Neurophysiology Flashcards
1
Q
What are the 3 planes and corresponding axes of rotation of extraocular muscles?
A
-horizontal = vertical
-vertical = horizontal
-torsional = visual
2
Q
what does Sherrington’s law of reciprocal innervation state?
A
For each eye, ‘antagonist’ muscles receive equal but opposite innervation
3
Q
what does herring’s law of motor correspondence state?
A
For conjugate movements, ‘synergist’ muscles receive equal innervation (from CNS), i.e. certain muscles must co-contract (or co-relax) = “yoked” pairs Oculomotor Coordination
4
Q
name the ipsilateral antagonists
A
-medial rectus
-lateral rectus
-superior rectus
-inferior rectus
-superior oblique
-inferior oblique
5
Q
for each of the RE extraocular muscles name the contralateral synergists so state the yoked muscle pairs of the two eyes
A
-medial rectus = lateral rectus
-lateral rectus = medial rectus
-superior rectus = inferior oblique
-inferior rectus = superior oblique
-superior oblique = inferior rectus
-inferior oblique = superior rectus
6
Q
why are there two sub divisions of the medial rectus?
A
because it is involved in both horizontal alignment and vergence
7
Q
how are eye movements different to other muscle movements in the body?
A
there is a lack of a monosynaptic stretch reflex in extraocular muscles
8
Q
give 3 devices that can measure eye movements and what are they all sampled at? What exactly can these measure?
A
-tobii pro spectrum
-eye link 1000+
-skalar
pupil boundary
pupil centre
gaze direction
9
Q
why does the optic nerve have to be cushioned and protected?
A
as it moves alot when the eyes move
10
Q
how do eye trackers work?
A
uses an image of the eye and by working out the center of the pupil and the geometry of the reflex, to find pupil boundary, centre and gaze direction, it can calculate how the eye is moving and where it’s looking.
11
Q
what is the function of eye movements in general?
A
to provide a good, stable image
12
Q
why do chickens move their bodies while keeping their heads completely still?
A
as they achieve stable image with their head instead of their eyes like us humans with foveal fixation
13
Q
give an example in animals of how eye orientation in the head affects how a stable image is achieved
A
pigeons have eyes on the side of their head as every time they take a step forward, the image moves back so they bob their head to compensate
14
Q
what are the two categories of eye movements and which eye movements fall in them?
A
-compensatory = stabilising
vestibulo-ocular reflex and optokinetic nystagmus
-targeting = fixation
saccades, smooth pursuit and vergence
15
Q
what is gaze
A
where the fovea is looking independent of where the eyes are in terms of orientation or head movement
16
Q
what is vestibulo-ocular reflex?
A
where your gaze remains unchanged even though the position of the eyes in the head changes due to fast, transient head movement
17
Q
give an example that explains what vestibular nystagmus is
A
if you were to rotate 360 degrees, then you get a slow phase to compensate for the head movement and then a quick phase to reset the eyes because you have ran out of room and this maximises the amount of time you get a stable view of the world
18
Q
what drives the vestibulo-ocular reflex?
A
a non visual stimulus - driven by afferent signal from inner ear canals
19
Q
what is optokinetic nystagmus?
A
where gaze gets stabilised by generating an eye movement that’s in the same direction as the movement of the field - Occurs in all animals. When it reaches its max limit, it resets (saccades)
20
Q
what is optokinetic nystagmus driven by?
A
retinal slip so has a visual stimulus
21
Q
what are the two types of saccade?
A
-involuntary = anticompensatory reset during head rotation (or in OKN)
-voluntary = redirecting the foveal line of sight via reflex, visual (normal scanning) and memory (making saccadic movements in the dark)
22
Q
what makes saccades different from other eye movements?
A
They are the only eye movement you can make to a non stimulus I.e. you don’t actually have to have something to look at for your eyes to make a saccade. This is the memory aspect of voluntary saccades
23
Q
what kind of movement are saccades?
A
a ballistic movement
24
Q
how long do saccades take to happen?
A
1/5 of a second
25
what are the two types of saccade
-Small saccade, short duration, lower frequency burst, occur at a lower velocity
-Large saccade, longer duration, higher frequency burst, occur at a higher velocity
26
what is smooth persuit?
-where you are following a small slow moving object as the visual stimulus by matching the velocity of the object as closely as possible
-only worries about how fast something is moving to track it not where it actually is
-Shows you can’t actually keep your eye on the ball so there's a slow phase initially and then saccade and then slow phase as its going at high speeds
27
what is the latency of saccades?
200 ms latency
28
what is the latency of VOR compared to retinal processing
10ms latency compared to 70ms
29
what does visual masking for saccadic suppression need to work?
presence of stationary, highly contoured visual background before
and after saccade
30
what happens in the brain to allow for saccadic supression?
selective suppression of low spatial frequencies as the striate cortex is impaired during saccades
31
what is saccadic suppression?
No sense of a blurred image during saccades
32
what drives smooth persuit?
a visual stimulus that is a slow moving target
33
what is vergence?
where the eyes move away or towards each other. Generally is the slowest of the eye movements unless if it is in concert with saccades as needing to change the orientation means the saccade increases the speed of vergence
34
what effect does eye movement have on perception?
If your eye moves and the object is stationary vs is your eye is stationary and the object moves, the brain can detect whether it’s motion in the real world or not
35
what are the stimuli for vergence?
-blur = accommodative vergence (lens)
-diparity = fusional vergence (prism)
36
what inputs are required for an appropriate sense of visual motion?
-visual signals of retinal image movement
-head movement signals
-eye movement signals
37
what does neural control consist of?
gaze shifts and gaze holding
38
how do our eyes respond to a moving object?
1. object in space moves
2. retinal image moves
3. head/ body moves
4. eyes move
5. appropriate perception of environmental motion requires multi-sensory input
39
what inputs are required for an appropriate sense of visual motion?
-signals of retinal image motion
-signals indicating head movement
-signals from eye movement
40
what other senses apart from vision are involved in self orientation?
-vestibular
-audition
-proprioception (motor and tactile)
41
what are MT and MST?
the middle temporal and middle superior temporal nuclei and these feed into the parietal lobe.
important in the visual pathways
42
what are the steps in the primary visual pathway and what is happening in parallel?
check page 9 of the op2501 term 2 google docs
43
what is proprioception?
having a sense of position of you body within the environment
44
what is efference copy?
the info sent to the brain of where the eyes are looking so the brain can determine where the object is in the world
45
what are the 4 gaze holding types of eye movement?
– Fixational
– Reflex (VOR, OKN)
– Smooth pursuit
– Vergence
46
what are the two gaze shifting types of eye movement?
-saccades
-fast phase of nystagmus
47
what are the three broad sections of the oculomotor system
-motor nuclei
-premotor circuitry systems (supranuclear gaze centers)
-common structures
48
what does the motor nucleus of the oculomotor system consist of?
CN 3, 4 and 6 and these control the EOM for eye movements connected via the MLF (a fibre tract not a nucleus)
49
what do the premotor circuitry systems of the oculomotor system consist of?
In the pons you have the PPRF. This nucleus controls horizontal gaze shifts. This is near abducens (makes sense as that’s what drives eyes side to side)
In the midbrain you have the riMLF and this nucleus controls vertical gaze shifts. This is near oculomotor and trochlear (make sense as that’s what drives eyes up and down)
MRF which controls vergence and is in the midbrain
50
what are the common structures of the oculomotor system?
Superior colliulus (tectum) in the midbrain brain (top of the brain stem)
Other cortical areas that project (frontal eye fields, supplementary eye fields and posterior parietal (LIP)
51
what nucleus controls slow phase eye movements?
vestibular nucleus
52
how can you move your eyes and hold gaze?
as it takes effort: the neural integrator calculates the position of the eyes in the orbit by taking into account the velocity of the eye movement
53
what happens in horizontal gaze control?
1. Signal pprf
2. Left goes to left lateral rectus
3. Interneurons cross the midline to go to the right medial rectus due to herrings law
4. drives both eyes to the left
pprf goes to the left lateral rectus, right pprf goes to the right medial rectus so driving eyes to the left which means the right medial rectus drives eyes to the left
(hence left LR and right MR are yoked muscles)
54
what are supranuclear, internuclear and infranuclear?
-premotor
-motor
-muscles
55
check brainstem diagram in screenshots
ok
56
what eye movements does the neural integrator deal with?
-horizontal
-vertical
-torsional
57
what eye movements do saccadic gaze generators do?
-horizontal
-vertical
-torsional
58
what eye movements do persuit generators do?
horizontal and vertical
59
in smooth persuit what side of the cortex does the persuit need to be stimulated to drive the eyes to the right?
the right side of the cortex
60
what is the difference between projection for saccades compared to projection for persuit?
for saccades its crossed whereas for persuit its on the same side of the brain
61
what happens in the brains for saccades to occur?
1Frontal eye field on the left
2.cross to the right pprf
3.Contract the right lateral rectus
4.interneuornes go across to left medial rectus and contract that
62
what happens in the brain for smooth pursuit to occur?
1. Projection is on same side
2.Goes to pons nucleus DLPN
3.Crosses to cerebellum and goes to medial vestibular nucleus
4. Goes across back to abducens so you end up on the same side
63
what is substantia nigra?
the first nucleus to generate in parkinson's disease and so produces a change in eye movements that can be monitored and measured
64
where is MLF and MRLF?
the midbrain
65
where is PPRF?
pons
66
what areas of the brain are involved in vergence?
-cortex (MT, MST And LIP)
-MRF
-cerebellum
-oculomotor nuclei
67
what law explains the fact that the same neuron that will activate one muscle will shut off when the opposite muscle is activated.
sherrington's law
68
what can cause a leaky neural integrator (so it does not work well)
can be a type of medication or cancer
69
what does the neural integrator do?
resists the elastic forces on the globe that would normally drive the eye back to midline by using continued tonic innervation of the extraocular muscles
70
what is pulse innervation?
phasic/ changing
where the eye movement requires a burst of energy to overcome inertia of the eyeball and signal is proportional to the size of the burst
71
what is step innervation?
tonic/ steady
steady firing required to maintain the new eye position where firing rate is proportional to eye position
72
how can you remember which extraocular muscles are yoked togther?
inferior oblique is yolked with the superior rectus, superior oblique is yolked with inferior rectus… superior, inferior, superior, inferior e.t.c.
73
what neural integrators are in the cerebellum?
flocculus and paraflocculus
74
what neural integrators control vertical and torsional movements?
interstitial nucleus of Cajal (INC)
75
what neural integrators control horizontal movements?
nucleus prepositus hypoglossi (NPPH)
and medial vestibular nucleus (MVN)
76
what does donder's law suggest?
the amount of torsion in the eye is not determined by the direction of line of site and instead is determined by the degree of rotation of the eye in the horizontal and vertical axes
77
what is listings law?
the 3d orientation of the eye and around its 3 axes
78
what is the binocular visual field?
When you simultaneously allow both eyes to see the same stimulus, you get increased firing of those cells compared to if each eye was looking at the stimulus monocularly
79
what does oblique penetration in V1 mean?
that you progress through ocular dominance groups 1-7 when using BV
80
what does the V1 graph of primates suggest?
some cells will be more responsive to one eye than others
81
how can two neural images provided by the visual cortex be combined?
through layering and averaging
82
describe ocular dominance columns looking down on the visual cortex
-alternate in an ordered way and the spacing between each column (re le) is equal
-Each hypercolumn is a processing module that works together with other hypercolumns to process lots of visual info, not just colour and contrast.
83
what is a hyper column? what does it do?
a chunk of cortex about 1mm square by 3mm thickness containing neurones with the same receptive field location but tuning to all possible selectivites and serves as a processing module for a particular area of the retina
84
where are the blobs and interblobs?
In v1 you get spots (blobs) which process info about colour and between the blobs is inter blobs - 2 categories
85
how can the thick and thin stripes in v2 be seen?
-Cytochrome oxidase staining allows you to see all of these stripes
-You can also see this using fMRI
86
what does v2 contain?
Thick stripes, thin stripes and interstripes where:
-Parvo goes from thin to inter stripes, magno goes to thick stripes
-Thin stripes = colour hence V4
87
what parts of vision does the temporal/ ventral (lower) pathway do?
-what pathway
-recognition
-shapes
-high acuity
-colour
88
what parts of vision does the parietal/ dorsal (upper) pathway do?
motion and location
89
where does most of the info in extrastriate area (V2) come from?
the striate cortex (v1)
90
what info is thick stripes?
magno info - disparity, orientation and movement
91
what kind of info is thin stripes?
parvocellular info - colour coded
92
what kind of info is interstripes?
parvocellular info - orientation sensitive but no colour coding (unlike the parvocellular info in thin stripes)
92
what does being able to adapt receptive fields of recognition cells allow you to do?
recognise the same people even after they age or change something about their face. Hence the cells are constantly creating new receptive field properties to recognise new things
92
what is aphantasia?
inability to have a mental image of anything in your head - something you are born with and may be more common than we think
92
give an example of a task someone with motion agnosia cannot do?
pour milk into a mug (they cannot identify moving objects)
93
what is achromatopsia?
means the person can recognise the shape but has 0 colour perception - can reproduce the shapes but cannot reproduce colours
94
what is apperceptive agnosia?
loss of form perception
95
what is associative agnosiia?
loss of form recognition
96
what is prosopagnosia?
inability to identify faces
97
what are some examples of perception problems?
-Inability to recognise shapes but has the ability to reproduce them
-Inability to reproduce shapes
-Orientation perception difficulty - reflexive motor response is not damages though
98
what can cause perception problems to arise?
CO poisioning
99
what are the two types of simultanagnosia?
-dorsal = where the px cannot percieve more than one image amongst overlapping pictures
-ventral = px can recognise shapes and objects but have no associative perception
100
what is visual hemifield neglect?
where one side of the parietal lobe has been damaged so the contralateral image cannot be seen, can be due to a stroke so people can recover over time - unilateral spatial neglect in a parietal patient
101
what is simultanagnosia?
impaired object recognition in an agnosia patient
102
what are the different cells in the different levels of the visual cortex?
-simple cells: respond best to stimuli at different angles/ orientations
-Complex cells respond to movement as well as orientation but are more responsive to movement so dont encode for absolute location but instead encode for texture
-In end stopped cell/ hyper complex cells the stimuli have to be at a particular orientation, be moving as well as be if a particular length
103
what are the two types of simple cells?
-edge detectors = when the inhibitory and excitatory stimuli lie side by side
-bar detectors = where the excitatory/ inhibitory bar is in the middle depending on which of the two bar detectors it is
104
how do simple cells work?
When the orientation is lined in the exact orientation of the detector then you get firing of the cell and if not then it does not fire
105
where do each of the cells in the different levels of the visual cortex arise from?
-simple cells arise from the convergence of the center surround of several cells in the lgn like ganglion receptive fields
-complex cells arise from the convergence of input of simple cells
-hypercomplex cells arise form the convergence of input of complex cells
106
how does resolution of the hypercolumn change throughout it?
Resolution of hypercolumn is lower in the peripheries of the visual cortex than in the center because there are less cells. So the density of cells determines how much foveal info is developed rather than the actual size of the hypercolumn as each hypercolumn is the same size. This is cortical magnification
107
what is needed for a stimulus to trigger a simple cell?
the stimulus has to be the correct orientation and fall within a specific part of the visual field
108
if an electrode penetrated the visual cortex obliquely, what will the receptive fields look like?
there is consistent drift in the position of the receptive field and the direction is dictated by the topographical map
109
if an electrode penetrated the visual cortex vertically, what would the receptive fields look like?
the receptive fields would overlap but would vary in size as different cells within each hypercolumn will have different sized receptive fields e.g. cells in layers 3,5 and 6 will have larger receptive fields than those in 2 and 4 as they are all in the same location column (where the receptive fields pile on top of each other in pretty much the same place but have different sizes )
110
how does the effect of a cortical shit on the receptive field position compare between the foveal region and peripheries of the primary visual cortex?
* For the foveal region of the primary visual cortex, a cortical shift of 1-2 mm moves the receptive field position by only 0.1 visual degrees.
* With increasing eccentricity, a cortical shift of 1-2 mm may move the receptive field position by several degrees.
111
what is bandwidth?
Bandwidth is the ratio of spatial frequencies at which contrast sensitivity is halved so one octave of bandwidth is a doubling of spatial frequency.
112
what is the bandwidth of LGN cells?
around 5 octaves
113
how can you determine bandwidth from a spatial frequency graph?
go to the half, find out where it intersects the curve, look at the spatial frequency and see how many doublings (octaves) have occurred at each point. The number of octaves is the bandwidth
114
what do the lobes of bar and edge detectors tell you?
smaller lobes have a higher/ optimal spatial frequency and more lobes mean a more narrow bandwidth so the more sharp the tuning is to spatial frequency
115
what is the blob? how do spatial frequencies change closer and further from the blob?
one of the sites of targeting in the parvocellular system and is where colour vision is processed. Away from the blob are higher spatial frequencies and closer to the blog are lower spatial frequencies
116
what aspects of vision are at the same level as that of an adult at birth?
-magno system
-colour perception
(orientation, contrast and stereopsis take years to develop)
117
how did teller cards originally be used to measure an infants visual acuity?
using preferential looking where the clinician stands behind a screen with a hole so they can look through and on the other side is a circle with lines on it and then allows the clinician to see where the baby is looking and ideally with decent visual acuity, they will look at the circle
118
what two techniques can be used to measure infant VA, which is better and why?
-preferential looking and visual evoked potential VEP
-VEP is better because its always accurate even at more reduced contrasts as it is objective
119
what is cone quantal efficiency?
the ability of cones to capture photons of light
119
how long after birth does rate of VA improvement start to level off
after around 6 moths to a year
120
why are babies born with poor vision?
-When a baby is born the inner segments of their cones are much fatter than what you see in the adult eye which means there is a lower density of cones in the fovea as less can fit, a lot of space where light is coming through but is not captured by the photoreceptor
-their outer cone segments being much shorter so they have a lower cone quantal efficiency to light - cone length 1/10th of an adult
-Small eye size
-Myelin sheath around the axons of the RGcs is still developing hence reduced efficiency of the RGCs sending impulses to the brain
-LGN and visual cortex continue to develop and progressively respond to higher frequencies, there are much less interconnections in the hypercolumns: brain itself is much smaller so as the size increases it will have an impact on the quality of the vision
121
what happens to the contrast sensitivity curve of babies once they are born?
the peak sensitivity shifts to higher spatial frequencies in the first 12 months allowing images to be seen with higher contrast
122
when does the refinement of the visual cortex occur?
general organisation of the visual pathways is completed before birth
once a baby opens their eyes and light reaches their retina as sensory input, the refinement begins at V1.
123
how can orientation perception in babies be determined?
via VEP using phase shifts and orientation shifts and if there is no change in brain activity between the phase shifts and orientation shifts, then that child does not have any orientation perception
124
how do growing axons of the developing optic nerve know where to go?
-need to grow along the correct pathway and select the right target
-via molecular sensing
-axons have a specialised tip (growth cones) that's guided by chemotaxis so cells can work out where they are supposed to be, and then undergo further refinement
125
what can cause visual deprivation in children?
-strabismus
-anisometropia
-Astigmatism
-Myopia
-neonatal cataract (most severe clinical deprivation: almost like lid closure)
this can all affect the development of the visual cortex
126
how do orientation columns change after birth?
The elements of the orientation column system are present at birth, but the selectivity of the individual cells within the system develops and fine tunes after birth.
127
how do ocular dominance columns change after birth?
At birth the input from the two eyes is overlapped in the cortex, segregation
into ocular dominance columns occurs after birth. when this occurs, stereopsis becomes present
128
what is monocular deprivation?
where you wipe out the receptive field properties of all the V1 cells in the eye that is covered during time of development -there's no cortical volume dedicated to the deprived eye due to severe amblyopia in the deprived eye
129
what causes severe amblyopia in the deprived eye in monocular deprivation?
due to major changes that occur in the projections from the LGN to the cortex
130
what does reversal of monocular deprivation show about the visual cortex?
he visual cortex is plastic because you can manipulate the receptive field properties depending which eye is being occluded - this is where eye patching arises from as in animal models, depriving the ‘good’ (eye that was open) eye shows the ‘weaker’ (eye that was occluded) can take up more cortical volume as it develops however if you deprive the ‘good’ eye for too long then you get reversal again.
131
give an example of an aspect of pattern vision that can be affected by visual deprivation and how
e.g. orientation which can arise from uncorrected astigmatism where they may have a bias to horizontal or vertical or oblique orientations.
132
how does uncorrected anisometropia affect contrast sensitivity?
as it causes the contrast sensitivity curve to ve depressed and shifted left as the parvocellular layer is smaller and has fewer connections hence causing images to be blurred.
133
what happens to axons of the LGN in normal development?
they separate to form ocular dominance columns
134
in animals how does monocular deprivation affect the size of ocular dominance stripes?
in normal, width of left and right eye ocular dominance stripes are equal whereas in monocular deprivation, width of ocular dominance stripes of normal eye is greater than that of the deprived as each eye is competing for cortical space
135
in strabismic animals, why does binocularity disappear?
binocularity disappears as the eyes are not going to be looking in the same direction causing a reduction in the number of binocular neurones. If an eye is misaligned, the binocular cells that are present have a horizontal orientation preference instead of vertical orientation preference.
136
why is it that when there is strabismus, binocular cells have a horizontal orientation preference?
because vertically tuned simple cells do not overlap so no pattern can stimulate both cells whereas for horizontally tuned cells, some overlap forming a bar stimulus which can activate both cells
137
what two aspects of vision are not easily changed by visual deprivation?
colour and motion
138
what is the critical period?
the period of time the visual system is plastic. visual stimulation is essential for normal visual development and visual function determines the exact timing of this period
139
how is plasticity different between the visual cortex layer and the temporal cortex?
the input layer (layer IVc) of the visual cortex is less plastic than the output layers ( II, III, V and VI) and in the temporal cortex, plasticity presumably continues indefinitely to allow storage of new visual memories.
