Macular sparing

Macular sparing is when the central 5-10 degrees of the visual field is unaffected in an otherwise hemianopic defect( a defect that affects one half of the field, if its two half of the temporal affected, it is bitemporal hemianopic and likewise for nasal). It is a common characteristic of visual field defects arising from supra- geniculate lesions.

Numberous explanations have been put forward to account for macular sparing, many of which have now been refuted as new evidence has come to light. Currently, there are three plausible theories:
(1) Shifts in ocular fixation.
(2) Separate blood supply
(3) Extent of macular representation

Up next, each theories explained.

(1) Shifts in ocular fixation
patients with hemianopic defects may learn to view objects of interest eccentrically in order to ensure that half of it is not lost within the field defect. In fact, such techniques are regularly taught to partially sighted patients with macular lesions. The theory goes that these patients, when asked to look at the fixation target of the perimeter, continue to view slightly to one side, which results in an apparent macular sparing.

Some recent work using a fundus perimeter - an instrument that allows the operator to view the fundus during perimetry and to locate the stimuli at a given retinal site - has demonstrated macular sparing in patients who do not show a shift in fixation( Rohrschneider, 1997). This theory cannot, therefore, explain all cases of macular sparing.

(2) Separate blood supply
The separate blood supplies theory follows from some work done by Smith and Richardson
(1996). They demonstrated two interesting points: (i) in some individuals the occipital pole of the visual cortex is supplied by the middle cerebral artery rather than the posterior cereberal artery and (ii) in some patients, there is a horizontal border at the macular between the areas supplied by the posterior temporal artery ( a branch of the posterior cerebral artery) and the area supplied by the middle cerebral artery.

Both these findings could explain macular sparing. If an occlusion occurs in either the posterior cerebral artery in a patient whose macular area is supplied by the middle cerebral artery, or in a branch of the posterior cerebral artery which does not supply the macular area, then some macular sparing would result. Some clinical evidence supporting the latter explanation has been provided by Ehlers (1957), who reported on eight cases in which the macular sparing was confined to either the upper or lower quadrant.

The separate blood supply theory must not be confused with an earlier theory based upon the belief that there is a dual blood supply to the visual cortex. There is no anatomic evidence of a dual blood supply to the visual cortex( Glaser, 1978)

(3) Extent of macular representation
The final theory to explain macular sparing simply states that the macular area has such a large cortical representation that in any incomplete lesion there is a high probability that some of the macular fibres will be left intact.

Please do further research if you are not sure on anything.

With references to David B. Henson PHD, Senior Lectureer ( Ophthalmology), The Medical School, The University of Manchester, Manchester, UK, Visual Fields (second edition), published by BUTTERWORTH HEINEMANN(BH).

Visual pathway defects

As not to be confused with the small 'curved in' portion(macular sparing) in defects of visual pathway, I have posted this for a clearer understanding. Note: lesion 3 is to be ignored as it is different from what we are taught. Up next, macular sparing.
With credits to mona.uwi.edu.

Pupillary pathway

Pupillary pathway

The pupillary reflex can be thought of as an afferent limb, a parasympathetic efferent limb, and a sympathetic efferent limb.

Afferent limb- Light stimulates photoreceptors and the signal is conveyed to a special set of ganglion cells that send their nerve impulses through the axons in a similar topographic distribution as those carrying other signals in the optic nerve (arrow 1 in the figure, please enlarge). Decussation occurs at the optic chiasm (arrow 2 in the figure) for the nasal fibers (arrow 4) . The big difference is that the afferent fibers do not enter the lateral geniculate body(LGN) but instead exit and pass through the brachium of the superior colliculus (arrow 5) where they synapse on the pretectal nuclei (arrow 7). These nuclei project bilaterally to the Edinger Westphal nuclei (arrows 6 and 7) via internuncial neurons by a process that has not been fully elucidated.

Efferent parasympathetic response- The Edinger Westphal nuclei (EWN) send fibers to join the oculomotor CNIII (arrow 8) and follow that course on the dorsomedial surface of the nerve (arrow 9). This is important because this is an outer surface which lies adjacent to the posterior communicating artery and is exposed to forces of herniation. After coursing thru the cavernous sinus these fibers emerge to enter the orbit with the inferior oblique branch of CNIII. These fibers synapse at the ciliary ganglion (arrow 10) and then enter the eye thru short posterior ciliary nerves to distribute fibers to the choroid, iris (arrow 11), and ciliary body. The red nucleus is shown in red and substantia nigra in black. The medial geniculate body is dark gray and medial to the brachium of the superior colliculus. The lateral geniculate body where the fibers responsible for vision will synapse lie lateral to the pupillary fiber pathway in another plane of section.

Efferent sympathetic response- This is believed to start in the hypothalamus and project in an uncrossed fashion with synapses in the mesencephalon and pons. These neurons project to and synapse upon the intermediolateral cell column from C8-T2 in the spinal cord. These exit the spinal cord and pass thru the stellate ganglion to synapse in the superior cervical ganglion. These fibers travel with the internal carotid artery, enter the cavernous sinus and travel with CN VI in the cavernous sinus to enter the superior orbital fissue with cranial nerve V. The fibers travel with the nasociliary branch of V, and pass thru the ciliary ganglion without synapsing. The fibers pass thru the long ciliary nerves to terminate on the dilator muscle. Some fibers diverge in the superior orbital fissue to innervate Muller's muscle.

Clinical significance? These pathways are important for the clinician to understand the basis for a blown pupil with a third nerve palsy. The pupillary fibers are compressed and this is most likely due to an aneurysm that affects the 3rd nerve at the posterior communicating artery.

PERRLA

Measuring of pupil size with PERRLA
PERRLA: Pupils Equal and Round; Reactive to Light and Accommodation
Pupils Equal and Round:




The pupil size is measured in scoptopic condition. The pupils are dilated and diameters of 4.8±1.0mm are observed for both eyes under low light condition.

The pupil size is measured in photopic condition. The pupils are constricted and diameters of 3.3±1.0mm are observed for both eyes under bright light condition. Both of the pupils are round and of the same diameter.

Reactive to Light:



The pentorch is shone onto the subject's eye and the constriction of the pupil is observed through the magnifier. This test is used to assess the reactivity of the pupil towards light.

The near triad test is used in observing the accomodation of the subject's eyes and two other aspects, namely convergence and miosis.

Accommodation - this is the focussing of the eye, which comes about through the change in shape of the lens inside the eye.

Convergence - this is the 'turning inwards' of the two eyes when looking at the object of regard, and it happens so that its image falls onto the fovea of each eye

Miosis - this is the decrease in size of the pupil that accompanies accommodation and convergence. No-one knows why this happens (although the mechanism is clear enough - there are neural links between the control centres of the three responses). It has the effect of increasing the depth of field of the eye, thereby reducing the amount of accommodation needed to see the object clearly, but whether this is by design or is just fortuitous is an unanswered question.

Marcus Gunn Pupil

Marcus Gunn Pupil

Marcus Gunn pupil which is also known as Afferent Pupillary Defect(APD) a condition of the eye where the pupil does not dilate appropriately to the level of light reaching it, resulting in one pupil appearing larger than the other.

Causes

Causes of APD include Optic Neuritis, glaucoma and optic nerve tumour. In multiple sclerosis, APD is usually associated with damage to the optic nerve resulting from Optical Neuritis.

Test

The Swinging Flashlight test is used to diagnose Marcus Gunn pupil, where there are abnormal pupil reflexes. Marcus Gunn pupil can also be seen in eyes with extensive retinal pathology.

Equal pupil size

When the light was shone to the left eye where the arrow is pointing to, it shows left relative afferent pupillary defect.

References and Credits

http://www-staff.lboro.ac.uk/~huph/nt.htm
http://www.wikipedia.com
http://www.mult-sclerosis.org/afferentpupillarydefect.html
http://www.fpnotebook.com/Eye/Exam/SwngngFlshlghtTst.htm
http://www.opt.indiana.edu/riley/HomePage/Pupil_Abnormal/1_Saint_Pupil_Abnormal.html
http://www.mrcophth.com/pupils/rapd.html
http://www.medrounds.org/ocular-pathology-study-guide/2005/11/pupillary-reflex-pathway.html

Header Background picture credit to Cheeky Photography