Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2817_Библиотеки_им_академика_М_И_Перельмана.pdf
7
‘On’ ganglion cell
‘Off’ ganglion cell
change of approximately 1 mV (by blocking the entry
of approximately 1 million Na+ ions). Thus, the overall response of the photoreceptor depends on the light
intensity; more light, less neurotransmitter. Rods/cones
are paradoxically most active during complete darkness!
The cascade is stopped by several mechanisms:
• TheintrinsicGTPaseactivityoftransducinconverts
GTP to GDP. The inactivation of transducin occurs
by a protein called RGS9 (regulator of G- protein
signalling 9). Inactivated transducin then recombines
with the βγ subunits, stopping the action of
phosphodiesterase.
• Photon-excitedrhodopsinmoleculesareinactivated
by phosphorylation by rhodopsin kinase, and by the
binding of arrestin, a protein whose sole function is to
block interactions between rhodopsin and transducin.
After prolonged exposure to light (a few seconds), the
link between rhodopsin and retinal is hydrolysed and
the all- trans- retinal dissociates. This is called bleaching, and the retinal is converted to retinol (vitamin A).
Vitamin A is reconverted to 11- cis retinal by retinal isomerase in the dark, and this then binds with the opsin to
reconstitute rhodopsin. This restores the sensitivity of the
photoreceptor and underlies dark adaptation.
Contrast detection in the retina: ‘on’ and ‘off’
channels
One crucial element in object recognition by the visual
system involves identifying the edges of objects, usually
by changes in light levels. Connections between bipolar
cells, horizontal cells, and ganglion cells act to increase
contrast between light and dark areas. Therefore, bipolar cells perform the initial data processing in the retina.
They receive input from groups of rods or a single cone.
There are two populations of cone bipolar cells, called
‘on’ and ‘off’ bipolar cells. These respond to input from
cone cells in different ways: ‘on’ cells depolarize and ‘off’
cells hyperpolarize in response to light. Along with the
horizontal cells, they enhance contrast.
There are two types of bipolar cell based on their
structure and response:
• Invaginatingbipolarcellsformspecializedsynapses,
called triad ribbon synapses, with the base of the
photoreceptors. The triad consists of the dendrites
of the bipolar cell and two horizontal cells. These
‘on’ bipolar cells are depolarised by light, due to the
reduced glutamate release from the photoreceptor.
These cells detect patches of brightness.
• Flatbipolarcellsformbasalsynapseswith
photoreceptors. In response to light, these ‘off’ bipolar
cells hyperpolarize. These cells detect dark regions of
the image.
Cone bipolar cells are termed midget bipolar cells, as
they are smaller than rod bipolar cells and depolarize in
response to light. All bipolar cells respond to a reduction
in glutamate release, but their different responses are
due to the different types of glutamate receptor (metabotropic in ‘on’ cells and ionotropic in ‘off’ cells) present in
their cell membranes.
Cone bipolar cells synapse with ganglion cells that
have the same response pattern. That is, ‘on’ bipolar cells
produce an increase in action potential firing rate in their
(‘on’) ganglion cells, and ‘off’ bipolar cells reduce the firing rate in their (‘off’) ganglion cells. This leads to two
channels. In response to light, the ‘on’ channel increases
the ganglion cell- firing rate, and the ‘off’ channel reduces
ganglion firing. So, in the dark, glutamate release inhibits
the ‘on’ channel and excites the ‘off’ channel. In the light,
the reverse happens; a reduction in glutamate excites the
‘on’ channel and inhibits the ‘off’ channel.
Each retinal ganglion cell is affected by light falling
on its circular receptive field (RF). The ganglion cells
show different responses depending on whether light
falls in the centre of the field or in the surrounding ring
(Fig. 7.15). An ‘on’ ganglion cell increases its firing rate
in response to illumination of the centre of its field and
decreases it in response to illumination of its periphery.
In diffuse illumination of both the centre and surround,
there is no change in the firing rate. For an ‘off’ ganglion cell, firing increases with surround illumination,
stops with light on the centre, and is unaffected by diffuse lighting. This property of ganglion cells is shared by
their bipolar cells, but because bipolar cells do not fire
action potentials, it is their graded potentials that vary.
This centre–surround antagonism is mediated in part
by horizontal cells, which, although they do not synapse
directly on bipolar cells, affect the glutamate release from
photoreceptors onto bipolar cells.
A
B
C
Fig. 7.15 Centre–surroundreceptiveeldsofganglioncells. (A)
Centreillumination.(B)Surroundillumination.(C)Diffuseillumination.
THE VISUAL SYSTEM
149THE NERVOUS SYSTEM
7
Less glutamate release
A
glutamate release
Hyperpolarizing
H = horizontal cell
THE VISUAL SYSTEM
Horizontal cells increase the contrast in the retina by
a mechanism called lateral inhibition. Horizontal cells
connect the outputs from neighbouring photoreceptors.
In the dark, they are excited by glutamate released from
the photoreceptors, which stimulates γ- aminobutyric
acid (GABA) release onto neighbouring photoreceptors.
GABA inhibits photoreceptors, reducing their glutamate
release (Fig. 7.16). This means that in response to centre
illumination, a neighbouring photoreceptor, which will
continue to release glutamate, will excite the horizontal
cell. This inhibits glutamate release from the centre photoreceptor, allowing bipolar cells to depolarize further
than they would without the horizontal cell effect. When
the surround is illuminated, the reduction in glutamate
release from the surround photoreceptors reduces GABA
release from the horizontal cell, and so the centre photoreceptor releases more glutamate, causing the centre
Light
C
Glutamate
GABA
‘On’ bipolar
cell
‘On’ ganglion
cell
B
C
Glutamate
‘On’ bipolar
‘On’ ganglion
Fig. 7.16 Horizontal(H)cellsreduceglutamatereleasefrom
neighbouringphotoreceptors. (A)Centreillumination:GABAergic
inhibitionbyhorizontalcellsenhancesthebipolarandganglioncell
responses;(B)surroundillumination:noGABAisreleasedfromthe
horizontalcell,sothe‘on’channelissuppressed.C,Centralcone;S,
surroundingcone.
No GABA
cell
cell
C = centre cone photoreceptor
S = surround cone photoreceptor
H
release
H
S
Depolarizing
response
Increased
firing
Light
S
Less
response
Reduced
firing
bipolar cell to be inhibited. The function of centre–surround inhibition is to exaggerate contrast at borders.
Rod cell signalling via amacrine cells
Rods are connected to depolarizing ‘on’ bipolar cells
that are connected to ganglion cells via amacrine cells.
Amacrine cells are a very diverse population of interneurons whose neurites have properties of both axons and
dendrites and use a wide variety of neurotransmitters to
modify synaptic transmission. They are implicated in rod
signalling, surround inhibition, and the detection of the
direction of motion, particularly in peripheral vision.
Rod signalling depends on light intensity; at high
light levels, rods are saturated, and all signalling occurs
through the cone cells ‘on’ and ‘off’ channels. In lower
light levels, such as at dusk, in the dark- adapted eye,
changes in rod membrane potential are transferred to
neighbouring cone cells through gap junctions to boost
cone function, to maintain colour vision and visual acuity at low light levels. However, at very low light levels, this boosting of cone cells is insufficient to maintain
colour vision, and all vision occurs via rod–amacrine cell
pathways.
Colour responses of retinal ganglion cells
Like bipolar cells, ganglion cells show ‘on’ and ‘off’ surround inhibition, but they differ from bipolar cells in producing action potentials, and thus their responses are
described in terms of action potential rate, not graded depolarization. They are also spontaneously active. Therefore,
inhibition of these cells decreases the resting rate of action
potentials and their centre–surround organization makes
these cells extremely sensitive to moving stimuli.
Ganglion cells can also be distinguished by their
responses to colour. Studies in monkeys (which have
a similar visual system to humans) have shown that
there are two major populations of ganglion cells, distinguished easily by their size, destination (see below),
and response characteristics. The most numerous cells
(80%) are small parvocellular (P) cells; these are found
near the fovea. Magnocellular (M) cells are larger and
less common (10%), and the remaining 10% are small,
non- M, non- P (K, or koniocellular) cells, which have low
spatial resolution. The RFs of P cells are smaller than
M cells, and they often show sustained responses compared with the transient responses of M cells. However,
the most striking difference is that they respond differently to coloured light. This is because P cells obtain
their input from single cones (or a group of cones with
the same wavelength sensitivity—S, M or L), while M
cells receive their input from rod cells. M cells are more
sensitive than P cells to low- contrast stimuli and are used
for motion detection and object fixation, while P cells
can distinguish fine detail and are important for spatial discrimination. This separation of functional detection of different features of the image at the first stage in
150 SYSTEMS OF THE BODY
7
f’
A
Red surround ‘on’
Yellow ‘off’
Blue ‘off’
the visual pathway is maintained throughout the visual
pathway.
Some non- M, non- P cells receive their input from M
and L cones together (but not S) and have larger RFs, so
they are good at measuring the brightness. The centre–
surround inhibition lets ‘on’ M cells respond best to green
(M cones) and red (L cones) light in the centre, while ‘off’
M cells fire when the light illuminates the surround.
The output of P ganglion cells shows colour opponency, that is, they are excited by one cone population
happens. Staring at this white box leaves the opponent colour unopposed, and so the white background
becomes that colour. For blue, the white background
becomes yellow; for red, it becomes green and vice versa.
Recently, a few retinal ganglion cells have been discovered that have melanopsin as their pigment rather
than rhodopsin or cone pigments. These cells’ axons
project to the suprachiasmatic nucleus in the hypothalamus and are associated with endocrine and circadian
rhythm functions.
THE VISUAL SYSTEM
and inhibited by another (Fig. 7.17). There are two populations of colour opponent P cells. The most common are
single red–green opponent.
Processing of visual information
There are four different possible responses, depending
on whether the ganglion cell is an ‘on’ or ‘off’ cell (Fig.
7.17A):
• red‘on’centre,green‘off’surround
• green‘on’centre,red‘off’surround
• red‘off’centre,green‘on’surround
Retinal ganglion cells are not mere relay cells for visual
information; they extract different aspects of the image.
What we ‘see’ depends on the features extracted in
the retina, and how this information is integrated and
interpreted by the brain. In the retina, the visual information splits into two streams, one for colour and one
for form and motion. This is parallel processing and is
• green‘off’centre,red‘on’surround.
Blue- yellow opponency compares input from S cones
with that of M and L combined (as the combined input
from M and L cones gives the perception of yellow).
These cells do not show a centre–surround response but
are either excited by blue light and inhibited by yellow
or vice versa (Fig. 7.17B) and are associated with K ganglion cells.
Perceived colour is based on the relative activities in
important because we view the world with two eyes,
providing two parallel streams of information, albeit
from slightly different angles. In the central visual
pathways, these streams are compared to give information about object depth, contrast and movement,
as well as image resolution. Because we use two eyes,
there are two separate images in the brain, and somewhere in the visual cortex they are merged (this is
known as the binding problem).
different ganglion cells, whose RF centres receive input
from the three different cones. This is easily demonstrated, for example, by staring at a red, green or blue
square for 30–60 seconds to fatigue the appropriate cone.
Then, if one stares at a white box, something strange
Visual processing in the lateral geniculate nucleus
The LGN has six layers (Fig. 7.18) which receive inputs
from the M and P ganglion cells. The two ventral layers,
called the magnocellular layers (M1– 2), are composed
M
L
L
M
of large cells and innervated by M ganglion cells (layer
1 from the contralateral eye, and layer 2 from the ipsilateral eye). The more dorsal parvocellular layers (P3– 6)
are composed of small cells and receive input from the P
Red ‘on’ centre
Green surround ‘off’
Green ‘on’ centre
Red surround ‘of
ganglion cells, with layers 3 and 5 ipsilateral and 4 and
6 contralateral. In between these layers are even smaller
cells, which comprise the K layers that receive input
M
L
L
M
from non- M, non- P cells that signal average illumination.
Just like the retinal ganglion cells, the LGN cells have
circular RFs and show the same centre–surround inhibi-
Red ‘off’ centre
Green surround ‘on’
Green ‘off’ centre
tion and colour opponency as the ganglion cells to which
they connect. Each layer shows precise topographical
mapping of the retina, with the majority of each layer
S
(M + L)
S
(M + L)
B
occupied by input from the fovea. The maps are in register, so at any vertical point through the LGN, the same
RF is represented. As only input from one half of the
visual field goes to each layer of the LGN, there are no
binocular responses.
Blue ‘on’
Fig. 7.17 Colouropponencyinganglioncells. (A)Red–greensingle
opponentcells.(B)Blue–yellowopponentcells.
Yellow ‘on’
There are two types of neuron in the LGN: geniculostriate neurons, which project to the visual cortex, and
a population of small interneurons. As well as receiving input from the retinal ganglion cells, these neurons
151THE NERVOUS SYSTEM
7
Koniocellular
P cellsIII–VI =
THE VISUAL SYSTEM
Contralateral
inputs
M cellsInput I–II =
Fig. 7.18 Layersinthelateralgeniculatenucleus. Magnocellular
layers(1and2)areshownshaded.InputsIandII:Mcells.InputsIII–VI:
Pcells.Inputtokoniocellularlayer:non-M,non-Pcells.
receive input from the visual cortex and reticular formation, so they may play a role in visual attention (see
below).
Visual attention selectively filters out irrelevant
information so the relevant detail is consciously perceived. The circuitry involved in attention is similar to
that involved in oculomotor control. The FEF; parietooccipital- temporal, primary visual (V1), and association
area (V2, V4) cortices; and SC are also involved (Fig. 7.3).
The earliest attentional activity occurs in the FEF neurons, suggesting that this is the source of the attentioncontrol signals. Experimental evidence also suggests that
three thalamic nuclei—the LGN and pulvinar and thalamic reticular nuclei (TRN)—are also strongly involved
in controlling attention. The pulvinar nucleus seems
to be very important, as it has neurons that respond to
colour, motion, and orientation. It receives input from
the LGN and SC and has reciprocal connections with the
visual cortex, and so can directly modulate the efficacy
of input from one region to another. Moreover, it modulates cortical neuron firing and so can synchronise firing
of different neurons involved in the parallel processing
of colour, motion and depth. This may be how the brain
solves the binding problem by integrating the parallel
streams of information to produce a visual percept of
the object. Pulvinar lesions lead to disturbances in visual
attention.
layers
VI
V
IV
III
II
I
Parvocellular layers
Magnocellular layers
non-M, non-P cellsInput to koniocellular =
Ipsilateral
inputs
Brain imaging studies also show that the LGN is
important in visual attention. As outlined in Chapter 1,
the thalamus is the ‘gatekeeper’ to the cortex and the
inhibitory TRN is the sentry to the thalamus. The TRN
receives input from the prefrontal and visual cortices, as
well as the SC. Attentional stimuli decrease TRN inhibition of the LGN. Additionally, corticothalamic activation of LGN from the FEF, V1 and V4 regions excite LGN
neurons, so that specific features from the M, P and K
cells can be selected for attention. In this way, the LGN
fulfils the gatekeeper role for vision.
Organization and response properties of cells in
the visual cortex
The V1 has six layers, each with specific inputs from
the parallel streams derived from the M, P and K layers
of the LGN. The different pathways carry information
regarding form, movement, colour and visual attention
in a topographic fashion. In this map, the fovea is disproportionately represented, and peripheral vision has little
representation. V1 is the first region in which input from
both eyes is combined.
Unlike neurons in the retina and LGN, those of the
visual cortex do not have circular RFs but respond to
lines of a particular orientation. Like many other regions
of the brain, the visual cortex is arranged in functional
columns. In a given column, which is 30–100 μm across,
all the neurons spanning layers 1–6 respond to bars of
light of a particular orientation; hence, the name orientation column. In each orientation column (Fig. 7.19),
there are two types of cell. Simple cells are found in layers 4 and 6. They have small, centre–surround RFs and
respond to stationary bars of a certain orientation from a
single visual field; that is, they are monocular and highly
sensitive to the position of a stimulus on the retina. In
layers 2, 3 and 5 are complex cells. These are not direction sensitive but respond preferentially to bars of light
of the same orientation as the simple cells moving across
the RF, parallel to the preferred orientation. However,
these cells are binocular, as they respond to input from
both eyes, although they show a preference for the visual
field of the simple cells. Moving across the cortex, each
successive column has a preferred orientation, which
changes by approximately 15 degrees. Across a distance
of approximately 1 mm, there are columns for each possible orientation for a single eye, from a given part of the
visual field. This set of orientation columns is called an
ocular dominance column. Columns with the same orientation are organized as stripes in the cortex. Parallel to
this are a similar set of columns representing input from
the same part of the visual field of the other eye. The area
of the cortex consisting of two ocular dominance columns, one from each eye, is called a hypercolumn (Fig.
7.19) and represents all of the input from a part of the
visual field to the primary visual cortex.
Arranged within the ocular dominance columns are col-
umns of complex cells, which are wavelength- sensitive.
152 SYSTEMS OF THE BODY
A single hypercolumn
(≈1 mm2)
500 µm
Blob
2 mm
V5 (MT)
V4
V3
V2
V1
LGN
Retina
detects form
detects colour
7
THE VISUAL SYSTEM
MST PP (7a) IT
I
II
C
I
C
Ocular
dominance
column
Fig. 7.19 Simpleandcomplexcellsarearrangedinorientation
columns,andtheseformoculardominancecolumnsand
hypercolumnsinthevisualcortex. C,Contralateral;I,ipsilateral.
30–100 µm
II
III
IV
V
VI
Orientation
column
These colour- sensitive cells are arranged in cylindrical
regions called blobs (based on metabolic staining with
cytochrome oxidase); they receive convergent input from
the parvocellular and koniocellular LGN layers. The areas
between the blobs are the interblob regions. The RFs of most
of the blob neurons are circular and show varying types of
colour opponency. The most complex of these are the double opponent cells, which signal colour contrast. There are
four types, depending on the preferred stimulus. For example, one type has a maximal ‘on’ response to a red spot on a
green background and an ‘off’ response to a green spot on
a red background. The other red–green type is the reverse,
and a similar combination occurs for blue and yellow.
Parallel processing in the visual cortex
Form
V5
Motion
Stereopsis
Colour
V4
Shape
Stereopsis
Form
V3
Motion
Binocular cells
Thick stripes
Motion
Binocular cells
Binocular
(Layers 4Cα, 4B, 6)
Magnocellular
system: detects motion
Fig. 7.20 Modellinghowwesee. IT,Inferiortemporalcortex;MST,
medialsuperiortemporalcortex;MT,Medialsuperiortemporalcortex;
PP,posteriorparietalcortex;RGC,retinalganglioncell. Integrationof
parallelprocessingofthedifferentstreamsofinformation.(Adapted
fromDeYoe,VanEssen.TINS.1988;11:219–226.)
V2 Interstripe
V1
Form
Motion
M1–2 P3–6 Koniocellular
M
RGCs
Shape
Colour
Stereopsis
Interblob
Binocular
Layers 2–3, 4Cβ
Parvocellular–
interblob system:
Colour
Form
P
RGCs
V2 Thin stripe
V1
Layers 2–3, 4Cβ
Non-M – non-P
Parvocellular–
blob system:
Colour
Colour
Colour
Blob
V4
The different streams of input from the LGN—motion,
form, and colour—are processed simultaneously in different layers of the visual cortex (Fig. 7.20). Inputs from the
M cells of the LGN, which synapse in different sublayers
of layer 4 to P cells, concern motion but not colour. Inputs
from P cells of the LGN are processed in two streams. One
stream in the parvocellular–blob pathway mediates colour
vision, while the other—the parvocellular–interblob pathway—performs high- resolution analysis of form. These
complex cells are binocular but not wavelength sensitive.
They are also important for depth perception.
Outputs from the primary visual cortex
Visual perception involves many different (extra- striate)
association regions of the occipital cortex that receive
output from the V1 (striate) cortex. In monkeys (and by
inference, humans), there are numerous areas known to be
involved in further processing of visual input (Fig. 7.21).
Many of these areas have some form of retinotopic map,
and there are complex interconnections between these
regions.
The parallel processing of different information
streams continues beyond V1. Many outputs go to the
secondary visual cortex (V2, Brodmann area 18), which,
on staining for cytochrome oxidase—a metabolic activity marker—shows a pattern of thick and thin stripes.
V2 has reciprocal connections with V1. Information
leaving V2 splits into two streams (Fig. 7.21). V2 thick
stripes receive inputs from the M pathway (via V1 layer
4) and analyse motion. This information is further processed in other regions, V3 and then V5 (also called the
153THE NERVOUS SYSTEM
7
IT– Inferior temporal
medial temporal, MT, cortex), and the medial superior
temporal (MST) cortex, before moving to other visual
association areas such as the posterior parietal cortex.
Cells in V5 are key motion detectors and are also important for depth perception. V5 damage causes loss of
motion perception.
The thin stripes of V2 receive inputs from blobs and
analyse colour. Output from this area goes to V4. Interblob neurons project to interstripe regions, which also
THE VISUAL SYSTEM
project to V3 and V4. Eventually, visual information
gets divided into two streams (Table 7.6, Fig. 7.21). The
‘where’ stream is carried dorsally, to the MST and posterior parietal cortices, and carries information about
an object’s location and motion, including one’s own
body and its spatial relationship to an object (visual
Fig. 7.21 Visualinformationfromtheprimaryvisual(V1orstriate)
cortexisprocessedbythevisualassociation(extra-striate)cortical
areasastwostreams.
“what?”
IT
PP – Posterior parietal
MT– Medial temporal
PP
“where?”
V4
MT
(V5)
V2
V3
V2
V1
guidance and reaching movements). The ventral ‘what’
stream projects to the inferotemporal (IT) cortex, which
can identify or recognize an object, pattern, or specific
face. V4 projects to V6 and activates cells that respond
to complex shapes and have a role in object shape
recognition.
The effects of selective lesions to the different areas and
functional imaging studies confirm the existence of these
two streams. Damage to the posterior parietal cortex causes
optic ataxia, where patients can recognize objects but cannot grasp them. Damage to the MST cortex and MT visual
cortex results in loss of visual motion perception (akinetopsia) in different directions. This has obvious lifestyle implications: think how difficult it might be to cross a busy road
or even to pour a drink without the cup overflowing.
In contrast, patients with damage to the IT cortex have
visual agnosia, where the position of an object is recognized, but it cannot be named or a copy drawn (except
from memory). In a particular form of this condition, called
prosopagnosia, patients cannot recognize individual faces,
however familiar. For example, a married person with
this condition would not recognize their spouse visually
but would recognize the sound of their voice. Alexia is
the inability to read written words. Damage to V4 results
in loss of colour vision—achromatopsia—while damage
to V6 causes an inability to distinguish two- dimensional
patterns.
In a particular condition called blindsight (cortical
blindness), patients who are totally blind due to the bilateral loss of V1 can still navigate to some extent through
space without colliding with objects that they reportedly
cannot see. This occurs due to a pathway which goes from
the magnocellular neurons of the LGN directly to the thick
stripes of V2, providing input to the ‘where’ pathway.
However, eventually the two streams (Table 7.6) inte-
grate to produce a coherent image of a three- dimensional
Table 7.6 Separationofvisualinformation
Function Motionperceptionandspatiallocation
Retinalganglioncelltype Mcells(non-macular) Pcells(fovea)
LGNcelllayers M1–M2 P3–P6
Corticalinputarea V1 V1
Visualassociationareas V2,V3,V5,MSTcortex,posteriorparietalcortex V2,V4,V6,anteriorinferiortemporallobe
Othercorticalareainvolvement Dorsolateralprefrontalcortex
Effectoflesion Opticataxia
LGN, Lateral geniculate nucleus; MST, medial superior temporal.
154 SYSTEMS OF THE BODY
Pathway
Dorsal stream: ‘Where things are or how they move’
Visualguidanceofhandandeyemovements
Frontaleyeelds
Ocularapraxia
Akinetopsia
Ventral stream: ‘What things are or
are like’
Colourandshapeperception
Objectrecognition
Ventrolateralprefrontalcortex
Medialtemporallobe
Visualagnosia
Prosopagnosia
Achromatopsia
Alexia
7
world. This processing of information in parallel streams
can explain how some visual illusions are produced. For
example, depth perception is much reduced in computergenerated pictures if the shading is produced by colour
contrast as opposed to luminance. This suggests that depth
information is processed by the magnocellular pathways.
Summary
The visual system is a complex system designed to extract
different features of an image: its colour, motion and
shape (Fig. 7.20). Some of this separation occurs early in
the pathway and information is processed in parallel
throughout the rest of the pathway. For example, colour
is detected by cones, which activate P cells that project via
parvocellular LGN layers to blob regions of the visual cortex, and onwards to V4. Rods, on the other hand, see only
in black and white, work best at low light levels, and are
excellent motion detectors. This information travels via
the M layers of the LGN to interblob regions of the visual
cortex and is forwarded to V5 and the posterior parietal
cortex. The parvocellular–interblob pathway is specialized
for shape perception, as cells in this pathway are sensitive
to the orientation of edges. Within the cortex, there are
many complex interactions between the many different
visual association regions. We get visual input from two
eyes, and the visual image is inverted and back- to- front
in the visual cortex. Somehow, somewhere in the cortex,
through the interactions between the various visual centres, the image is inverted again to appear the ‘right way
up’, and binocular input is transformed into one seamless
three- dimensional percept of the outside world.
Self- assessment case study
A 35- year- old man reported blurred vision and headaches. The ophthalmoscopic examination is normal, with
no signs of papilloedema or retinopathy. There are no
signs of cataracts or other opacities. Direct and consen-
sual pupillary reflexes are normal as are conjugate eye
movements. However, there is mild diplopia. Visual field
examination shows a bitemporal heteronymous hemianopia (tunnel vision). A magnetic resonance imaging
(MRI) MRI scan is scheduled and a blood sample is taken
for endocrine evaluation.
After studying this chapter, you should be able to
answer the following questions:
1. Where is the lesion located?
As the visual field deficit occurs in both eyes, the lesion
must occur at, or posterior to, the optic chiasm. Any lesion
occurring after the optic chiasm produces a homonymous
deficit, so this patient has a lesion at the level of the optic
chiasm. Compression of the optic chiasm affects only those
fibres that decussate. These fibres arise from the nasal side
of the each retina, so the part of the visual field affected is
the temporal visual field in both eyes. The patient does not
notice this extensive lesion, as the temporal visual field of
one eye appears in the nasal visual field of the other eye.
Examination of each eye separately reveals the deficit.
2. What is the possible cause of the compression and
what will the investigations show?
The optic chiasm lies above the pituitary gland, and
tumours of the pituitary cause compression of the optic
chiasm. Pituitary adenomas are mostly benign and are
classified as either non- secretory (more common) or secretory, depending on whether they produce anterior pituitary hormones such as prolactin, growth hormone and
ACTH. In this patient the symptoms seem to be entirely
due to the presence of a mass, which suggests a nonsecretory tumour. The headaches are caused by the stretching of the dura mater, whilst diplopia can be caused by
pressure on the ocular motor nerves (3rd, 4th and 6th)
due to the lateral extension of the tumour. Imaging of the
brain using MRI will show any significant pituitary mass.
Analysis of hormone levels in blood will show whether
this is a secreting or non- secreting tumour. Non- secreting
tumours may also present with inadequate hormone
secretion—hypopituitarism.
THE VISUAL SYSTEM
155THE NERVOUS SYSTEM
This page intentionally left blank
HEARING AND
BALANCE: THE
AUDITORY AND
VESTIBULAR SYSTEMS
Chapter summary
1. The auditory and vestibular systems both use mechanosensory hair
cells to transduce stimuli.
2. The outer ear collects and funnels sound waves to induce vibrations
of the tympanic membrane. The sound waves are converted into
mechanical vibrations by three middle ear bones (malleus, incus and
stapes) that amplify the signal. The stapes transfers the sound waves
to the inner ear via the oval window where they are converted to
fluid pressure waves that stimulate the sensory apparatus.
3. The cochlea contains three fluid filled chambers. The outer two
contain perilymph and the inner one contains endolymph. The
outer two provide a pathway for pressure waves to flow through
the system while the inner chamber contains the auditory sensory
apparatus, the organ of Corti.
4. The organ of Corti contains rows of hair cells that sit on the basilar
membrane. They have stereocilia that project into the chamber or
embed into the tectorial membrane. When the fluid waves cause
the basilar membrane to vibrate, the stereocilia bend. Adjacent
cilia are connected by tip links and tensing these links opens
mechanosensitive K+ channels, causing the cell to depolarise and
release glutamate to stimulate cochlear afferents.
8
5. The basilar membrane is tapered in shape to provide a spatial map
based on resonance frequency. This tonotopic map is preserved
along all the neural relay pathways to the auditory cortex (via the
brainstem and thalamus).
6. The vestibular system detects head movements. It has three
semicircular canals arranged at right angles to each other and
two otolith organs that detect changes in rotational and linear
8
movements, respectively. The system also produces compensatory
eye movements during head movement for image stabilization and
object tracking.
7. Vestibular sensory hair cells are also connected by tip links that open
or close K+ channels when they are displaced by endolymph fluid.
8. Damage to the auditory system results in conduction or sensorineural
deafness. Specific tests are used to assess the functional integrity of
the auditory system.
9. Damage to the vestibular system results in vertigo, nausea and
nystagmus. The integrity of the system can be assessed in several
ways (e.g. vestibulo- ocular reflex, caloric test and Hallpike’s
manoeuvre).
Introduction
Hearing is one of our most important senses, because of
its roles in the perception of speech and the ability to communicate. Hearing deficits are common, particularly in the
young and the elderly, and the prevalence increases with
age. In the UK, approximately one in six of the popula-
HEARING AND BALANCE: THE AUDITORY AND VESTIBULAR SYSTEMS
tion have some form of hearing impairment; 8 million are
aged over 60 years and 900,000 have profound deafness,
including 50,000 children. Worldwide, the World Health
Organization reports that 432 million adults and 34 million children have ‘disabling’ (>35 dB loss in their good ear)
hearing loss, and these numbers will drastically increase
by 2050. Nearly 80% of people with disabling hearing loss
live in low- and middle- income countries. The symptoms of
hearing loss—earache, tinnitus (ringing in the ears), vertigo
and otorrhea—are associated with ear problems.
Hearing loss is hardest for young children. They are
deprived of the normal acquisition of speech and consequently require other forms of communication (e.g.
sign language or lip reading). Acute deafness in adolescents can have a significant psychological impact, as it
deprives them of social contact with their peers. In the
elderly, deafness causes increased isolation and estrangement from family and friends. People with hearing loss
ranging from mild to severe are termed ‘hard of hearing’.
They usually communicate through spoken language
and can benefit from hearing aids, cochlear implants and
other assistive devices. ‘Deaf’ people mostly have profound hearing loss, which implies very little or no hearing. They often use sign language for communication.
The vestibular system is intimately involved in
maintaining balance, and the most frequently reported
symptoms of vestibular disorders are dizziness,
unsteadiness when walking, vertigo and nausea. These
symptoms can range from mild, lasting minutes, to
severe, resulting in total disability. As the vestibular system interacts with many other parts of the nervous system, symptoms may manifest as problems with vision,
movement, thinking and memory. Vestibular disorders
occur frequently and affect people of all ages. Balance
disorders are increased in frequency in the elderly and,
by the age of 75 years, become one of the most common
reasons for visiting the doctor. In many cases the cause
lies in the inner ear.
The impact of deafness and balance disorders in society is significant in terms of financial and emotional
costs: the cost of diagnosis and treatment, hearing aids,
speech therapy or vestibular rehabilitation, and lost
work potential. This chapter reviews the anatomy and
physiology of the auditory and vestibular systems and
describes clinical signs and symptoms associated with
their dysfunction (Box 8.1).
Auditory system
The auditory system is a specialized sensory system with
two main functions: to detect and localize sound and to
decode sounds into meaningful language. It comprises
the cochlea, the afferent auditory pathways and the auditory cortex in the temporal lobe and can detect frequencies from 20 Hz to 20 kHz. The auditory pathway uses
both ears to detect and signal the location of the sound.
Complex inhibitory circuitry magnifies the differences
in the timing and intensity of sounds that occur between
the two sides during normal hearing.
158
SYSTEMS OF THE BODY