Visual Pathways Flashcards

1
Q

What and where are the components of the visual pathway? What can be the effect of tumours in any of these components?

A
  • The optic nerve goes from the eye
  • The two optic nerves meet at the optic chiasm.
  • The axons pass through the optic chiasm and form the optic tract.
  • The optic chiasm lies immediately above the pituitary: pituitary tumours cause bilateral loss of peripheral receptive fields
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2
Q

Where do axons from cells in the lateral geniculate nucleus project to?

A

Axons from cells in the lateral geniculate nucleus project to the visual cortex (striate cortex) via the optic radiation. The axons from the lateral geniculate cells project anteriorly and then posteriorly along the side of the posterior horn of the lateral ventricle eventually to reach the occipital cortex. The primary visual cortex is known as the striate cortex or area 17

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3
Q

Why is the visual cortex called area 17?

A
  • Korbinian Brodmann (1868 - 1918) was a German neuroanatomist who became famous for his division of the cerebral cortex into 52 distinct anatomical regions from their cytoarchitectonic (histological) characteristics. These areas are now usually referred to by the numbers Brodmann gave them.
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4
Q

What is conscious visual perception and how is it mediated?

A
  • Conscious Visual perception is mediated by the lateral geniculate-occipital cortex pathway. If this pathway is damaged (eg by an infarct in the posterior cerebral artery, a person will be blind.
  • Cells in the primary visual cortex send cortico-cortical axons into the surrounding ‘visual association cortex’ (areas 18 & 19) which is where the data from the retina is converted into conscious perception

See diagram in lecture notes

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5
Q

What project to the superior colliculi, what are they necessary for and what do they connect to? How is it tested? What can damage to the superior colliculis cause? Which tract arises here and what does this mediate?

A
  • Some optic nerve fibres project to the superior colliculi in the midbrain. The superior colliculi are necessary for the ability to track a moving object. (You test this when you ask someone to follow your finger with their eyes). The superior colliculi connect to the medial longitudinal fasciculi (MLF) which links together and synchronises the oculomotor nuclei.
  • Damage to the superior colliculus pathway means that a patient has difficulty tracking a moving object.
  • Remember the tectospinal tract TST arises in superior colliculi and mediates neck reflexes triggered by seen objects

See diagram in lecture notes

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6
Q

How is visual perception mediated? How is visual fixation and tracking mediated?

A
  • Visual perception is mediated by cortical pathways through area 17
  • Visual fixation and tracking is mediated by the superior colliculus acting on the oculomotor nuclei and the neck muscles via the tectospinal tract

See diagram in lecture notes

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7
Q

What is Meyer’s loop? Where do these fibres travel? What can damage Meyer’s loop?

A
  • Fibres in the optic radiation mediating vision from the upper quadrants loop more anteriorly around the side of the lateral ventricle. This path is known as Meyer’s Loop. Fibres mediating vision from the lower quadrants travel more directly back to the visual cortex. Strokes or tumours can sometimes selectively damage Meyer’s loop on one or other sides of the brain

See diagrams in lecture notes for nature of damage

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8
Q

Which visual fields do each eye contribute to? How is each visual field see?

A

Both eyes contribute to both visual fields.

  • Everything to the left of your fixation point in both eyes is called the left visual field. It is seen by the right visual cortex
  • The left visual field projects to the right visual cortex and vice versa.
  • How does this happen? The nasal hemiretina from the left eye projects to the right visual cortex; the temporal hemiretina from the right eye projects to the same right visual cortex. Both hemiretinae view objects in the left visual field.

See diagram in lecture notes

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9
Q

What are the 7 types of optic lesions and how are they caused?

A
  • 1 Partial optic nerve lesion: Ipsilateral scotoma*
    o (*A scotoma is a patch of blindness).
  • 2 Complete optic nerve lesion: Blindness in that eye
  • 3 Optic chiasm lesion: Bitemporal hemianopia
  • 4 Optic tract lesion: Homonymous hemianopia
  • 5 Damage to of Meyer’s Loop: Homonymous upper quadrant anopia
    o (axons are arranged with upper part of visual field anterior)
  • 6 Optic radiation lesion: Homonymous hemianopia
  • 7 Visual cortex lesion: Homonymous hemianopia (Macular sparing)
    o The central parts of the eye (macula and fovea) have a bilateral projection to the visual cortex, so a lesion on one side will often not affect central vision; this is called macular sparing

See diagram in lecture notes

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10
Q

What pathway mediates the visual recognition (perception) of an object? What does damage to this pathway cause? What else does these pathways mediate?

A
  • The visual cortical pathway mediates the visual recognition (perception) of an object. If this pathway is damaged the person is blind. In a very few cases however despite loss of visual cortex (due to a stroke) a patient will insist they can still see (although they cannot). This strange condition is called Anton-Babinski syndrome. No-one knows why it happens. The patient’s brain believes they can still see, so the brain makes up (confabulates) their visual surroundings.
  • The visual pathways to the brain stem mediate visual reflexes. These can persist although visual perception does not exist.
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11
Q

You need to know the neuroanatomy and physiology of certain key visual reflexes. What are these reflexes?

A

o The pupillary light reflex
o The accommodation reflex
o The vestibulo-ocular reflex
o The blink reflex

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12
Q

Which nerves mediate the visual reflexes?

A

III, IV, & VI Oculomotor nerves

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13
Q

Which nuclei and fibres are involved in the pupillary light reflex? Which muscles do these act on? What are the key points to remember about this reflex?

A
  • Axons in the optic nerve project to the pretectal nuclei and then bilaterally to the Edinger-Westphal nuclei.
  • Parasympathetic preganglionic fibres project from the E-W nuclei to the ciliary ganglia in the orbit behind each eye. From here postganglionic fibres enter the eye and act on sphincter muscles around the pupil to constrict it. This is the pupillary light reflex.
  • Key points:
    o a) Remember the mnemonic “In on II, out on III”.
    o b) Remember this is a ‘consensual’ reflex in that stimulation of one eye produces constriction in both eyes
    o c) Remember Atropine (muscarinic antagonist drug) blocks the pupillary light reflex.

See diagrams in lecture notes

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14
Q

When can the accommodation reflex occur? What is it controlled by? What are the three components of this reflex?

A
  • Accommodation is an act of will and can only occur in a conscious person. It is controlled by the Frontal Eye Fields (FEF) which are specialised parts of the premotor area that are dedicated to motor control of the extraocular eye muscles Damage to FEFs leads to an inability to direct gaze from one object to another. (Also loss of fast phase of nystagmus)
  • This reflex has three components:
    o Thickening of lens
    o Convergence
    o Pupil constriction
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15
Q

How is thickening of the lens achieved during the accommodation reflex?

A
  • When viewing a distant object the ciliary muscle sphincter is relaxed and the lens is under tension from a ring of suspensory ligaments which pull on it to stretch and flatten it. In the accommodation reflex the ciliary muscle contracts and opposes the tension in the suspensory ligaments
  • When this tension is reduced the lens thickens passively towards its wider relaxed shape. This wiser lens enables the eye to focus on nearby objects
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16
Q

How is convergence of the eyes achieved during the accommodation reflex?

A
  • Convergence is controlled from frontal eye fields. It involves simultaneous activity in the medial rectus muscles on each side. This convergence is mediated by the oculomotor nerve (CN III) bilaterally.. Convergence cannot be triggered in an unconscious patient.
  • The convergence part of the accommodation reflex is very delicate and can be disturbed by fatigue, trauma, alcohol, drugs, etc.
  • If it occurs incorrectly or not at all we see double; this is diplopia
17
Q

How is pupil constriction achieved during the accommodation reflex?

A
  • a) Pupillary constriction: output pathway is same (CN III) pathway as for pupillary light reflex. Input to cause this constriction is from descending projections from frontal eye fields in premotor cortex.
  • Why is there pupillary constriction when viewing near objects?
  • Pupillary constriction improves focusing on objects closer than the ‘near point’
  • The near point is the nearest point seen clearly when lens is at maximum convexity (technically pupil constriction improves ‘depth of field’)
18
Q

What is the vestibulo-ocular reflex (VOR) and which nerves are involved? What happens when this reflex is absent?

A
  • If you turn your head to the side while looking at a distant object your eyes rotate in the opposite direction to the head to keep the direction of gaze constant and the object kept in view.
  • This is the vestibulo-ocular reflex (VOR). The input (afferent) arc of this reflex is the vestibulo-cochlear nerve (CN VIII) which receives signals from the semicircular canals. The output is the abducens nerve (CN VI) and the oculomotor nerve (CN III).
  • The vestibulo-ocular reflex is sometimes called ‘dolls eye reflex”. It is tested by holding someone’s eyes open and gently rotating the head from side to side; in a normal person the eyes should rotate in the head to keep the gaze direction constant. With the reflex absent (as below) the eyes stay fixed in the head.
  • It is important to realise that the VOR involves the oculomotor nerve in one eye (the one moving inwards) and the abducens nerve in the other eye (moving outwards). This is another example of co-operation between oculomotor nuclei mediated by the medial longitudinal fasciculus
  • This is a YouTube video nicely illustrating some normal eye movements and the vestibulocular reflex https://www.youtube.com/watch?v=rRDDKKqkdTg
19
Q

How do you test the vestibulo-ocular reflex?

A

Testing the vestibulo-ocular reflex: The Caloric Stimulation Test

  • Warm water is irrigated into the external auditory canal with a syringe. The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal.
  • In a normal subject:
  • If the water is warm (44°C or above) this mimics a head turn to the ipsilateral side. Both eyes will turn slowly away from the irrigated ear toward the contralateral ear, followed by horizontal fast flick (nystagmus) towards the irrigated ear.
  • If the water is cold (30°C or below), this mimics a head turn to the contralateral side. The eyes then turn slowly toward the ipsilateral ear, with horizontal fast flicks towards the non-irrigated ear.
  • Direction of flick is given by ‘COWS’.
  • Cold=flick to other ear: Warm=flick to same ear.
  • MUST SEE VIDEO!! Doing Caloric test on a med student: https://www.youtube.com/watch?v=Vo00ZYOXDrQ
20
Q

What is nystagmus and how can it be elicited?

A
  • Nystagmus is a form of the VOR caused by continuing rotation of fluid in the semicircular canals. It shows as an initial slow rotation followed by a fast flick back. The direction of the nystagmus is always given by the direction of the fast flick.
  • Nystagmus can be elicited by spinning someone around for a few minutes (eg on a rotating chair). The fluid in the semicircular canals has inertia and does not at first rotate, but after a while friction with the walls starts the fluid rotating. When the rotation stops the fluid continues to rotate for a while, inducing post-rotational nystagmus. The slow component of the nystagmus follows the movement of the fluid, so the direction of the fast phase of the nystagmus is against the direction of rotation
    (see picture in notes)
  • Example of (optokinetic) nystagmus: note slow movement to right of picture followed by fast flick back to left
21
Q

What is the purpose of the blink reflex and which nerves contribute to its input and output?

A
  • Protects eyes from foreign bodies (grit etc)
  • Input: sensory nerve endings in cornea or conjunctiva; these are branches of the ophthalmic branch (V1) of the trigeminal (V) nerve.
  • Output: motor fibres in the facial (VII) cranial nerve to the obicularis oculi muscle which pushes the eyelids together.
22
Q

Summarise the key eye reflexes.

A
  1. Pupillary constriction (light) reflex. Consensual.
  2. Vestibulo-ocular reflex (VOR)
    o When we move our head while looking at an object our eyes automatically move to compensate for the head movement. This is the VOR.
    o If rotation continues further than eyes can move, a single nystagmus occurs to flick eyes to new fixation point.
  3. Accommodation reflex (only in conscious subject)
    o When viewing near objects, get:
    a) accommodation (thickening of lens)
    b) convergence
    c) pupillary constriction.
    - Caloric testing for vestibulo-ocular reflex COWS:
    o Cold Opposite, Warm Same. Cold water = FAST phase of nystagmus to the side Opposite from the cold water filled ear, Warm water = FAST phase of nystagmus to the Same side as the warm water filled ear.