based on the chapter "Disorders of the Eye" from Harrison's Principles of Intern al Medicine (17th edition) Sebastian Kuepper skuepper@uni-muenster.de Content Anatomy of the Eye General Eye Examination 3 5 Symptoms: red and painful eye corneal abrasion ................................. ........ 8 .................................................. .................. ............ 8 subconjunctival hemorrhage ................. .................... .............................. ............................. 8 ................. .. Blepharitis .................................................. .............. .................................... ........ .................................. ...... 9 Dakrozystitis .................................................. 9 .... ............................. ............... conjunctivitis ................... ............................... ................................................ .. ...... .......................................... 10 Keratitis .............. .................................... ..................................... 11 .. ........ herpes simplex .................................................. ..... ............................................. ........ ......................... .............. 12 Herpes Zoster ................................................ .. ............................... 12 ................. uveitis ................ .................................. ............................................. ..... .............. 13 acute angle-closure glaucoma ........................... ...... .................................................. Endophthalmitis ...... ......... 13 ................................. ................................. ................. ................................. 14 symptom: acute visual dis turbance 15 Amaurosis fugax and Zentralarterienverschluss ....... .............. .................................... .......... 15 anterior ischemic optic neuro pathy (AION )................................. Optic neuritis .................. ............. 16 ................. ............................................. ..... .................................................. .16 toxic optic neuropa thy .............................................. ............................. ..................... .17 papilledema .......................................... ..... .................................................. .................... 17 ............................ vitreous detachment .............................. .................... ............................... 17 ................. retina l detachment .................................................. ................ .............................. 18 migraine with aura ........................... ....................... .................................................. strok e and TIA ............... 18 ............................... ................... ............................... ............................. 18 symptom: chroni c vision impairment 19 cataract (cataract ).......... .......................... ........................ ............................................... 19 glau coma. .................................................. ....................... ........................... ........................... 20 age-related macular d egeneration (AMD )................. ............................................ ...... ....... ........................................ 21 diabetic retinopathy .................................................. Retinitis pigmentosa ........ .......................... ............. 22 .................................... .............. melanoma and other tumors, 23 .......................... ........ ........... .................................................. ................. ........ 23 symptom: movement of the eyeball 24 endocrine ophthalmopathy ....... ........ .................................................. .................... .................... 24 pseudotumor orbit ....... .............................. .................... .................................................. Horner's Syndrome ............................................ .. 25 ................... ............................... ...................... 25 symptom: drooping eyel id ptosis congenita .................... 26 .................................... .............. .............................................. 26 myogenic ptosis . .................................................. ........................... ....................... ................ 26 neurogenic ptosis .................. ............. .................................................. ............... ................... 26 symptoms: double vision, motility disorders and nystagmus 27 myasthenia gravis ..... .................................................. . ................................................. 27 N. ........ oculomotor (thi rd cranial nerve )............................................ .........N. ..... ................................... 27 trochlear (cranial nerve IV )............ ................................ ............................................... ... 28 ..... N. abducens (cranial nerve VI ).................................... ........ .................................................. Strabismus ......... ................................. ...... 29 .................................... .............. ................................ 29 ................ nystagmus .. ................................................ ............................... ................... Literature ........ 30 31 2 ANATOMY Structure of the eye OF EYE EYE The visual system consists of eyeball, annex parts (lids, lacrimal apparatus, co njunctiva), and visual pathway. The globe (eyeball) is composed of functionally ● ● Refractive (cornea, lens, vitreous) and perceiving light units (retina). The eyeball is surrounded by a three-layer wall. From outside to inside: ● Tunica fibrosa: ○ ○ Sclera (sclera): design and resistance. Cornea (cornea) with a refraction lens d iopters from 43rd Iris (Iris): optical aperture for the regulation of light. Cil iary body (ciliary body): accommodation, suspension of the lens, the production of aqueous humor. Choroid (choroidal) blood supply to the outer layer of the ret ina. Pars caeca (stratum pigmentosum): Light filters and metabolism. Pars optica (Str and Str pigmentosum nervosum): pay the photoreceptors. Sclera choroid ● Tunica vasculosa (= uvea): ○ ○ ○ ● Tunica interna (= retina): Conversion to optical neural signals. ○ ○ Schlemm canal Irisfortsätze Zonulafasern cornea iris pupil anterior chamber, posterior chamber Ciliary body, retina, vitreous, optic nerve Figure 1: Schematic cross section th rough the eye. Source: Wikipedia.de http://de.wikipedia.org/wiki/Bild:Eye_scheme.svg () Lens 3 The interior of the eye is divided into three functionally and anatomically sepa rate rooms: ● ● ● anterior chamber, posterior chamber and vitreous. Anterior and posterior chamber containing the aqueous humor (nutrition of the le ns and cornea, immune functions), which is formed in the posterior chamber by ci liary body, passes through the pupil opening in the anterior chamber and from th ere through the Schlemm's canal into the venous system. Through a balance of aqu eous humor production and absorption is usually a constant intraocular pressure of 12 will receive up to 20 mmHg upright. The vitreous is 98% water and is used for light refraction (dpt 1.33). Visual pathway first Neuron: sensory cells of t he retina (rods and cones). 2nd Neuron: bipolar cells. 3rd Neuron: ganglion cell s, with their projections to the N. Optic (CN II) form. About optic chiasm and o ptic tract to the geniculate body (Latin thalamus), where the results for the fo urth Neuron is then over optic radiation to the visual cortex. Accommodation To both distant and near objects can be reproduced sharply, then the refractive pow er of the eye are adjusted accordingly. For this purpose the lens is distorted. ● ● Distant view: By train the zonules (relaxed ciliary muscle), the lens is stretch ed to an ellipse. The refractive power decreases. Nahblick: By discharge of zonu le (ciliary muscle tense, parasympathetic fibers of the oculomotor nerve [III. C N]) is the lens of their own elasticity and is replaced by a more "spherical" sh ape. The refractive power increases (= accommodation). Pupillary reflex goal: Constant light by adjusting the pupil size (part of the a daptation). ● Afferents: Retina → N. → Optic chiasm → Tr. opticus. Before the Latin corpus gen release of fibers to praetectalis Area. Redirecting to Edinger-Westphal nuclei on both sides (allows Isokorie and consensual light reaction). parasympathetic e fference: Edinger-Westphal nucleus → N. oculomotor (III) → Ciliary ganglion → Nn . short ciliary → M. pupil sphincter. sympathetic efference: hypothalamus, medul la oblongata → → → sympathetic ganglion superior cervical ganglion → internal ca rotid artery / A. ophthalmic (accompanying nerve plexus) → N. ciliary longi → pu pil dilator. ● ● Fremdreflex corneal reflex to protect the eye from drying out and debris by eyel id closure. ● ● Afferents: N. ophthalmicus (branch of trigeminal nerve V) Red nucleus → → → brai nstem reticular formation (facial nucleus). Efference: N. facialis (CN VII) → M. orbicularis oculi. When strong light is also on the afferent nerve Optic (CN II). 4 GENERAL EYE EXAMINATION EYE EXAMINATION Case history ● ● ● ● ● Updated: red eye, pain (stabbing, dull, or eye movement), visual disturbance (ac ute or chronic), double vision, injury? One or both sides? Eye History: glasses, amblyopia, strabismus, surgery,Trauma? Past history: if a general disease with ocular involvement in such Diabetes mellitus, hypertension, infection, rheumati c disease? Drugs History: e.g. Cortisone, Resochin, amiodarone, chlorpromazine? Family history: refractive errors, strabismus, cataract, glaucoma, retinal detac hment? Visusprüfung The resolving power of the sound eye is an arc minute. For the diag nosis of visual loss should first be ruled out a refraction. As a quick test, th e "stenopaic gap" (a kind of punch cards are used): If the visual acuity improve s as seen through the 2 mm pinhole, a refractive error is likely. A correction i s done with plus glasses for hyperopia (farsightedness, the eyeball is too short ), with minus lenses in myopia (nearsightedness, the eyeball is too long). The m easured and corrected visual acuity is known as "cum correctione visual acuity ( corrected visual acuity) called. The determination of visual acuity is carried o ut separately for each eye. The exact test of visual acuity with refraction is d one by the specialist. Orienting to the visual acuity with the Snellen table (6 m spacing) or the Rosenbaum card for the coat pocket (36 cm) can be determined. The patient indicates which row he made six meters away (or 36 cm distance in th e Rosenbaum card) can not read just yet. Visual acuity can then be read from the table. Myopia, hyperopia Snellen T-t ation Figure 2: refractive errors and their correction. Snellen table for determinatio n of visual acuity. Source: Wikipedia.de (http://de.wikipedia.org/wiki/Bild:Myopia.svg, ... / Image: Hypermetropia.svg, ... / Image: Snellen06.png) Where: visual acuity = Istentfernung Sollentfernung Normal: 6 20 = 1.0 and (when given in ft). 6 20 If the visual acuity even after correction <1.0, this must be further clarified. With a visual acuity below 5 / 50, the "counting fingers" at 1 m (possibly 30 c m), with even poorer vision "hand movements" and finally "light a torch - the di rection of recognized" documented. Blindness is in visual acuity ≤ 0.02 or restriction of the visual field to ≤ 5 d egrees. 5 The review of diagnostic pupillary pupillary reflex is one of them to any physic al examination. They are being guided information on the functions of retina, N. optic (II), midbrain and nerve oculomotor (III). A normal result does, however, a partial damage of individual structures is not enough. ● ● ● Miosis (small pupil): light, parasympathetic tone (sleep, fatigue, narcosis), op ioids, Naheinstellungsreaktion (Konvergenzmiosis), Horner's syndrome. Mydriasis (dilated pupil): dark, sympathetic (fear, joy, surprise: making "big eyes"), ocu lomotor palsy, medications. Anisocoria (unequal dilated pupils): Note to efferen t pupil defect, eg central paralysis, mass, intracranial pressure, head injury, in various syndromes (eg, Adie's syndrome) but also idiopathic. direct light reaction Both eyes of the patient are covered. If one eye be released, the pupil narrows to about 0.2 s (miosis) because of the incident light. consensual (indirect) light reaction By placing the edge of the hand to the nose of the patients examined eye is shie lded from direct light. The other eye is now illuminated. The shielded, non-illu minated pupil should constrict it too. A blinded eye shows no reaction in direct lighting (amaurotic pupil). The consensual reaction to light when illuminated t he healthy eye will remain. "Swinging-flashlight test" Used in diagnosis of discrete unilateral disorders of retinal or optic nerve. Ca n e.g. be with retrobulbar neuritis and other optic neuropathies, the only refer ence. If only a partial injury before the sensory structures, ranging mostly fro m the residual function to allow a direct reaction to light. Only in (side) comp arison of the pupils can have the disorder may be clinically apparent. These two eyes are alternately with the same distance, lit the same time and same intensi ty of light slanting down. Observed, the initial constriction and subsequent dil ation of the pupil. A pathological finding, also known as "Marcus-Gunn pupil" me ans (a relative afferent pupillary defect). Motilitätsprüfung patient is asked t o follow an object with the eyes (eg, pen tip). In the nine main areas are exami ned: right top right bottom right top left top left bottom left straight down Visual field testing (confrontation test) doctor and patient sit facing the same amount. Both cover the opposite eye. The doctor takes an object from the outsid e to the center line (all four quadrants).In normal vision can see both the obj ect simultaneously. 6 Direct ophthalmoscopy With direct ophthalmoscopy see an upright, 16 times magnif ied image of the retina. This one goes with the electric ophthalmoscope as close as possible to the patient's eye. It may not accommodate the examiner. One shou ld recognize optic disc (where light reflected from temporal), and mean macular periphery. The papilla (optic nerve head, outlet of artery and vein centralis, " blind spot") is extremely sharp, vital colored (yellow-orange), in the retinal l evel and possibly has a central depression (excavation). 1 2 The vessel caliber money Arte Source: National Eye Institute, National Institute s of Health rie: vein is 2:3, spontaneous venous pulsation in the arterial pulse Ggs. to normal. At intersections, the vessels are not constricted. The macula l utea ("yellow spot") with the avascular fovea centralis has the greatest density of photoreceptors and is the point of sharpest vision. Figure 3: Fundus. (1) papilla, and V. A. centralis. (2) fovea centralis of the m acula lutea. papillae important pathological findings ● ● ● fuzzy boundary (edge blurring): papilledema. Paleness: e.g. with optic atrophy. enlarged cupping: glaucoma. Assessment of intraocular pressure is with both index fingers probed with closed eyes, the upper eyelid. The important thing is the page comparison. Palpation i s only a stone-hard globe in acute angle-closure glaucoma is not detected a slig ht increase in pressure would not. The tonometrische measurement of intraocular pressure is performed by an ophthalmologist. There are various methods, most of the Goldmann tonometer is used. Is a physiological intraocular pressure of 10 mm Hg to 21. Slit lamp examination and gonioscopy with the slit lamp to lens, corne a and anterior chamber can be assessed. The non-direct vision chamber angle can be evaluated by the glaucoma diagnosis with the gonioscopy. Both studies will be conducted by an ophthalmologist. 7 Symptom: General RED AND PAINFUL EYE EYE The symptoms "red eye" and "pain" may have a number of causes that need to be cl arified by differential diagnosis. Grob are: for glaucoma, inflammation, hemorrh age, trauma, and mechanical irritation. It is important to ask about side effect s. A palpable hard eye can continue to think of a reaction-free pupil must glauc oma (emergency, cause blindness!). In conjunctival injection, glued eyes in the morning and secretion conjunctivitis is likely. A red eye without side effects c an be with the appropriate local findings and medical history (such as heavy lif ting, exertion, warfarin-dosing) on a bruising back. Erosion General CORNEA A corneal abrasion of the cornea is as erosion (English corneal abrasion refers) . It is the result of a violation (eg, fingernail, branches), or foreign objects from the left vertical scratches on the cornea. Strong clinical pain, tearing ( epiphora), foreign body sensation, blepharospasm, eyelid swelling and conjunctiv al injection. Diagnosis of corneal staining with fluorescein, an epithelial defe ct in the blue light is then visible. Always looking for a foreign body (eversio n of the upper and lower eyelid)! Antibiotic ointment therapy union or hospitali zation for recurrent erosion. The prognosis is good, it usually comes within a f ew days for healing. Subconjunctival Hemorrhage hemorrhage General A subconjunctival hemorrhage (syn. Hyposphagma) from rupture of small bl ood vessels occurs either spontaneously (especially the elderly), trauma (histor y), or by coughing, straining, bending, etc. before. Extensive clinical bleeding under the conjunctiva, even with impressive local findings mostly harmless. Vis ual acuity is not affected. Spontaneous regression therapy within two weeks. Whe n thinking of recurrent hypertension or coagulation disorders! 8 Blepharitis General An inflammation of the eyelid is known as blepharitis. Common causes: se borrheic dermatitis (blepharitis squamosa) are, barley grain (Hordeolum, painful bacterial infection of Zeis or Moll's glands) and Hailstone (chalazion, painles s Chronic-granulomatous inflammation of the meibomian gland). Think For refracto ry lesions in basal cell carcinoma or squamous cell carcinoma! Clinic ● ● ● Blepharitis squamosa: low inflamed eyelid margins, scales, glued eyelashes, ofte n accompanying chronic conjunctivitis. Hordeolum: painful nodules, pus central p oint, the cause: often S. aureus. Chalazion: painless, coarse nodes. Therapy ● ● ● Blepharitis squamosa: warm compresses, strict hygiene, topical antibiotics. Good prognosis, but often lengthy process. Hordeolum: antibiotic ointment, dry heat (red light). Fast cure. Chalazion: Injection of corticosteroids, but are general ly operative incision necessary. DAKROZYSTITIS General The most common disease of the lacrimal organs is the inflammation of th e lacrimal sac (Dakrozystitis), mostly due to nasolacrimal outflow obstruction o f the duct. Clinic ● acute Dakrozystitis: highly flammable (pressure), painful swelling. Under pressu re to drain pus. Pathogens are usually staphylococci, pneumococci and Pseudomona s. chronic Dakrozystitis: epiphora, often lack signs of inflammation. Occurrence in the context of Wegener's granulomatosis, and chronic. Nasenschleimhautentz. ● After diagnosis of the acute symptoms: Rö. contrast for the representation of th e outflow obstruction and surgical planning. Therapy ● Dakrozystitis acute: acute: targeted antibiotic therapy (local and systemic), di sinfecting envelopes, with abscess: incision. Later: most OP, e.g. nasolacrimal by Toti: creation of a direct connection between the lacrimal sac and nasal muco sa, bypassing the bile duct. chronic Dakrozystitis: Surgery after Toti or sac-ex tirpation. ● 9 Conjunctivitis General The most common cause of a "red eye", the conjunctival inflammation (con junctivitis) is. This results in vasodilation, cellular infiltration and exudati on. Pain is usually only minimally present, visual acuity is hardly restricted. Differences are infectious (bacterial, viral, parasitic, mycotic) and non-infect ious forms. Red Eye Clinic, sticky eyelids, eyelid swelling, foreign body sensat ion, eyes burning. Possibly. Photophobia, and epiphora. In an allergic cause sev ere itching is likely a blepharospasm suggests corneal involvement (keratoconjun ctivitis). Diagnostic slit lamp (extent of vascular injection, nature of secreti on, conjunctival swelling), Evert (follicle? Papillae? Foreign?), Smear (diagnos tic agent) and Epithelabstrich (Ausstrichzytologie limit for the differential). DD-conjunctivitis of the individual forms ● infectious conjunctivitis: ○ ○ viral (most adenoviruses): watery discharge, epiphora and LK-swelling. In the Au sstrichzytologie: lymphocytes and monocytes. bacteria (many poss. pathogen): pur ulent discharge, hyperemia and conjunctival swelling (chemosis) are at the foref ront. Granulocytes and bacteria in the Ausstrichzytologie. Chlamydia D-K: mucopu rulent secretion, follicles in the tarsal conjunctiva. In the Ausstrichzytologie : intracellular inclusion bodies. (The A-C, the chlamydia cause us not occurring trachoma: in tropical countries leading cause of blindness!) Allergic conjuncti vitis: viscous secretions, itching and papillae of the conjunctiva (cobblestone) are typical. Eosinophils in the smear. Often, as part of "hay fever" (rhinoconj unctivitis) or by triggering contact lenses (Riesenpapillenkonjunktivitis). nons pecific conjunctivitis: caused by external stimuli or dry eye (keratoconjunctivi tis sicca, such as Sjogren's syndrome. diagnosis: including the Schirmer test. C omplete: corneal ulcer). Most foreign body sensation and epiphora. ○ ● non-infectious conjunctivitis: ○ ○ Therapy ● ● ● ● ● Viral: symptomatic with cool compresses. Prevention through hygiene (eg, no comm on towels to use, do not rub the eyes). bacteria: antibiotic-containing ointment , possibly in combination with cortisone (leads to faster relief, but only under strict control). Chlamydia: tetracycline eye drops or ointment (4-6 wk). Danger of "ping-pong infection, therefore mitbehandeln partner. allergy: desensitizati on, possibly corticosteroid eye drops. non-specific: avoid artificial tears, the triggering stimulus. 10 Keratitis General In the investigation of the superficial cornea (keratoconjunctivitis) an d deeper, ulcerative inflammation to be distinguished. The latter cause vision p roblems due to possible scarring, opacity or perforation of the cornea and provi de an ophthalmic emergency dar. The cause can be identified infectious and non-i nfectious forms. Clinic ● Infectious keratitis: ○ bacteria (90% of cases): purulent discharge, pain, photophobia, reduced visual a cuity, epiphora, hypopyon (pus in the lower anterior chamber). Pathogens are v.a . Staphylococci, pneumococci, Pseudomonas and Moraxella. Hazardous-onset form is the ulcer serpens with rapid progression (a few hours!) And intraocular involvement. Can lead to loss of the eye. ○ ○ ○ ● Viral: watery discharge, often severe pain (especially in herpes simplex). Mycot ic: slight discomfort.Pathogen: Aspergillus and Candida albicans. Protozoa: sev ere pain, photophobia, epiphora. Mostly in contact lens wearers (Acanthamoeba). non-infectious keratitis: risk of erosion in the course of superinfection → → → ulcer perforation. Among the non-infectious keratitis includes Superficial punct ate keratitis (corneal punctate lesions due to wetting), keratitis sicca (dry ey e), keratitis incomplete eyelid closure (eg facial paralysis) and keratitis neur oparalytica (paralysis of the ophthalmic nerve, by loss of sensation of the corn ea with reduced blinking frequency). Rapid diagnosis diagnosis and treatment are crucial. Using slit lamp may epithel ial, turbidity, cell and possibly pus are shown in the anterior chamber. Swabs f or the detection of pathogens and resistance testing to perform! Therapy ● bacteria: local antibiotics (broad spectrum are known to agents and resistance), with hypopyon (anterior chamber involvement) shows therapeutic mydriasis of iri s and ciliary body to immobilize ("Zykloplegie"). In advancing ulcer hospitaliza tion. If necessary. OP (coverage of large epithelial defects with conjunctiva, c ornea transplantation in perforated ulcer). Viral: local Antivirals for system w ith varicella zoster (zoster ophthalmicus) possibly. Mycotic: local antifungal a gents (for intraocular involvement systemic), if necessary, surgery. Acanthamoeb a: Propamidin local, antibiotic eye drops and Zykloplegie. non-infectious: if po ssible, treat the cause, artificial tears, infection prophylaxis. When paralysis / paresis possibly OP: lateral Lidvernähung (tarsorrhaphy). ● ● ● ● 11 HERPES General SIMPLEX A primary infection with herpes simplex (usually Type I) runs on the eye as conj unctivitis and blepharitis. An HSV keratitis is always a secondary infection (re lapse by virus persistence in the ganglion gasseri), which can also lead to corn eal ulcer. A primary infection can easily be confused with an adenovirus conjunc tivitis, if the characteristic periocular vesicles (vesicles do not occur). Dend ritic branching corneal epithelial lesions are pathognomonic for a secondary inf ection. Clinic Very painful eye, photophobia, eyelid swelling, epiphora. Dependi ng on the location and possible visual loss. Forms of HSV keratitis ● ● ● Dendritica keratitis: epithelial branching tree-like, characteristic of HSV recu rrence, repealed corneal sensitivity. Keratitis disciformis: central corneal dis c. Vascularization, and iridocyclitis possible (especially if recurrent). endoth elial keratitis: caused by viruses in the aqueous humor. Swelling of endothelial cells, corneal opacity. In chamber angle involvement: sec. Glaucoma. Diagnostic slit lamp, Fluoreszinfärbung shows corneal lesions. Topical antiviral therapy agents (eg Trifluridin, acyclovir). In K. disciformis and intraocular i nvolvement and systemic acyclovir. Cortisone is contraindicated in Hornhautläsio n allowed with intact epithelium against. Cortisone prevents scarring, but it in creases the risk for secondary glaucoma, corneal and prolonged course. HERPES General Zoster As with herpes simplex may occur in the varicella-zoster virus to an endogenous relapse. To an eye involvement (zoster keratitis), it comes when the first Trige minal branch (ophthalmic nerve) is concerned. Clinically, it shows an ocular inv olvement by Hutchinson's sign: skin sores to go nose → N. nasociliaris affected (including the inside of the eye care). Painful vesicular dermatitis clinic, lim ited to one dermatome. Red eye, decreased sensitivity of the cornea. The corneal lesions may resemble HSV keratitis. Later: anterior uveitis, secondary glaucoma , scarring and neuralgia possible. Local therapy: acyclovir (mostly additional s ystemic administration for the treatment of dermatitis). With intact epithelium and cortisone allowed (see HSV keratitis). 12 Uveitis General Depending on the affected section, we distinguish anterior uveitis (irit is), uveitis intermedia (Zyklitis) and posterior uveitis (choroiditis). Mixed fo rms are iridocyclitis and panuveitis. Clinic ● Iridocyclitis: dull pain, visual loss, photophobia, Reizmiosis, epiphora, or mix ed ciliary injection (conjunctiva is involved). Even chronic course possible. Ch oroiditis: no pain, since choroid does not contain sensitive nerves. Visual loss , visual disturbances (veil). ● In contrast to iridocyclitis with glaucoma the anterior chamber of normal depth and the pupil is narrow (Reizmiosis). Etiology and pathogenesis of uveitis is of ten an immunological one (system) underlying disease, eg Ankylosing spondylitis, M. Reiter, Crohn's disease, psoriasis (all HLA-B27-associated), sarcoidosis,rh eumatoid arthritis or Behçet M.. Acute anterior uveitis may also be infectious t o conditions (rare), eg in herpes infection, syphilis, tuberculosis and leprosy. A choroiditis may also be infectious due, for example, Cytomegalovirus (CMV), s yphilis, brucellosis and toxoplasmosis. Diagnosis ● Iridocyclitis: slit-lamp examination showed Tyndall phenomenon (protein accumula tion and cellular infiltration of the anterior chamber → visual loss), and corne al edema. Choroiditis: ophthalmoscopy shows whitish, ill-defined foci. ● Therapy ● Iridocyclitis: It is important to avoid synechiae (adhesions of the iris and len s and iris and cornea): therapeutic mydriasis and steroid therapy. In systemic erregerbedingter I.: antibiotic or antiviral therapy (if any). ● Choroiditis: depending on the cause, steroids or antibiotics (local and systemic ). ACUTE ANGLE BLOCK BLOCK ANGLE GLAUCOMA GLAUCOMA Rather rare and often misdiagnosed general cause of a red, painful eye. Suscepti ble patients with flat anterior chamber (for example, are due to short bulb with hyperopia or large pupil during cataract). A sudden blockage of aqueous outflow , there is a paroxysmal increase in intraocular pressure to a multiple of the st andard. Emergency, as threatened blindness in the affected eye! 13 Clinic ● general: acute pain (possibly by projection misinterpreted as headache), nausea and vomiting (by stimulation of the vagus). General symptoms can be so much in t he foreground, that is first thought of appendicitis or brain tumor. Eye: mixed injection, corneal edema, eye dull, flat anterior chamber entrundete, reactionle ss pupil, rock hard eyeball, severe visual loss is (may not notice, because the healthy eye laminated). ● Diagnostic triad of red eye, pupil-free reaction on palpation and hard eyeball. Treatment goals are the reduction in pressure within 6 hours, pain relief and cl earing up of the cornea (the causal surgical treatment to enable). ● drugs: osmotic reduction of vitreous volume (mannitol iv, glycerol oral), reduci ng aqueous production (carbonic anhydrase inhibitors: acetazolamide iv; local be ta-blockers, eg timolol) and extract the iris from the anterior chamber angle (l ocal miotics: pilocarpine 1%). Mechanical: dent of the cornea with a glass rod ( aqueous pressed in the periphery, thereby opening the chamber angle). operativel y: shunt between the front and back room, for example, Laser iridotomy. ● ● Endophthalmitis General After perforating trauma or endogenous infection via hematogenous spread of pathogens (bacteria, viruses, fungi). Risk are v.a. chronically ill, immunos uppressed or diabetic patients. It threatens the loss of the eye (within hours!) . Hospital Deep, dull pain in the eye, acute visual loss, severe redness. Typica l clinical history and diagnosis. Slit lamp: mixed injection, hypopyon. Ophthalm oscopy: yellowish discoloration vitreous, whitish spots with hemorrhagic retinal edge, possibly retinal detachment. Think For intravenous drug users and patient s with indwelling catheter-visual defect on Candida endophthalmitis! Pathogen-sp ecific antibiotic therapy (systemic, local and intravitreal). The course is vari able. 14 Symptom: General ACUTE Visual disorder visual disorder The sudden loss of vision is always an emergency, even if it lasts only a few se conds. differences have to be visual disturbances, emanating primarily from the eye (eg, retinal detachment, Zentralarterienverschluss), and those who have a ne urological cause (eg, cerebrovascular disease, migraine). Differential diagnosis , the distinction is important in: ● painless visual disturbance: for example at Zentralarterienverschluss, temporal arteritis, retinal detachment, acute ischemic optic neuropathy, retrobulbar neur itis, vitreous detachment. painful visual disturbance (often with "red eye"): ac ute angle-closure glaucoma, acute iritis, verblitzung (photoelectrica keratitis) , corneal ulcer, trauma. ● Moreover, can be symptoms of groundbreaking diagnostic (eg, hard eyeball in glau coma attack, Rußregen and black curtain to see in retinal detachment). Amaurosis General Fugax AND ZENTRALARTERIENVERSCHLUSS ZENTRALARTERIENVERSCHLUSS Blindness in one eye by ischemia of the retina, eg in embolism of ipsilateral in ternal carotid artery. When it comes to amaurosis fugax dissolution or washing o ut of the embolus for full recovery of visual acuity within a short time. In con trast, there is persistent occlusion after about an hour to irreversible retina damage (infarction) with blindness in the affected eye. Rapid painless unilatera l visual loss clinic ("falling curtain", "lights out") at Zentralarterienverschl uss.Visual loss or visual field loss when only one branch is affected. The dire ct pupillary reflex is abolished. Ophthalmoscopy Diagnosis: ● ● Amaurosis fugax: inconspicuous ophthalmoscopic findings. Zentralarterienverschlu ss (infarction): narrow vessels, gray-white retina (edema). Only the fovea centr alis appears as cherry stain. Bulbusmassage therapy to flush the embolus in a peripheral retinal vessel. Hemod ilution to improve blood flow. The prognosis is unfavorable, with complete Zentr alarterienverschluss is the blindness of the eye to prevent almost never. Lysis is due to the possible side effects and the low likelihood of success usually no t carried out. More important is the search for the source of embolism (eg atria l fibrillation), for example to prevent a stroke. 15 Anterior ischemic Optic neuropathy (AION), optic neuropathy General Acute ischemia of the optic disc, arteriosclerotic, or (rarely) arteriti c due. The latter occurs as a complication of temporal arteritis (M. Horton befo re). Hospital Sudden, unilateral, painless loss of vision (occasionally slow-pro gressing) or visual field defects (wedge). Afferent pupil defect. In addition, t emporal arteritis, headache, tender and pulseless temporal artery Kausch Merz. A history of weight loss and Reduction. Allg.zustand. Diagnosis OPHTHALMOSCOPY pa pilledema with sectoral accented edge blur. Therapy ● ● AION: none. Hemodilution can be tried. AION in temporal arteritis: protect high- dose systemic corticosteroids immediate (especially around the second eye). Optic neuritis General inflammation of the optic nerve in the (papillitis) or behind the eye (r etrobulbar neuritis). Most younger patients are affected. Causes are infections (eg Lyme disease), autoimmune diseases (eg lupus erythematosus, Crohn's disease, M. Wegener), toxic injury (eg, methanol, lead, chloramphenicol) or idiopathic. The retrobulbar neuritis is often a multiple sclerosis (encephalitis disseminata advance). Hospital Sudden vision loss with central scotoma (often after exercis e: Uhthoff's phenomenon), pain on eye movement and pressure on the eyeball. In a ddition, afferent pupil defect and red-green color blindness-. Ophthalmoscopy Di agnosis: ● ● Papillitis: edema and hyperemia of the optic nerve head, blurred disc margin. Re trobulbar neuritis: inconspicuous findings ("the patient sees nothing and the do ctor does not"). Delayed latency visual evoked potentials (VEP) in demyelination. Therapy is ofte n spontaneous improvement. If possible, treat underlying disease. To accelerate the Visuserholung: steroid therapy (but does not affect the final result). The p rognosis depends on the underlying disease. 16 TOXIC Optic neuropathy General Toxic damage of the optic nerve can lead to acute loss of vision by bila teral swelling of the optic nerve head. Substances are, for example Ethambutol, methanol, chloramphenicol, amiodarone, streptomycin, lead, arsenic, D-penicillam ine, isoniazid and sulfonamide. At a similar picture can lead thiamin, vitamin B 12 and folic acid deficiency. Papilledema General Most-sided swelling of the optic nerve exit point (English papilledema), eg with chronically elevated intracranial pressure. Because of the potentially life-threatening increase in intracranial pressure for an immediate diagnosis is necessary (neurosurgical, neurological, internist). Clinic Reversible darkening phenomena (Obskurationen), enlarged blind spot, ongoing headache. Diagnosis OPHTHALMOSCOPY randunscharfe papilla excavation is no longer distinguishable. Of ten discrepancy between (good) and functional (pathological) ophthalmoscopic fin dings. Further diagnostics (eg imaging) to clarify the increase in pressure cause. Ther apy to treat underlying disease. After normalization of intracranial pressure, p apilledema is back, but it can remain an optic atrophy. Vitreous detachment General Partial or complete detachment of the vitreous from its base (English vi treous detachment). At the age fluid-filled lacunae occur in the vitreous, which may cause a collapse of the vitreous. This leads to densities that are perceive d as free moving opacities (floaters). the vitreous from incomplete sets aside f rom the retina, can develop on the remaining connections traction forces, which in turn can lead to rupture or detachment of the retina. Clinic floaters ("float ers"). Light flashes and chills indicate a retinal defect and must be clarified. Ophthalmoscopy to exclude diagnosis of retinal damage.Treatment vitreous detac hment is not dangerous in itself, as long as the retina is not involved. 17 Retinal detachment General elevation of the neurosensory retina from the retinal pigment epithelium (syn. retinal detachment, Eng. Retinal detachment). Can cause retinal (rhegmato genous retinal detachment), train through the vitreous strands (Traktionsamotio) or liquid between the retina and retinal pigment epithelium (exudative retinal detachment, such as M. Coats be). Risk factors include high myopia, Z.n. Trauma and family history. Clinic light flashes, floaters, Rußregen, shadows in the visual field (like a cu rtain from top to bottom falling or ascending from below). For infestation of th e retina center: rapid visual loss. Diagnosis OPHTHALMOSCOPY bubble retinal detachment, possibly bright red retinal hole. Alwa ys the other eye mituntersuchen because retinal holes can occur bds. In therapy with low hole retinal detachment: Laser (attachment of the retina aro und the hole). For more extensively findings: OP (Silikonplombe is sewn to the s clera, the eyeball and to einzudellen so as to restore the contact between the r etina and pigment epithelium). If necessary. Vitrectomy with replacement of the vitreous by silicone oil to tampon to the eye from the inside. The rhegmatogenou s retinal detachment is probably not a good prognosis, the other forms. MIGRAINE General MIT AURA AURA In the 20-minute visual migraine aura, there is visual disturbances, such as vis ion loss, flashes of light and perception of jagged colored lines (even with clo sed eyes). Typically, the headache occurring after the aura. The described visua l disturbances may be confused with amaurosis fugax in, come in contrast, howeve r, on both sides and take longer. STROKE General AND TIA An insufficiency of the posterior circulation can result in homonymous visual di sturbances. A circulatory disorder of the visual cortex 'leads to hazy vision an d possibly for the perception of flashes of light to those of a migraine aura ma y be similar. Double vision, dizziness, weakness, dizziness, and dysarthria have to think of a brainstem ischemia. When a heart attack in the area of the visual cortex, "It is a homonymous visual field defect, which ends exactly on the vert ical axis. 18 Symptom: General CHRONIC Visual disorder visual disorder The most common cause of chronic deterioration of vision in most age-related len s opacity (cataract). Thus, the already known since ancient times "cataract surg ery" one of the most frequently performed operations in general. In the cataract and glaucoma family history is often positive. Differential importance of the d istinction between central (eg macular degeneration), peripheral (eg for glaucom a) and total loss of vision (eg cataract). Another possible cause of reduced vis ion for a slow, which should not be forgotten, check the "old glasses (refractio n and any new prescription). Cataract (GREY STAR) (STAR GREY General Creeping, clouding of the lens. Most age-related, but more frequently in systemic diseases such as diabetes mellitus, renal insufficiency, and M. Wilson , after trauma / surgery or iatrogenic (especially steroid, radiation). Rarely h as a congenital cataract, e.g. inherited or due to intrauterine injury (rubella, mumps, toxoplasmosis). The classification of senile cataract is based on morpho logical criteria: ● ● ● ● Nuclear cataract: hardening and discoloration of the lens nucleus, slow progress ion. Figure 4: cataract. Source: Wikipedia.de (.../ Image: Cataract_in_human_eye.png) Cortical cataract: cortical changes (vacuoles, water columns), is proceeding fas ter than the nuclear cataracts. Special: rear shell opacity. Cataract matura: di ffused white lens, shadowy yellow nucleus, visual acuity at light-dark perceptio n reduced. Cataract hyper matura: complete liquefaction of the cortex, capsule s inks, so that the upper edge is visible in the pupil, frequently secondary open angle glaucoma (glaucoma phakolytisches). Very independent variable clinic: insidious visual loss, graying ("all gray to g ray) vision, blurred or distorted, altered color perception, glare. Diagnosis At tenuated red reflex of the fundus ophthalmoscopy and at Spaltlampenunters. The o nly effective therapy treatment: surgical removal of the opaque lens (usually an outpatient basis under local anesthesia). Most inserting an artificial lens. Th e posterior lens capsule remains in the OP i.d.R. (Received extracapsular catara ct extraction, ECCE). This may deteriorate secondary (cataract, occurs in every third patient). Treatment of cataract: clouded posterior chamber is cut by laser in the optical axis. If no artificial lens usedmay, at bilateral aphakia ("len sless"), the refraction can be corrected with cataract glasses. This is now the exception. 19 GLAUCOMA General Creeping optic neuropathy, usually due to a chronically elevated intraoc ular pressure. After the second leading cause of blindness diabetes mellitus in industrialized nations. Differences are open-angle glaucoma (90%) and angle clos ure glaucoma (see acute angle-closure glaucoma). Glaucoma is the previously heal thy eye (primarily occur) and as a result of various eye diseases (secondary), e g iridis in hyper mature cataract, rubeosis. Pathogenetically usually there is a n increased outflow resistance, rarely increased aqueous humor production. Figure 5: glaucoma. Clinic Source: Wikipedia.de (.../ Image: Glaukompapille2.jpg) The open-angle glaucoma runs in Ggs. to angle-closure glaucoma insidious, painle ss and often asymptomatic. Occasionally, nonspecific symptoms (headache, burning eyes). In a symptomatic visual field defect of the optic nerve damage is alread y advanced. The early diagnosis is so crucial! It is therefore recommended that the first reading glasses prescribed by an ophthalmologist always allow to measu re the opportunity in the eye pressure (glaucoma screening). Diagnosis Slit lamp and gonioscopy: common shallow anterior chamber. Enger (with narrow-an gle) or closed (with angle-closure glaucoma) chamber angle. OPHTHALMOSCOPY chara cteristic is the crisp, faded, with enlarged papilla excavation and in the depth kinked vessels. Tonometry: increased intraocular pressure (> 21 mmHg). Perimetr y: paracentral nasal visual field defects (early sign). Therapeutic goal of treatment of chronic glaucoma is the reduction of intraocula r pressure in order to prevent the progression of optic atrophy and visual field defects. Drugs Basically, there are the following possibilities of conservative treatment of gl aucoma: ● ● Inhibition of aqueous humor production and improving the aqueous outflow. Be used as eye drops, alpha-2 agonists (eg clonidine), cholinergics (eg pilocarp ine), beta blockers (eg timolol), carbonic anhydrase inhibitors (eg dorzolamide) and prostaglandins (eg latanoprost), and combinations. Operation Laser trabeculoplasty (scar contraction in trabecular meshwork leading to dilata tion of the spaces) with open anterior chamber angle or filtering surgery (aqueo us humor is derived by Skleraöffnung under the conjunctiva) are available. 20 Age- MACULAR DEGENERATION (AMD) MACULAR DEGENERATION General Progressive, degenerative disease of the macula. Differences are exudati ve (wet) and non-exudative (dry) macular degeneration. With over 65 years, the A MD is a common cause of chronic, painless bilateral visual loss. Slow visual los s clinic. In exudative form of macular edema and sudden loss of vision with poss ible distortion of vision and micro-or macropsia. The peripheral vision usually remains preserved, as a rule only the macula is affected. Etiology and pathogene sis are the starting points of the action pigment epithelium and choroid. Aging of the retinal pigment epithelium leading to increased deposition of products fr om the photoreceptor metabolism (Druze): dry form. For perfusion of the choroid, it is mediated by tissue hypoxia VEGF *- a vascular neoplasm with bleeding unde r the retina: wet form. Diagnosis Ophthalmoscopy: drusen, serous detachment of the retina. The choroidal neovascul arization can be represented by means of fluorescein angiography. If one patient before an Amsler card and see this instead of the checkerboard pa ttern of wavy or distorted lines, this indicates a macular edema. Figure 6: Amsler card (left: normal, right: AMD patient). Source: National Eye Institute, National Institutes of Health. Therapy ● ● Dry AMD: No known effective therapy that can stop a possibly high-dose vitamin a dministration (C, E, beta carotene) progression. wet AMD: laser or photodynamic therapy can be deserted newly formed vessels. Monoclonal antibodies against VEGF are currently in clinical trials. * VEGF: vascular endothelial growth factor. 21 DIABETIC RETINOPATHY RETINOPATHY General Until 1921 this was a rare disease. After the discovery of insulin and t he associated dramatically improved life expectancy of diabetic patients, diabet ic retinopathy is now one of the most common causes of blindness in developed na tions. We distinguish the following forms: ● non-proliferative: microaneurysms, moderate bleeding, venous caliber changes. pr oliferative: neovascularization or vitreous hemorrhage, rubeosis iridis. diabet. Maculopathy: macular edema. Figure 7: Diabetic retinopathy. Source: National Eye Institute, NIH ● ● In diabetes mellitus, it is inter alia to changes in small vessels (microangiopa thy). With the invention of the ophthalmoscope by Hermann von Helmholtz (1850), it was possible, small vessels in the living directly visualize and detect patho logical changes. The regular examination of the fundus is an important measure t o determine the extent of microangiopathy and to intervene early therapeutically to further damage (not only for the eye) averted. Asymptomatic hospital. In the late stage by participating in the macula, or vitreous hemorrhage sudden blindn ess or visual loss. Blindness can occur through: rubeosis iridis (neovascularisa tion on the iris), or diabetic macular edema Traktionsamotio. The etiology and p athogenesis of diabetic retinopathy is a microangiopathy. With hyperglycemia it comes to the vascular basement membrane thickening, capillary occlusions and ret inal ischemia later with the formation of angiogenic factors (VEGF, IGF). The ne wly formed blood vessels tend to be inferior microaneurysms, increased permeabil ity and haemorrhage. Diagnosis Ophthalmoscopy: microaneurysms, macular hemorrhages, yellow spots ("hard exudate s" from the vessel leaked blood components, eg lipids). Optimal glycemic control therapy (HbA1C <7%), laser treatment (with macular edem a: centrally, in proliferative retinopathy: panretinal). When vitreous hemorrhag e vitrectomy. Are important for each diabetic regular ophthalmological controls! 22 Retinitis General Pigmentosa Heterogeneous group of (usually hereditary) diseases of the retina, where photor eceptors are based. Despite the name, this is not an inflammatory process. The a ge of onset depends on the mode of inheritance, most affected patients are young . First clinic increased glare sensitivity and night blindness. Later, visual fi eld defects (especially in the periphery: "Tunnel vision") and visual loss. Diag nosis OPHTHALMOSCOPY proliferations of the retinal pigment epithelium, optic atrophy, close together arteries, relfexarmer fundus. Electroretinogram: greatly reduced or abolished. Treatment None. Optimization of Restsehvermögens through magnifying glasses. MELANOMA General AND OTHER Tumors Tumors The most common primary intraocular malignant Uveamelanom is. Depending on locat ion we distinguish iris melanoma (often without symptoms, possibly secondary gla ucoma), Ziliarkörpermelanom (accommodation and refraction) and uveal melanoma (p ossibly falls on by Begleitamotio in macular Participation: visual loss). In ord er to determine position and expansion of the tumor, ultrasound and indocyanine green angiography can be used. The metastasis is hematogenous, v.a. in the liver . Treatment options to remove the tumor, enucleation, radiotherapy and laser thera py is possible. More common than primary tumors are metastases that infect the eye, such as Mamm a-Ca. Even leukemia and lymphoma can infiltrate the structures of the eye. 23 Symptom: LOCATION CHANGE LOCATION CHANGE General OF Eyeball eyeball Oculi Asymmetrical appearance of the eyeballs is to first clarify what the eye is chan ged, Is it a clear eye (exophthalmos) or is the other eye in the orbit sunken (e nophthalmos)? Delineate the Pseudoexophthalmus (long eyeball with high myopia) a nd the Pseudoenophthalmus (eyeball is smaller). By Exophthalmometer (by Hertel) can be measured, how far the eyeball protrudes over the bony orbital rim and sid e differences are observed. In diseases of the orbit usually is an interdiscipli nary cooperation (otolaryngologist, neurosurgeon, internist) is required. Causes of exophthalmos (protrusion of the eyeball) are: ● ● ● ● thyroid eye disease (most frequently, such as Graves' disease), inflammatory cha nges (eg, orbital cellulitis, Orbitaabszess, cavernous sinus thrombosis), vascul ar changes (such as arteriovenous fistula, orbital hematoma) and tumors of the o rbit (eg hemangioma dermoid, Optikusgliom, metastases ). Orbita (most common cau se, such as blow-out fracture), neurogenic changes (such as Horner's syndrome) a nd symmetrical wasting of the Orbitagewebes (eg, senile atrophy, dehydration). Endocrine Causes of enophthalmos are: ● ● ● Eye disease eye disease General autoimmune inflammatory disease with involvement of the orbit, eg with a utoimmune thyroiditis. Most of asymmetric exophthalmos, sometimes even unilatera lly. In adults the most common cause for both unilateral and for bds exophthalmo s. Deposits of glycosaminoglycans in the orbit and inflammatory involvement of o rbital fat tissue and muscles lead to exophthalmos. Clinic Reddened,dry eyes, r educed Bulbusmotilität, double images. Diagnosis Clinical: exophthalmos, impaired convergence property (Möbius's sign), typical L idzeichen (Dalrymple: retraction of the upper eyelid, from Gräfe: retraction of the upper lid in lower view; Stellwag: blink less often; Cooker: Gaze; Gifford: difficulty in eversion of the upper lid). Sonography thickened: extraocular eye muscles. Prednisone therapy (60 mg / d for 4 weeks), X-ray irradiation of the orbit. If n ecessary. surgical Orbitadekompression to pressure injuries of the N. to prevent optic. 24 PSEUDO TUMOR General ORBITA Idiopathic, inflammatory with lymphocytic and eosinophilic infiltration Orbitasy ndrom. A special case is the Tolosa-Hunt syndrome (granulomatous inflammation of the orbital apex with painful ophthalmoplegia). Clinic Painful inflammation, ey elid swelling, limited Bulbusmotilität. Diagnosis difficult. Sonographically are the swollen eye muscles (myositis) with enlarged tendons. The MRI shows a diffu se soft tissue swelling. The definitive diagnosis is confirmed by biopsy. High-d ose therapy, systemic glucocorticoid administration (in the case of dramatic imp rovement is based this finding, the diagnosis ex juvantibus). HORNER SYNDROME SYNDROME General Trias of (pseudo) enophthalmos (paralysis or paralysis of the orbital M. rudimentary Lidretraktoren: lower is higher, the eye looks smaller), ptosis (pa ralysis of the Müller M. tarsalis) and miosis (paralysis of the pupil dilator). Cause is an injury in the course of the ipsilateral Sympathikusbahn: ● ● ● central: e.g. Tumors, encephalitis, multiple sclerosis. preganglionic: e.g. Trau ma, goiter, aneurysm, Pancoast tumor. postganglionic: e.g. Internal carotid aneu rysm. Diagnosis Clinical: direct and consensual light reaction intact (in contrast to Parasympat hikusschädigung), pupil is far slower (Dilatationsdefizit). Cocaine eye drops: p upil on the affected side does not react with dilatation. Therapy to treat underlying disease. 25 Symptom: General HANGING LID LID A (one-or two-sided), drooping of the eyelid is called ptosis. It can be made be tween congenital and acquired ptosis. Unilateral ptosis rather indicates a neuro genic, bilateral ptosis out more on a myogenic cause. By frown the patient attem pts to extend the lids. Operational raising the upper eyelid ● ● ● Fasanella-Servat operation for: v.a. to mild ptosis. Cut a portion of the rear v ertical Lidblattes → Lidverkürzung. Levatorresektion: shortening of the levator palpebrae M.. Frontalis suspension: Connect with the upper eyelid tissue in the area of the brows using a sling (autologous fascia lata or plastic threads). Ptosis General Congenital Underdeveloped and hanging by congenital upper eyelid (usually unilateral) levat or defect. If a pupil is masking Amblyopiegefahr! Case of bilateral ptosis recli ned the baby's head so that both eyes can see. In Waardenburg syndrome is ptosis , epicanthus and blepharophimosis. Surgical therapy raising the upper eyelid. MYOG Ptosis ptosis General main cause of myogenic ptosis is myasthenia gravis. Usually both sides a re affected, but not always equally strong. Typically, an increase of ptosis in the course of the day (abnormal fatigue) is. This can be used diagnostically: En trapment of ptosis by rapidly opening and closing of the eyelids or fatigue duri ng prolonged looking up (Simpson-test). (The further diagnosis and treatment are neurological.) NEURO GENE Ptosis ptosis General Most-sided eyelid drooping due to damage to the innervation of the two e ye-opener: Müller-muscle (sympathetic ptosis in Horner's syndrome) or LevatorMus kel (paralytic ptosis with oculomotor injury). When Horner's syndrome is the pup il is narrow and the Augenmotilität normal. When motility is disturbed oculomoto r paralysis of the eye and affected the pupil normal width (external paralysis: only external eye muscles) or extended (complete paralysis and ciliary muscle an d sphincter pupil concerned, therefore absolute pupil, mydriasis, paralysis of a ccommodation). Treatment depends on the underlying disease. 26 Symptom: DOUBLE IMAGE, DOUBLE IMAGE motility motility General AND Nystagmus Nystagmus First, must persist between monocular (double vision when one eye is covered, fo r example, keratoconus, cataract or uncorrected refractive error) and disappear binocular diplopia (double vision when one eye is covered, cause a deviation of the eyes of Parallel stance can be distinguished). Binocular diplopia can neurog enic (eg, sixth nerve palsy), myogenic (egwith myasthenia) or by mechanical con straint (eg blow-out fracture of the orbit, mass) may be caused. (Think mell If nerve damage and diabetes.!) Motility disorders can by nerve damage (eg, third nerve palsy) or by an imbalanc e of the eye muscles (eg, caused in squint). When nystagmus (eye tremor) occurs ruck or pendulum involuntary rhythmic eye mov ements, which may be acquired or congenital. Myasthenia General GRAVIS In myasthenia gravis, it may not only to the drooping eyelid (see myogenic ptosi s), but also to get double vision. Many myasthenia patients, only the eye muscle s are affected, a systemic muscle weakness exists. Clinic Intermittent double vi sion that can not be assigned to a single nerve. The pupils are always normal. I f necessary. Accompanying myogenic ptosis. Diagnosis Tensilon test (temporary improvement by administering a cholinesterase inhibitor ) and detection of acetylcholine receptor antibodies. DD: Botulinum toxin poison ing. Cholinesterase inhibitor therapy, glucocorticoids, azathioprine, and plasmaphere sis in severe cases, immunoglobulin administration. If necessary. Thymectomy (th ymoma is often a cause of antibody formation). The purely ocular form of myasthe nia has a good prognosis. N. Oculomotor (third cranial) nerve General The (rare), oculomotor palsy is mainly by vascular disease (eg, aneurysm ) caused. The N. oculomotor muscles following supplies: ● motor fibers → external eye muscles: ○ ○ M. rectus superior, inferior, and medial and inferior oblique eye movements → al l down to the bottom lateral (N. IV) and lateral (N. VI). Levator palpebrae → le vator. M. ciliaris → accommodation. Sphincter pupil → miosis. ● parasympathetic fibers → inner eye muscles: ○ ○ 27 Clinic differences, the following diseases: ● O.-complete paralysis: complete interior and almost all external eye muscles aff ected (loss of motor function and pupil accommodation, mydriasis, ptosis). Becau se of the ptosis, the patient has no diplopia. O. partial outer-paresis: isolate d paralysis of the extraocular muscles supplied with squint to the outside botto m. Because of the ptosis no double images. O. partial inner-paresis: paralysis o f the isolated internal muscles supplied with mydriasis and lack of accommodatio n. No double vision, since there is no squint. ● ● V.a. participation of pupils in a motor diagnostic imaging is indicated to aneur ysms, to exclude space-occupying processes and Clivuskantensyndrom. (More diagno stics and therapy is neurosurgical, neurological and radiological.) Figure 8: nerves of the eye area. Source: Wikipedia.de http://de.wikipedia.org/wiki/Bild:Augennerven.jpg () N. General Trochlear (IV CN) CN The N. trochlear nerve supplies the superior oblique (moving laterally down and internal rotation). An injury occurs v.a. after trauma. Vertical double vision c linic, v.a. Looking down at the nasal (eg climbing stairs). Double images disapp ear when looking upward. The patient attempts by compensatory head posture to av oid double images (up to the ocular torticollis). Diagnosis Bielschowsky Kopfneigetest: When inclination of the head on the side of the para lyzed eye and fixation with the healthy eye deviates from the paralyzed eye upwa rd. For slope on the healthy side produced no difference in the height. 28 N. Abducens (CN VI) nerve General The N. abducens supplies the rectus lateralis (lateral motion). Causes o f injury are vascular diseases (diabetes mell., Hypertension), meningitis, subar achnoid hemorrhage, and tumors with increased intracranial pressure. The long co urse at the base of the skull makes the nerve vulnerable to damage. A sixth nerv e palsy can always have to think a brain booster! Clinic Einwärtsschielstellung, horizontal double vision (largest in the attempted abduction), compensatory hea d posture rotated toward the affected side. Occlusion therapy of the affected ey e until the paralysis wears off. If no treatable underlying disease is found or not the paralysis of regressing, may be a 1-year corrective eye muscle surgery. Strabismus General A deviation of the axis of vision in one eye from the normal is known as squint (strabismus). In contrast to the paralysis squint (strabismus paralytic) is the squint angle for accompanying squint (strabismus concomitant) the same f or all eye movements. During early childhood strabismus syndrome is not fixating eye is suppressed central nervous system, to avoid double vision. In children, it can then come to amblyopia (visual acuity reduction in organically apparently healthy eye,to optical even with optimal correction persists). An untreated Am bylopie can lead to a visual acuity <0.02 (one-eyed blindness), which mainly be relevant is if the other eye illness (eg, trauma). The spatial vision is with on e eye is not possible (relevance for certain professions, such as pilot). The cl inic early childhood strabismus syndrome is asymptomatic, as caused by the suppr ession of the non-fixating eye is no double images. More important, therefore, t he routine eye examination, particularly one microstrabismus (due to the small a ngle squint squint inconspicuous) to diagnose early. In the (rare) normosensoris chen strabismus binocular vision is already well developed, not fixating eye can no longer be suppressed and it is therefore of double images, which are avoided by screw up of the eye. By early surgery, the binocular vision restored. Diagno sis A squint of the eyes may be replaced by non-central corneal light reflex (ex amination with a flashlight after Hirschberg) and pathological covered (at conce aling one eye does not do an adjustment here covered eye) was diagnosed. 29 A latent strabismus (balance disorder of the eye muscles, which can lead under c ertain circumstances, to squint, eg fatigue, alcohol, stress) is diagnosed by th e revealed. The reaction of the just covered eye is still observed in Wiederaufd ecken. Does that just covered eye, even a merger movement recording, the test is pathological. Without symptoms no treatment of latent squint is necessary becau se there is always a primary Parallel stance and full binocular vision. A more p recise diagnosis (exact determination of squint angle, testing of binocular visi on and stereopsis) is done by an ophthalmologist. During early childhood strabis mus syndrome therapy is performed on the Prevention and Treatment of amblyopia i n early childhood, the occlusion treatment. This mainly leading eye is covered i ntermittently and poorly trained the seeing eye. It is important that while the sehtüchtige eye loses vision. After the amblyopia treatment is completed success fully, a surgical correction of squint to be done (strabismus surgery). By reduc ing or relaxing the eye muscles, the position of the eyes is corrected at rest. Nystagmus General Sided, involuntary rhythmic nystagmus (jerk or a pendulum). Occur sponta neously or provoked lagerungsabhängig. There are numerous causes, for example: ● acquired: ○ ○ ○ Central nervous: inter alia Stroke, cancer, multiple sclerosis, encephalopathy. toxic-metabolic, alcohol, lithium, barbiturates, benzodiazepines, ketamine. vest ibular: M. Ménière, labyrinthitis. ocular: inter alia Albinism, cataracts, color blindness. idiopathic: no identifiable cause. ● : Congenital ○ ○ Differences are many different forms, including these are: ● ● physiological: for example Optokinetic Nystagmus as seen from a moving train. Th e direction of view-N.: Occurs when looking at in a certain direction, the expre ssion of a brainstem or cerebellar damage (multiple sclerosis, stroke, tumor). ○ ○ ○ blickparetischer N. sudden blow by Blickhalteschwäche form, eg in stroke, trauma , tumor (nothing to do with palsy!). dissociated nerve: both eyes affected in di fferent ways, eg in internuclear ophthalmoplegia (lesion of the medial longitudi nal fasciculus). Rebound-N.: After prolonged excessive turning of counter-regula tion. ● ● ● peripheral vestibular nerve: a horizontal spontaneous nystagmus in peripheral Ve stibularisläsion (eg Menière), visible through Frenzel glasses. Central vestibul ar nerve: "up-beat" - or "down-beat", eg with brain stem lesions. N storage.: Pr ovoked by specific head position. Treatment depends on the underlying disease, may help prism glasses. 30 LITERATURE General Ophthalmology ● ● Horton JC (2008): "Disorders of the Eye", in Kasper DL, Braunwald E, Fauci AS et al.: Harrison's Principles of Internal Medicine. 17th Edition. New York: McGraw -Hill. Lang GK (2004): Ophthalmology. 3rd Edition. Stuttgart: Thieme. Special Ophthalmology ● ● Augustin AJ (2007): Ophthalmology. 3rd Edition. Berlin: Springer. Kanski JJ (200 8): Clinical Ophthalmology. 6th Edition. London: Elsevier. is the current version of this script are available for download at the address http://www.harvey-semester.de/ 31