Pupillary Reflexes and Visual Pathways Notes

Function of the Pupil

  • Regulates light input.
    • Constriction (light): Decreases glare, increases depth of focus, reduces pigment bleaching via parasympathetic nerves (CN III).
    • Dilation (dark): Increases light entering eye via sympathetic nerves.

Pupillary Light Reflex

  • Direct: Constriction of stimulated eye's pupil.
  • Consensual: Constriction of the other eye's pupil.

Pupillary Light Reflex Pathways

  • Afferent: Photoreceptors → bipolar cells → ganglion cells → optic nerve/chiasm/tract → pretectal nucleus → Edinger-Westphal nuclei.
  • Efferent: Edinger-Westphal nucleus → oculomotor nerve → ciliary ganglion → short ciliary nerves → constrictor pupillae muscle → pupillary constriction.
  • Afferent stimulation on one side stimulates efferent pathways bilaterally, causing constriction in both eyes.

Defects of the Afferent Pathway

  • Weak pupillary constriction in both eyes when the affected eye is stimulated but normal constriction when the other eye is stimulated. (e.g., damage to left optic nerve)

Swinging Torch Test and RAPD

  • Relative Afferent Pupillary Defect (RAPD): Partial pupillary response when damaged side is stimulated.
  • Swinging torch test: Alternating light stimulation.
    • Pupils constrict when light swings to undamaged side; paradoxically dilate when light swings to damaged side.
  • Causes: Optic neuropathy, retinal damage.

Defects of the Efferent Pathway

  • Anisocoria: Unequal pupil size due to sympathetic or parasympathetic damage.
    • Examples: Horner’s syndrome (sympathetic damage), CN III palsy (parasympathetic damage).
  • Damage to left CNIII: Left pupil doesn't constrict regardless of which eye is stimulated; right pupil constricts normally.

Near Reflex

  • Adaptation for near vision; near response triad:
    • Pupillary constriction.
    • Convergence.
    • Accommodation.
  • Pathway: Visual pathway → visual cortex → frontal cortex → oculomotor nucleus and Edinger-Westphal nucleus → ciliary ganglion → short ciliary nerves → constrictor pupillae.

Visual Pathway Anatomy

  • Eye → Optic Nerve → Optic Chiasm (partial decussation) → Optic Tract → Lateral Geniculate Nucleus (LGN) → Optic Radiation → Visual Cortex.

Retina

  • First order neurons: Rods and Cones.
  • Second order neurons: Bipolar cells.
  • Third order neurons: Ganglion cells (→ Optic nerve).
    • Destination: Lateral geniculate nucleus (LGN) in the thalamus.

Optic Chiasm

  • Lesions anterior to chiasm affect one eye; posterior lesions affect both.
  • Partial decussation: 53% of fibers cross.
    • Crossed fibers (nasal retina) for temporal visual field.
    • Uncrossed fibers (temporal retina) for nasal visual field.

Retro-chiasmal Visual Pathway

  • Optic tracts: Connect chiasm to LGN (fibers from ipsilateral temporal retina and contralateral nasal retina).
  • Lateral geniculate nucleus: Receives input from both retinas.
  • Optic radiations: LGN to visual cortex.

Primary Visual Cortex

  • Location: Calcarine sulcus in occipital lobe (striate cortex).
  • Superior visual field projects below calcarine fissure; inferior field above.
  • Right hemifield projects to left cortex; left hemifield to right cortex.
  • Large area represents macula (posteriorly located).

Extrastriate Cortex

  • Surrounds primary visual cortex.
  • Dorsal pathway: Spatial orientation and movement.
  • Ventral pathway: Object/face/color recognition.

Visual Field Defects

  • Optic nerve lesion: Unilateral defect.
  • Optic chiasm lesion: Bitemporal hemianopia (temporal field defect in both eyes).
  • Posterior to chiasm lesion: Contralateral homonymous field defects.

Additional Notes on Visual Field Defects

  • Bitemporal hemianopia: Often from pituitary gland enlargement.
  • Homonymous hemianopia: Often from stroke.

Macular Sparing Homonymous Hemianopia

  • Damage to primary visual cortex (often stroke) leads to contralateral homonymous hemianopia with macula sparing.
  • Macula has dual blood supply (posterior and middle cerebral arteries).