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Articles > The Physiological 'Blind Spot' as a Measure of Cortical Activation


24 Aug 2010

 

The Physiological ‘Blind Spot’ as a Measure of Cortical Activation
Functional Neurology for Practitioners of Manual Therapy page 17-18
Randy W. Beck, BSc (Hons), DC, PhD, Clinical Director Murdoch University
Chiropractic Clinic, Perth, Australia

 

 


A visual image inverts and reverses as it passes through the lens of the eye and
forms an image on the retina. Image from the upper visual field is projected on
the lower retina and from the lower visual field on the upper retina. The left
visual field is projected to the right hemiretina of each eye in such as fashion
that the nasal hemiretina of the left eye and the temporal hemiretina of the right
eye receive the image. The central image or focal point of the visual field falls
on the fovea of the retina, which is the portion of the retina with the highest
density of retinal cells and as such produces the highest visual acuity. The fovea
receives the corresponding image of the central 1°- 2° of the total visual field but
represents about 50% of the axons in the optic nerve and projects to about 50%
of the neurons in the visual cortex.


The macula comprises the space surrounding the fovea and also has a relatively
high visual acuity. The optic disc is located about 15° medially or towards the
nose on each retina and is the convergence point for the axons of retinal cells as
they leave the retina and form the optic nerve. This area although functionally
important has no photoreceptors. This creates a blind spot in each eye about
15° temporally from a central fixation point.


When both eyes are functioning, open, and focused on a central fixation point,
the blind spots do not overlap so all the visual field is represented in the cortex
and one is not aware of the blind spot in one’s visual experience. The area of
the visual striate cortex which is the primary visual area of the occipital lobe,
representing the blind spot and the monocular crescent which are both in the
temporal field, does not contain alternating independent ocular dominance
columns. This means that these areas only receive information from one eye. If
you close that eye, the area representing the blind spot of the eye that remains
open will not be activated due to the lack of receptor activation at the retina.


It would be expected that when one eye is closed the visual field should now
have an area not represented by visual input and one should be aware of the
absence of vision over the area of the blind spot. However, this does not occur.
The cortical neurons responsible for the area of the blind spot must receive
stimulus from the other neurons that create the illusion that the blind spot is not
there. This is indeed the case and is accomplished by a series of horizontal
projection neurons located in the visual striate cortex that allow for neighboring
hypercolumns to activate one another.


The horizontal connections between these hypercolumns allow for perceptual
completion of ‘fill in’ to occur (Gilbert & Wiesel 1989; McGuire et al 1991).
The blind spot is therefore not strictly monocular, but it is dependent on the
frequency of firing of horizontal connections from neighboring neurons. These
may be activated via receptors and pathways from either eye.


Perceptual completion refers to the process whereby the brain fills in the region
of the visual field that corresponds to a lack of visual receptors. This explains
why one generally is not aware of the blind spot in everyday experience.


The size and shape of the blind spots is dependent to some extent on the Central
Integrative State of the horizontal neurons of the cortex that supply the stimulus
for the act of completion to occur. The integrative state of the horizontal
neurons is determined to some extent by the activity levels of the neurons in the
striate cortex in general. Several factors can contribute to the CIS of striate
cortical neurons; however, a major source of stimulus results from
thalamocortical activation via the reciprocal thalamocortical optic radiation
pathways involving the lateral geniculate nucleus (LGN) of the thalamus.


Only 10-20% of the projections arriving in the LGN nucleus are derived directly
from the retina. The remaining projections arise from the brainstem reticular
formation, the pulvinar, and reciprocal projections from the striate cortex.


It is clear from the above that the majority of the projection fibers reaching the
LGN are not from retinal cells. This strongly suggests that the LGN acts as a
multimodal sensory integration convergence point that in turn activates neurons
in the striate cortex appropriately. The level of activation of the LGN is
temporally and spatially dependent on the activity levels of all the multimodal
projections that it receives.


In 1997, Professor Frederick Carrick discovered that asymmetrically altering the
afferent input to the thalamus resulted in an asymmetrical effect on the size of
the blind spot in each eye. The blind spot was found to decrease on the side of
increased afferent stimulus. This was attributed to an increase in brain function
on the contralateral side due to changes in thalamocortical activation that
occurred because of multimodal sensory integration in the thalamus.


The stimulus utilized by Professor Carrick in his study was a manipulation of the
upper cervical spine which is known to increase the FOF of multimodal neurons
in areas of the thalamus and brainstem that project to the visual striate cortex.
These reciprocal connections lower the threshold for activation of neurons in the
visual cortex.


By decreasing the threshold for firing of neurons in the visual cortex the blind
spot became smaller because the areas surrounding the permanent geometric
blind spot zone is more likely to reach threshold and respond to the receptor
activation that occurs immediately adjacent to the optic disc on the contralateral
side. The size and shape of the blind spot will also be associated with the
degree of activation of neurons associated with receptors adjacent to the optic
disc. The receptors surrounding the optic disc underlie the neurons that form
the optic nerve exiting by way of the optic disc.

The amplitude of receptor potentials adjacent to the optic disc may therefore also be decreased due to
interference of light transmission through the overlying fibers even though they
should have lost their myelin coating during development; otherwise,
interference would be even greater. This interference results in a decreased
receptor amplitude, which in turn results in decreased FOF of the corresponding
primary afferent nerve. This may result in a blind spot physiologically larger than
the true anatomical size of the blind spot.


This lead to the understanding that the size and shape of the blind spots could
be used as a measure of the CIS of areas of the thalamus and cortex due to the
fact that the amplitude of somatosensory receptor potentials received by the
thalamus will influence the FOF of cerebellothalamocortical loops that have been
shown to maintain a CIS of the cortex.


Therefore, muscle stretch and joint mechanoreceptor potentials will alter the FOF
of primary afferents that may have an effect on visual neurons associated with
the cortical receptive field of the blind spot when visual afferents are in a steady
state of firing. Professor Carrick proposed that ‘A change in the FOF of one
receptor-based neural system should effect the central integration of neurons
that share synaptic relationships between other environmental modalities,
resulting in an increase or decrease of cortical neuronal expression that is
generally associated with a single modality’ (Carrick 1997).


Care should be taken not to base too much clinical significance on the blind spot
sizes until any pathological or other underlying cause that may have resulted in
the changes in blind spot size are ruled out. The blind spot has been found to
increase in size due to the following conditions;
 Multiple evanescent white dot syndrome;
 Acute macular neuroretinopathy
 Acute idiopathic blind spot enlargement (AIBSE) syndrome;
 Multifocal choroiditis;
 Pseudo presumed ocular histoplasmosis;
 Peripallary retinal dysfunction; and
 Systemic vascular disease.


An ophthalmoscopical examination is therefore an important component of the
functional neurological examination.

Randy W. Beck, BSc (Hons), DC, PhD

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