Pupillary and visual pathway

423 views 36 slides Oct 16, 2020
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About This Presentation

OPHTHALMOLOGY


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VISUAL AND PUPILLARY PATHWAY ASWIN SATHIYAN ROLL NO.31

INTRODUCTION-VISUAL PATHWAY The  visual pathway  begins with photoreceptors in the retina and ends in the  visual  cortex of the occipital lobe.  Once the potential is generated, it is going to pass through the neural pathway, ultimately to visual cortex from where the image is perceived …then we are able to comprehend it. This whole pathway is k/a visual pathway

RETINA OPTIC NERVE LATERAL CHIASMA NASAL FIBRES TEMPORAL FIBRES RODS &CONES – 1 st order neurons BIPOLAR CELLS– 2 nd order neurons GANGLION CELLS– 3 rd order neurons OPTIC CHIASMA Decussating to opposite side OPTIC TRACT I/L C/L

LGB- 4 th order neuron OPTIC RADIATION TEMPORAL LOBE Inferior fibres PAREITAL LOBE Superior fibres VISUAL CORTEX

OPTIC NERVE Continuation of nerve fibre layer of retina 1.2 million axons Doesn’t have neurilemma (can’t regenerate) Total length 47-50 mm Divided into 4 parts Intraocular – 1mm, optic nerve head,shortest part Intraorbital /extraocular/retrobulbar – 3 mm, longest part Intracanalicular – 6-9mm, optic canal part, along with ophthalmic artery Intracranial – 10mm, brain, above the cavernous sinus

OPTIC CHIASMA Flattened structure 12mm Horizantally 8mm Anterio -posteriorly It lies over diaphragma sella Continues posteriorly as optic tracts and forms anterior wall of third ventricle Nerve fibers arising from nasal halves of the two retinae decussate at the chiasma

OPTIC TRACT Bundles of nerve fibers running outwards and backwards from postero -lateral aspect of optic chiasma Consist of temporal fibers of retina of same eye and nasal half of opposite eye Each optic tract end in LGB

LATERAL GENICULATE BODY (LGB) 6 layers --- no. 1 to 6 Layers 1,4,6 --- receive inputs from C/L hemiretina Layers 2,3,5 --- receive inputs from I/L hemiretina Magnocellular & parvocellular pathways Magnocellular Parvocellular Layers 1&2 layers 3 to 6 Large cells small cells Motion and stereo form BLOOD SUPPLY : Anterior and lateral choroidal artery

OPTIC RADIATION Extend from LGB to visual cortex Fibers of optic radiation spreads out fanwise to form medullary optic lamina Superior fibers of radiation ( which subserve inferior field) proceed directly posteriorly through parietal lobe

VISUAL CORTEX Located on medial aspect of occipital lobe Subdivided into - Visuosensory area (striate area 17) - Visuopsychic area (striate area 18 and 19) BLOOD SUPPLY : posterior cerebral artery except at the tip of cortex which has dual blood supply middle cerebral artery & posterior cerebral artery.

OPTIC NERVE Lesion of optic nerve- -characterised by complete blindness on affected side - Cause: Trauma, tumor , optic neuritis

Lesion of optic chaisma - 1.Central chiasmal lesion- -Bitemporal hemianopia -Bitemporal hemianopic paralysis of pupillary reflex -Also leads to partial descending optic atrophy Cause: Pituitary tumors Craniopharyngioma, Suprasellar aneurysm. OPTIC CHIASMA Lesion of optic chaisma - 1.Central chiasmal lesion- -Bitemporal hemianopia -A type of heteronymous hemianopia Cause: Pituitary tumors Craniopharyngioma Suprasellar aneurysm .

2.Lateral chiasma lesion- - Binasal hemianopia -Heteronymous hemianopic Cause: Hydrocephalus, Posterior communicating artery atheroma

OPTIC TRACT Lesions of optic tract- -Incongruous homonymous hemianopia - Causes- syphilitic meningitis or gumma , tubercular meningitis, aneurysm of PCA and tumors of optic thalamus.

LATERAL GENICULATE BODY Lesions of LGB- incongruous homonymous hemianopia -contralateral HH. Causes : lesion of anterior and lateral choroidal artery

OPTIC RADIATION Features varies depending on site of lesion 1.Involvment of total optic radiation- complete homonymous hemianopia ( more congruous)

2. Involvement of part of optic radiation in temporal lobe - Superior quandrantic hemianopia ( pie in the sky)

3. Involvement of part of optic radiation in parietal lobe – Inferior quandrantic hemianopia (pie on the floor)

VISUAL CORTEX Anterior occipital cortex Homonymous hemianopia(sparing macula) Cause – occlusion of posterior cerebral artery Tip of occipital cortex Homonymous hemianopia(macula defect) Causes – head injury, gunshot injury involving tip of cortex

INTRODUCTION-PUPILLARY PATHWAY The pupils are controlled by two muscles of ectodermal origin—the sphincter and dilator pupillae. The sphincter is supplied by cholinergic nerves of the parasympathetic system through the third cranial nerve. The fibres start in the Edinger–Westphal nucleus near the third nerve nucleus in the floor of the aqueduct of Sylvius. The dilator pupillae is supplied by the adrenergic fibres of the cervical sympathetic nerve. The dilator tract probably commences in the hypothalamus not far from the constrictor centre and also has connections with the cerebral cortex.

INTRODUCTION THE PUPILLARY REFLEXES The pupils participate in several reflexes, three of which are of clinical importance: The light reflexes: If light enters an eye, the pupil of that eye contracts (the direct light reflex ), an activity shared equally by the pupil of the other eye (the consensual light reflex ). b) The near reflex: A contraction occurs on looking at a near object, a reflex largely determined by the reaction to convergence but in which accommodation also plays a part. c)The psychosensory reflex: A dilatation of the pupil occurs on psychic and sensory stimuli.

PUPILLARY REFLEX LIGHT REFLEX DIRECT L.R ACCOMODATION REFLEX INDIRECT L.R OR CONSENSUAL L.R Light and reflex in the same eye Light and reflex in the opposite eye

PATHWAY OF LIGHT REFLEX RETINA OPTIC NERVE (afferent) OPTIC TRACT PRETECTAL NUCLEUS EWN (R) SPHINCTER PUPILLAE CILIARY GANGLION III N. EWN (L) III N. CILIARY GANGLION SPHINCTER PUPILLAE Bilateral innervation from pretectal nucleus is the reason for indirect light reflex

PATHWAY OF ACCOMODATION REFLEX OPTIC TRACT LGB OPTIC RADIATION STRIATE CORTEX EWN (R) SPHINCTER PUPILLAE CILIARY GANGLION III N. EWN (L) III N. CILIARY GANGLION SPHINCTER PUPILLAE OPTIC NERVE RETINA

ABNORMAL PUPILLARY REACTIONS ARGYLL ROBERTSON PUPIL Seen in neurosyphilis,tabes dorsalis,DM B/L lesion of pretectal nucleus Light reflex : absent Accomodation reflex : present B/L irregular and constricted pupil : ISOCHORIA Light near dissociation

FEATURES OF ARP Involvement is usually Bilateral but Asymmetrical The retinae are sensitive to light The pupils are small in size and irregular in shape The light reflex is absent but near reflex is present Dilate poorly with mydriatics like Atropine Physiostigmine may cause further constriction

2. ADIE’S TONIC PUPIL Lesion in the post ganglionic ciliary ganglion U/L Seen in viral infections Pupillary reflex Affected side Other side DLR - + ILR - + AR - /slow + ANISOCHORIA

3. RAPD/RELATIVE AFFERENT PUPILLARY DEFECT Also k/a Marcus Gunn pupil Earliest manifestation of optic N. disease Tested by swinging flash light test

Optic neuritis Anterior ischemic optic neuropathy Compressive optic neuropathy Glaucoma Optic Nerve Tumors Orbital Diseases Ischemic Retinal Diseases : CRAO CRVO BRAO BRAVO Ocular Ischemic Syndrome Central serous retinopathy or cystoid macular edema Retinal detachment Chiasmal compression Optic tract lesion Postgeniculate damage Midbrain tectal damage ETIOLOGY OF RAPD

 Grade 1+ : A weak initial pupillary constriction followed by greater redilation Grade 2+ : An initial pupillary stall followed by greater redilation Grade 3+ : An immediate pupillary dilation Grade 4+ : Immediate pupillary dilation following 6 sec illumination Grade 5+ : Immediate pupillary dilation with no constriction at all  However, most subjective grading of RAPDs has serious limitations, such as some large-scale errors that arise from age variations in pupil size and pupil mobility GRADING SCALE

4. HUTCHISON’S PUPIL Etiology : raised ICT ( trauma,TB meningitis,tumors ) Causes third nerve irritation ultimately nerve palsy 3 phases Affected side Other side Phase 1 Pupil constricts Normal Phase 2 Pupil dilates Constricts Phase 3 Dilated Dilated

5. WERNICKE’S REACTION Disease of optic tract Both DLR & ILR are absent if the light is shown to the temporal half of the same side and nasal half of the opposite side If we able to stimulate that part of retina which is carrying the impulses to the defective optic tract, then no DLR no ILR

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