Sistim Faal Penglihatan Manusia

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SISTIM PENGLIHATAN Dr H SONNY PAMUJI LAKSONO. M Biomed

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Faal Penglihatan

Transcript of Sistim Faal Penglihatan Manusia

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SISTIM PENGLIHATANDr H SONNY PAMUJI LAKSONO. M Biomed

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SUSUNAN OPTIK MATA

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*MEMISAHKAN COP & COA

*DI BLKG KORNEA & DIDEPAN LENSA

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ANATOMI MATA

CORNEA TRANSPARANT

CHOROID LAP PIGMENT,

>> PEMB DARAH

RETINA SEL RESEPTOR

LENSA KRISTALINA

TRANPARANT,

DIFIKSASI OLEH

ZONULA ZINII

KE CILIARY

BODY

CILIARY BODY : TDD OTOT SIRKULER & LONGITUDINAL

IRIS : OTOT SIRKULER

DILATASI PUPIL

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*MENGISI SEBAGIAN BESAR BOLA MATA,

KONSISTENSI LUNAK

*PEMB DRH - , Bag luar : membran hyaloid, Bag tengah :

sal hyaloid. Nutrisi : dari khoroid, badan siliar&retina

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STRUKTUR LAPISAN RETINA

INTI (NUKLEUS)

KORTEKS

BAG EQUATOR

There are about 6.5 to 7 million cones in each eye, and they are sensitive to bright light and to color.  The highest concentration of cones is in the macula.  The fovea centralis, at the center of the macula, contains only cones and no rods.  There are 3 types of cone pigments, each most sensitive to a certain wavelength of light: short (430-440 nm), medium (535-540 nm) and long (560-565 nm).  The wavelength of light perceived as brightest to the human eye is 555 nm, a greenish-yellow.  (A “nanometer”—nm—is one billionth of a meter, which is one millionth of a millimeter.)  Once a cone pigment is bleached by light, it takes about 6 minutes to regenerate

SEL KERUCUT:

RETINA : These are the main cells in the retina: ·

1.Photoreceptors (rods & cones) 2.Horizontal cells (lateral inhibition at the level of the photoreceptors) 3.Bipolar cells ("on" and "off" cells) connect photoreceptors to retinal ganglion cells 4.Amacrine cells (lateral inhibition at the level of the retinal ganglion cells) 5.Retinal ganglion cells (the axons of which form the optic nerve

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The macula lutea is the small, yellowish central portion of the retina, and it is the area providing the clearest, most distinct vision.  When one looks directly at something, the light from that object forms an image on one’s macula.  A healthy macula ordinarily is capable of achieving at least 20/20 (“normal”) vision or visual acuity, even if this is with a correction in glasses or contact lenses.  Not uncommonly, an eye’s best visual acuity is 20/15; in this case, that eye can perceive the same detail at 20 feet that a 20/20 eye must move up to 15 feet to see as distinctly.  Some people are even capable of 20/10 vision, which is twice as good as 20/20.  Vision this acute may be due to there being more cones per square millimeter of the macula than in the average eye, enabling that eye to distinguish much greater detail

The Macula

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fovea centralisThe very center of the macula is called the fovea centralis, an area where all of the photoreceptors are cones; there are no rods in the fovea.  The fovea is the point of sharpest, most acute visual acuity.  (The center of the fovea is the “foveola.”)  Because the fovea has no rods, small dim objects in the dark cannot be seen if one looks directly at them.  For this reason, to detect faint stars in the sky, one must look just to the side of them so that their light falls on a retinal area, containing numerous rods, outside of the macular zone.

There are about 110,000 to 115,000 cone cells in the fovea and only about 25,000 cones in the tiny foveola.  The macular/foveal area is the main portion of the retina used for color discrimination.  Color vision deficiencies, which occur in less than 8% of males and in less than 1% of females, are usually hereditary, although they also can result from certain diseases, injury, or as a side effect of some medications or toxins

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BLIND SPOT ( BINTIK BUTA)The beginning of the optic nerve in the retina is called the optic nerve head or optic disk.   Since there are no photoreceptors (cones and rods) in the optic nerve head, this area of the retina cannot respond to light stimulation.  As a result, it is known as the “blind spot,” and everybody has one in each eye.  The reason we normally do not notice our blind spots is because, when both eyes are open, the blind spot of one eye corresponds to seeing retina in the other eye.  Here is a way for you to see just how absolutely blind your blind spot is.  Below, you will observe a dot and a plus. 

   

 Follow these viewing instructions:

1.Sit about arm’s length away from your computer monitor/screen. 2.Completely cover your left eye (without closing or pressing on it), using your hand or other flat object. 3.With your right eye, stare directly at the     above.  In your periphery, you will notice the     to the right. 4.Slowly move closer to the screen, continuing to stare at the    . 5.At about 16-18 inches from the screen, the     should disappear completely, because it has been imaged onto the blind spot of your right eye.  (Resist the temptation to move your right eye while the     is gone, or else it will reappear.  Keep staring at the    .) 6.As you continue to look at the    , keep moving forward a few more inches, and the     will come back into view. 7.There will be an interval where you will be able to move a few inches backward and forward, and the     will be gone.  This will demonstrate to you the extent of your blind spot. 8.You can try the same thing again, except this time with your right eye covered stare at the     with your left eye, move in closer, and the     will disappear.

If you really want to be amazed at the total sightlessness of your blind spot, do a similar test outside at night when there is a full moon.  Cover your left eye, looking at the full moon with your right eye.  Gradually move your right eye to the left (and maybe slightly up or down).  Before long, all you will be able to see is the large halo around the full moon; the entire moon itself will seem to have disappeared.Like any other ocular structure, certain pathologies can have an adverse affect on the optic disk and optic nerve.  Although there are too many to list completely, a few will be included here.

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There are about 120 to 130 million rods in each eye, and they are sensitive to dim light, to movement, and to shapes.  The highest concentration of rods is in the peripheral retina, decreasing in density up to the macula.  Rods do not detect color, which is the main reason it is difficult to tell the color of an object at night or in the dark.  The rod pigment is most sensitive to the light wavelength of 500 nm.  Once a rod pigment is bleached by light, it takes about 30 minutes to regenerate.  Defective or damaged cones results in color deficiency; whereas, defective or damaged rods results in problems seeing in the dark and at night.

SEL BATANG

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COLOR VISIONTo see any color, the retinal cone cells first must be stimulated by light.  “Red-sensitive” cones are most stimulated by light in the red to yellow range, “green-sensitive” cones are maximally stimulated by light in the yellow to green range, and “blue-sensitive” cones are maximally stimulated by light in the blue to violet range.  Accordingly, due to their respective sensitivities to long (L), medium (M), and short (S) wavelengths, they also are referred to as “L” cones, “M” cones, and “S” cones.  Collectively, the photoreceptors in the human eye are most sensitive to wavelengths between 530 and 555 nanometers, which is bright green tending toward yellow.

“Red-sensitive” or “L” cones

                                                       

“Green-sensitive” or “M” cones

                                                       

“Blue-sensitive” or “S” cones

                                                       

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TRICOLOR THEORY YOUNG-HELMHOLTZ

* TEORI WARNA NYA TERDIRI DARI 3 MACAM SEL KERUCUT* MASING MASING SEL KERUCUT TERDIRI DARI FOTOPIGMENT YANG BERBEDA, DAN MASING MASING HANYA SENSITIF TERHADAP SALAH SATU WARNA DASAR ( BIRU, HIJAU, MERAH) *PIGMENT PERTAMA : BIRU SENSITIVE THD WARNA BIRU ATAU PIGMENT PANJANG GELOMBANG PENDEK MENYERAP CHY MAX BIRU- VIOLET *PIGMENT KEDUA : HIJAU SENSITIVE THD WARNA HIJAU ATAU PIGMENT PANJANG GEL MENENGAH MENYERAP CHY MAX HIJAU*PIGMENT KETIGA : MERAH SENSITIVE THD WARNA MERAH ATAU PIGMENT PANJANG GEL YANG PANJANG MENYERAP CHY MAX KUNING*SEL KERUCUT YANG SENSITIF THD SPEKTRUM KUNING, CUKUP SENSITIF THD MERAH SBG RESPON THD CHY MERAH PD AMBANG YG LEBIH RENDAH DARI WARNA HIJAU

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The brain must compare the input from the three different kinds of cone cells, as well as make many other comparisons.  This comparison begins in the retina (which is an extension of the brain), where signals from “red” and “green” cones are compared by specialized red-green “opponent” cells.  These opponent cells compute the balance between red and green light coming from a particular part of the visual field.  Other opponent cells then compare signals from “blue” cones with the combined signals from “red” and “green” cones.  When one type of cone does not work properly, the proper color calculations cannot take place.

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RECEPTOR CELLS Rods are responsible for "scotopic" or low intensity vision. Cones are responsible for "photopic" or high intensity vision. Both rods and cones contain a photopigment which absorbs the light. There are 4 photopigments, one in rods and one in each of 3 cones. The photopigment is called rhodopsin and consists of two parts - a filter called an opsin and a light sensitive chromophore called retinal. Retinal is common to all four photopigments. [See graph of distribution of cells across retina]

PHOTORECEPTIONIn the dark the concentration of cGMP (cyclic guanosine monophosphate) in rods and cones is high. This opens cyclic nucleotide gated (non-selective cation) channels (CNG channels). Sodium (Na+) and calcium (Ca2+) enter the cell and this depolarizes, resulting in an increase in transmitter release.In the light, a G-protein, transducin, is activated starting a cascade of biochemical events and resulting in a fall in cGMP. The receptor operated channels close and the cells hyperpolarise (receptor potential), resulting in a fall in transmitter release

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MEKANISME PHOTORESEPTOR

* POTENSIAL AKSI DIDALAM RETINA DITIMBULKAN OLEH AKTIFITAS CAHAYA

PADA SENYAWA FOTOSENSITIF DIDALAM SEL BATANG & KERUCUT.

* PADA SAAT CAHAYA DI ABSORBSI OLEH SENYAWA INI , MAKA AKAN

MENIMBULKAN PERUBAHAN –PERUBAHAN PADA STRUKTUR SENYAWA TSB,

DAN HAL INI AKAN MEMULAI TIMBULNYA AKTIFITAS DIDALAM SYARAF.

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RESPON LISTRIK SEL-SEL DIRETINA* RESPON SEL BATANG, KERUCUT DAN

SEL HORIZONTAL : HIPERPOLARISASI

* RESPON SEL BIPOLAR : HIPERPOLARISASI

ATAU DEPOLARISASI

*AMACRINE SEL : POTENSIAL DEPOLARISASI

( SEBAGAI GENERATOR POTENSIAL)

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DASAR-DASAR IONIK POTENSIAL FOTORESEPTOR * CHANNEL ION NATRIUM PADA SEGMENT

LUAR SEL BATANG SEL KERUCUT

TERBUKA PADA KEADAAN GELAP

SEHINGGA TERJADI ALIRAN LISTRIK

DARI DALAM KE LUAR

* POMPA Na+-K+ PADA SEGMENT BAG

DALAM BERPERAN MEMPERTAHANKAN

KESEIMBANGAN ION

* PADA SAAT ADA CAHAYA PADA BAG

LUAR SEGMENT, MAKA BEBERAPA

CHANNEL NATRIUM TERTUTUP

HIPERPOLARISASI POTENSIAL RESEPTOR

ME < KAN PELEPASAN NEUROTRANSMITER DI

SINAPS POTENSIAL AKSI DI SEL GANGLION>

IMPULS KE OTAK

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SENYAWA-SENYAWA FOTOSENSITIF* SENYAWA-SENYAWA FOTOSENSITIF PROTEIN( OPSIN & RETINENE 1)

* RETINENE 1 MERUPAKAN ALDEHIDA DARI VIT A RETINAL

RHODOPSIN

* PIGMEN FOTOSENSITIF DIDALAM SEL BATANG : RHODOPSIN ( VISUAL

PURPLE)

* OPSIN NYA DISBT : SCOTOPSIN

* SENSITIF TERHADAP CAHAYA DGN PANJANG

GELOMBANG 505 nm

* BM : 41,00, BANYAK TERDAPAT DI BAGIAN

DISK SEL BATANG

* PADA KEAD GELAP : RETINENE 1 DLM

RHODOPSIN BER BTK: 11 CIS ALL TRANS

METARHODOPSIN II PENUTUPAN

CHANNEL ION NATRIUM

* PEMISAHAN RETINENE 1 DARI

OPSIN (SCOTOPSIN)

CAHAYA

PEMBTK

LGS

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HUBUNGAN RHODOPSIN DAN CHANNEL ION NATRIUM

* RHODOPSIN AKAN MENGAKTIVASI TRANSDUCIN(= G PROTEIN)

BERIKATAN DGN GTP AKTIVASI PHOSPODIESTERASE

KATALISIS( cGMP 5 GMP), c GMP BERPERAN UNT MEMPERTAHANKAN

AGAR CHANNEL ION NATRIUM TERBUKA, PE<< c GMP MENYEBABKAN

CHANNEL ION NATRIUM TERTUTUP HYPERPOLARISASI

SETIAP 1 MOL RODOPSIN

TDD 7 CROMOFOR

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STRUKTUR RHODOPSIN

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MEKANISME PENGAKTIFAN RODOPSIN

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CHANEL Na terbuka & ion masuk

Perubahan GTP menjadi cGMP O/ guanilate cyclase

Dalam keadaan malam

1

2

Pada saat ada cahaya

Pengaktifan rodopsin oleh cahaya transducin

3

4

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Perubahan GDP GTP phospodiesterase cGMP

Channel tertutup Na tidak bisa masuk

5

6

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EFEK DEFISIENSI VITAMIN A TERHADAP PENGLIHATAN

* VITAMIN A SINTHESIS RETINENE / RETINAL

* DEFISIENSI VIT A RABUN SENJA / NIGHTBLINDNESS /NYCTALOPIA

* FUNGSI SEL BATANG & KERUCUT TERGGG

* DEFISIENSI KRONIS DEGENERASI

STRUKTUR LAPISAN SEL RETINA.

* TERAPI DGN VIT A HANYA BER

MANFAAT BILA BELUM TERJADI PE-

RUBAHAN STRUKTUR ANATOMI SEL

PADA LAPISAN RETINA/ RESEPTOR

PADA RETINA RUSAK

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BIPOLAR CELLS

The release of transmitter either inhibits "depolarising" or (+) bipolar or stimulates "hyperpolarizing" or (-) bipolar cells which then relay the receptor potential to the retinal ganglion cells which increase/decrease their firing rate as appropriate. [Therefore, (+) bipolars lose their transmitter inhibition and depolarize in light, whereas (-) bipolars lose their stimulus and hyperpolarize in light. Nb. light causes photoreceptors to hyperpolarize and transmitter release, at synapses with bipolar cells, falls].

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VISUAL CODINGThe retina analyses the visual image in terms of (a)

colour, (b) form, (c) movement, (d) luminance and (e) depth.

a. Colour; green, blue and red cones. Cones contain a filter (opsin) and a light-sensitive bit

(chromophore, called retinal). Green cones have green filters, red cones have red filters etc.• red cones maximally sensitive to 559nm light • green cones to 531nm • blue cones to 419nm

   

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Colour opponency. Red/green and blue/yellow "centre-surround" receptive fields of retinal ganglion cells (see below) mean that there are retinal ganglion cells sensitive to red/green contrasts and others sensitive to blue/yellow differences. (Yellow is made up of output from red/green cones combined). This aids in colour contrast definition. Colour-blind people usually lack either a red or green opsin and have trouble distinguishing red from green (both appear the same).

b. Form; edge detection, centre-surround receptive fieldsEach retinal ganglion cell has a receptive field that corresponds to input from part of the visual field (a small region of the retina). This receptive field is made up of information from one to 1000s of photoreceptors arranged in a "centre-surround" fashion (see diagram).

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RECEPTIVE FIELDS"ON" and "OFF" cells

                                                                

[Exercise: draw a line down a sheet of paper; (1) light on left, dark on right; assuming that a constant illumination gives a net output of the centre-surround receptive field of zero, determine the net output at the border, for an "ON" centre retinal ganglion cell - as on the left in the diagram above. You will see that this retinal ganglion cell detects edges. (2) Now do the same for red on the left, green on the right, for a (+)green centre/(-)red surround retinal ganglion cell. You will find that this cell detects red/green edges].

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STRUKTUR RETINA

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STRUKTUR RETINA

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COLOR DEFICIENCY ( BUTA WARNA )If all the cone receptors work, but one type does not work as well as the other two, an “anomalous trichromatism” results.  A weakness in the long wavelength (“red” or “L”) cones causes “protoanomaly,” where more long wavelength light is required in order to perceive colors the same as a person with normal color vision.  A weakness in the medium wavelength (“green” or “M”) cones causes “deuteranomaly,” where more medium wavelength light is required in order to perceive colors the same as a person with normal color vision.  A weakness in the short wavelength (“blue” or “S”) cones causes “tritanomaly,” where more short wavelength light is required in order to perceive colors the same as a person with normal color vision.When one type of cone receptor does not work at all, an “anomalous dichromatism” results.  In “protanopia,” there is a lack of the receptors sensitive to long (reddish) wavelengths of light.  In “deuteranopia,” there is a lack of the receptors sensitive to medium (greenish) wavelengths of light.  In “tritanopia,” there is a lack of the receptors sensitive to short (bluish) wavelengths of light.  These conditions are portrayed as follows:

•protanopia (difficulty distinguishing between blue/green and red/green) •deuteranopia (difficulty distinguishing between red/purple and green/purple) •tritanopia (difficulty distinguishing between yellow/green and blue/green)

When only one cone receptor functions, the color deficiency is “monochromatism.”  Very few people (about 3 in a million) have total “color blindness” or “achromatopsia”; they see things only in shades of white, gray and black.  Color deficiencies usually are genetic.  However, sometimes such deficiencies are acquired due to retinal diseases such as glaucoma or diabetes or by retinal poisoning by certain medications

ASPEK KLINIS :

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About 7% of males have a red-green deficiency, compared to about .4% of females.  The genes for the red and green receptors (cones) are carried on the X chromosome.  As a result, a male with a defect in one of these genes does not have another X chromosome to compensate and, therefore, will be color deficient.  On the other hand, a female with such a defective gene has another X chromosome which, as a rule, will have a compensating normal gene.  With a red-green deficiency, a person might have difficulty distinguishing between things such as red and green traffic lights or electrical wiring.  Red-green color perception is altered in conditions such as optic neuritis.People with a less common type of deficiency cannot distinguish between blues or yellows.  The gene for the blue receptor (cone) is carried on Chromosome #7.  Blue-yellow color vision is diminished in many disorders, including glaukoma, diabetic retinopathy, cataract, and retinal disease.  In some cases, a reddish “X-chrome” contact lens, worn in one eye, can help a color deficient person discern more easily between colors.You might wish to check your color vision.  If so, go to color vision testing.

COLOR DEFICIENCY ( BUTA WARNA )

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Color Vision TestingPseudo-Isochromatic Plates frequently are used by eye specialists to get an idea of one’s color efficiency or deficiency.  To a color-deficient person, all the dots in one or more of the plates will appear similar or the same—“isochromatic.”  To a person without a color deficiency, some of the dots will appear dissimilar enough from the other dots to form a distinct figure (number) on each of the plates—“pseudo-isochromatic.”In the following plate, even a color-deficient person will be able to distinguish an orange “25” on a turquoise background:

                                                   

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Pemeriksaan fundus oculi

1. ALAT YANG DIPAKAI OFTALMOSKOP: OFTALMOSKOP DIREKT & OFTALMOSKOP INDIRECT.

2. YANG DIPAKAI : OFTALMOSKOP DIRECT

3. PROSEDUR PEMERIKSAAN :

A. PEMERIKSAAN DILAKUKAN DIRUANGAN GELAP

B. ATURLAH ALAT OFTALMOSKOP SEHINGGA BERADA

PADA POSISI F

C. SESUAIKAN UKURAN LENSA PADA OFTALMOSKOP

SESUAI DENGAN KEADAAN REFRAKSI ANDA(PEMERIKSA)

DAN KEADAAN REFRAKSI PASIEN. MIS NYA : PEMERIKSA

MIOP - 2 D DAN PENDERITA EMETROP MAKA PAKAILAH

LENSA PADA OFTALMOSKOP –2. BILA BAIK PENDERITA MAUPUN

PASIENNYA EMETROP, PAKAILAH LENSA PADA OFTALMOSKOP 0

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OFTALMOSKOP DIREKT

OFTALMOSKOP

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FUNDUSCOPI ARTERI RETINALISVENA RETINALIS

PAPILA NERVI OPTICI

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ASPEK KLINIS: OPTIC ATROPHY.“Optic atrophy” of the optic disk (visible to an eye doctor looking inside the eye) is the result of degeneration of the nerve fibers of the optic nerve and optic tract.  It can be congenital (usually hereditary) or acquired.  If acquired, it can be due to vascular disturbances (occlusions of the central retinal vein or artery or arteriosclerotic changes within the optic nerve itself), may be secondary to degenerative retinal disease (e.g., optic neuritis or papilledema), may be a result of pressure against the optic nerve, or may be related to metabolic diseases (e.g., diabetes), trauma, glaucoma, or toxicity (to alcohol, tobacco, or other poisons).  Loss of vision is the only symptom.  A pale optic disk and loss of pupillary reaction are usually proportional to the visual loss.  Degeneration and atrophy of optic nerve fibers is irreversible.

.

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GAMBARAN FUNDUS OCULI PASIEN RETINOPATHY DIABETICUM

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GAMBARAN FUNDUS OCULI PASIEN GLAUKOMA

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GLAUKOMA“Glaucoma” is an insidious disease which damages the optic nerve, typically because the “intraocular pressure” (IOP) is higher than the retinal ganglion cells can tolerate.  This eventually results in the death of the ganglion cells and their axons which comprise the optic nerve, thereby causing less and less visual impulses from the eye to reach the brain.  In advanced glaucoma, the peripheral retina is decreased or lost, leaving only the central retina (macular area) intact, resulting in “tunnel vision.”  Elevated IOP—which can be measured by a “tonometry” test—is a result of too much fluid entering the eye and not enough fluid leaving the eye. Normally, fluid enters the eye by seeping out of the blood vessels in the ciliary body.  This fluid eventually makes its way past the crystaline lens, through the pupil (the central opening in the iris), and into the irido-corneal angle, the anatomical angle formed where the iris and the cornea come together.  Then the fluid passes through the trabecular meshwork in the angle and leaves the eye via the canal of Schlemm.

If too much fluid is entering the eye, or if the trabecular meshwork “drain” gets clogged up (for instance, with debris or cells) so that not enough fluid is leaving the eye, the pressure builds up in what is known as “open angle glaucoma.”  Open angle glaucoma also can be caused when the posterior portion of the iris, surrounding the pupil, somehow adheres to the anterior surface of the lens (creating a “pupillary block”), preventing intraocular fluid from passing through the pupil into the anterior chamber.  On the other hand, if the angle between and iris and the cornea is too narrow or is even closed, then the fluid backs up, causing increased pressure in what is known as “closed angle glaucoma.”An internal pressure more than that which the eye can tolerate can deform the lamina cribrosa, the small cartilaginous section of the sclera at the back of the eye through which the optic nerve passes.  Deformation of the lamina cribrosa seems to “pinch” nerve fibers passing though it, eventually causing axon death.  Untreated glaucoma eventually leads to optic atrophy and blindness

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Eye pressure is measured by using a “tonometer” (with the test being called “tonometry”), and the standard tonometer generally is considered to be the “Goldmann tonometer.”  The normal range of intraocular pressure (IOP) is 10 mm Hg to 21 mm Hg, with an average of about 16 mm Hg.  Typically, eyes with intraocular pressure measurements of 21 mm Hg or higher, using a Goldmann tonometer, are considered suspect for glaucoma.  However, although glaucoma typically is associated with elevated IOP, the amount of pressure which will cause glaucoma varies from eye to eye and person to person.  Many people with glaucoma have IOP’s in the normal range (“low tension” glaucoma), possibly indicating that their lamina cribrosas are too weak to withstand even normal amounts of pressure; whereas, many people with IOP’s which would be considered high have no evidence of glaucomatous damage.

Visual field loss, caused by optic nerve damage, is measured by using a “visual field analyzer” or “perimeter.”  The procedure is known as “perimetry.”  Field loss due to glaucoma usually is not even measurable until 25% to 40% of the optic nerve’s axons have been destroyed. 

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PROSES AKOMODASI

*MATA DLM KEADAAN ISTIRAHAT: SINAR

SEJAJAR YG BERASAL DARI BENDA TAK BER

HINGGA (> 6 M) MEMP FOKUS TEPAT DIRETINA

(TANPA AKOMODASI)

*SINAR YANG DATANG SECARA DIVERGEN

AKAN DIFOKUSKAN PADA TITIK DIBELAKANG

RETINA BAYANGAN BENDA TIDAK JELAS

*UNTUK DAPAT MELIHAT SUATU BENDA PADA

JARAK LEBIH DEKAT LAGI DARI 6M DENGAN

JELAS MAKA MATA HARUS BERAKOMODASI

< 6M

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MEKANISME AKOMODASI

* LENSA ELASTIS : DLM KEADAAN ISTIRAHAT DIREGANGKAN OLEH ZONULA ZINII

*M.SILIARIS BERKONTRAKSI( SRBT SIRKULER & RADIAL BAG BLKG ZONULA ZINII BER GERAK KEDEPAN & KEDALAM MENGENDOR LENSA LEBIH CEMBUNG PADA SAAT TATAPAN DIARAHKAN PADA OBJEK YG LEBIH DEKAT

ZONULA ZINII

OTOT SILIARIS (SIRKULER & RADIAL)

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FOCUSSING Focussing involves:

1.moving the lens towards the back of the eye 2.turning the eyes inward towards the nose (convergence) 3.pupil constriction 4.fattening of the lens

ACCOMODATTIONWhen the ciliary muscle in the ciliary body relaxes, the ciliary processes pull on the suspensory ligaments, which in turn pull on the lens capsule around its equator.  This causes the entire lens to flatten or to become less convex, enabling the lens to focus light from objects at a far away distance.  Likewise, when the ciliary muscle works or contracts, tension is released on the suspensory ligaments, and subsequently on the lens capsule, causing both lens surfaces to become more convex again and the eye to be able to refocus at near.  This adjustment in lens shape, to focus at various distances, is referred to as “accommodation” or the “accommodative process” and is associated with a concurrent constriction of the pupil

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REFRAKSI MATA

1. MATA EMETROP

2. MATA MYOP

3. MATA HIPERMETROP

4. MATA ASTIGMATISMUS

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The eye allows us to see and interpret the shapes, colors, and dimensions of objects in the world by processing the light they reflect or emit.  The eye is able to see in bright light or in dim light, but it cannot see objects when light is absent.Light from an object (such as a tree) enters the eye first through the clear cornea and then through the pupil, the circular aperture (opening) in the iris

 Next, the light is converged by the crystalline lens to a nodal point immediately behind the lens; at that point, the image becomes inverted.  The light progresses through the gelatinous vitreous humor and, ideally, back to a clear focus on the retina, the central area of which is the macula.  (If the eye is considered to be a type of camera, the retina is equivalent to the film inside the camera.)  In the retina, light impulses are changed into electrical signals and then sent along the optic nerve and back to the occipital (posterior) lobe of the brain, which interprets these electrical signals as visual images.  Actually, then, we do not “see” with our eyes but, rather, with our brains; our eyes merely assist with the process.

MATA EMETROP

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MATA EMETROP

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The Nearsighted Eye (Myopia)Myopia is the most common refractive condition and affects one in four people in North America.  Myopic individuals are nearsighted:  they see near objects clearly, but distant objects are blurry.  Myopia occurs when light rays entering the eye are focused in front of your retina instead of directly on it.  Nearsightedness can be corrected by eyeglasses, contact lenses, or refractive surgery.  The tendency to develop myopia runs in families.  Myopia (nearsightedness) usually starts in childhood and typically stabilizes in the late teens or early adulthood

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MATA MYOP

Far Source Near Source

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THE FAR-SIGHTED EYE

Hyperopia (far-sightedness), is the opposite of myopia. Here, your eye is too short or your cornea is less curved. Consequently, light rays entering your eye fall behind the retina. This results in blurred vision – which is worse at near distances than far. 

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MATA HIPERMETROP

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THE ASTIGMATIC EYE Astigmatism occurs when your cornea is shaped like a football with two different curvatures. Images appear blurred or ghost-like because light rays are refracted unequally. In extreme cases, images both near and far appear blurred. Many people who have myopia also have astigmatism.

In the case of “astigmatism,” one or more surfaces of the cornea or lens (the eye structures which focus incoming light) are not spherical (shaped like the side of a basketball) but, rather, are cylindrical or toric (shaped more like the side of a football).  As a result, there is no distinct point of focus inside the eye but, rather, a smeared or spread-out focus.  Astigmatism is the most common refractive error

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MATA ASTIGMATISMUS

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MATA PRESBYOP

PRESBYOPIAAfter age 40 in most people, and by age 45 in virtually all, a clear, comfortable focus at a near distance becomes more difficult with eyes which see clearly (whether with or without glasses) at a far distance.  This normal condition is known as “presbyopia,” and it is due both to a lessening of flexibility of the crystalline lens and to a generalized weakening of the ciliary muscle which causes the lens to accommodate (change focus).  By the time one reaches age 65 or so, the crystalline lens is virtually incapable of changing shape.  Unless one is nearsighted, it is not possible to focus objects (such print on a page) clearly at even an arm's length distance.

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Note that “presbyopia” is not the same as “hyperopia” (farsightedness).  Presbyopia is an age-related condition, resulting in difficulty keeping a clear, comfortable focus at a near distance, even with an eye which is not hyperopic (farsighted).  On the other hand, hyperopia is a refractive error which makes it more difficult than normal to maintain a focus at a near distance than at a far away distance at any age (although, if one has a moderate to high degree of hyperopia, even maintaining a clear focus far away is difficult).

MATA PRESBYOP

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REFLEK-REFLEKS PENGLIHATAN

1. REFLEKS PUPIL / CAHAYA

2. NEAR RELEKS

3. OCCULOCEPHALIC

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JALUR LINTASAN REFLEK PENGLIHATAN

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NEAR REFLEKS

PUPIL : MYOSIS

GERAKAN MATA : KONVERGEN

LENSA : BERTAMBAH CEMBUNG

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dark: main iris muscle set involved is RADIAL

radial

                              light: main iris muscle set involved is CIRCULAR

circular

                              

MYOSIS

MIDRIASIS

LIGHT REFLEX / REFLEK CAHAYA :In bright light, the parasympathetic nervous system causes the circular sphincter muscle of the iris to contract and pupil constriction occurs. In dim light, the sympathetic nervous system causes the radial muscle to contract, dilating the pupil

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REFLEK CAHAYA:

LANGSUNG TIDAK LANGSUNG

* PADA KEADAAN PATOLOGIS DAPAT TERJADI : PUPIL TIDAK

MENIMBULKAN RESPON (MYOSIS) TERHADAP CAHAYA TETAPI RESPON

AKOMODASI MASIH BAIK PUPIL ARGYLL ROBERTSON

LESI PADA DAERAH TECTAL

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PEMERIKSAAN TAJAM PENGLIHATAN(VISUS)

• VISUS SESEORANG DITENTUKAN DGN CARA MEMBANDINGKAN KETAJAMAN ORANG TERSEBUT DENGAN ORANG NORMAL

• ALAT YANG DIPAKAI UNTUK MEMERIKSA VISUS ADALAH OPTOTIPE SNELLEN : BESAR HURUF-HURUF YANG ADA SUDAH DITENTUKAN/DITERA SESUAI DGN JARAK YANG DIPERLUKAN OLEH ORANG NORMAL UNTUK DAPAT MELIHATNYA DENGAN JELAS.

• PADA PINGGIR SETIAP BARIS TERDAPAT KODE ANGKA DGN SATUAN FEET/METER, YANG MENUNJUKAN BERAPA METER HURUF SEBESAR ITU OLEH MATA NORMAL MASIH DAPAT DIBACA

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OPTOTIP SNELLEN

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PROSEDUR PEMERIKSAAN VISUS

1. ORANG PERCOBAAN DUDUK PADA JARAK 6 METER TEPAT DIDEPAN OPTOTIPE SNELLEN

2. PERIKSALAH MATA KANAN TERLEBIH DAHULU, KEMUDIAN MATA SEBELAH KIRI(MONOKULER)3. MINTALAH ORANG PERCOBAAN UNTUK

MENGINDENTIFIKASI HURUF YG ADA PADA OPTOTIPE MULAI DARI ATAS SAMPAI HURUF PADA BARIS 6/6

4. BILAMANA ORG PERCOBAAN HANYA DPT MEMBACA DENGAN JELAS & BENAR HURUF-HURUF PADA BARIS BERKODE 20 METER MISALNYA & JARAK OP KE OPTOTIPE ADALAH 6 METER MAKA PENULISAN VISUSNYA ADALAH : 6/20

5. BILA HURUF E TIDAK DAPAT TERBACA MAKA LAKUKAN PROSEDUR : FINGER COUNTING, HAND MOVEMENT DAN LIGHT PERCEPTION

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KESIMPULAN PEMERIKSAAN VISUS

1. BILA DIDAPAT HASIL PEMERIKSAAN VISUS MATA KANAN ADALAH = 6/6 ( VOD=6/6),

KESIMPULAN : MATA KANAN OP EMETROP ATAU HIPERMETROP.

UNTUK MEMASTIKAN DIAGNOSA LAKUKAN PEMERIKSAAN DENGAN LENSA SFERIS NEGATIF 0,12D, BILA OP MENGATAKAN DGN LENSA TSB HURUF DI OPTOTIPE PADA BARIS 6/6 MENJADI LEBIH JELAS MAKA DIGNOSA OP : HIPERMETROP

SEBALIKNYA BILA HURUFNYA MENJADI LEBIH BURAM MAKA DIGNOSA MATA KANAN OP = EMETROP / NORMAL

2. BILA DIDAPAT HASIL PEMERIKSAAN VISUS MATA KANAN ADALAH = 6/9 (VOD=6/9) ,

KESIMPULAN : MATA KANAN OP MYOP

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KOREKSI KELAINAN VISUS

1. BILA DIAGNOSA KELAINAN REFRAKSI ADALAH MYOP MAKA DILAKUKAN KOREKSI DENGAN LENSA SFERIS NEGATIF.

PROSEDURE :

- GUNAKAN LENSA SFERIS NEGATIF DENGAN KEKUATAN

YANG TERKECIL DAHULU (-0,12 D) LALU TENTUKAN

BERAPA VISUSNYA

- TAMBAHKAN KEKUATAN LENSA NEGATIF SECARA

BERTAHAP –0,12, -0,25, -0,50, -0,75 DST SAMPAI OP DAPAT

MEMBACA HURUF-HURUF PADA BARIS KE 7 ATAU 6/6

- BESAR KEKUATAN DIOPTRI LENSA YANG DIPAKAI ADALAH :

LENSANEGATIF DENGAN KEKUATAN TERKECIL YANG

MASIH DAPAT MEMBERIKAN DAYA PENGLIHATAN TERJELAS

PADA OP.

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size of a 20/20 letter(=6/6)When an eye doctor sets up an examination room, care should be taken in calibrating the size of the letters on the visual acuity chart (which usually is projected onto a highly reflective screen).  The correct size of a 20/20 letter can be calculated using the diagram below, where

•the letter’s visual angle subtended at the eye is 5' of arc (one-half of which is 2.5' of arc), •d is the distance (or virtual distance, if using a mirror), along the line of sight, from the eye to the chart in feet, and •h is one-half the height of the 20/20 letter in millimeters.

As an example, let’s say that the viewing distance, d, is 20 feet.

Since a right angle is formed by the line of sight and the plane of the acuity chart, then simple trigonometry can be used:

1.2.5' of arc ÷ 60 = 0.04167° 2.tangent 0.04167° = h ÷ d = h ÷ 20 feet 3.0.0007272 = h ÷ 6,096 millimeters 4.h = 4.433 millimeters 5.2h = total height of a 20/20 letter at 20 feet = 8.866 millimeters

In general, the size of a 20/20 letter (in millimeters) is .4433 × d (where d is the viewing distance in feet).

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20/20 or 6/6 visual acuityThe reason that the number “20” is used in visual acuity measurements is because, in the United States, the standard length of an eye exam room (that is, the distance from the patient to the acuity chart) is about 20 feet.  (In Great Britain, where meters are used instead of feet, a typical eye exam room is about 6 meters long; 6 meters is 19.685 feet, which is close to 20 feet, since this is considered to be close enough to optical infinity.  Therefore, instead of using 20/20 for normal vision, they commonly use 6/6.)Someone with 20/20 or 6/6 vision (visual acuity) is just able to decipher a letter that subtends a visual angle of 5 minutes of arc (written 5') at the eye.  (5' of arc is 5/60 of a degree, because there are 60' of arc in 1 degree.)  What this means is that if you draw a line from the top of a 20/20 letter to the eye and another line from the bottom of the letter to the eye, the size of the angle at the intersection of these two lines at the eye is 5' of arc.  (Also, the individual parts of the letter subtend a visual angle of 1' of arc at the eye.)  It does not matter how far away something is from the eye; if it subtends an angle of 5' of arc at the eye, then a person with 20/20 visual acuity will just be able to determine what it is.A person with 20/20 vision could stand 30 feet away from a test chart and just decipher a 20/30 letter on the chart, since at that distance a 20/30 letter would subtend an angle of 5' of arc at the person’s eye.  That same person could stand 80 feet away from the chart and be able to decipher a 20/80 letter, or 200 feet away to be able to decipher a 20/200 letter.

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20/20 compared with other acuitiesNow, someone with 20/20 visual acuity does not have “perfect” vision, since it is quite possible to see better than 20/20.  The less the bottom number in the visual acuity ratio, the better the acuity; and the greater the bottom number, the worse the acuity.  Therefore, 20/15 acuity is better than 20/20 acuity, and 20/30 acuity is worse than 20/20 acuity.  Also, 20/15 acuity is equivalent to 6/4.5 acuity, while 20/30 acuity is the same as 6/9 acuity.As noted before, although 20/20 is "normal" visual acuity for most people, it is possible (and, in fact, very common) to be able to see better than that.  For instance, many people have 20/15 visual acuity.  A person with 20/15 acuity can stand 20 feet away from an object and see it as well as a person with 20/20 acuity moving up to 15 feet away from the object to view it.  If that is true, let’s take a person with 20/15 vision looking at an object from 100 feet away.  Where would a person with 20/20 vision need to stand to see the object just as well?  The answer is 75 feet away from the object.  (That is, 15/20 × 100 feet = 75 feet.)It is even possible, although not too common, for someone to have 20/10 visual acuity.  Let’s say a person with 20/20 vision can just barely detect a ship which is 25 miles away out on the ocean.  A person with 20/10 acuity could be 50 miles away from the ship and still be able to just detect it.  That is, if a person with 20/10 acuity can just tell what an object is, a person with 20/20 vision would need to stand half that distance away to be able to see what it is.You can use the same rationale when considering someone with less than 20/20 acuity.  Consider a person with 20/40 visual acuity (which is what someone needs in most states to get a driver’s license).  If a person with 20/20 acuity can just read a sign which is 60 feet down the road, the person with 20/40 acuity would have to be 30 feet away to read the same sign.  Also, a person with 20/15 acuity could be 80 feet away, and a person with 20/10 acuity 120 feet away, to read the same sign

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PERGERAKAN DAN PERSARAFAN BOLA MATA

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OTOT-OTOT EXTRAOCULER

GERAKAN OTOT : medial rectus (MR)—moves the eye toward the nose

•external rectus (ER)—moves the eye away from the nose •superior rectus (SR)—primarily moves the eye upward and secondarily rotates the top of the eye toward the nose •inferior rectus (IR)—primarily moves the eye downward and secondarily rotates the top of the eye away from the nose •superior oblique (SO)—primarily rotates the top of the eye toward the nose and secondarily moves the eye downward •inferior oblique (IO)—primarily rotates the top of the eye away from the nose and secondarily moves the eye upward

PERSARAFAN OTOT :Each extraocular muscle is innervated by a specific cranial nerve:

•medial rectus (MR)—cranial nerve III •external rectus (ER)—cranial nerve VI •superior rectus (SR)—cranial nerve III •inferior rectus (IR)—cranial nerve III •superior oblique (SO)—cranial nerve IV •inferior oblique (IO)—cranial nerve III

The following can be used to remember the cranial nerve innervations of the six extraocular muscles:

ER6(SO4)3.

Ada 6 otot extraoculer yang berperan untuk gerakan rotasi mata kearah : Vertikal ,Horizontal, dan anteroposterior. Otot tersebut adalah :

medial rectus (MR), the external rectus (ER), the superior rectus (SR), the inferior rectus (IR), the superior oblique (SO), and the inferior oblique (IO).

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cardinal positions of gazeThe “cardinal positions” are six positions of gaze which allow comparisons of the horizontal, vertical, and diagonal ocular movements produced by the six extraocular muscles.  These are the six cardinal positions:

•up/right •right •down/right •down/left •left •up/left

                                                                                              

                 MR = Medial Rectus     ER = Exteral RectusSR = Superior Rectus     IR = Inferior Rectus

SO = Superior Oblique     IO = Inferior Oblique

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STRABISMUS (HETEROTROPIA)The angle of deviation of the strabismus is measured in “prism diopters.”  If the angle of deviation remains the same in all cardinal positions of gaze (see the previous section), the strabismus is classified as “concomitant” (or “nonparalytic”).  If the angle of deviation is not the same in all cardinal positions of gaze, the strabismus is classified as “nonconcomitant” (or “paralytic”).Below, views of the two most common types of strabismus—esotropia and extropia—are displayed:

Esotropia Exotropia

                                                                                       

Esotropia can be congenital (a muscle imbalance present from birth), and usually the angle of deviation is large.  Management involves surgical correction (at age six months or earlier).  Some cases of low-angle esotropia respond successfully to visual therapy, especially in a child or an adult for which the esotropia is of recent onset and for which there is no macular damage (that is, the strabismic eye is capable of good visual acuity).

ASPEK KLINIS :

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LINTASAN PERSARAFAN PENGLIHATAN DAN

KELAINANNYA

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The Optic Nerve

visual pathwayAs the optic nerve leaves the back of the eye, it travels to the optic chiasm, located just below and in front of the pituitary gland (which is why a tumor on the pituitary gland, pressing on the optic chiasm, can cause vision problems).  In the optic chiasm, the optic nerve fibers emanating from the nasal half of each retina cross over to the other side; but the nerve fibers originating in the temporal retina do not cross over.From there, the nerve fibers become the optic tract, passing through the thalamus and turning into the optic radiation until they reach the visual cortex in the occipital lobe at the back of the brain.  This is where the visual center of the brain is located.  The visual cortex ultimately interprets the electrical signals produced by light stimulation of the retina, via the optic nerve, as visual images. 

     

The optic nerve (also known as cranial nerve II) is a continuation of the axons of the ganglion cells in the retina.  There are approximately 1.1 million nerve cells in each optic nerve.  The optic nerve, which acts like a cable connecting the eye with the brain, actually is more like brain tissue than it is nerve tissue

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NEURAL PATHWAYS

* AXON DARI SEL-SEL GANGLION NERVUS OPTICUS DAN TRACTUS OPTICUS, MENUJU KE GENICULATUM LATERALIS (DI TALAMUS)* SERABUT-SERABUT DARI MASING-MASING HEMIRETINA NASAL BERPOTONGAN DIDAERAH CHIASMA OPTICUM* DIDALAM GENICULATUM BODY , SERABUT-SERABUT YANG BERASAL DARI SETENGAH BAGIAN NASAL RETINA DAN SETENGAH BAGIAN TEMPORAL AKAN BERSINAPS PADA SATU SEL YANG AKSONNYA AKAN MEMBENTUK TRACT GENICULOCALCARINA, DAN TRACT INI AKAN MENUJU KE LOBUS OCCIPITAL CORTEX CEREBRI * AKSON AKSON SEL GANGLION DARI TRACT OPTICUS AKAN MENUJU KE REGIO PRETECTAL(MIDBRAIN) DAN SUPERIOR COLICULUS( MEMPERANTARAI- REFLEK PENGLIHATAN)* AKSON-AKSON LAIN DARI CHIASMA OPTICUM AKAN MENUJU KE NUKLEUS SUPRACHIASMATIC DI HIPOTALAMUS( MEMPERANTARAI HUBUNGAN ANTARA BERBAGAI MACAM HORMON DAN IRAMA SIRKADIAN DENGAN SIKLUS GELAP-TERANG

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NEURAL PATHWAY

* SERABUT-SERABUT YANG BERASAL DARI HEMIRETINA BAGIAN TEMPORAL SATU MATA DITERUSKAN SEJALAN DENGAN N OPTICUS YANG IPSILATERAL* SERABUT YANG BERASAL DARI HEMIRETINA BAG NASAL AKAN DITERUSKAN DAN BERJALAN BERSAMA N OPTICUS SISI YG KONTRALATERAL * N OPTICUS TRACT OPTICUS, BERHUBUNGAN DENGAN : NUKLEUS GENICULATUM LATERAL,COLICULUS SUPERIOR, NUKLEUS TRCT OPTICUS, NUKLEUS TRACT OPTICUS ACESSORIUS, PRETECTAL REGION DAN HIPOTALAMUS* PROYEKSI DARI RETINA BERHUBUNGAN DENGAN NUKLEUS GENICULATUM LATERAL, YG TDD : 6 LAP SEL YAITU : 2 LAP MAGNOSELULER & 4 LAP PARVOSELULER. AKSON DARI ½ HEMIRETINA TEMPORAL YG IPSILATERAL AKAN BERAKHIR PADA 3 LAPISAN INI DAN AKSON YG ½ HEMIRETINA KONTRALATERAL AKAN BERAKHIR DI 3 LAP LAINNYA

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NEURAL PATHWAY* AKSON-AKSON DARI NUKLEUS GENICULATUM MELALUI RADIATIO OPTICA AKAN BERHUB DGN SEL SYARAF DI CORTEX PENGLIHATAN PRIMER(AREA 17 CORTEX OCCIPITAL), AREA INI BERHUB DGN CORTEX PENGLIHATAN SECUNDER, CORTEX PENGLIHATAN TERTIER & DAERAH INTEGRASI PENGLIHATAN OCCIPITOPARIETAL / OCCIPITOTEMPORAL). PROYEKSI JALUR PENGLIHATAN DI NUK GEN LAT MELIPUTI PENGENALAN : WARNA, GERAKAN BENDA DAN KWALITAS PERSEPSI PENGLIHATAN STEREOSKOPIK* HUB ANTARA RETINA DAN HYPOTHALAMUS BERHUBUNGAN DENGAN: PERUBAHAN SIANG DAN MALAM DENGAN HORMONAL DIDALAM TUBUH MELALUI PENGATURAN IRAMA SIRKADIAN ATAU IRAMA BANGUN & TIDUR , OLEH KARENA ITU RETINA JUGA MEMPENGARUHI PIGMENTASI PADA KULIT( HORMON MSH)* HUB ANTARA RETINA & PRETECTAL REGIO : BERHUB DGN UKURAN / DIAMATER PUPIL (MYOSIS & MIDRIASIS)

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KELAINAN LINTASAN PERSARAFAN

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LAPANG PANDANG BINOKULER

PERIMETRI

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LAPANG PANDANG BINOKULER

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