Tunnel vision and macular sparing

 I used to think psychogenic at once, then I added migraines to the differential. Of course, there are plenty of organic reasons to develop tunnel vision and the differential should be stratified along the duration of symptoms. There seems to be no proper literature on this neuroophthalmological classic, except for the few sentences every textbook spends on psychogenic visual field disturbances. Here is what I came up with after reading case reports:

Functional cerebral

  • Psychogenic
  • Migraine

Vascular (see below for a more extensive discussion)

  • Bilateral PCA stroke – typically post top-of-the-basilar
  • Hemodynamic disturbance in the vertebrobasilar area, when no posterior communicating arteries are present
  • Near death experience in cardiac standstill


  • Retinitis pigmentosa
  • Chorioretinitis
  • Glaukoma
  • Pseudotumor cerebri
  • AION

Chiasma lesions (produce incomplete tunnel vision)

  • Pituitary adenomas


A few words on macular sparing field defects: the literature is not consistent about the anatomical and physiological basis of this phenomenon. Yet it exists. Several explanations have been put forward.

  1. Artifact: it might be an artifact due to the way field defects are proven – perimetry. But more advanced methods tend to also show macular sparing.
  2. Retinal overlap: both retinal hemifields might give have fibers of the other halves’ macular region – this is very hard to prove.
  3. Bilateral representation: this should be due to an early crossing branch of the optic tract or radiation.
  4. Vascular: myth has it that the occipital pole is supplied by early branches of the PCA or branches of the Sylvian artery (coming from the MCA). While the latter seems to be rare in the only existing studies (see reference below), the former could be more frequent. The visual cortex is supplied by  four main branches of the PCA: the anterior and posterior temporal arteries, the parietooccipital artery and the calcarine artery.

Reference: here is a cool article on the history and theory of macular sparing.


Unilateral mydriasis

This is a straightforward diffential, so that you won’t find any recent reviews on the topic. We are stuck with our textbooks – you can probably judge the  quality and the uptodateness of your favorite textbook by it’s handling of this classic question.

Here are some remarks:

  •  Anisokoria: You can use apraclonidine if you have it to find out which side is the bad one.
  • Pathologically small: DD of Horner’s – too broad (separate CME session)
  • Pathologically big: can be pharmacological (use Pilocarpine to prove that further anti-M3 doesn’t change the big pupil), ophthalmological (use slit slamp), Adie’s/Ross syndrome or symptomatic ciliar ganglion disease (only after reinnervation the denervated pupil becomes tonic and accommodating, whereas in the acute phase often both is not true), peripheral oculomotor (compression mostly, can occur w/o other third nerve problems), mesencephalic.