### Concave (minus lenses ): - diverge the rays - used for correction of myopia. ### B. Cylindrical lens - It is a piece of glass cut from a cylinder in a plane parallel to its axis. - The cylindrical lens may be concave or convex (minus or plus cylinder). - The image is in the form of line perpendicular on the axis of the lens - Cylindrical lenses are used in the treatment of regular astigmatism. ## The lens power: - The unit of lens power is the dioptre. - One dioptre: is defined as the power of a lens which brings parallel rays falling on it to a focus at a distance of one meter. ## Emmetropia - (The Normal State of Refraction) - It is the condition of refraction in which the parallel rays come to a focus on the retina (when the accommodation is completely relaxed) - The diopteric power of the eye is 60D (cornea 42 D & lens 18 D) ## Ametropia - (Error of refraction) - It is the condition of refraction in which with accommodation completely relaxed, parallel rays do not come to a focus on the retina. - It may be: 1. Myopia 2. Hypermetropia 3. Astigmatism 4. Anisometropia 5. Aphakia ## Myopia (Short Sight) - It is the condition of refraction of the eye in which the parallel rays come to a focus in front of the retina (with accommodation completely relaxed). - Rays coming from a point on the retina leave the eye convergent and meet at a point nearer than infinity (PR is infront of the eye ). ### Etiology 1. **Axial Myopia**: the most common cause of myopia - It is due to an increase of the antero- posterior diameter of the eye. - The increase in length affects the posterior part of the eye behind the equator. 2. **Refractive Myopia**: - The refractive system becomes more powerful. - It may be: - Curvature Myopia: Caused by an increase in the curvature of the cornea or the lens - Index Myopia: Caused by an increase in the refractive index of the ocular media (most important is the lens as in nuclear sclerosis and nuclear cataract) ### Types of myopia 1. **Simple myopia**: the commonest type - Starts at the age of 14 years (at puberty) and progress slowly till the age of 25 years and then becomes stationary. - Rarely exceeds - 6 D - is not accompanied by degenerative changes in the fundus and is not liable to complications 2. **Progressive (degenerative or malignant ) myopia**: - It starts at the age of 5 - 10 years, progress rapidly and continue to progress after the age of 25 years. - May reach - 25 D or more - It is accompanied by degenerative changes in the fundus and is liable to complications. 3. **Developmental (congenital) myopia**: - It is rare - It dates since birth, soon reaches -10 D and then become stationary for life. - Rarely leads to complications. ## Clinical Picture ### Symptoms: 1. **in simple myopia**: - Indistinct vision for far: - it is the only symptom, in simple myopia - some improvement of vision occurs if the patient screws his eyes to narrow the palpebral fissure into a slit. 2. **In high degrees**: - Photopsia & Musca volitantes: due to vitreous degeneration