Occipital lobe and clinical effects of its dysfunction

OCCIPITAL LOBE AND CLINICAL EFFECTS OF ITS

DYSFUNCTION

CONTENTS

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.

CORTEX

› 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.

Layers of the cerebral cortex.

Regional variations in cerebral cortex

Variations of cortical layers

› 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.

Surface anotomy of occipital lobe:

› 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.

Anatomy of occipital lobe

Functional anatomy

FUNCTIONAL ANATOMY OF OCCIPITAL LOBE:

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.

› Stimulation or ictal activity produces simple visal hallucinations.

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.

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

CLINICAL EFFECTS OF DYSFUNCTION

Visual field defects:

Macular sparing

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.

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.

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.

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.

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.

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

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

Left hemisphere occipital cortex invoved in more local processing.

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.

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

BALINT SYNDROME

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.

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

BALINTS SYNDROME

Prosopagnosia

› 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.

ALEXIA WITH OUT AGRAPHIA

ALEXIA WITH OUT AGRAHIA

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

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

COLOR AGNOSIA

› 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.

› 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.

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

Malingering and organic visual loss

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.

SUMMARIZATION OF EFFECTS OCCIPITAL LOBE DYSFUNCTION:

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.

› Visual object agnosia.

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

orientation.

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

[parieto-occipital]

THAN Q