GENERAL NEUROLOGY

Pupillary response in consciousness disorders

Updated on 25/11/2023, published on 22/11/2023

The primary goals of the neuro-ophthalmic exam are to determine the etiology, location, and severity of the consciousness disorder

Normal pupils

  • normal pupils are round and regular, equal in size (isocoric) under both light and dark illumination   Normal pupils
    • in adults, the typical pupil size ranges from 2 to 4 mm in diameter in bright light and 4 to 8 mm in the dark
  • normal direct and consensual response to light stimulus
    • pupils constrict to direct illumination (direct response) and the illumination of the fellow eye (consensual response)
    • in darkness, the pupils dilate
  • an intact near response (accommodation reflex)
    • the test requires voluntary effort
    • both pupils constrict when the eyes focus on a near object, accompanied by accommodation (lens thickening and eye convergence
  • absence of a RAPD

Pupillary light reflex

  • the pupillary light reflex (PLR) is easily tested in unconscious patients:
  • first, observe the pupil size in ambient and dim lighting to check for anisocoria
  • shine a bright light into one eye and then alternate between each eye, observing the reactivity of both pupils
  • note if the pupils react briskly, sluggishly, or show no response
  • a relative afferent pupillary defect (RAPD) can be detected by swinging the flashlight from one eye to the other

Abnormal pupils

  • abnormal pupil shape
    • an oval pupil in a comatose patient is always indicative of a midbrain lesion or compression   Oval pupil due to mesencephalic hemorrhage
    • rule out other causes like ocular surgery, trauma, acute glaucoma, or congenital conditions   Post-cataract surgery defect
  • inadequate miosis or mydriasis  Uncal herniation
    • bilateral, small but reactive pupils are nonspecific
      • may suggest a metabolic etiology, diencephalic lesion, or the effect of certain toxins/drugs
    • bilateral nonreactive mydriasis can indicate midbrain lesions or bulbar coma
  • anisocoria  Anisocoria
    • unilateral mydriasis
      • uncal herniation – compression of the N III e at the Kernohan notch with the ipsilateral (rarely contralateral) nonreactive mydriasis (Hutchinson pupil)   (Agrawal, 2020)
      • any compressive lesion along the third nerve (e.g., ruptured posterior communicating artery aneurysm) may cause ophthalmoparesis with nonreactive mydriasis
      • exclude pharmacologic dilation (administration of topical 1% pilocarpine will not constrict an atropinized, pharmacologically dilated pupil)
    • unilateral, small but reactive pupil
      • Horner syndrome is caused by damage to the ipsilateral oculosympathetic pathway
        • the descending pathway from the hypothalamus to Budge´s ciliospinal center in the C8-T2 segments of the spinal cord
        • ascending sympathetic chain that returns to the internal carotid artery, the cavernous sinus, cranial nerve VI, and then via CN V1 to the eye
        • anisocoria worsening in the dark and mild ipsilateral ptosis (semiptosis) support the diagnosis of Horner syndrome (confirmation using cocaine drops is possible )
  • abnormal reaction to light
  • absent accommodation reaction
  • light-near reflex dissociation
    • an impaired pupillary light reaction while the near reaction remains intact
    • unilateral or bilateral (dorsal midbrain lesion)
diencephalon
  • homolateral miosis of 2 mm, hemianhidrosis, and often ptosis, i.e., central Horner syndrome due to a lesion of the subthalamic sympathetic center and the initial segment of the efferent pathway for pupillodilation
  • light reflex is preserved
  • bilateral miosis in thalamic hemorrhages is caused by a defect in the central inhibitory impulses to the Edinger-Westphal (E-W) nucleus
mesencephalon
(midbrain)
  • tectum/pretectum lesion

    • no light reaction with preserved accommodation response (light-near dissociation)
    • preserved ciliospinal (CS) reflex
    • isocoria with mydriasis 4-6 mm
  • tegmental lesions

    • damage to the E-W nucleus and sympathetic and parasympathetic pupillomotor pathways
    • pupils are distorted, often anisocoric, 3-5 mm or mydriatic (depending on the preservation of sympathetic tracts)
    • pupillary light reflex and ciliospinal reflex are absent
    • unilateral tegmental lesion with mydriatic, reactive homolateral pupil, and contralateral hemiparesis may mimic the temporal cone. A distinguishing feature may be the preserved frontoorbicular reflex
  • compressive lateral mesencephalic syndrome (uncal herniation)
    • progressive homolateral mydriasis 5-9 mm (Hutchinson´s pupil)
    • initially, the light reaction is preserved; later, the pupil becomes nonreactive and external oculomotor paresis with ptosis follows
      • predominant pupillomotor involvement in the initial stage of CN III compression is due to anatomical predisposition – pupillomotor fibers, located on the upper dorsomedial side of the oculomotor nerve, are compressed against surrounding structures
pons
  • primary pontine lesions
    • bilateral miosis ( pinpoint pupils) ~ 1 mm
    • due to lesion of sympathetic pupillodilator pathways with facilitation of intact pupilloconstrictor fibers
    • the light reaction is preserved
    • as the pontine hemorrhage progresses, the pupils dilate and become nonreactive (probably due to the extension of the lesion into the midbrain)
  • pontine stage of rostrocaudal deterioration syndrome
    • pupils are nonreactive, diameter 3-5 mm
medulla
oblongata
  • lateral bulbar lesions
    • ipsilateral Horner syndrome with 1-2 mm miosis
    • the light reaction is preserved
  • terminal stage of rostrocaudal deterioration (bulbar coma)
    • bilateral nonreactive mydriasis (induced by systemic norepinephrine washout due to anoxia)

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