BUTA KORTIKAL

PRESENTAN PEMBIMBING
Dr. dr. ENDANG
AULIA RACHMAN RAHMAWATI, Sp. S (K)
 The two occipital lobes
Are the smallest of four paired lobes in
the human cerebral cortex.
Separated from parietal lobe by: Parieto-
occipital sulcus.
The OL 3 landmarks:
Calcrine fissure: Div. The upper and
lower halves of the visual world.
Lingual Gyrus
Fusiform Gyrus
Four Lobes on the Lateral Surface

Parieto-occipital
Sulcus

PARIETAL
FRONTAL LOBE
LOBE The occipital lobe
is
separated from the
parietal
TEMPORAL
OCCIPITAL and temporal lobes
LOBE
LOBE by the
line between the
Preocci parieto-
pital occipital sulcus and
Notch the
preoccipital notch
 Parieto-occipital
Sulcus

The parieto- PARIETAL

occipital sulcus
divides the parietal OCCIPITAL
and
occipital lobes on the
medial surface.
 Subdivisions of the OL
1. (6+
V1Areas)
Primary Visual
2. V2 Cortex

3. V3

4. V3A Secondary Visual

Cortex
5. V4

6. V5
 The occipital lobe

is the visual processing center of the mammalian

brain containing most of the anatomical region of
the visual cortex.
The primary visual cortex is Brodmann area 17,
commonly called V1 (visual one).
Human V1 is located on the medial side of the
occipital lobe within the calcarine sulcus;
the full extent of V1 often continues onto the
posterior pole of the occipital lobe. V1 is often
also called striate cortex because it can be
identified by a large stripe of myelin, the Stria of
Gennari.
 Extrastriate regions
Visually driven regions outside V1 are
called extrastriate cortex.

There are many extrastriate regions,

and these are specialized for
different visual tasks, such as
visuospatial processing, color
discrimination, and motion
perception.
 Connections of the Visual
Cortex
Connections
-Primary Visual Cortex
(V1)
-Input from LGN
-Output to all other
levels
-Secondary Visual
Cortex (V2)
Output to all other
levels
-After V2
Output to the parietal Dorsal Stream
Visual Guidance of Movements
lobe - Dorsal Stream Ventral Stream
Output to the inferior Object Perception
temporal lobe - STS
Ventral Stream Visuospatial functions (bio
movement
Output to the superior
temporal sulcus (STS)
- STS Stream
 Connection
s
V1- Largest area, called striate
cortex.
Receives the largest input from the
LGN and projects to ALL other
occipital
V2 -
regions. Alsoprocessing
1st projects tolevel.
all other
occipital areas. Segregates info from
V1.
 Pathways into the visual
brain
Geniculo-striate system
Tecto-pulvinar system
Dorsal (ParL)
1 How or Where
Visual Guidence of mov.
LGN V1V2

Eye dial
Me
Tectum Pulvinar
(Sup Colli) (Thal)
Ventral (TempL)
La What
2 te Obj. perception & recog.
r al
 Functions
A significant functional aspect of the occipital
lobe is that it contains the primary visual cortex.
Retinal sensors convey stimuli through the optic
tracts to the lateral geniculate bodies, where
optic radiations continue to the visual cortex.
Each visual cortex receives raw sensory
information from the outside half of the retina on
the same side of the head and from the inside
half of the retina on the other side of the head.
 O.L Function

V1 & V2 - function like mailboxes:

segregating info to other areas.,
receives primary visual impressions
Color/Form/Motion/Size and illumination.

V3, V3A, V4, V5- Visual association

areas- Recognition and identification of
objects, storage of visual memories, it
functions in more complex visual
recognition and perception,
revisualization, visual association and
 The primary visual cortex (Brodmann
area 17 or,
according to more recent nomenclature, V1)
is located almost entirely on the medial surface
of the occipital lobe; just a small portion (perhaps
1 cm long) extends around the posterior pole onto
the lateral surface.
The visual cortex also is called the striate
cortex because a white myelinated fiber layer,
the white stria of Gennari,is characteristic of this
area.
The calcarine fissure extends from the parieto-
occipital sulcus to the posterior pole, dividing the
visual cortex into an upper portion (the cuneus
gyrus) and a lower part (the lingual gyrus)
most of the primary visual cortex is buried in
the tissue within the calcarine fissure.
 Combines and analyzes the visual information
relayed from the LGN and transmits this
information to the higher visual association
areas (the extrastriate cortex), which
provide further interpretation.
These areas surround the striate cortex and
are located on the lateral aspects of the
occipital cortex.
Historically called Brodmann areas these
areas now are known to contain several
distinct cortical areas (designated V2, V3, V4,
and V5) in which visual processing occurs.
 Clinical Effects of Occipital Lobe Lesions

Visual Field Defects

Cortical blindness
Visual Anosognosia
Visual Illusions
Visual hallucinations
Visual Agnosias
 Cortical Blindness

With bilateral lesions of the occipital lobes

(destruction of area 17 of both hemispheres),
there is a loss of sight that can be
conceptualized as bilateral hemianopia.
The degree of blindness may be equivalent to
that which follows severing of the optic nerves.
The pupillary light reflexes are preserved
because they depend upon visual fibers that
terminate in the midbrain, but reflex closure of
the eyelids to threat or bright light may be
preserved
 No changes are detectable in the retinas.
The eyes are still able to move through a
full range and, if there is macular sparing
as there usually is with vascular lesions,
optokinetic nystagmus can be elicited
Visual imagination and visual imagery in
dreams are preserved.
With rare exceptions, no cortical potentials
can be evoked in the occipital lobes by
light flashes or pattern changes (visual
evoked response), and the alpha rhythm is
lost in the electroencephalogram
 Less-complete bilateral lesions
leave the patient with varying degrees of visual
perception.
There may also be visual hallucinations of either
elementary or complex types.
The mode of recovery from cortical
blindness:There will be a regular progression from
cortical blindness through visual agnosia and
partially impaired perceptual function to recovery.
Even with recovery, the patient may complain of
visual fatigue (asthenopia) and difficulties in
fixation and fusion.
 The usual cause of cortical
blindness
is occlusion of the posterior cerebral arteries (most
often embolic) or the equivalent, occlusion of the
distal basilar artery.
Macular sparing may leave the patient with an
island of barely serviceable central vision.
The infarct may also involve the mediotemporal
regions or thalami, which share the posterior
cerebral artery supply, with a resulting Korsakoff
amnesic defect and a variety of other neurologic
deficits referable to the high midbrain and
diencephalon (drowsiness, akinetic mutism etc )
Patients with bilateral occipital lobe
damage
may have complete cortical blindness.
Some patients with cortical blindness are
unaware that they cannot see, and some
even confabulate visual descriptions or
blame their poor vision on dim lighting or
not having their glasses (Anton syndrome,
originally described in 1899).
Patients with Anton syndrome may describe
objects they see in the room around them
but walk immediately into the wall.
 Visual Anosognosia (Anton
Syndrome)

The main characteristic of this disorder is the

denial of blindness by a patient who obviously
cannot see.
The patient acts as though he could see, and in
attempting to walk, collides with objects, even to
the point of injury.

The lesions in cases of negation of blindness

extend beyond the striate cortex to involve the
visual association areas.
 Kasus
Seorang perempuan 52 tahun datang
dengan keluhan sulit membuka mata
setelah terjatuh dirumah +/- 6 hari
yang lalu, saat pasien jatuh sedang
beraktivitas, Muntah (+), sakit kepala
(+), penurunan kesadaran (+),
kelemahan anggota gerak pada
awalnya kemudian membaik.
TD : 180/100 Pernapasan : 18x/i
HR : 95 x/i T : 36,5
 Pemeriksaan fisik
GCS : E4M6V5
Mata pupil isokor 3mm/3mm, RCL (+), RCTL (+),
VOD (0/60), VOS (0/60)
TRM (-)
Parese n. Cranialis : n. IV centralis sinistra
Kekuatan motorik (4444 /4444) , Sensorik (+ /+)
5555 / 5555 + /+
Refleks Fisiologis (+ /+), Refleks patologis (-/-)
+/+
Otonom : BAB (+), BAK (+)
CT SCAN

Chronic
Thromboemboli
infarction di lobus
occipital sinistra
 Diagnosis Klinis : Stroke Iskemik +
Buta kortikal + Paraparese UMN
Diagnosis Topis : Korteks Occipital
(Brodmann 17/V1)
Diagnosis Etiology : Thromboemboli
 Therapy & Plans
Perfussion:
O223L/i

ManagementofHypertension
Calciumantagonist/CalciumChannelBlocker
ARB

ManagementofStroke:
RTPA(ifonset<4hr)
Anticoagulan(Lovenox/Arixtraifonset48hr)
Antiplatellet(Aspilet&CPGif>8hr)

Neurovitamins
Citicholin2x1000mg
Methylcobalamin1x500mg
 ANALISA KASUS
Kas
us Teori
KELEMAHAN
Occlusionofthearteri
ANGGOTAGERAK
ATAS cerebrimedia
Kas Teori
us
PENURUNAN ARAS(ACTIVATING
KESADARAN RETICULARSYSTEM)
Teor
Kasus i
Occlusion of the posterior
PENURUNANJARAK cerebral arteries (most
PANDANG often embolic) or the
equivalent, occlusion of
the distal basilar artery.
TERIMAKASIH