Visual Pathways
Visual signals exit the retinas via the optic nerves.
At the optic chiasm:
Nasal retinal fibers cross to the opposite side.
Temporal retinal fibers remain ipsilateral.
Fibers form the optic tracts, synapsing in the dorsal lateral geniculate nucleus
(LGN) of the thalamus.
From the LGN, geniculocalcarine fibers (optic radiations) transmit signals to the
primary visual cortex in the calcarine fissure area of the medial occipital lobe.
Other visual projections:
To suprachiasmatic nucleus (hypothalamus) — circadian rhythm regulation.
To pretectal nuclei (midbrain) — pupillary light reflex and eye focusing.
To superior colliculus — rapid eye movements.
To ventral lateral geniculate nucleus & basal brain regions — behavioral control.
Divided into:
New system: direct signals to visual cortex — conscious visual perception.
Old system: midbrain and forebrain structures — reflexive and primitive visual
responses.
Function of the Dorsal Lateral Geniculate Nucleus (LGN)
Relays visual signals from optic tract to visual cortex with precise point-to-point
fidelity.
Keeps signals from each eye segregated in six layers:
Layers II, III, V: from lateral half of ipsilateral retina.
Layers I, IV, VI: from medial half of contralateral retina.
Maintains parallel, corresponding transmission from both eyes.
Second function: “Gating” visual information
Controlled by:
Corticofugal fibers from primary visual cortex.
Reticular areas of the mesencephalon.
Both act as inhibitory control circuits to regulate signal flow.
Layer-specific functions:
Magnocellular layers (I & II):
Receive from Y retinal ganglion cells.
Fast conduction, black-and-white, low spatial fidelity.
Parvocellular layers (III–VI):
Receive from X retinal ganglion cells.
Color, high spatial detail, moderate conduction speed.
Organization and Function of the Visual Cortex
Located on medial aspect of occipital lobes.
Divided into:
Primary visual cortex (V1 / striate cortex):
In calcarine fissure area.
Signals from macula near occipital pole.
Upper retina → superior calcarine fissure.
Lower retina → inferior calcarine fissure.
Fovea: disproportionately large representation due to high acuity.
Secondary visual areas (visual association areas):
Surround V1 (mainly Brodmann’s area 18 / V2).
Extend over lateral, anterior, superior, and inferior occipital cortex.
Progressively process and interpret visual information.
Includes areas V3, V4, V5, etc.
Primary Visual Cortex Structure
Has six distinct layers, like other cerebral cortical areas.
Geniculocalcarine fibers (from lateral geniculate nucleus) mainly terminate in
layer IV.
Y ganglion cell signals → Layer IVcα.
X ganglion cell signals → Layers IVa and IVcβ.
Signals are transmitted vertically both toward the cortical surface and deeper levels.
Vertical Neuronal Columns
Cortex organized into millions of vertical columns, each 30–50 µm wide.
Each column acts as a functional processing unit (~1000+ neurons per column).
Signals process along these columns to decipher bits of visual information at
successive stations.
Outward to layers I–III for local lateral transmission.
Inward to layers V–VI for long-distance signal transmission.
Color Blobs
Specialized column-like regions interspersed among visual columns.
Activated specifically by color signals.
Key sites for decoding color information.
Interaction of Signals from Both Eye
Signals from each eye remain separate in layer IV, in alternating 0.5 mm wide
stripes.
Deciphers whether visual images from both eyes are in register.
Crucial for stereopsis (depth perception) and adjusting eye positions for fusion.
Two Major Visual Analysis Pathways
Fast “Position-Form-Motion” Pathway (via Y fibers)
Analyzes 3D position, motion, and gross form.
Projects to posterior midtemporal and occipitoparietal cortex.
Black-and-white, rapid, no color info.
Accurate “Detail-Color” Pathway (via X fibers)
Analyzes fine detail, texture, letters, and color.
Projects to ventral, inferior, and medial occipital & temporal cortex.
Visual Image Analysis Patterns
Primary visual cortex responds mainly to contrasts, not to uniform illumination.
Sharp contrast borders stimulate neurons proportionally to contrast intensity.
Adjacent equally stimulated retinal receptors inhibit each other → only borders
activate signals.
Detection of Orientation and Shape
Simple cells in layer IV detect specific line orientations (vertical, horizontal,
oblique).
Complex cells detect the same orientations, even if displaced laterally/vertically.
Higher-order neurons in outer layers and secondary areas respond to specific
shapes, angles, and line lengths.
Color Detection
Based on color contrast (e.g., red vs. green).
Enables color constancy: perceived color remains stable despite changes in lighting.
Simple, complex, and hypercomplex cells handle progressively complex color
contrasts.
Effects of Primary Visual Cortex Removal
Causes loss of conscious vision (cortical blindness).
Some subconscious visual reflexes may persist (e.g., reacting to light or movement).
Mediated via older visual pathways: mainly through superior colliculi and other
midbrain structures.
Fields of Vision & Perimetry
Field of vision: area seen by an eye at any instant.
Nasal field: towards the nose.
Temporal field: towards the side (lateral).
Perimetry: method to chart the field of vision for each eye.
Subject focuses on a central spot; a light/object moves in the field.
Blind spot (~15° lateral to central vision) due to optic disc (no rods/cones).
Scotomata: abnormal blind spots outside optic disc area.
Causes: glaucoma, retinal allergies, toxins (e.g., lead, tobacco).
Retinitis pigmentosa:
Degeneration of retina + melanin deposition.
Begins with peripheral vision loss, progressing to central vision.
Lesions of the Optic Pathway
Optic nerve destruction → total blindness in affected eye.
Optic chiasm destruction → bitemporal hemianopsia (loss of temporal fields of both
eyes).
Often due to pituitary tumors
Optic tract lesion → homonymous hemianopsia (loss of same visual field in both
eyes).
Eye Movements & Their Control
Muscular Control
Six muscles control eye movement:
Medial & lateral recti → side-to-side.
Superior & inferior recti → up & down.
Superior & inferior obliques → rotation (maintain upright visual fields).
Neural Pathways
Cranial nerves III, IV, VI control ocular muscles via brainstem nuclei.
Medial longitudinal fasciculus connects nuclei for coordinated movements.
Cortical control via occipital cortex → pretectal/superior colliculi → oculomotor
nuclei.
Vestibular system also sends signals via medial longitudinal fasciculus.
Fixation Movements
Voluntary fixation:
Controlled by premotor frontal cortices.
Allows choosing new visual points.
Involuntary fixation:
Controlled by secondary occipital visual areas.
Keeps eyes locked on object.
Lesions impair the ability to maintain fixation
Mechanism of Involuntary Fixation
Negative feedback keeps object on the fovea.
Continuous micro-movements:
Tremor: 30–80 cycles/sec.
Drift: slow movement.
Flick: rapid corrective motion if object moves off fovea.
Controlled largely by superior colliculi (damage impairs this ability).
Saccadic Movements
Rapid jumps from one fixation point to another (2–3/sec).
90% of time: fixation; 10% of time: eye movement.
Brain suppresses vision during saccades → no awareness of the jumps.
Occur during:
Reading: multiple saccades per line.
Viewing art: multidirectional saccades between points of interest.
Pursuit Movements
Eyes track moving objects smoothly.
Initially irregular, followed by saccadic jumps.
After a few seconds, smooth pursuit develops.
Requires advanced cortical computation for speed/direction matching.
Superior Colliculi & Visual Orientation
Responsible for turning eyes and head toward sudden visual disturbances.
This function persists even after visual cortex destruction, but not if superior colliculi
are also damaged.
Retinal points are mapped topographically in superior colliculi (less precise than
visual cortex).
Signals transmitted to oculomotor nuclei direct eye movements.
Superior colliculi also map somatic and acoustic signals to assist directional
movement.
Y optic nerve fibers conduct these rapid-turning visual signals; type W fibers' role is
unclear.
Superior colliculi relay signals via medial longitudinal fasciculus to move
head/body toward stimuli (visual, auditory, somatic).
Fusion of Visual Images
Visual images normally fuse at corresponding retinal points for coherent perception.
Visual cortex processes signals from lateral geniculate body to align images.
Misaligned images excite specific interference neurons → triggers corrective eye
movements.
Fusion achieved when interference excitation ceases.
Stereopsis (Depth Perception)
Due to 2+ inch separation between eyes → images differ slightly.
Disparity increases as object nears → provides depth cues.
Different optic pathways register images for specific distances (e.g., 2m, 25m).
This non-register/register pattern enables depth perception (stereopsis) up to 200 feet
(60m).
Strabismus (Cross-eye)
Failure of eyes to fuse in one or more coordinates (horizontal, vertical, torsional).
Can result from improper early visual system alignment.
Types: horizontal, torsional, vertical — can occur in combination.
May cause suppression of one eye’s image → poor development of that eye’s visual
acuity.
Neural connections to visual cortex reduce for the suppressed eye, especially in adults.
Autonomic Control of Eye Functions
Parasympathetic (via Edinger-Westphal nucleus):
Controls ciliary muscle (accommodation) and sphincter pupillae (pupil constriction).
Sympathetic (from T1 to superior cervical ganglion):
Controls radial iris fibers (pupil dilation) and eyelid smooth muscle.
Control of Accommodation (Focusing)
Lens adjusts for best focus through ciliary muscle contraction/relaxation.
Negative feedback mechanism rapidly fine-tunes lens strength.
Cues for adjustment:
Chromatic aberration (focus difference between red & blue light).
Eye convergence when fixating near objects.
Foveal clarity difference (center vs. edge).
Oscillating accommodation (up to 2 Hz) helps detect focus quality changes.
Brain areas: Brodmann’s areas 18 & 19 → pretectal area → Edinger-Westphal
nucleus.
Pupillary Diameter Control
Miosis (constriction): Parasympathetic (Edinger-Westphal nucleus → sphincter
pupillae).
Mydriasis (dilation): Sympathetic (superior cervical ganglion → radial iris fibers).
Pupillary Light Reflex
Light on retina → optic nerve → pretectal nucleus → Edinger-Westphal nucleus →
constriction.
Reflex adapts eye rapidly to changing light (range of about 30:1 in light entry).
CNS diseases (e.g., neurosyphilis, alcoholism) may block this reflex.
Argyll Robertson Pupil
Pupils fail to constrict to light but constrict during accommodation.
Characteristic of CNS diseases like neurosyphilis.
Horner’s Syndrome
Results from interruption of sympathetic pathway.
Features:
Miosis (constricted pupil)
Ptosis (drooping upper eyelid)
Vasodilation (flushed skin)
Anhidrosis (lack of sweating)