 Special somatic afferent nerve

 Transection leads to blindness and no direct

pupillary light reflex
 Optic chiasma has decussating fibers from two
nasal hemiretinas
 Non crossing fibers from two temporal
hemiretinas
 Projects fibers to suprachiasmatic nucleus of
hypothalamus
 Midsagittal transection or pressure leads to
BITEMPORAL HEMIANOPIA
 Binasal hemianopia by bilateral lateral
compression(calcified ICAS)
 It contains fibers of contralateral nasal
hemiretina and ipsilateral temporal
hemiretina
 It projects to ipsilateral lateral geniculate
body,pretectal nuclei and superior colliculus
 Transection causes CONTRALATERAL
HEMIANOPIA
 Six layered nucleus
 Layers 1,4 and 6 receive crossed fibers;layers
2,3 and 5 receive uncrossed fibers
 Receives input from layer VI(multiform) of
striate cortex (area 17)
 Receives fibers from contralateral nasal
hemiretina and ipsilateral temporal
hemiretina
 It projects to layer IV of striate cortex through
geniculocalcarine tract
 It projects to visual cortex through two
divisions upper and lower
 Upper division Projects to upper bank of
calcarine sulcus(cuneus)
 It contains fibers from superior retinal
quadrants (inferior visual field quadrants)
 Transection causes contralateral lower
quadrantanopia
 Bilateral destruction of cunei will lead to
lower altitudinal hemianopia
 Loops from lateral geniculate body
anteriorly(Meyer’s loop),then posteriorly to
end in lower bank of calcarine sulcus(lingual
gyrus)
 It contains fibers from inferior retinal
quadrants (superior visual field quadrants)
 Transection causes contralateral upper
quadrantanopia(pie in the sky)
 Bilateral destruction of lingual gyri will lead to
upper altitudinal hemianopia
 It consists of upper bank(cuneus) and lower
bank(lingual gyrus)
 Lesions cause CONTRALATERAL
HEMIANOPIA with macular sparing
 Posterior area receives macular input(central
vision)
 Intermediate area receives paramacular
input(peripheral input)
 Anterior area receives monocular input
 Retina – the deepest tunic
 Composed of two layers
 Pigmented layer – single layer of melanocytes
 Neural layer – sheet of nervous tissue
▪ Contains three main types of neurons
▪ Photoreceptor cells
▪ Bipolar cells
▪ Ganglion cells
 Two main types
 Rod cells – more sensitive to light
▪ Allow vision in dim light
 Cone cells – operate best in bright light
▪ Enable high-acuity, color vision
 Considered neurons
 Structures in the eye bend light rays
 Light rays converge on the retina at a single
focal point
 Light bending structures (refractory media)
 The lens, cornea, and humors
 Accommodation – curvature of the lens is
adjustable
 Allows for focusing on nearby objects
 Most visual information travels to the
cerebral cortex
 Responsible for conscious “seeing”
 Other pathways travel to nuclei in the
midbrain and diencephalon
 Pathway begins at the retina
 Light activates photoreceptors
 Photoreceptors signal bipolar cells
 Bipolar cells signal ganglion cells
 Axons of ganglion cells exit eye as the optic nerve
 Optic tracts send axons to:
 Lateral geniculate nucleus of the thalamus
▪ Synapse with thalamic neurons
▪ Fibers of the optic radiation reach the primary visual
cortex
 Some axons from the optic tracts
 Branch to midbrain
▪ Superior colliculi
▪ Pretectal nuclei
 Other branches from the optic tracts
 Branch to the suprachiasmatic nucleus
 The pupillary light reflex is a reflex that
controls the diameter of the pupil, in
response to the intensity (luminance) of light
that falls on the retina of the eye. Greater
intensity light causes the pupil to become
smaller (allowing less light in), whereas lower
intensity light causes the pupil to become
larger (allowing more light in). Thus, the
pupillary light reflex regulates the intensity of
light entering the eye
 Visible colored part of the eye
 Attached to the ciliary body
 Composed of smooth muscle
 Pupil – the round, central opening
 Sphincter pupillae muscle (constrictor or circular)
 Dilator pupillae muscle (dilator or radial)
▪ Act to vary the size of the pupil
 The optic nerve is responsible for the afferent limb of the pupillary reflex - it senses the incoming
light. The oculomotor nerve is responsible for the efferent limb of the pupillary reflex - it drives
the muscles that constrict the pupil.
 Neuron 1
 The pupillary reflex pathway begins with retinal ganglion cells, which convey information from 
photoreceptors to the optic nerve (via the optic disc).
 The optic nerve connects to the pretectal nucleus of the upper midbrain, bypassing the lateral
geniculate nucleusand the primary visual cortex.
 Neuron 2
 From the pretectal nucleus, axons connect to neurons in the Edinger-Westphal nucleus,(crossed
and uncrossed fibers) whose axons run along both the left and right oculomotor nerves.
 Neuron 3
 Oculomotor nerve axons (preganglionic parasympathetic fibers)  synapse on ciliary
ganglion neurons.
 Neuron 4
 Ciliary ganglion gives rise to post ganglionic parasympathetic fibers which innervate the
constrictor muscle of the iris.

 First Order – Retina to Pretectal Nucleus in
B/S
(at level of Superior colliculus)
 Second Order – Pretectal nucleus to E/W
nucleus
(bilateral innervation!)
 Third Order – E/W nucleus to Ciliary Ganglion
 Fourth Order – Ciliary Ganglion to Sphincter
pupillae (via short ciliary nerves)
 Constricted (mioisis) Dilated (mydriasis)
Parasympathetic (pupilloconstrictor)
 Sympathetic denervation
Lesion of the third CN
(pupillodilator) Drugs
denervation Atropine
Cocaine
 Drugs
▪ Pilocarpine
▪ Morphine
 Oculosympathetic paresis

 Ptosis
 Miosis
 Ipsilateral anhidrosis
 Does not dilate with cocaine
4%
 First Order – Posterior (paraventricular
nuclei)Hypothalamus to ciliospinal centre of
Budge (C8-T2)
(Uncrossed in Brainstem)
 Second Order – Ciliospinal centre of Budge to
Superior Cervical Ganaglion
 Third Order – Superior Cervical Ganglion to
dilator pupillae muscle. (Close to
ICA and joins V1 intracranially)
 Central – B/S lesions (tumours, vascular and
MS ) Syringomyelia,
 Preganglionic – Pancoast tumour, Carotid &
Aortic aneurysms, Neck lesions/trauma,ca
lung
 Postganglionic – Cluster headaches,
Nasopharyngeal tumours, Otitis media,
Cavernous sinus mass and ICA disease.
 Miscellaneous – Congenital (brachial plexus
injury) Idiopathic.
 Argyll-Robertson pupil Miotonic pupil (Adie’s syndrome)
Dilated
 Small, irreg Poor response to light and
convergence.
 Does not react to light
Constricts with weak
 Reacts to Pilocarpine
accommodation Holmes-Adie syndrome
Reduced tendon reflexes
 Causes (Knee, ankle)
▪ syphilis - Orthostatic hypotension
▪ diabetes
 Defective adduction of the ipsilateral
eye
 Nystagmus of the contralateral
(abducting) eye
 NORMAL CONVERGENCE
 Causes
 Young patients
▪ Bilateral
▪ Demyelination
 Older patients
▪ Unilateral
▪ Vascular, tumours
 Localising the lesion

• Monocular visual field defects indicate

lesions anterior to the optic chiasm
• Bitemporal defects are the hallmark of
chiasmal lesions
• Binocular homonymous hemianopia result
from lesions in the contralateral
postchiasmal region
• Binocular quadrantanopias reflect optic
tract lesions
 Area 17 visual association
area(18,19) superior colliculus and
pretectal nucleus oculomotor complex
of midbrain
 Rostral Edinger Westphal nucleus for
pupillary constriction via ciliary ganglion
 caudal Edinger Westphal nucleus for ciliary
muscle contraction
 Medial rectus subnucleus for convergence
 Frontal eye field area in poterior partof
middle frontal gyrus(8) for voluntary saccadic
movements of eyes
 Irritative lesion contralateral
conjugate deviation of eyes
 Destructive lesion transient ipsilateral
deviation of eyes
 Area 18, 19 concerned with involuntary track
and persuit movements of eyes
 Stimulation contralateral conjugate
deviation of eyes
 Located in abducent nuclei of pons or
paramedial reticular formation of pons
 Input from contralateral frontal eye field
 Projects to ipsilateral lateral rectus muscle
and contralateral medial rectus subnucleus of
oculomotor complex via MLF