VISUAL PATHWAY Visual Pathway is the nervous pathway that transmits impulses from retina to visual centre in cerebral cortex. Components: Optic Nerve Optic Chiasma Optic Tract Lateral Geniculate Bodies Optic Radiations Visual cortex
VISUAL PATHWAY ANATOMY Visual sensations rods and cones visual cortex 1 st order neurons –BIPOLAR CELLS 2 nd order neurons –RETINAL GANGLION CELLS TO LGN IN THALAMUS 3 rd order neurons- LGN TO VISUAL CORTEX
Extends from optic disc to optic chiasma. It is about 45 to 50mm in length. It is backward continuation of NFL of retina consists of 1 million myelinated axons originating from ganglion cells & contains Afferent fibres of pupillary light reflex. It is covered by meningeal sheath of the brain, does not regenerate when cut. PARTS OF OPTIC NERVE Intraocular part - 1mm Intraorbital part - 25mm Intracanalicular part - 9mm Intracranial part -10mm OPTIC NERVE
INTRAOCULAR PART Starts from optic disc, pierces the choroid and sclera converting into sieve like structure the lamina cribrosa & At back of eyeball it becomes continuous as intraorbital part. 4 layers
INTRAORBITAL PART Extends from the back of the eyeball to optic foramina, covered dura, arachnoid & pia. Anteriorly - separated from the ocular muscles by orbital fat. Posteriorly near optic foramina, closely surrounded by annulus of zinn & origin of rectus muscle. Some fibres of SR muscle are adherent to its sheath here & accounts for painful ocular movements in retrobulbar neuritis. RELATIONS: B/w optic nerve & LR –ciliary ganglion, nasociliary nerve, branch of 3,6 CN, & sympathetic nerve. Central retinal artery with accompanying vein enter the nerve on inferomedial aspect 10mm from eyeball.
INTRACANALICULAR PART Lies within the optic canal Inferolateral - ophthalmic artery & crosses obliquely over it as it enters the orbit to lie on medial side Medial - posterior ethmoid sinus & sphenoid sinus separated by thin bony lamina. This accounts for retrobulbar neuritis following infection of sinuses.
INTRACRANIAL PART RELATIONS Inferior- cavernous sinus, diaphragma sellae, pituitary gland. Superiorly- anterior perforated substance, medial root of olfactory tract & anterior cerebral artery. Laterally – internal carotid artery. Ophthalmic artery originates from internal carotid artery under the optic nerve. AA- carotid artery aneurysms compress nerve.
OPTIC CHIASMA It is flattened structure. Fibres originating from the nasal halves of the retina , divides at the chiasma. Relations: Anterior- anterior cerebral artery, anterior communicating artery. Posteriorly- infundibulum, hypothalamus, mamillary body & pituitary. Superior- 3 rd ventricle. Inferior- pituitary gland. Lateral – extracavernous internal carotid artery. A- sagittal section, B - superior view
OPTIC TRACT These are cylindrical bundle of nerve fibres . Lies b/w tuber cinereum & anterior perforated substance & joins the cerebral peduncle. Each optic tract consists of fibres from the temporal half of the retina of the same eye and the nasal half of the opposite eye. Pupillary reflex fibres pass on to superior colliculus through superior brachium from here.
LATERAL GENICULATE BODY It is a mushroom-shaped structure in the posterior thalamus . It receives approximately 70% of the optic tract fibers within its 6 alternating layers of grey and white matter (the other 30% of the fibers go to the pupillary nucleus). Layers 1, 4, and 6 of the LGN contain axons from the contralateral optic nerve. Layers 2, 3, and 5 arise from the ipsilateral optic nerve. The 6 layers, numbered consecutively from inferior to superior, give rise to the optic radiations. 2 nd order neurons from optic tract relay here.
OPTIC RADIATIONS Fibres spread out fanwise to form medullary optic lamina, first vertical later becomes horizontal. Superior fibres which subserve inferior visual fields proceed directly posteriorly through parietal lobe to visual cortex. Inferior fibres which subserves superior visual fields,1st sweep anteroinferiorly in meyer loop around anterior tip of temporal horn of lateral ventricle then into temporal lobe.
VISUAL CORTEX Located on the medial aspect of the occipital lobe, above and below calcarine fissure. Visuosensory area V1 (Brodmann area 17) receives fibres of optic radiations. Surrounding it is visuopsychic area 18(peristriate) V2,V3 and 19(parastriate)V4,superior temporal gyrus V5.
VISUAL PATHWAY The macular fibres typically receive vascular supply at the occipital cortex from the middle cerebral artery& posterior cerebral artery.
Visual fields & Retina have INVERTED & REVERSED relationship. TERMINOLOGIES CONGRUOUS –Alike in both eyes, size, shape. eg -Post optic radiation lesions INCONGROUS– Different in both eyes. eg -Optic tract & LGB lesions HOMONYMOUS- Both eyes with same laterality. HETERONYMOUS- Both eyes with different laterality.
ANOPIA Loss of vision in one visual field (Right anopia )
HEMIANOPIA Loss of vision in one half of visual field. Heteronymous hemianopia
QUADRANTANOPIA Loss of vision in a quadrant of visual field. HOMONYMOUS TYPE
ARRANGEMENT OF NERVE FIBRES IN RETINA
FIELD DEFECTS IN RETINAL LESIONS Central scotoma . Ring scotoma . Nonspecific focal depression . Gen e ral ised constriction .
CENTRAL SCOTOMA Involves fixation only CAUSES Papillitis Leber’s hereditary optic atrophy Drug toxicity – ethambutol, ethyl alcohol, chloroquine Compressive lesions of optic nerve
PARACENTRAL SCOTOMA – Involves a region next to but not including fixation CAUSES Myelinated nerve fibres Congenital optic nerve head hypoplasia .
CENTROCECAL SCOTOMA – Extends from fixation to blind spot Papilloedema – centrocecal scotoma with sloping edges
OPTIC NERVE FIBRE ARRANGEMENT Arrangement of distal optic nerve fibre just behind eyeball. Arrangement of proximal nerve fibre near chiasma.
FIELD DEFECTS IN LESIONS OF OPTIC NERVE Cause Traumatic avulsion of optic nerve Optic atrophy Head injury Optic neuritis. Clinical features Ipsilateral anopia (loss of vision) Loss of direct pupillary reaction (same side) loss of consensual pupillary reaction (other side) Near or accommodation reflex is present
LESION OF PROXIMAL PART OF OPTIC NERVE OR ANTERIOR CHIASMAL SYNDROME Involves ipsilateral optic nerve fibers and contralateral inferonasal fibres . Type- junctional scotoma (combination of central scotoma/complete scotoma in one eye and temporal hemianopia in the other) .
OPTIC CHIASMA- NFL TEMPORAL FIBRES Uncrossed temporal fibres , run backwards in lateral part. NASAL PERIPHERAL FIBRES 3/4 th of fibres cross over to enter medial part of opposite tract in following manner- 1.Lower nasal fibres in optic tract traverse chiasma low & anteriorly. 2.Upper nasal fibres in optic tract traverse chiasma high & posteriorly.
MACULAR FIBRES Some fibres crossed & run backwards in opposite optic tract. Some fibres uncrossed and run on same side in optic tract.
CENTER CHIASMA Produced by lesions involving the decussating fibres in the body of chiasma. Bitemporal hemianopia. Bitemporal hemianopic paralysis of pupillary reflexes. Optic atrophy CAUSES Pituitary adenoma or malignancy Craniopharyngioma Chronic chiasmal arachnoiditis Fracture of the base of skull Suprasellar aneurysms & meningioma.
LESION LATERAL TO OPTIC CHIASMA Binasal hemianopia Binasal hemianopic paralysis of pupillary reflex Optic atrophy. CAUSES IIIrd ventricle enlargement causing pressure on each side of chiasma. Atheroma of carotids or posterior communicating arteries on both sides.
FIELD DEFECTS IN LESIONS OF OPTIC TRACT- 5 Right incongruous homonymous hemianopia Afferent pupillary conduction defect present. C/L hemianopic pupillary response Optic atrophy Association with right hemiplegia and left 3 rd nerve paralysis indicates a left optic tract lesion involving left cerebral peduncle and left 3 rd nerve.
CAUSES OF OPTIC TRACT LESION Syphilitic meningitis Tuberculous meningitis Tumors of thalamus Temporal lobe glioma Aneurysm of superior cerebellar or posterior cerebral arteries.
BOW-TIE” OPTIC ATROPHY Cause – involvement of fibres entering optic disc nasally & temporally. it occurs lesions of chiasma & c/l optic tract involving crossed retinal fibres nasal to fovea.
LATERAL GENICULATE BODY Macular fibres wedge shaped area broadening towards caudal plate . Upper retinal – M edial ½ of anterior LGB. Lower retinal – L ateral ½ of anterior LGB.
FIELD DEFECTS IN LESIONS OF LATERAL GENICULATE BODY 6- Incongruous homonymous hemianopia Sparing of pupillary reflexes. Optic disc pallor may occur due to partial descending atrophy.
CAUSES AV malformations Arterial inflammations Injuries Vascular occlusions
OPTIC RADIATION Upper retinal fibres Upper part of optic radiations Lower retinal fibres Lower part of optic radiations Macular fibres Central part of optic radiations
OPTIC RADIATIONS OF THE TEMPORAL LOBE From the LGN, inferior visual fibers first course anteriorly and then laterally and posteriorly to the meyer loop of the temporal lobe. Superior fibers course more directly posteriorly in the parietal lobe. Lesions affecting the meyer loop thus produce superior incongruous homonymous visual field defects- pie in the sky. Damage to the temporal lobe anterior to the meyer loop does not cause visual field loss. Lesions affecting the radiations posterior to the loop produce homonymous hemianopic defects that extend inferiorly.
OPTIC RADIATIONS OF THE PARIETAL LOBE Lesions of the parietal lobe, which often result from stroke or neoplasms, tend to involve superior fibers first, causing contralateral inferior homonymous hemianopic defects. More extensive lesions affect the superior visual fields but remain denser inferiorly. Other neurologic effects Agnosia- unable to recognise objects (inability to interpret sensations). Apraxia- unable to make movements. Acalculia- loss of ability to perform simple calculations. Agraphia – inability to write letters,symbols . Left–right confusion. Optokinetic nystagmus
OPTIC RADIATIONS OF THE OCCIPITAL LOBE As the visual fibers approach the occipital lobes, the visual field becomes congrous . The central fibers become separate from the peripheral fibers and course to the occipital tip, whereas the peripheral fibers travel to the anteromedial cortex. The anteromedial region of the occipital lobe subserves a monocular “temporal crescent” of visual field in the far periphery(60°–90° from fixation). Visual field defects resulting from occipital lobe lesions may have the following characteristics in the hemifields contralateral to the lesion: • congruous homonymous hemianopia, possibly sparing the fixation region • monocular defect of the temporal crescent involving only the most anterior portion of the occipital lobe.
VISUAL FIELD DEFECT OF OPTIC RADIATIONS 7. Anterior temporal lobe, inferior fibres are involved - Superior quadrantanopia Pie in the sky. 8. Parietal lobe, superior fibres are involved- Inferior quadrantanopia- Pie on the floor. 9. Total fibres of optic radiations are involved- Complete homonymous hemianopia. 10. Posterior part of Internal capsule (Ant occipital cortex)-homonymous hemianopia with macular sparing.
COMMON CAUSES OF LESIONS OF OPTIC RADIATIONS Vascular occlusions Cerebral tumours Injury by fall on the back of head Temporal lobectomy for epilepsy
VISUAL CORTEX Called cortical retina, since true copy of retinal image is formed here. Right & left visual fields are represented within left & right occipital lobe respectively. Fibres from macular area relay posteriorly in visual cortex. Fibres from superior & inferior peripheral retina end upper & lower part of calcarine sulcus.
FIELD DEFECTS IN LESIONS OF VISUAL CORTEX LESIONS IN VISUAL CORTEX TIP OF OCCIPITAL ANTERIOR VISUAL ANTERIOR MOST PART CORTEX CORTEX OF VISUAL CORTEX CONGRUOUS HOMONYMOUS HEMIANOPIA with macular sparing. Ex : pca occlusion.
Bilateral homonymous macular defects, presenting like bilateral central scotoma occur in bilateral lesions of occipital cortex.
COMMON CAUSES OF LESIONS OF VISUAL CORTEX Vascular lesions in territory of PCA Trauma- fall on the back of head or gunshot injury Cerebral tumours - primary or metastatic.
HALF- MOON SYNDROME / TEMPORAL CRESCENT SYNDROME Only example of a monocular field defect from a retrochiasmal lesion Most likely infarction of the anterior 10% of the occipital cortex Measured by kinetic perimetry from 60- 90°
REFERENCE AK KHURANNA ANATOMY & PHYSIOLOGY WOLFF’S ANATOMY OF EYE AND ORBIT( 8 TH EDITION)