Module two - Machado Flashcards
1
Q
orientation of the midbrain
A
anterior/rostral
posterior/caudal
superior/dorsal
inferior/ventral
2
Q
lateral
A
towards the side
3
Q
medial
A
toward the midline
4
Q
ipsilateral
A
on the same side
5
Q
contralateral
A
on the opposite side
6
Q
dorsal/superior
A
top
7
Q
ventral/inferior
A
below
8
Q
rostral/anterior
A
front
9
Q
caudal/posterior
A
back
10
Q
terms for slices of the brain
A
horizontal, coronal, sagittal
11
Q
fissure
A
longitudinal (down the middle)
12
Q
corpus callosum
A
white matter allowing the two hemispheres to speak to other.
13
Q
cerebellum
A
just above the brain stem at the front of the brain
14
Q
thalamus
A
a subcortical structure that relays and filters information from the senses and transmits the information to the cerebral cortex.
15
Q
brain stem structures
A
midbrain (superior and inferior colliculi)
pons
medulla.
16
Q
ventricular system
A
consists of inter-connected cavities with cerebrospinal fluid.
17
Q
cerebral cortex
A
divided into two hemispheres and four lobes (frontal, parietal, occipital, temporal)
18
Q
what is the brain made of?
A
10% neurons, 90% glial cells
19
Q
structure of neurons
A
dendrites, cell body, axon, axon terminals.
20
Q
dendrites
A
extend from the cell body. receive input from other neurons.
21
Q
soma
A
cell body
22
Q
axon
A
extends from the cell body and sends messages to other cells (some are covered in myelin)
23
Q
myelin
A
a fatty substance formed by oligodendrocytes - speed up the electric signals between cells.
24
Q
axon terminals
A
where the axon comes into contact with another neuron
25
synapse
where two neurons meet, there is a tiny gap called a synapse. signals cross this gap using chemicals released by a neuron. the chemical diffuses across the gap makes the next neuron transmit an electrical signal
26
pre- and post-synaptic.
pre (before the synapse, goes from electrical to chemical) post (after the synapse, goes from chemical to electrical signals)
27
three main types of glial cells
astrocytes, oligodendrocytes, microglial cells.
28
astrocytes
form blood brain barrier.
29
oligodendrocytes
produce myelin in CNS to cover axons.
30
microglia
remove debris left by dead brain cells.
31
what is an action potential?
electrical impulse that travels down the axon triggering the release of neurotransmitters.
32
what causes action potentials
sensory input
33
single cell recording
recording the action potential from a single neuron
34
receptive field
cells only respond to stimuli in a region of space (receptive field) of that cell.
35
when do we use functional imaging (fMRI)
when multiple cells will be firing at once. it gives us an overall representation of the active cells. we can then estimates the number of cells there.
36
maps of neural activity
we can map different action in auditory cells and when we're smelling things etc.
37
what is cognitive neuroscience
branch of neuroscience that focussed on brain function and dysfunction - relates behaviour to brain function
38
what is cognitive psychology
branch of psychology that focuses on complex mental processes such as perception learning and memory.
39
brain lesion analysis
uncovers how the brain works by studying those lesions in specific regions. if we can find a commonality between impairments of a group of people with damage to one area then we can attribute that impairment to the damaged area of the brain. a control group is needed.
40
electroencephalography (EEG)
recording of the electrical activity of the brain, pattens are usually really similar across people (unless there is something wrong). this means we can use this to pick up abnormal activity as seizures.
41
event related potentials (ERP)
Based on EEG. involves time locking an event so we can see how the brain responds to certain events.
42
how do we remove noise from ERP
averaging a large number of trials.
43
latency, amplitude, topography
speed of activity, how much activity, where was the activity.
44
ERP strengths and weaknesses
strength: temporal resolution (timing).
weakness: spatial resolution (where)
45
neuroimaging
the use of various techniques to provide pictures of the structure and function of the living brain.
46
structural imaging
computed tomography, magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI).
47
positron emission tomography (PET)
patient needs to be injected with radioactive material, invasive, shows a concentration of radioactive substance showing a functional view of the brain.
48
functional magnetic resonance imaging (fMRI)
adaptation of MRI that records changes related to metabolic activity in successive images in order to produce a functional view of the brain, non-invasive, magnets are used.
49
transcranial magnetic stimulation
non-invasive, uses a coil to stimulate parts of the brain. can be excitatory (causes movement) or inhibitory (stops movement).
50
converging methods with brain scanning
it is best to combine information from all these tools to gain clearer conclusions
51
how do we hear (simple terms)
ear captures sound waves and auditory receptors turn this mechanical energy of vibrations caused by sound waves into electrical signals that get transmitted to the brain
52
parts of the outer ear
pinna (ear folds) and auditory canal (ends at the eardrum)
53
middle ear parts
ear drum and ossicles (middle ear bones that transfer energy to the inner ear)
54
inner ear parts
cochlear (spiral shaped fluid filled tube) that contains hair cells that act as receptors for sound. the vibrations cause the fluid to move that moves the hair cells that transform the mechanical energy into electrical energy.
55
spiral ganglion cells
tuned to a specific frequency of sound.
56
tinnitus
hearing sound where there is none in the external environment such as a buzzing or ringing (caused by disease of spontaneous activity such as loud music)
57
how does auditory information get to the brainstem.
it travels through the vestibulocochlear nerve which is also related to balance.
58
is hearing bilateral
yes, the information can stay on the same side of the brain or cross over. this is why when we have damage to one cortex it doesn't affect hearing except localisation of sound can sometimes be harder.
59
which is the first region of the cortex to process sound
primary auditory cortex located in the superior temporal lobe (cells are laid out in order of frequencies making it easier to interpret different frequencies.
60
how do we tell where a sound comes from? (localisation)
related to the slight difference in time it takes to arrive at the two ears (sounds on the right will get to the right ear before the left). The time difference is called intramural time.
61
sound localisation on the vertical plane
not as good in humans but is related to the shape of our ears. our brain recognises and learns the shape of our own ear and the patterns in where the sound is coming from vertically. if the pinnae are covered our vertical lateralisation is impaired.
62
pathway of sound
external ear ->>> middle ear ->>> inner ear ->>>> brain stem ->>>>> thalamus ->>>>> cortex.
63
sclera
the white of the eye - continuous with the cornea.
64
macula
the central area of the retina that is specialised for central vision.
65
fovea
the visual image received by the fovea is the least distorted; marks the centre of the retina and the centre of the macula.
66
muscles of the eye
there are three pairs of extra ocular muscles which are inserted into the sclera enabling the eye to move.
67
the flow of visual information within the retina
photoreceptors, bipolar cells, ganglion cells.
68
information about light flows in what direction
nerve fibres, to ganglion cells, to bipolar cells, to photoreceptors (rods and cones).
69
blind spot in the eye.
where light hits the optic nerve, there are no cells there to receive information.
70
optic disk
where axons of retinal ganglion cells exit from retina and then form optic nerve.
71
temporal view
the half of the retina furthest away from the nose (temporal hemiretina)
72
nasal view
half of the retina close to the nose (nasal hemiretina)
73
what happens if the left optic nerve is cut
vision from the left eye will be lost completely.
74
what happens if the optic chiasma is transected
peripheral vision will be lost.
75
what happens if the left optic tract is cut
vision of the right hemifield will be completely loss
76
optic nerve
axons of ganglion cells are called this before the cross as the optic chasm.
77
optic tract
axons of the ganglion are called this after they cross at the optic chasm.
78
retinotectual pathway
retina, thalamus, primary visual cortex.
79
lateral geniculate pathway
the left and right LGN re the two major targets of the two optic tracts.
80
primary visual cortex
receives visual inputs, first region of the cortex to process visual information.
81
phosphene threshold for people on ecstasy and not
those on ecstasy had a lower phosphene threshold.
82
sensory integration
different senses can be integrated into vision to influence our perception - example seeing a puppet speaking because you can hear the voice and see the mouth moving.
83
cells responding to a receptive field
each cell has it's own limited region of space. the cell will fire when something is in that region.
84
what are neuron in the MT selective for?
direction and speed of motion.
85
subtraction methods
there is a lot of other activity going on in the brain so we need to isolate certain activity to what we are looking at. Experimental condition (activity of interest) minus the control condition (assists towards isolating the activity linked to event of interest)
86
what does the dorsal stream code
motion and location (where)
87
what does the ventral stream code
detailed stimulus features and object identification (what).
88
interconnectivity of the extra striate cortex
different areas (V1-V5) are not all connected with each other and do not flow sequentially from one area to the next (there are some projections directly from V1 to V5). This information is all integrated to provide a coherent visual experience.
89
area V4
located along the ventral stream, selective for colour and form.
90
area V5
located along the dorsal stream, also called area MT, selective for direction and speed of motion.
91
what pathway is subcortical vision
retinotectual pathway
92
what pathway is cortical vision
retinogeniculostriate pathways (90% of axon in the optic tract)
93
which cortical system evolved first
the subcortical system, the cortical system evolved later on.
94
sprague effect
the restoration of orienting towards the cortically blind hemifield - results from cutting fibres that originate in another nearby structure and project to the superior colliculus on the same side as a cortical lesion.
95
important points for the sprague effect
removing visual cortex was devastating for the cat, subcortical visual pathways were unable to compensate for the damaged cortical visual pathways until the ipsilateral superior colliculus was released from normal inhibition (thus disinhibiting the subcortical visual pathway on the side of the cortical damage)
96
visual cortex vs. superior colliculus damage
in a localisation task cortical damage didn't matter but subcortical damage did and vice versa for a discrimination task.
97
what does complete damage to V1 within one hemisphere do?
renders patient hemianopic
98
hemianopic
the rods and cones are still firing but the patient has no conscious, awareness of anything in the ipsilateral hemisphere of vision.
99
blindsight
the term coined to residual vision where people still see things outside their own conscious awareness
100
what does blindsight suggest
the subcortical visual pathway in human may play an important role in orientating towards visual stimuli.
101
activity of neurons in the deeper layers of the superior colliculus - monkeys.
recorded deeper neurons during eye movement, found that these neurons have a movement field they move even when in darkness, a large population of broadly tuned cells are active for each eye movement.
102
what is a saccade
a rapid eye movement.
103
overall conclusion about neurons in deeper layers
they can have vasomotor or pure motor capabilities.
104
superior colliculus lesion experiment in humans
eye movements were recorded, results suggested that the superior colliculus plays an important role in generating rapid eye movement towards stimuli that appear in the contralateral hemifield.
105
reflective eye movements.
helps survival, often referred to as exogenous eye movements because they are driven by external stimuli
106
fixation reflex
triggered by an external visual stimulus projecting onto central vision, superior colliculus is important for this.
107
saccade and fixation reflexes
eye movements and fixation are opponent processes.
reflexive saccades help our eyes move in order to foveate a sudden change in the visual periphery, whereas the fixation reflex helps our eyes maintain their position.
108
fixation offset experiment
the fixation offset effect provides a measure of responsiveness of the fixation reflex, they found that having the original stimulus present made looking at the target stimulus a lot slower than if it disappeared when the target appeared.
109
voluntary eye movements.
choosing to move our eyes towards something whether or not there is external stimulation.
called endogenous.
110
endogenous eye task.
fixate on centre, an arrow head will appear pointing towards a box on the screen, look at the box and then fix gaze back to centre.
111
exogenous eye task
this is reflex eye movements. fixate in centre and move gaze to where the object appears.
112
effects of TMS over cortex on saccades (REM)
for endogenous task saccades direct towards the contralateral hemifield were delayed when TMS was over the prefrontal cortex. TMS over the parietal lobe did not affect the speed. for the exogenous task the TMS did not produce a response.
113
conclusion of the delay in contralateral endogenous saccade
was a consequence of disrupting the normal operation of the frontal eye field.
114
experiment where patients had lesions
those that had lesions in the frontal eye field had delayed eye movements to the contralateral hemifield.
115
conclusion of the experiment with frontal eye lesions
frontal eye fields are normally involved in generating voluntary eye movements.
116
reflexive eye movements depend more on what?
subcortical structures.
117
voluntary eye movements depend more on what
cortical structures.
118
why so reflexive eye movements happen faster
because less connections need to be made - fewer neural connections need to be made. less processing compared to voluntary eye movements.
119
reflexive orienting
humans rely on reflexive orienting to avoid danger but reflexive behaviours are not always advantageous.
120
cortex and subcortex at birth
newborns are believed to have mature subcortical structure but cerebral cortex is not fully developed.
121
fixation offset effect in infants
compared to the older infants 1.5 month olds showed slower responses indicating the fixation reflex was stronger. maturation of the cortex in older babies allowed better strategic control.
122
when do frontal lobes fully develop
15-20 years of age
123
anti-saccade task
fixate on centre, when stimulus appears move eyes in the opposite direction, return eyes to centre - this required inhibition of a reflexive saccade followed by execution of a voluntary saccade.
124
who performs better on the anti-saccade task in children
those aged 15 performed better than children 5-8 years who had the most directional errors.
125
why are younger children worse at the anti saccade task
because of delayed maturation of the frontal lobes. damage to frontal lobes in adults should cause the poorer performance to return.
126
reflexive saccades in those with damage to one frontal eye field
poor performance on contralateral stimuli but performed fine for ipsilateral stimuli, supports hypothesis that frontal eye field normally imposes inhibitory control over the ipsilesional oculomotor circuitry that generates reflexive saccades.
127
relationship between frontal eye field and superior colliculus
each SC controls reflexive eye movements towards the contralateral field.
128
healthy aging
neurons die over time so performance in anti saccade tasks decrease over time.
129
frontal lobe enables what
efficient voluntary control over visual orienting.
130
the oculomotor system
oculomotor behaviour is determined by cells in a number of brain areas at the subcortical and cortical levels.
subcortical cells mediate more primitive reflexive oculomotor responses.
phylogenetically newer cortical cells impose control over primitive reflexes via projections to subcortical cells, facilitating them when advantageous and inhibiting them when disadvantageous.
131
visual attention is determined by what
things in our external environment (exogenous influences) and internal factors (endogenous influences)
132
which visual task take more control (exogenous/endogenous)?
endogenous (more conscious control and awareness, voluntary not as reflexive)
133
overt vs. covert shifts of attention
overt is looking directly at something and paying attention to it whereas covert is paying attention but not looking directly.
134
effects of covert attention on occipital lobe activity found that
there was a stronger response when stimulus appeared where participants were covertly focusing their attention (indicates that focusing on one part means we lose focus of other parts of our visual field).
135
movements of attention difference between exogenous and endogenous.
exogenous shifts are elicited by an external stimulus (superior colliculus is responsible) endogenous shifts of attention are elicited internally (cortical neurons are important).
136
facilitation
if there is something indicating where a stimulus is going to appear we react quicker when the stimulus does appear (attention facilitates responses).
137
inhibition of return
when attention is directed towards a location and there is a long delay before a target appears, the reaction time is longer because inhibition of return discouraged us from looking at the location again because there was nothing there earlier.
138
what is the flanker task used for?
assessing the efficacy of strategic control over attention (how easily distracted a participant is) - measured by RT on incongruent trials minus congruent trials.
139
steps of brain development
cell division
cell migration
cell differentiation
140
cell division
stem cells divide into two cells, newly divided cells migrates away to take up position in the cortex and stem cell remains to undergo more division.
141
cell migration
we form one layer at a time, as new cells come they move past already formed cells to a newly formed layer.
142
cell differentiation
newly divided cells take on the appearance and characteristics of a neuron of glial cells.
143
plasticity
refers to the ability of the nervous system to change and learn new things, plasticity declines as we get older.
144
results of the study rewiring the brain of newborns
after the animals were raised to adulthood the neurons in PAC in the rewired hemisphere behaved like visual neurons in response to visual stimuli.
145
results fo the effects of stimulating visual cortex in adults with impaired vision
results indicated that the effect of activating the visual cortex is altered in people with severe visual impairment, as evidenced by a reduction in the ability to elicit light flashes in people with a high degree of visual impairment (especially if those people have been blind since birth).
146
results of study on mental imagery in sighted and congenitally blind adults
in both congenitally blind and sighted participants, the production of mental images was associated with activation of the visual cortex (even if they'd never seen before).
147
training and plasticity in humans study - results
greater changes to blood flow occurred in the contralateral primary motor cortex for trained than for untrained sequences after only three weeks of training and greater changes still occurred even after 8 weeks of no training.
148
conclusion about training and plasticity in the human brain
in the human adult brain, training can induce relatively rapid changes in brain activity that reflect the plastic ability of the nervous system to acquire and retain new information and skills.
149
the ageing brain and plasticity
brain becomes less plastic, size of hippocampus reduces, this can be combatted with engagement in aerobic exercise which increases the size of hippocampus.
