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PART ONE REVISION. > ANATOMY - Pupil and Pupillary pathways (reflexes) > Flashcards

ANATOMY - Pupil and Pupillary pathways (reflexes) Flashcards

1
Q

What is simple anisocoria?

A

<0.4mm difference in pupil size - present in 25% of the population and may change sides.

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2
Q

What is physiological tremor in pupil known as?

A

Hippus (pupillary athetosis)

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3
Q

What is physiological anisocoria?

A

When the difference in size is usually 1mm in diameter or less
1. pupil size disparity is same in the light as in the dark
2. pupils react normally to light.

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4
Q

If anisocoria is greater in the light, which pupil is abnormal?

A

the larger pupil, the pupil which failed to constrict.

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5
Q

What are the causes of abnormally dilated pupil (ie greater anisocoria in the light?) (4)

A
  1. Traumatic iris sphincter muscle - torn pupillary margin or iris transillumination defects.
  2. Adie Tonic pupil - irregular pupil, reacts minimally to light, and slowly to convergence. Hypersensitivity to pilocarpine 0.125%.
  3. Third nerve palsy - always associated ptosis or extraocular muscle palsies
  4. Mydriasis drops
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6
Q

If anisocoria is greater in the dark, which pupil is abnormal

A

Smaller pupil (pupil fails to dilate).

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7
Q

What are the causes when abnormal pupil is constricted?

A
  1. Uveitis
  2. Horner syndrome - mild ptosis on side of small pupil
  3. Argyll Robertson pupil - bilateral irregularly round miotic pupils but mild degree of anisocoria
  4. Pharmacological miosis
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8
Q

What scenarios does mydriasis occur in ?

What scenarios does miosis occur in? (3)

A

Mydriasis: low light, excitement, fear

Miosis: illumination, convergence, sleep.

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9
Q

What are the effects of pupillary dilation? (5)

A
  1. Reduces depth of field
  2. Reduces depth of focus
  3. Reduced diffraction of light
  4. Increased Stiles-Crawford Effect
  5. Increased chromatic aberration
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10
Q

What is the Stiles-Crawford Effect?

A

Light entering the edge of the pupil is less effective at stimulating photoreceptors than light entering centrally because it meets the receptors obliquely rather than axially.

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11
Q

What is the difference between Stiles-Crawford effect 1 and Stiles-Crawford effect 2?

A

effect 1 - greater stimulus effectiveness (brightness) of a ray passing paraxially compared to a ray entering eccentrically.

effect 2: change in hue and saturation of monochromatic light depending on angle of incidence

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12
Q

What is the latency period of the pupil?

A

Duration from exposure to response - on average 0.2-0.5 seconds

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13
Q

What is the latency period affected by? (2)

A
  1. Light intesity - decreases with increasing light intensity
  2. Accomodation (pupil reacts faster to light than to accomodation)
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14
Q

What is pupil size affected by? (2)

A
  1. Iris colour (blue larger than brown)
  2. Autonomic nervous system (fatigue, exercise, light intensity)
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15
Q

What are the two types of light reflex?

A
  1. The direct pupillary reflex
  2. Consensual pupillary reflex
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16
Q

What is the afferent pathway of the light reflex?

A

FROM RETINA TO PRETECTAL NUCLEUS

  1. Fibres leave tract and synapse in pretectal olivary nucleus near superior colliculus
  2. Each pretectal nucleus only receives ipsilateral input.
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17
Q

What are the 3 pathways of the light reflex?

A
  1. Afferent (from retina to pretectal nucleus)
  2. Internuncial neuron/centre (from pretectal to edinger westphal nucleus)
  3. Efferent (from edinger westphal, third nerve, ciliary ganglion and short ciliary nerve to sphincter pupillae)
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18
Q

What is the role central pathway of the light reflex? (internuncial neurons)

A
  1. Axons from pretectal nucleus nerve cells will cross/synapse towards the edinger westpal nucleus (parasympathetic) of the oculomotor nerve on BOTH sides of the midbrain
  2. Each prectal nucleus will give fibres to both edinger westphal nuclei –> this is responsible for the direct AND consenusal reflex.
19
Q

What is the efferent pathway of the light reflex?

A
  1. Preganglionic fibres travel with oculomotor nerve (through its inferior division to inferior oblique) to ciliary ganglion and synapse
  2. Postganglionic fibres travel in short ciliary nerves to sphincter pupillae muscle and both pupils constrict.
20
Q

What are the causes of an efferent pupillary defect (fixed dilated pupil) (6)

A
  1. Brain stem lesions at level of superior colliculus and red nucleus (accompanied by long tract signs
  2. Third nerve lesions, usually compressive (20% of microvascular palsies involve the pupil)
  3. Ciliary ganglion/short ciliary nerve lesions
  4. Iris damage due to surgery
  5. Grossly elevated IOP
  6. Mydriatic drugs –> pilocarpine will only constrict a pupil affected by a neurological lesion)
21
Q

What conditions can cause RAPD? (3)

A

LESIONS OF RETINA
1. Large retinal detachments
2. Ischaemia (CRVO/CRAO)
3. Dense Macular Lesion

LESIONS OF ANTERIOR OPTIC PATHWAY (retina to pretectal nucleus)
1. Lesions of optic nerve (optic neuropathy, glaucoma)
2. Lesions of optic chiasm
3. Lesions of optic tract
4. Lesions of pretectum

22
Q

Which areas of visual pathway would not be affected by RAPD?

A
  1. Lateral geniculate body
  2. Optic radiations
23
Q

What happens to the affected eye when there is RAPD in light swinging test?

A

Paradoxical dilatation of affected eye, also of consensual eye.

24
Q

What is Reverse RAPD?

A

Used to test efferent defects

Paradoxical dilatation ONLY in CONSENSUAL EYE as AFFECTED eye is FIXED DILATED –> means there is RAPD in fixed dilated eye.

Paradoxical dilatation occurs as does not receive light input from AFFECTED eye for consensual light reflex.

25
Q

What is wernicke’s hemianopic pupil?

A

It is an AFFERENT PUPILLARY DEFECT with a lesion in the OPTIC TRACT which presents with contralateral hemianopia

26
Q

What are the causes of Argyl Robertson Pupil?

A

Lesion in the internucial neurons of the light pathway (in the midbrain) –> specifically the DORSAL (posterior) aspect of the edinger westphal nucleus

27
Q

What is the argyl robertson pupil?

A

It is smaller, irregular in shape,
Little to no constriction to light (absent light reflex) and BRISK near reflex

ARP –> Accomodation reflex present

PRA –> pupillary reflex absent

28
Q

Why are the argyl robertson pupils miotic?

A

There is disruption of the supranuclear/dorsal adrenergic fibres that inhibit the edinger westphal nucleus

therefore… uninhibited parasympathetic neurons of edinger westphal nucleus leads to miosis (spinal miosis)

29
Q

What are the causes of argyll robertson pupil?

A

Diabetes
Neurosarcoidosis
MS
Lyme Disease
Encephalitis
Chronic alcoholism
Tertiary neurosyphilis

30
Q

What is Adie Tonic Pupil (Holmes-Adie Syndrome)

A

It is parasympathetic denervation of the pupil which causes poor/absent light reflex but with near reflex present (tonic reaction)

Adie tonic pupil + decreased deep tendon reflexes

31
Q

What is the cause of adie tonic pupil?

A

Damage to ciliary ganglion –> upregulation of postsynaptic receptors to allow re-innervation –> abnormal/abberant innvervation/regeneration –> tonic miosis on near reflex along with accomodation.

32
Q

How do you diagnose adie tonic pupil?

A

Anisocoria, worsening of anisocoria in light.

Responds supersensitive to 0.125% diluted pilocarpine –> after 30-60 minutes the dilated pupil will now constrict more than the normal pupil

This is because of increased receptors due to denervation hypersensitivity.

33
Q

What is the difference between argyll robertson pupil and adie tonic pupil?

A

Both have light-near dissociation, but argyll robertson the pupil is smaller, in Holmes/Adie the pupil is larger.

34
Q

What are the three main types of aetiologies of Horner’s syndrome?

A
  1. Central brainstem lesions
    (First Order - neuron from hypothalamus terminating at ciliospinal centre of budge)
  2. Preganglionic lesions
  3. Post-ganglionic lesions
35
Q

What are the first order causes of Horner’s syndrome? (7)

A
  1. CVA
  2. Lateral Medullary Syndrome
  3. Arnold-Chiari malformation
  4. Encephalitis/Meningitis
  5. Syringomyelia
  6. Intracranial tumors (pituitary or basal skull)
  7. Spinal trauma above T2/T3
36
Q

What are the pre-ganglionic (second order) causes of Horner’s syndrome (7)

A

From the ciliospinal centre of budge to the superior cervical ganglion at C3/C4 level.

  1. Pancoast tumour (malignancies)
  2. Subclavian artery lesions
  3. Cervical rib injuries
  4. Mediastinal lymphadenopathy
  5. Trauma of branchial plexus
  6. Dental absess involving mandibular region
  7. Iatrogenic - thyroidectomy, CABG
37
Q

What are the post-ganglionic (third order) causes of Horner’s syndrome?

A

From superior cervical ganglion –> V1 of trigeminal nerve –> long ciliary nerve –> sphincter dilator muscle and superior tarsal muscle and sweat glands.

  1. Carotid cavernous fistula
  2. Internal carotid artery dissection / aneurysm
  3. Cluster headache/migraine
  4. Herpes zoster infection
  5. GCA
  6. Raeder paratrigeminal syndrome (unilateral facial pain)
  7. Cavernous sinus thromboss
38
Q

What are the signs of Horner’s syndrome?

A

Miosis - reaction of pupils to light and accomodation is normal

Ptosis - partial due to muller’s muscle involvement and reverse ptosis (lower lid involvement)

Anhidrosis- First order neurons (full body), second order (face), third (ipsilateral brow)

39
Q

When is cocaine used for pharmacological test for Horner’s syndrome? What is the mechanism?

A

For all 1st/2nd/3rd order neurone testing to confirm horner’s –> there is an EXAGERRATION OF ANISOCORIA.

Prevents reuptake of noradrenaline from synapse –> in all 1st/2nd/3rd order cases there is no noradrenaline in the synapse so cannot act therefore Horner pupil does not dilate and normal pupil dilates.

40
Q

When is apraclonidine 0.1% used in testing Horner’s syndrome?

A

causes REVERSAL OF ANISOCORIA –> Horner’s pupil dilates and normal pupil does not dilate.

A2-agonist and weak A-1 agonist –> due to sympathetic denervation –> there is hypersensitivity of A1-Receptor within pupillary dilator muscle to cause DILATATION.

Should not be used in paediatrics due to risk of CNS/respiratory depression.

41
Q

When is Hydroxyamphetamine 1% test used in Horner’s syndrome?

A

THIRD ORDER NEURON - no response

1ST/2ND - the Horner pupil dilates.

Hydroxyamphetamine 1% Releases stored noradrenaline from the third-order neuron pre-synaptic terminal within the iris –> increased dilatation (1st/2nd order)

In 3rd-order neuron, there is a lesion in this neuron, so there is no stored noradrenaline so there is no pupillary response to hydroxyamphetamine drops.

42
Q

When is phenylephrine used in Horner’s syndrome?

A

to confirm location of Horner’s syndrome.

adrenergic agonist –> acts on hypersensitive A-1 receptors so will see dilatation of pupil (in THIRD-ORDER neuron)

There is no denervation hypersensitivty in 1st/2nd order neuron so no dilatation of pupil with phenylephrine

42
Q

Whats the difference between argyll-robertson pupil and Adie pupil?

A

Argyll pupil is small, unresponsive to light, Adie pupil is large, slow responsive to light.

Both pupils have strong near reponse.

Argyll robertson has associated with absent tendon reflexes and iris atrophy.

PART ONE REVISION. (80 decks)

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