Kelompok 7

Putri Ayu Helni

Regi
Abdul Wahyu Yudhistira
Rahmat Fajri
Vera Oktapiani
Ayu Fadhilah
Erinnah Yunvinnah Permatasari
Monick Mahndasari
Freshcillia Oktaviani
Tomi Edwardo
KM Azka
Vivi Kurnia

SKENARIO D
Mrs. Y, 30 years old, cone to your practice cause of ptosis. She has got trauma on palpebra
superior since one year ago. She could not do binocular vision.
From physical examination: M. Levator action (-) cause of N. III

I. KLARIFIKASI ISTILAH
1. Ptosis : prolapsnya organ atau bagian atau turunnya kelopak mata atas akibat kelumpuhan
2. Trauma on palpebra superior: luka atau cedera pada kelopak mata bagian atas
3. Binocular vision: Berhubungan dengan kedua mata
4. Musculus levator action: otot yang mengangkat organ
5. N. III: Nervus occulomotor yang mempersyarafi bagian wajah, leher

II. IDENTIFIKASI MASALAH

1. Mrs. Y, 30 tahun, menderita ptosis dan mendapat trauma di palpebra superior sejak 1 tahun
yang lalu
2. Dia tidak bisa melakukan binocular vision
3. Hasil pemeriksaan fisik: aksi musculus levator (-) karena N.III

III. ANALISIS MASALAH

1. Anatomi dan fisiologi regio orbitalis?
2. Bagaimana persyarafan di daerah tersebut?
3. Hub umur dan JK dengan ptosis?
Sex
No sexual predilection has been described.
Age
Acquired ptosis can occur at any age, but it is commonly seen in older adults. Congenital
ptosis occurs at birth.
4. Hub trauma 1 tahun lalu dengan ptosis?
5. Penyebab tidak bisa melihat secara binocular vision? Karena terjadi kelumpuhan nervus III
yang turut mempersyarafi otot2 ekstrinsik bola mata seperti : m. rectus medialis. Sehingga
terjadi ketidakseimbangan pada mata.
6. Apa hubungan tidak dapat melihat secara binocular dengan ptosis?
Nervus III selain mempersyarafi bagian palpebra, juga mempersyarafi bagian dari otot-otot
ekstrinsik pada bola mata. Hal ini yang diasumsikan berhubungan dengan binocular ny,
karena selain palpebra yang tidak bisa terangkat, bola mata juga tidak bisa memutar secara
normal.Kedudukan bola mata harus otroporia.
7. Interpretasi hasil pemeriksaan fisik? Kelumpuhan pada nervus III
8. DD?
9. Pem. Penunjang?
10. WD? Ptosis
11. Etiologi?
12. Epidemiologi?
13. Patogenesis?
14. Manifestasi klinis?
15. Tata laksana? Terapi, operasi 3. Severe: operasi segera (tetap di observasi selama 6 bulan).
Mild (2mm): takutnya pada akan menutup axis visual (amblioplia). Klo pada org dewasa
 tidak terlalu dikhawatirkan karena perkembangan fisus telah selesai. Pada Mild, axis visual
tidak tertutup, jadi dikasih obat-obat yang bisa memperkuat metabolism tonus otot.
Lensa kontak: kornea tertutup, sehingga kalo kesenggol tidak erosi. Tarsus dijahit,
digantung di musculus frontalis.
16. Prognosis?
Perbaikan congenital ptosis dengan operasi mengembalikan fungsi otot levator palpebra
yang baik dan juga dari segi kosmetik.Dengan observasi dan pengobatan yang benar,
amblyopia d apat diperbaiki dengan sukses.
17. Komplikasi?
18. KDU?
Tingkat Kemampuan 2
Mampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan
pemeriksaanpemeriksaan tambahan yang diminta oleh dokter (misalnya : pemeriksaan
laboratorium sederhana atau X-ray). Dokter mampu merujuk pasien secepatnya ke spesialis
yang relevandan mampu menindaklanjuti sesudahnya

Bleparospasme: Tonus muscular orbicularis yang kuat. Menutup tidak bisa buka
DD: chalazion, tumor palpebra  mekanik

IV. HIPOTESIS
Mrs Y, 30 tahun, menderita ptosis akibat parese dari occulomotoris

V. KERANGKA KONSEP

Mrs Y, 30

Trauma palpebra superior

Parese N.
III

M. levator Otot eks dan in

palpebra superior bola mata

Binocular vision
Ptosis
terganggu
081373727753
VI. LEARNING ISSUES
What I know What I don’t What I’ve to How I will learn
know prove
Anfis orbitalis Regi, Vivi
(anatomi),
Monick, Tomi
(Fisiologi)
Syaraf Eci, Vera, Azka
Ptosis Puey, yudis, erin,
ari, fadeg

VII. SINTESIS

ANATOMI DAN FISIOLOGI REGIO ORBITALIS

INERVASI REGIO ORBITALIS

N. Opticus (N. II) : Sensoris

- Berfungsi untuk penglihatan
- Keluar dari cranium melalui canalis opticus

N. Oculomotorius (N. III): Motoris

- Berfungsi untuk mengangkat palpebra superior, memutar bola mata ke atas dan ke bawah dan
medial, mengecilkan pupil dan akomodasi
- Tempat keluar dari cranium melalui Fissura orbitalis superior

N. Trochlearis (N. IV): Motoris

- Berfungsi membantu memutar bola mata ke bawah dan lateral
- Keluar dari cranium melalui Fissura orbitalis superior

N. trigeminus (N. V) divisi ophtalmicus: Sensoris

- Berfungsi pada cornea, kulit dahi, kulit kepala, palpebra dan hidung, juga membrana mucosa
sinus paranasalis dan cavum nasi
- Keluar dari cranium melalui Fissura orbitalis superior

N. abducens (N. VI) : motoris

- berfungsi pada M. Rectus lateralis, memutar bola mata ke lateral
- Keluar dari cranium melalui Fissura orbitalis superior

Pada kasus ini nervus yang terkena adalah N. III

Nervus oculomotorius
N. III adalah saraf motoris dan mempersarafi otot-otot ekstrinsik bola mata berikut ini yang
terdapat di dalam orbita: m.levator palpebrae superior, m. Rectus superioris, m. Rectus superior,
m. Rectus medius, m. Rectus inferior, dan m. Obliquus inferior. Saraf ini juga mempersyarafi m.
Sphincter pupillae dan m. Ciliaris bersama dengan serabut parasimpatis.
N. III keluar dari aspek anterior mesencephalon, medial terhadap pedunculus cerebri
 Gbr. 1. Pandangan lateral tengkorak, memperlihatkan falx cerebri, tentorium cerebelli, batang otak dan ganglio
trigeminus
Saraf ini berjalan dekat dan di antara A. Cerebri posterior dan A. Cerebelli superior
 Gbr. 2. Arteri dan saraf otak dilihat pada permukaan inferior otak.

Kemudian berjalan ke depan di dalam dinding lateral sinus cavernosus dan bercabang dua
menjadi ramus superior dan ramus inferior, yang akan menuju orbita melalui Fissura orbitalis
superior.
Ramus superior masuk ke orbita melalui bagian bawah fissura orbitalis superior di dalam
annulus tendineus.
 Gbr 3
Cabang ini mempersyarafi m. Rectus superior, kemudian menembus otot ini dan mempersyarafi
M. Levator palpebrae superioris yang ada di atasnya.
Ramus inferior masuk ke orbita dengan cara yang sama dan memberikan cabang-cabang ke m.
Rectus inferior, m. Rectus medialis, dan m. Obliquus inferior. Saraf ke m. Obliquus inferior
membrikan sebuah cabang yang berjalan ke gangglion ciliaris dan membawa serabut-serabut
parasimpatis ke m. Sphincter pupillae dan m. Ciliaris.

Otot-otot yang dipersyarafi oleh N. III

Otot-otot ekstrinsik bola mata (otot lurik)
M. Rectus superior
- Origo: Annulus tendineus communis pada dinding posterior orbita
- Insersio: Permukaan superior bola mata tepat posterior terhadap taut corneo-scleral
- Fungsi: Mengangkat cornea ke atas dan medial

M. Rectus inferior
- Origo: Annulus tendineus communis pada dinding posterior orbita
- Insersio: Permukaan inferior bola mata tepat posterior terhadap taut corneo-scleral
- Fungsi; Menurunkan cornea ke bawah dan medial

M. Rectus Medialis
- Origo: Annulus tendineus communis pada dinding posterior orbita
- Insersio: Permukaan medial bola mata tepat posterior terhadap taut corneo-scleral
- Fungsi: memutar bola mata sehingga cornea menghadap ke medial

M. obliquus inferior
- Origo: Dasar orbita
- Insersio: Permukaan lateral bola mata, profunda terhadap m. Rectus lateralis
- Fungsi: Memutar bola mata sehingga cornea menghadap ke atas dan lateral

Otot-otot Intrinsik Bola Mata (Otot Polos)

M. sphincter pupillae
- persyarafan: syaraf parasimpatis melalui n. Occulomotorius
- Fungsi: Konstriksi pupil
M. Ciliaris
- Persyarafan: syaraf parasimpatis melalui n. Occulomotorius
- Fungsi: Mengatur bentuk lensa, pada akomodasi membuat lensa lebih bulat

Otot-Otot Palpebra
- M. Levator palpebrae superioris
- Origo: Belakang orbita
- Insersio: Permukaan anterior dan pinggir atas tarsus superior
- Persyarafan: Otot lurik oleh n. III, dan otot polos (otot-otot Muller) oleh syaraf simpatis
- Fungsi: Mengangkat palpebra superior

Ramus superior yang kena

BINOCULAR VISION
The way humans see is influenced by the fact that we have binocular vision.
Most people find this concept confusing. The word binocular conjures up an image of the hand-
held, dual-eyepiece telescope that is used for birdwatching and at sports competitions to see the
action up close.
Binocular vision, however, refers to a particular perspective or way of seeing the world.
In binocular vision, the eyes are used together to produce a view that is stereoscopic or three
dimensional (3-D). This means that we can see things in terms of their length, width, and depth.
We share this feature with other animals, such as monkeys, hawks, cats and dogs.
Our eyes are located forward in the head and some distance apart,
with the nose serving as a divider in between. This attribute
enables us to obtain two distinct views of the same object, each
seen from a slightly different angle or parallax. Our brain
combines these images to create a stereoscopic, three-dimensional
reference in our visual field.
The figure shows the area of visual overlap defined by fuchsia-
colored lines. Within this region of overlap, three-dimensional
vision (stereopisis) is possible. Outside of the region of overlap, it is not. The figure also shows
the line of sight out to the focal point, defined by red lines.
In technical terms, we call this fused (our brain combines both images into one), simultaneous
(separate views of the same image are obtained simultaneously) binocular vision (both eyes are
used).
Binocular vision has three primary advantages over monocular vision, or vision in which only
one eye is used.
• A wider horizontal visual field (one eye = 150°; two eyes = 180°+)
• It gives binocular summation or an enhanced ability to detect faint images
• It gives stereopsis or precise depth perception.
The eyes must be pointed correctly and move in a coordinated manner in order to maintain
stereopsis and singleness of vision. To achieve this, the position of each eye in its
socket is controlled by six muscles called extraocular muscles.
Small differences in the length of the extraocular muscles in the two eyes, their strength, or their
points of connection can cause one eye to move to a different position in its socket relative to the
other. This is known as phoria.
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dependable resource for books and products. You can find these materials at the Eye-Care Store.

PTOSIS
Definisi
Ptosis adalah kondisi kelopak mata yang tidak dapat membuka dengan optimal seperti mata
normal ketika memandang lurus ke depan (Drooping eye lid). Secara fisik, ukuran bukaan
kelopak mata pada ptosis lebih kecil dibanding mata normal. Normalnya kelopak mata terbuka
adalah = 10 mm. Ptosis biasanya mengindikasikan lemahnya fungsi dari otot levator palpebra
superior ( otot kelopak mata atas ). Rata – rata lebar fisura palpebra / celah kelopak mata pada
posisi tengah adalah berkisar 11 mm, panjang fisura palpebra berkisar 28 mm. Rata – rata
diameter kornea secara horizontal adalah 12 mm, tetapi vertikal adalah = 11 mm. Bila tidak ada
deviasi vertikal maka refleks cahaya pada kornea berada 5,5 mm dari batas limbus atas dan
bawah. Batas kelopak mata atas biasanya menutupi 1.5 mm kornea bagian atas, sehingga batas
kelopak mata atas di posisi tengah seharusnya 4 mm diatas reflek cahaya pada kornea. Jika batas
kelopak mata atas menutupi kornea 1 atau 2 mm kebawah masih dapat dikatakan normal,
termasuk ptosis ringan, jika menutupi kornea 3 mm termasuk ptosis sedang, dan jika menutupi
kornea 4 mm termasuk ptosis berat.

Jenis / tipe ptosis

Ptosis secara garis besar dibagi menjadi 2 type:
1. Congenital Ptosis (dibawa sejak lahir).
2. Acquired Ptosis (didapat).

Ptosis kongenital ada sejak lahir dan biasanya mengenai satu mata dan hanya 25%
mengenai ke 2 mata. Ptosis terjadi karena kesalahan pembentukan (maldevelopment) otot
kelopak mata atas dan tidak adanya lipatan kelopak mata, tetapi kerusakan mendasarnya
kemungkinan timbul pada persarafan dibandingkan otot itu sendiri, karena sering ditemukan
lemahnya otot rektus superior yang dipersarafi oleh Saraf / Nervus III. . Ptosis yang terjadi pada
masa perkembangan bayi dapat menyebabkan amblyopia, yang terjadi pada satu atau kedua mata
dimana kelopak mata menutupi visual axis, terutama jika berhubungan dengan ptosis kongenital
(ptosis yang didapat dari lahir). Amblyopia dari ptosis berhubungan dengan astigmatisme tinggi.
Ptosis menimbulkan tekanan pada kelopak mata dan dengan waktu dapat merubah bentuk kornea
yang menimbulkan cylinder tinggi. Anak – anak dengan congenital ptosis dan amblyopia harus
dipertimbangkan untuk melakukan operasi ptosis, dan kelainan refraksi yang mereka miliki harus
diterapi dengan kontak lens, dan untuk amblyopianya harus dilakukan terapi oklusi (tutup mata).
Acquired ptosis sering terlihat pada pasien berusia lanjut. Umumnya disebabkan
bertambah panjangnya (stretching) otot levator palpebra (otot yang berfungsi mengangkat
kelopak mata), trauma/pasca kecelakaan, pertambahan usia, pengguna contak lens dan luka
karena penyakit tertentu seperti stroke, diabetes, tomor otak, kanker yang mempengaruhi saraf
atau respon otot, horner sindrom dan myasthenia gravis.
Etiologi
Ptosis can be caused by problems with the elevator muscles of the eyelid, the aponeurosis
of the levator, nerve abnormalities either central or peripheral, trauma, inflammation, or lesions
of the lid or orbit.
Aponeurotic ptosis is the most common cause of acquired ptosis. Senescence, involutional
changes, dehiscence, or disinsertion of the levator aponeurosis are common. Chronic
inflammation or intraocular surgery (eg, cataract surgery) can incite stretching of the levator
aponeurosis and dehiscence from the anterior surface of the tarsal plate. Long-term use of
contact lenses has also been implicated. Patients maintain normal or near-normal levator
function, with a high upper eyelid crease. The attachments from the levator to the skin remain
intact, and this forms the crease.
Neurogenic blepharoptosis may be congenital or acquired in origin. Congenital neurogenic
ptosis is usually due to Horner syndrome or a third nerve palsy. Acquired neurogenic ptosis
causes include Horner syndrome, third nerve palsy, or myasthenia gravis.
Congenital Horner syndrome can result in mild ptosis associated with ipsilateral miosis,
iris and areola hypopigmentation, and anhidrosis. The cause is paresis of the Mueller muscle,
secondary to an embryologic lesion of the sympathetic pathway.
Congenital third nerve palsy has a variety of causes. Patients can present with aberrant
regeneration and a small pupil. Often, parents believe that this is secondary to birth trauma.
Acquired Horner syndrome can be secondary to trauma, neoplastic insult, or vascular
disease of the sympathetic pathway. All stigmata of congenital Horner syndrome, excluding iris
and areola hypopigmentation, are present. Raeder paratrigeminal syndrome occurs in middle-
aged men with daily ipsilateral headaches and the stigmata of acquired Horner syndrome.
Dysfunction of the third cranial nerve can result from a myriad of acquired insults.
Trauma, multiple sclerosis, vasculopathy, and infection are all potential etiologies. Extraocular
muscle dysfunction, pupillary abnormalities, and the presence of aberrant regeneration may aid
in establishing the correct diagnosis.
Synkinetic neurogenic ptosis is the product of innervational anomalies. Marcus-Gunn jaw
winking and posttraumatic ptosis are 2 examples of this interesting etiology. Microvascular
diabetic neuropathies never result in synkinetic neurogenic ptosis.
 Myogenic blepharoptosis usually is congenital, but it can be associated with acquired
disease processes.
Congenital myogenic ptosis is secondary to levator dysgenesis.
Acquired myogenic ptosis can be found in myasthenia gravis, chronic progressive external
ophthalmoplegia, oculopharyngeal dystrophy, and myotonic dystrophy.
Traumatic blepharoptosis can ensue after an eyelid laceration with transection of the upper
eyelid elevators or disruption of the neural input.
Mechanical ptosis can stem from the presence of eyelid neoplasms, for example,
neurofibromas or hemangiomas or cicatrization secondary to inflammation or surgery

Epidemiologi

Patofisiologi
Blepharoptosis, which is a droopy upper eyelid, is the result of dysfunctioning of one or
both upper eyelid elevator muscles. These elevator muscles are the levator palpebrae superioris
and its aponeurosis and the Mueller muscle. The levator palpebrae superioris is a striated muscle
that is innervated by the superior division of the oculomotor nerve (cranial nerve III). This
muscle is about 40 mm long and originates from the lesser wing of the sphenoid. It continues
anteriorly, and at the Whitnall ligament, it travels inferiorly as an aponeurosis. This aponeurosis
is 14-20 mm long and inserts into the anterior aspect of the tarsal plate. It also sends attachments
to the skin, forming the upper eyelid crease. The levator muscle and aponeurosis is the major
elevator of the upper eyelid.
The Mueller muscle, a sympathetically innervated smooth muscle, has its origins from the
undersurface of the levator superioris. Approximately 12 mm long, it inserts superiorly on the
tarsal border and elevates the upper eyelid by approximately 2 mm.

Manifestasi Klinis

Diagnosis
Diagnosis Banding
Anophthalmos Hemangioma, Capillary
Apraxia of Lid Opening Horner Syndrome
Bell Palsy Laceration, Eyelid
Blepharospasm, Benign Essential Lyme Disease
Cellulitis, Orbital Marcus Gunn Jaw-winking Syndrome
Cellulitis, Preseptal Multiple Sclerosis
Chalazion Myasthenia Gravis
Chronic Progressive External Ophthalmoplegia Neuro-ophthalmic History
Conjunctivitis, Giant Papillary Neurofibromatosis-1
Corneal Abrasion Oculomotor Nerve Palsy
Corneal Foreign Body Orbital Fracture, Apex
Dermatitis, Atopic Orbital Fracture, Floor
Duane Syndrome Ptosis, Congenital
Exophthalmos Thyroid Ophthalmopathy

Tata Laksana
Untuk kasus adalah dengan terapi dilihat 6 bulan, setelah itu lalu dilakukan operasi.

Prognosis
• Perbaikan congenital ptosis dengan operasi mengembalikan fungsi otot levator palpebra yang
baik dan juga dari segi kosmetik.Dengan observasi dan pengobatan yang benar, amblyopia
dapat diperbaiki dengan sukses.

Complications
• Uncorrected congenital ptosis can result in amblyopia secondary to deprivation or
uncorrected astigmatism.
1. An abnormal eyelid position can have negative psychosocial effects, especially in young
children and teenagers.
2. Ostracism can lead to poor academic performance, loss of self-esteem, and alienation.
• In some cases, uncorrected acquired blepharoptosis results in decreased field of vision and
frontal headaches.
1. The decreased visual field can affect one's ability to perform activities of daily life.
2. Driving, reading, and navigating a flight of steps can be particularly difficult.
• If correction of blepharoptosis is undertaken, complications related to the surgery can ensue.
1. Because most ptosis surgery is performed with the patient under local anesthesia and with
monitored anesthesia care, reactions to anesthetic agents are possible complications.
2. Bleeding and poor response to anesthetic agents are potential intraoperative
complications.
3. Bleeding and infection can be devastating complications in the early postoperative
period. Prolonged bruising, edema, undercorrection or overcorrection of the ptosis, eyelid
asymmetry, and corneal foreign body sensation can be later complications

KDU
Tingkat Kemampuan 2
Mampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaanpemeriksaan
tambahan yang diminta oleh dokter (misalnya : pemeriksaan laboratorium
sederhana atau X-ray). Dokter mampu merujuk pasien secepatnya ke spesialis yang relevan
dan mampu menindaklanjuti sesudahnya

SEKEDAR BACAAN..... 
(1) The combination of exotropia, hypotropia, limitation of adduction, elevation, and depression
in association with ptosis is diagnostic for a third nerve paralysis. Abduction and incycloduction
are the only remaining oculomotor functions. Depending on the degree of ptosis, the patient may
or may not see double.
(2) Congenital paralysis may be unilateral or bilateral. The unilateral form is the more common
one.
(3) Lid elevation on attempted adduction and depression with or without constriction of the pupil
are signs of aberrant regeneration of the third nerve. Aberrant regeneration is seen in about two
thirds of congenital third nerve paralyses. It is a common finding in third nerve paralysis
acquired early in life.
(4) The pupil reaction may be normal or the pupil is fixed and dilated. In congenital third nerve
palsy, the pupil may be constricted.
(5) Occasionally, patients with a congenital third nerve paralysis fixate with the paralyzed eye.
This causes a large combined exodeviation and hyperdeivation of the normal eye, which may
become deeply amblyopic.
(6) Associated ocular or systemic abnormalities may be associated with congenital third nerve
paralysis and should be searched for, including neuroimaging.
(7) A leading cause of nontraumatic third nerve paralysis is diabetes. The pupil is spared and no
aberrant regeneration occurs. The condition is usually self-limiting and associated with diplopia
unless ptosis is complete.
(8) Third nerve paralysis can occur from extrinsic fascicular defects, caused by pressure,
vascular lesions, or nerve interruptions. This may be related to systemic disease or trauma.
Aberrant regeneration is common and occurs in two thirds of patients.
(9) Traumatic third nerve paralysis is usually associated with a fixed and dilated pupil. Aberrant
regeneration may occur and diplopia is frequent unless visual acuity is decreased by associated
ocular injuries or ptosis.
(10) The surgical treatment of third nerve paralysis presents a formidable challenge to the
ophthalmic surgeon. A complete third nerve paralysis with complete ptosis is best left
untreated. When the paralysis is partial, especially when some adduction is preserved, the
patient may benefit from maximal recession of the lateral and resection of the medial rectus
muscles. This may be combined with upward transposition of the muscle insertions to
counteract the hypotropia. Transfer of the superior oblique muscle to the insertion of the medial
rectus muscles with or without fracture of the trochlea has also been recommended.24, p.300 Ptosis
surgery is postponed until alignment of the eyes has been achieved by surgery. Caution with
regard to ptosis surgery is advised if elevation is impaired because of exposure problems.
NEURO VISION REHABILITATION INSTITUTE

Definition of Neuro-Optometric Rehabilitation

Neuro-Optometric Rehabilitation is an individualized treatment regimen for patients with visual
deficits as a direct result of physical disabilities, traumatic and / or acquired brain injuries.
Neuro-Optometric Therapy is a process for the rehabilitation of visual / perceptual / motor
disorders. It includes, but is not limited to, acquired strabismus, diplopia, binocular dysfunction,
convergence, and / or accommodation, paresis / paralysis, oculomotor dysfunction, visual spatial
dysfunction, visual perceptual and cognitive deficits, and traumatic visual acuity loss.

Patients of all ages who experienced neurological insults require Neuro-Optometric

Rehabilitation. Visual problems caused by Traumatic Brain Injury, Cerebrovascular Accidents,
Cerebral Palsy, Multiple Sclerosis, etc. may interfere with performance causing the person to be
identified as Learning Disabled or as having Attention Deficits Disorder. These visual
dysfunctions can manifest themselves as psychological sequela such as anxiety and panic
disorders as well as spatial dysfunctions affecting balance and posture.

A Neuro-Optometric Rehabilitation treatment plan improves specific acquired vision dysfunction

determined by standardized diagnostic criteria. Treatment regimens encompass medically
necessary noncompensatory lenses and prisms with and without occlusion and other appropriate
medical rehabilitation strategies.

VISION IS OUR DOMINANT SENSE

More than just sight is measured in terms of visual acuity; vision is the process of deriving
meaning from what is seen. It is a complex, learned and developed set of functions that involve a
multitude of skills. Research estimates that eighty to eighty five percent of our perception,
learning, cognition and activities are mediated through vision.
The ultimate purpose of the visual process is to arrive at an appropriate motor, and/or cognitive
response.

There is an extremely high incidence (greater than 50%) of visual and visual-cognitive disorders
in neurologically impaired patients (traumatic brain injury, cerebral vascular accidents, multiple
sclerosis etc.) Rosalind Gianutsos, Ph.D.

"Visual-perceptual dysfunction is one of the most common devastating residual impairments of

head injury". Barbara Zoltan, M.A., O.T.R.
"The majority of individuals that recover from a traumatic brain injury will have binocular
function difficulties in the form of strabismus, phoria, oculomotor dysfunction, convergence and
accommodative abnormalities". William Padula, O.D.

The process of vision can be broken down into three general categories; 1) visual acuity and
visual field, 2) visual motor abilities and 3) visual perception.

1) VISUAL ACUITY and VISUAL FIELD

Visual Acuity - This refers to clarity of sight. It is commonly measured using the Snellen chart
and noted, for example, as 20/20, 20/50, 20/200 etc. Visual acuity becomes blurred in various
refractive conditions, for example, myopia (nearsighted), hyperopia (far-sighted), astigmatism
(mixed), and presbyopia (age related loss of focusing).

Visual Field - This is the complete central and peripheral range, or panorama of vision. Various
neurological conditions, such as stroke, cause characteristic losses of the visual field, for
example hemianopsia. The person may, or may not, concurrently demonstrate a visual neglect
which is a perceptual loss of vision and visual motor integration to the side of the visual field
loss.

2) VISUAL MOTOR ABILITIES

Alignment - This refers to eye posture. If the eyes are straight and aligned the eye posture is
termed phoric. If an eye turns in, out, up or down compared to the other eye then the eyes are not
straight or aligned and the condition is termed strabismus. Exotropia is a form of strabismus
where an eye turns out, esotropia is where an eye turns in, hypertropia is where an eye turns up,
and hypotropia is where an eye turns down. These can also occur in combination, such as hyper-
exotropia, or hyper-esotropia.
• Fixation - The ability to steadily and accurately gaze at an object of regard. This is most
dysfunctional in nystagmus which is an uncontrollable shaking of the eyes.
• Pursuits - The ability to smoothly and accurately track, or follow, a moving object
• Saccades - The ability to quickly and accurately look, or scan, from one object to another
• Accommodation - The ability to accurately focus on an object of regard, sustain that
focusing of the eyes, and to change focusing when looking at different distances
• Convergence - The ability to accurately aim the eyes at an object of regard and to track
an object as it moves towards and away from the person
• Binocularity - The integration of accommodation and convergence
• Stereopsis - Depth perception

3) VISUAL PERCEPTION
Visual-Motor Integration - Eye-hand, eye-foot, and eye-body coordination
• Visual-Auditory Integration - The ability to relate and associate what is seen and heard
• Visual Memory - The ability to remember and recall information that is seen
• Visual Closure - The ability "to fill in the gaps", or complete a visual picture based on
seeing only some of the parts
• Spatial Relationships - The ability to know "where I am" in relation to objects and space
around me and to know where objects are in relation to one another
• Figure-Ground Discrimination - The ability to discern form and object from background
•

THE THREE MOST DEVASTATING AND INTOLERABLE VISUAL PROBLEMS

RESULTING FROM BRAIN INJURY AND STROKE
Although there are many visual problems that arise from brain injury and stroke, three are more
devastating and impairing than the rest. These are visual field loss, intractable double vision, and
visual / balance disorders.
Visual Field Loss
With a visual field loss the patient is literally blind to half of their field of vision. This places the
person at increased risk of further injury and harm from bumping into objects, being struck by
approaching objects, and falls.

A two fold approach is used to treat visual field loss. Visual rehabilitation activities are
prescribed by the doctor and administered by the therapist to teach scanning of the hemianopic
field loss. This is a difficult task. It is the act of seeing something that brings our visual attention
and scanning to bear. However, these patients do not see to the field they are being trained to
scan and attend. Therapy is aimed at teaching that and several approaches have been developed
to assist in this, but remediation still requires a lot of effort and patience.

Special visual field awareness prism lenses are used in treating visual field loss. As the patient
scans into the prism the optics are shifted so as to perceptually gain about 15 to 20 degrees of
visual field recognition. Since diplopia is perceived when scanning into the prism, fixation in the
prism must be brief. These are used as spotting devices only to determine if there is an object in
the periphery that deserves further visual attention. When such an object is spotted, the patient
turns their head to view it in detail with their intact central vision.

Double Vision (Diplopia)

Double vision (diplopia) is a serious and intolerable condition that can be caused by strabismus,
ophthalmoplegia, gaze palsy, and decompensated binocular skills in patients with brain injury,
stroke and other neurologically compromising conditions. Prisms, lenses and / or vision therapy
can oftentimes help the patient achieve fusion (alignment of the eyes) and alleviate the diplopia.
If and when these means are not employed, the patient may adapt by suppressing the vision of
one eye to eliminate the diplopia. If lenses, prisms, and / or therapy are not successful and the
patient does not suppress, intractable diplopia ensues.

In this population of patients, patching has frequently been used to eliminate the diplopia.
Although patching is effective in eliminating diplopia it causes the patient to become monocular.
Monocular as opposed to binocular vision will affect the individual primarily in two ways;
absence of stereopsis and reduction of the peripheral field of vision. These limitations will
directly cause problems in eye hand coordination, depth judgments, orientation, balance,
mobility, and activities of daily living such as playing sports, driving, climbing stairs, crossing
the street, threading a needle etc.

A new method of treating diplopia that does not have these limitations has been successfully
evaluated. It is called the "spot patch" (invented and named by this author) and is a method to
eliminate intractable diplopia without compromising peripheral vision. It is a small, usually
round or oval, patch made of dermacil tape, 3-M blurring film (or another such translucent tape).
It is placed on the inside of the lenses of glasses and directly in the line of sight contributing to
the diplopia. The diameter is generally about one centimeter, but will vary on the individual
angular subtense required for the particular strabismus, or gaze palsy.

Visual Balance Disorders

Visual balance disorders can be caused by a Visual Midline Shift Syndrome (VMSS), oculo-
motor dysfunction in fixations, nystagmus, and disruptions of central and peripheral visual
processing. A full description of these disorders is beyond the scope of this paper. The treatment
will depend on the visual diagnosis and etiology. Lenses, prisms and visual rehabilitation
activities are used in the remediation of these disorders.
OVERVIEW OF THE PATHOPHYSIOLOGY OF VISION PROBLEMS FOLLOWING
BRAIN INJURY OR STROKE

Traumatic Brain Injury can have devastating effects on the visual system. Vision is frequently
disrupted following head injury, stroke and other neurologically compromising conditions (e.g.
multiple sclerosis, cerebral vasculitis, aneurysm, hypoxia etc). The anatomy and physiology of
the visual system, the vascular network of the brain, and the dynamics of head trauma all
contribute to the incidence of ocular trauma and visual dysfunction.

Injury to the visual system can be diffuse and / or focal and can localize to any, or a combination
of the ocular structures, cortical areas, mid brain, or nerve nuclei. Brain injuries affecting vision
typically occur via axonal shearing, hemorrhage, infarct, inflammation, and / or compression.

The third cranial nerve and third nerve nuclei seem to be particularly vulnerable to injury
following trauma and stroke. These innervate eight of the twelve extra-ocular muscles (the
medial, inferior and superior recti, and inferior oblique muscles), the ciliary (focusing) muscle
inside of the eye, the levator (eyelid) muscle, and the pupillary sphincter muscle. Consequently,
injury to this area causes some classic signs and symptoms that will manifest as:
• Exotropia
• Exophoria
• Convergence Insufficiency
• Convergence Infacility
 • Accommodative Insufficiency
• Accommodative Infacility
• Ptosis
• Fixed and Dilated Pupil

Limited Motility (Abduction, Sursumduction, Infraduction) of the affected eye

The sixth cranial nerve and nuclei are also prone to injury in TBI and stroke. These control two
of the twelve extra-ocular muscles (the lateral recti muscles) which are responsible for abduction
of the eye. Injury to the communication pathways between sixth nerve nuclei and their paired
third nerve nuclei can also occur. This is termed an internuclear ophthalmoplegia (INO). Sixth
nerve problems will manifest as:
• Esotropia
• Esophoria
• Divergence Insufficiency
• Divergence Infacility
• Limited Abduction of the Affected Eye
•

Internuclear Ophthalmoplegia will manifest as:

• Exotropia
• Limited Adduction of the Affected Eye
• Paralysis of Gaze to the Affected Side

The fourth cranial nerve is less frequently injured in TBI and stroke. It is more frequently injured
by direct trauma. The fourth nerve and nucleus control two of the twelve extra-ocular muscles,
the superior obliques. These muscles are responsible for inferior gaze of the eye when it is
adducted. Damage to this area will manifest as:
• Hypertropia
• Limited Down Gaze of the Affected Eye when Adducted

The optic nerve (second cranial nerve) and its radiations and pathway back to the occipital and
associated corticies can be injured in TBI and stroke. The location of the injury will determine
the nature of the deficit. Visual field loss is the manifestation of these injuries.

If the optic nerve is damaged between the eye itself and the optic chiasm, there will be a
monocular loss of sight and a pupillary defect. This is seen in direct trauma and multiple
sclerosis.

When the damage is at the chiasm there will be a classic bi-temporal visual field loss. This is
found frequently in pituitary disorders.

If the injury occurs in the optic radiations coursing back from the chiasm to the lateral geniculate
nucleus (LGN), there will be an incongruous (unequal) bilateral visual field loss. Although this
can be a hemianopsia (half visual field loss) or quadrantanopsia (quarter field loss), it will more
frequently show as a quadrantanopsia.

When the injury is posterior to the LGN and ranging back to the occipital cortex there will be a
homonymous bilateral visual field loss. The visual field loss will show more frequently as a
hemianopsia, but can also be a quadrantanopsia.

Visual fibers feed forward to other areas of the brain. One in particular is the parietal cortex
which is frequently referred to as the association cortex. It is called this because it integrates
information from the various senses in an attempt to derive meaning from the "whole picture".
When there is damage to this area, one will frequently find a visual neglect.

Visual neglect is a perceptual loss of vision. The person is unaware of their sight, or lack of sight
to the affected side. If the nerve pathways and occipital cortex are spared and only the parietal
cortex is affected there will a sparing of vision (to a good degree), but the person will "ignore"
and not attend to vision on the affected side. If the pathways and / or occipital cortex are injured
as well as the parietal cortex, then there will be an actual visual field loss in addition to the
person having a neglect, and / or denial of loss of vision.

Injury to the frontal cortex can affect vision. The frontal eye fields are in the frontal cortex and
so eye movement disorders can occur from injury here. This can also cause a perceptual deficit
in visual memory.

Parietal and occipital-parietal injuries can cause visual perceptual deficits. These include visual-
motor integration, figure-ground discrimination, spatial relations, topographic orientation and
form perception and constancy.

Vision integrates with and affects balance. Approximately twenty percent of the visual fibers are
involved in this process. Following brain injury and stroke problems with nystagmus, ocular
motor control and strabismus will disrupt balance and can cause dizziness and vertigo.

Visual Midline Shift Syndrome {(VMSS) Padula}, is a condition that affects balance, posture,
orientation and mobility can occur following TBI and stroke In VMSS the persons' visual
perception of the world will appear compressed in one portion and expanded in another. Their
perception of the world will therefore appear slanted, or tipped, and walls may appear bowed and
distorted. Balance is disrupted when attempts are made to orient to that perception of the visual
world. For example, imagine a patient who has suffered a left cerebral vascular accident (CVA)
with right hemiparesis and right hemianopsia. This patient will be observed to weight bear left. A
shift of the visual perception of their midline to the non-affected side will often be found. A
mismatch results between the visual perception of self, spatial relations and the physical and
kinesthetic feedback received. Since vision is the dominant sense attempts are to orient to the
visual perception. As a result, VMSS will cause, and / or, exacerbate problems with balance,
orientation and mobility. VMSS can also be found in patients showing extensor and flexor
postures. In these cases the VMSS will be shifted either up, or down.
PTOSIS
(Kelopak Mata Yang Menggantung)
Definisi

Symptoms / Gejala
- Jatuhnya / menutupnya kelopak mata atas yang tidak normal.
- Kesulitan membuka mata secara normal.
- Peningkatan produksi air mata.
- Adanya gangguan penglihatan.
- Iritasi pada mata karena kornea
terus tertekan kelopak mata.
- Pada anak akan terlihat guliran
kepala ke arah belakang untuk
mengangkat kelopak mata agar
dapat melihat jelas.

Pemeriksaan
Ketika melakukan pemeriksaan, yang pertama kali diperhatikan adalah penyebab dari
ptosis itu sendiri. Dibawa sejak lahir atau disebabkan oleh penyakit tertentu atau disebabkan oleh
trauma. Kemudian dokter akan melakukan pemeriksaan:
- Tes tajam penglihatan, tes kelainan refraksi, hasil refraksi dengan sikloplegic juga harus
dicatat.
- Kelainan strabismus / mata juling.
- Produksi air mata (Schirmer test).
- Diameter pupil dan perbedaan warna iris pada kedua mata harus diperiksa pada kasus
Horner Syndrome.
- Tinggi kelopak mata atau fissure palpebra diobservasi dan diukur. Pengukuran dilakukan
dalam millimeter (mm), di ukur berapa besar mata terbuka pada saat melihat lurus / kedepan,
melihat ke atas dan kebawah.
- Foto lama dari wajah dan mata pasien dapat dijadikan dokumentasi untuk melihat perubahan
pada mata.

Treatment / pengobatan
Observasi hanya dibutuhkan pada kasus congenital ptosis sedang (mild congenital
ptosis), jika tidak terdapat tanda amblyopia, strabismus dan jika terdapat ketidaknormalan posisi
kepala.
• Pasien harus dievaluasi setiap 3 atau 4 bulan untuk menangani amblyopia pada congenital
katarak. Foto luar mata dapat membantu memonitor pasien.
• Guliran kepala harus diperhatikan , jika pasien sering mengangkat dagunya (chin up posture),
menandakan bertambah buruknya ptosis, disarankan untuk melakukan operasi.
• Pasien harus diperiksa akan adanya astigmatisme disebabkan tekanan dari kelopak mata.

Operasi ptosis/ surgical care

Ptosis biasanya tidak terperbaiki dengan waktu, dan membutuhkan operasi sebagai
penyembuhan, khususnya operasi plastic dan reconstructive. Operasi ini ditujukan untuk
memperkuat otot levator palpebra.
Koreksi ptosis dengan operasi pada kasus congenital ptosis dapat dilakukan pada
berbagai usia, tergantung dari keparahan penyakitnya. Intervensi awal dibutuhkan jika terdapat
tanda – tanda amblyopia dan ocular torticollis. Beberapa kasus ocular torticollis menghambat
pergerakan (mobility) pada bayi dan anak – anak disebabkan masalah keseimbangan pada
posture kepala dan dagu yang terangkat. Jika tidak terlalu mendesak /urgent, operasi dapat
ditunda hingga usia 3 atau 4 tahun.

Prognosis/ masa depan

• Perbaikan congenital ptosis dengan operasi mengembalikan fungsi otot levator palpebra yang
baik dan juga dari segi kosmetik.Dengan observasi dan pengobatan yang benar, amblyopia
dapat diperbaiki dengan sukses.

*************** Mahendra Indonesia ***************

Ptosis
.a Defenisi :
Posisi satu atau kedua palpebra superior yang terlalu rendah .
Posisi normal palpebra superio adalah ditengah – tengah antara limbus superior dan
tepian atas pupil atau pada saat mata berada dalam posisi memandang primer (sewaktu
 kepala dan mata terletak sejajar dengan benda yang dlihat ) maka palpebra superior
menutupi bagian atas cornea sejauh lebih kurang 2 mm.

Secara fisik, ukuran bukaan kelopak mata pada ptosis lebih kecil dibanding mata normal.
Normalnya kelopak mata terbuka adalah = 10 mm. Ptosis biasanya mengindikasikan
lemahnya fungsi dari otot levator palpebra superior ( otot kelopak mata atas ). Rata – rata
lebar fisura palpebra / celah kelopak mata pada posisi tengah adalah berkisar 11 mm,
panjang fisura palpebra berkisar 28 mm. Rata – rata diameter kornea secara horizontal
adalah 12 mm, tetapi vertikal adalah = 11 mm. Bila tidak ada deviasi vertikal maka
refleks cahaya pada kornea berada 5,5 mm dari batas limbus atas dan bawah. Batas
kelopak mata atas biasanya menutupi 1.5 mm kornea bagian atas, sehingga batas kelopak
mata atas di posisi tengah seharusnya 4 mm diatas reflek cahaya pada kornea. Jika batas
kelopak mata atas menutupi kornea 1 atau 2 mm kebawah masih dapat dikatakan normal,
termasuk ptosis ringan, jika menutupi kornea 3 mm termasuk ptosis sedang, dan jika
menutupi kornea 4 mm termasuk ptosis berat.

klasifikasi
berdasarkan onset dibagi menjadi :
Konginental ( paling sering disebabkan kelainan myogenik )
Ptosis kongenital ada sejak lahir dan biasanya mengenai satu mata dan hanya 25%
mengenai ke 2 mata. Ptosis terjadi karena kesalahan pembentukan
(maldevelopment) otot kelopak mata atas dan tidak adanya lipatan kelopak mata,
 tetapi kerusakan mendasarnya kemungkinan timbul pada persarafan dibandingkan
otot itu sendiri, karena sering ditemukan lemahnya otot rektus superior yang
dipersarafi oleh Saraf / Nervus III. . Ptosis yang terjadi pada masa perkembangan
bayi dapat menyebabkan amblyopia, yang terjadi pada satu atau kedua mata
dimana kelopak mata menutupi visual axis, terutama jika berhubungan dengan
ptosis kongenital (ptosis yang didapat dari lahir). Amblyopia dari ptosis
berhubungan dengan astigmatisme tinggi. Ptosis menimbulkan tekanan pada
kelopak mata dan dengan waktu dapat merubah bentuk kornea yang menimbulkan
cylinder tinggi. Anak – anak dengan congenital ptosis dan amblyopia harus
dipertimbangkan untuk melakukan operasi ptosis, dan kelainan refraksi yang
mereka miliki harus diterapi dengan kontak lens, dan untuk amblyopianya harus
dilakukan terapi oklusi (tutup mata).

Didapat ( paling sering disebabkan kelainan aponeuretik )

Acquired ptosis sering terlihat pada pasien berusia lanjut. Umumnya disebabkan
bertambah panjangnya (stretching) otot levator palpebra (otot yang berfungsi
mengangkat kelopak mata), trauma/pasca kecelakaan, pertambahan usia,
pengguna contak lens dan luka karena penyakit tertentu seperti stroke, diabetes,
tomor otak, kanker yang mempengaruhi saraf atau respon otot, horner sindrom
dan myasthenia gravis.

Berdasarkan etiologi dibagi menjadi :

Table.1 klasifikasi ptosis beard
Kelainan perkembangan levator
Digolongkan sebagai ptosis konginental sejati .
Terjadi akibat distrofi otot – otot levator yang mempengaruhi kontraksi dan relaksasi
serat – serat otot .
Ditandai dengan :
Ptosis pada posisi primer memandang
Palpebra hanya sedikit bergerak saat memandang keatas dan terjadi gangguan
putupan saat melihat kebawah .
Keterlambatan palpebra saat memandang kebawah adalah petunjuk penting untuk
diagnosis kelaian perkembangan levator .
Ptosis konginental terkadang sering disertai dengan adanya strabismus dan pada 25 %
kasus sering disertai bersamaan dengan distrofi muskulus rektus superior yang
berakibat kelemahan pandangan keatas .

Ptosis myogenik lainnya

 Blepharophimosis
Adalah Penyempitan fisura palpebra
abnormal pada arah horizontal , disebabkan
oleh pergeseran lateral kanthus internus.
Penyebab 5 % kasus ptosis konginental ,
bersifat familier , merupakan penyakit
autoso- maldominant hereditary, yang
ditandai dengan ptosis bilateral (3) . normalnya
lebar fisura palpebra adalah 28 – 30 mm tetapi pada keaadaan ini lebar fisura bisa
hanya mencapai ½ lebar normal

2. Oftalmopolegia eksternal menahun

Anamnesa:
Pasien mengeluh sulit mengangkat kelopak mata atasnya sehingga lapangan pandang
pasien jadi berkurang (Kesulitan membuka mata secara normal dan Adanya
gangguan penglihatan.)
Pasien mengeluhkan matanya seperti mata malas
jatuhnya / menutupnya kelopak mata atas yang tidak normal.
Peningkatan produksi air mata.
Iritasi pada mata karena kornea terus tertekan kelopak mata.
Pada anak akan terlihat guliran kepala ke arah belakang untuk mengangkat kelopak
mata agar dapat melihat jelas.

Penjelasan dr. H. Ibrahim, SpM

Pemeriksaan klinis