3.1.9 Assesses pupil reactions.

Question 1

How do we assess pupils?

Answer 1

• Dim but DO NOT turn off the room lights, explain to patient
• Assess D=N
• THEN do swinging flashlight to assess RAPD. This is to compare the relative strengths of the signals reaching the brain from the eyes hence why RAPD can be detected
• DO NOT block the view of the spot target with your head or body, otherwise they will accommodate!
• can be quantified using neutral density filters but nobody really does this!

Question 2

Bilateral RAPD?

Answer 2

• If the condition is bilateral and symmetrical, there will not be a RAPD but bilateral APD
• Afferent pupillary defects do not cause anisocoria (different pupil sizes), but may produce abnormal pupillary light reflexes. Efferent pupillary defects produce anisocoria and are caused by lesions to the motor neurone system, which carries signals from the central nervous system to the iris via the third cranial nerve.

Question 3

Cause of RAPD

Answer 3

• Optic nerve ischaemia, compression, optic neuritis, asymmetric glaucoma
• Large RD
• CRAO or Ischaemic CRVO

Question 4

Absolute Afferent Pupillary Defect:

Answer 4

• Involved eye is completely blind i.e. no LP
• Both pupils equal in size
• No reaction to light so no direct or consensual of affected eye
• Near reflex normal though and working eye will cause direct & consensual response?

Question 5

Abnormalities of the pupil such as anisocoria is in College management guidelines

Answer 5

• Must know about how pupils react in each syndrome
• argyll - accomodating but reactionless
• horners - looks like 3rd nerve palsy but doesn’t have motility issues, sympathetic problem so ptosis, small pupils (less contraction). This condition can happen the other way around

Question 6

Physiological Anisocoria

Answer 6

• No underlying cause, Longstanding, Increased prevalence with age, between 0.5-1.00mm
• Degree of anisocoria stays relatively constant in light & dark

Question 7

Tonic (Adie’s) Pupil

Answer 7

• No underlying cause (normally) but can be caused by infection, trauma or surgery (SIT) to ciliary ganglion. Sometimes in Sjogrens syndrome
• Caused by parasympathetic denervation at the level of the ciliary ganglion (bundle of neurons)
• When associated with absent or poor tendon reflexes known as Holmes-Adie syndrome
• Associated in women, aged 20-40
• SYMPTOMS:
  
  • Sudden blurring of vision
  • Photophobia
• SIGNS:
  
  • Pupil may become smaller with time
  • May be oval shaped or have segmental constriction
  • Unilateral - fellow pupil may be involved later
  • Affected pupil normally does not constrict very much or not at all in response to direct light. Non affected eye will react to light but consensual response may not be as visible

Question 8

Horner’s Syndrome

Answer 8

• Congenital or acquired
• Caused by interruption of the oculosympathetic innervation at any point along the neural pathway from the hypothalamus to the orbit
• Potential causes in adults include neoplasia, demyelination and carotid artery disease. May occur after surgery (for example, to the neck)
  
  • In children, birth trauma is the most common cause of Horner’s syndrome.
• SIGNS:
  
  • TRIAD: 1. MIOSIS 2. PTOSIS 3. ANHYDROSIS
    
    • Mild ptosis is due to a weakness of Muller muscle
      Elevation of the lower eyelid is due to a weakness of the inferior tarsal muscle
      Miosis is due to the unopposed action of the sphincter pupillae (used to constrict pupil parasympathetically)
  • Dilation lag of miosed pupil - turn lights off, wait a minute, then whilst it is dark, shine light into previously miosed eye & it won’t constrict as much as you might expect
  • Anisocoria more pronounced in dark - normal pupil dilates quick whilst the affected one takes its time but once there, it becomes less pronounced
  • Anhydrosis varies to being whole half of face or small patch depending on lesion location
  • Reduced IOP on affected side
  • If it occurs early in life, then iris heterochromia possible
  • Pupil responses normal, just lagged dilation!

Question 9

Argyll Robertson Pupil

Answer 9

• Associated with neurosyphilis (normally near final stage of disease). Diabetes & MS, Encephalitis, Myotonic dystrophy
• Often irregular shape to pupils
• Attenuated response to topical mydriatics
• Thought to result from a lesion in the midbrain that disables the pathway for the pupillary light reflex but does not affect the more ventral (nearer the front of the brain) pathway mediating the near reaction
• In bright light neither pupil constricts, but on accommodation (near target) both constrict
• In dark conditions, lack of dilation

Question 10

MANAGEMENT

Answer 10

• Good to take photographs if monitoring anisocoria
• Patients with suspected Horner’s syndrome may require MRI of the brain with contrast, as well as CT or MRI of the chest and neck
• Suspected Argyll Robertson pupil requires serological tests for syphilis
• Physiological anisocoria or Tonic pupil require no referral normally

Question 11

Compare the pupillary signs of the conditions:

Answer 11

• Physiological anisocoria: Unequal pupil sizes 0.5-1mm, asymmetry, similar in light/dark
• Tonic pupil: affected pupil larger, decreased response to light but normal near response. Idiopathic, when associated with poor tendon reflexes: Holmes adie syndrome
• Horner’s syndrome: Miosis of affected pupil. Mild ptosis and anhydrosis on affected side, heterochromia if congenital.
• Argyll-Robertson pupil: Bilateral miosis, minimal or no reaction to light but normal near response. Can be associated with neurosyphilis.