occipital lobe and clinical effects of its dysfunction

2.  Layers of cerebral cortex and its
variations.
 Surface and functional anotomy of
occipital lobe.
 Clinical effects of occipital lobar
dysfunction.
 Differentiation between malingering and
organic visual loss.

3. › One third of the cerebral cortex is on the
exposed part of gyri remaining is buried in
sulci and gyri.
› 15 to 30 billion nerve cells.
› Thickness of the cortex from 4.5 mm in the
frontal area to 1.3 mm in the occipital area.

6. › The areas of where six layers can not be
identified are called as heterotypical
different from homotypical.
› Supragranular cortex high level cortical
functions.
› Archicortex and paleo cortex.
› Granular and agranular cortex.

7. › Superiolateraly occupies a small area
behind the parieto occipital sulcus.
› Medially area behind the occipetoparietal
sulcus.
› Inferiorly limited by collateral sulcus.
› medially occipital lobe is devided in to
cuneus and lingual gyrus.

10. Consists of Broadmann areas 17,18,19.
 Primary visual cortex or striate cortex or
area 17
› Well devoloped layer 4 a thick layer of
external band of ballirager.
› Lips of calcarine with adjacent areas cuneus
and lingual gyrus.
› Perception of simple sensation
color, size, shape, motion and illumination.

11. › Stimulation or ictal activity produces simple
visal hallucinations.

12.  Associative visual cortex:
› Parastiriate [area 18] and peristriate [area
19]
› receives and interprets impulses.
› Have extensive connections.
› Concerned with more complex visual
functions of perception, spatial orientation,
visual association, and visual memory.
› Stimulation produces formed or complex
visual hallucinations.

13. › In humans occipital eye field is present in the
visual association cortex concerned with
reflex eye movements.

14.  Visual field defects:

15.  Unclear .
 Dual representation of macula in each
occipital pole.
 Collateral blood supply from anterior
and middle cerebral artery.
 Extensive cortical representation at
occipital pole and depths of anterior
calcarine fissure.

16.  Cortical blindness:
› Bilateral lesions of the occipital lobe there is
loss of sight and reflex closure of eyelids to
threat and light with sparing of pupilary light
reflex.
› Most common cause bilateral pca infarcts.
› Other causes are PRES, CJD, PML and
gliomas.

17.  Visual anasagnosia or Antons syndrome:
› Denial of blindness.
› Occurs with bilateral PCA infarcts.
› Sparing of tiny islands of vision
› Patient complains of fluctuation of images as
the vision is captured in spared islands of
cortex.

18.  Visual illusions:
› Size, shape, movement or combination of
three.
› Occipital lesion or in combination
occipitotemporal and occipitoparietal
areas.
› Illusion of movement occurs with
occipetotemporal lesions.
› Polyopia with lesions in occipital lobe.
› Palinopsia with lesions in occipitoparietal
lesions.

19.  Visual hallucination:
› Elimentary or simple visual hallucination is the
feature of striate cortex
› Includes flashes of light, luminous lightened
candles, multiple stars and geomatric forms.
› Complex or formed visual hallucination is a
feature of association cortex or its
connections
› Includes objects, animals, persons and
scenes.

20.  VISUAL OBJECT AGNOSIA:
› Failure to recognize objects by vision with
preserved ability to recognize them through
touch or hearing and in the absence of
impaired primary visual perception or
dementia

21.  Aperceptive visual agnosia:
› Perceived elements of object are
synthesized to whole image.
› Pick out features of the object correctly such
as lines, angles,colors or movement but fail
to appreciate the whole object.
› Examples : spectacles
› Right hemisphere particularly lingual gyrus
involved in global processing of the object

22.  Left hemisphere occipital cortex
invoved in more local processing.

23.  ASSOCIATED VISUAL AGNOSIA:
› Is more closely related to aphasia than
primary disorder of vision.
› Patients can copy and match the drawing
of objects but can not name them.
› They can be identified by tactile or auditary
modality.
› have associated color agnosia and
prosagnosia.

24. • Bilateral posterior hemispheric lesions involving
occipitotemporal gyrus some times lingual gyri
and adjacent white matter.

25.  Charecterised by
› Simultagnosia is a disorder of visual attention
especially to peripheral field associated
inability to perform orderly visual scanning of
the environment and attention to other
sensory stimuli are intact.
› Optic ataxia is the loss of hand eye co-
ordination with difficulty in touching or
reaching the objects under visual guidance.

26. • Optic apraxia is inability project gaze voluntarily
in the peripheral field despite intact
occulomotor movements.

28. › Inability to recognise familiar faces or
pictures.
› Associated with inability to memorise new
faces.
› Inability to name the species of birds,
animals or car model.
› Bilateral ventromesial occipital lesions.

31.  The classic syndrome of pure alexia
without agraphia is caused by a left
posterior cerebral artery occlusion in a
right-handed individual
 All visual information enters only the right
hemisphere
 The right visual cortex perceives the
written material but cannot transmit it to
the left hemisphere because of the
callosal lesion

32.  The inferior parietal lobule in the dominant
hemisphere (primarily area 39, the angular
gyms) is the association cortex that combines
the visual and auditory information necessary
for reading and writing
 A second distinct type of alexia, classically
called alexia with agraphia, results from
damage to the inferior parietal lobule itself
(angular gyrus and environs).
 This lesion renders the patient unable to read or
write

33. › Differentiated between perceptual color
disturbance or anomia
› Congenital retinal color blindness is the most
common type tested by using ishihara
charts.
› Acquired color blindness due to cerebral
lesion is called central achromatopsia.
› Associated visual field defects and
prosopagnosia.

34. › Most often the lesions are bilateral and tend
to affect the upper quadrants with lesions in
bilateral ventro mesial temporal lobes and
lower part of the striate cortex.

35.  Color anomia can be a part of pure
word blindness or anomic aphasia.

36.  Signing
 Shmidt Rimpler test
 A functionally blind person ignorant of
laws of reflection may have much
improved vision reading an acuity chart
held at his chest in a mirror 10 ft away
than reading the chart 20 ft away.
 Optokinetic nystagmus.
 Photic drive on eeg and VER.

37. 1. Effects of unilateral disease:
› Contraletral homonymous hemianopia,
which may be central or peripheral.
› Visual hallucinations.
2. Left occipital disease:
› Rt. Homonymous hemianopia
› Alexia with out agraphia, color anomia.

38. › Visual object agnosia.
3. Rt. Occipital disease:
› Lt. Homonymous hemianopia.
› Visual illusinations and hallucinations
› loss of topographic memory and visual
orientation.

39. 4. Bilateral occipital disease:
› Cortical blindness.
› Anton syndrome.
› Achro motopsia.
› Prosopagnosia [tempero-occipital]
› Simultagnosia and balints syndrome [parieto-
occipital]

40. THAN Q