Past paper 1 Section C Flashcards
A) Neural correlates of prediction error
B) Dorsal stream in language processing
C) The somatic marker hypothesis
The somatic marker hypothesis (SMH) arose from studies of patients with neurological damage – in particular, those with damage to the amygdala, and those with damage to the orbitofrontal cortex/ventro-medial prefrontal cortex. (The anatomical and functional distinctions between the OFC and vmPFC are disputed.)- the somatic marker is the prior memories linked to emotions
Regarding the amygdala:
* Patients DR and SE, with bilateral damage, showed selective impairment in the recognition of “fear” from face photographs (mean 4/10 correct vs. 8.6/10 for controls; performance was normal for other emotions; Calder et al., 1996).
* Lesions to the amygdala abolish/reduce the acquisition of fearful responses to initially neutral stimuli which are repeatedly paired with aversive outcomes (e.g., Blanchard & Blanchard, 1972)
* Patients with amygdala lesions show less declarative memory for emotional material. For example, participants were shown a slide show with accompanying narrative which included some emotional elements (scenes of surgery) and 24 hours later answered questions about what they had seen. Controls showed better memory for the most evocative slide than for the other slides; patients with amygdala damage did not (Adolphs et al., 1997).
* The superior recall of information about emotionally arousing pictures (both pleasant and unpleasant) relative to retrieval of neutral information has been found to correlate with the size of the amygdala activation during encoding (Hamann et al., 1999)
Regarding the vmPFC:
* Lesion patients show increased emotional reactivity (e.g., frustration, irritability) and decreased emotionality (i.e., they are judged to be less responsive, show blunted affect, socially withdraw; Anderson et al. (2006).
* Patients also fail to show the elevation in skin conductance response (SCR – a measure of sweating) that usually accompanies viewing a socially-evocative slide image (e.g., a mutilated body; Damasio et al., 1990).
* When faced with moral dilemmas which pit the emotionally-charged sacrifice of one person against the greater loss of other lives, lesion patients were more likely to choose the “utilitarian” response (e.g., shoving one person under a train to save five others; Koenigs et al., 2007)
Amydgala and vmPFC damage and decision-making
Phineas Cage after damaged the amygdala, he makes poor decisions.
Emotions are key for making rational decisions since the amygdala are actually used for both emotions and decision making. Without weighing decision back and forth by using conscious cue of emotions. The prior memories linked to emotions are called somatic marker.
Antonio Damasio and colleagues noted that vmPFC patients often show impaired “real life” decision-making, but are indistinguishable from “normal” participants in terms of general intellect and performance on a range of neuropsychological tests.
D) Unilateral neglect
Inattention to side of
space opposite lesion
(more severe following
right sided lesions)
¡ Ignore food on left of plate
¡ Groom only right side
¡ Damage to Posterior
Parietal Cortex..
A) Interocular Transfer of Adaptation
interocular transfer. Refers to a change in threshold in one eye which had been occluded, similar to, but of lower magnitude, than that in the fixating eye in response to a visual stimulation.
No interocular transfer: colour + light/dark adaptation
Yes : tilt after effects, motion aftereffect
We have seen in previous lectures that adaptation to specific visual attributes
(a direction of motion, a particular wavelength of light or a particular orientation) can help to specify
the nature of the neural mechanisms underpinning these aspects of vision. In this lecture, we discuss
the interocular transfer of the effects of adaptation, to help understand where in the visual system
these adaptation effects occur. When an adapting stimulus is viewed with only one eye, the
aftereffects of the adaptation on subsequent perception can be measured separately for a test stimuli viewed with the same adapted eye, versus the test stimuli viewed with the unadapted eye.
If the site of adaptation in the eye/brain is pre-cortical (along the geniculostriate pathway), the affected cells
are monocular (receiving input only from one eye) and an aftereffect should only be seen in the
adapted eye.
Conversely, if the site of adaptation is in the visual cortex, the affected cells are much
more likely to be binocular (receiving input from two eyes) and we should then expect the aftereffect
to be similar when viewed in the adapted versus unadapted eyes.
B) Arousal
Arousal generally refers to the experience of increased physiological (inside-the-body) activity. This can include an increased (faster) heart rate, perspiration, and rapid breathing. Within the context of social psychology, the experience of arousal has implications in a number of areas, including the experience of emotion, attitudes, lie detection, aggression, attraction, and love.
C) Outer and inner hair cells
We know from Lecture 1 that the hair cells in the organ of Corti are responsible for transducing physical
vibration into electrical impulses, but we didn’t discuss their functions. There are two types of hair cells, inner
hair cells (closest to the centre of the cochlea spiral) and outer hair cells.
Outer hair cells play a critical role in actively amplifying the incoming sound. In particular, when their
stereocilia are stimulated they contract, pulling the tectorial membrane with them and adding vibration
energy to the organ of corti. They contain a remarkable motor protein (prestin) that is one of the fastest
acting biological motors known to man (much faster than the myosin molecules that contract muscle). They
have been observed to contract and expand over 70,000 times per second, but may be able to go faster!
Their movement was beautifully demonstrated by Jonathan Ashmore at UCL – using a patch clamp pipette
on a single outer hair cell from a guinea pig, they injected an electrical current waveform of “Rock around the
clock” – demonstrating movements that mirror changes in sound level.
The amount of active amplification provided by the outer
hair cells is not constant – it amplifies low intensity
sounds a lot (~50 dB) and the gain reduces as the input
intensity increases. This change of amplification is a
significant non-linearity in cochlea behaviour. The
‘active process’ of amplification can introduce new
frequency information on the Basilar Membrane. You
should hope your music system is linear – you don’t want
it introducing its own frequencies to your favorite tunes,
but the human auditory system is anything but linear!
The active amplification process makes the relationship
between input and output curved (a compressive
nonlinearity).
The behaviour of the outer hair cells can be
diagnostically very useful. We can stimulate the ear with
two pure tones, and then record the sound information
that comes back from the ear. If the hair cells are
working correctly, then we can measure sounds coming
out of the ear that contain frequencies that weren’t in the
input. These sounds are referred to as otoacoustic
emissions – and nowadays they form the basis of the
new-born hearing screen.
Damage to the outer hair cells significantly reduces
active amplification with the result that individuals can
have significant hearing impairments. Thus, the outer
hair cells play a key role in normal hearing.
The inner hair cells have a quite different function and
are critically involved in the fast transmission of sound
information to the brain. Outer hair cells generally form
synapses to a single ganglion cell which pools responses over several hair cells. Inner hair cells however
speak to multiple ganglion cells, and they don’t share their audience! Each individual inner hair cell has
synaptic connections to around 20 ganglion cells which send fast axons through the auditory nerve to the
cochlea nucleus.
The organisation of the cochlea nerve is tonotopic, with individual axons responding most to a particular
sound frequency (the characteristic frequency) and only responding to a limited range of frequencies (i.e.,
band pass filters). The ganglion cells that connect with a given hair cell have different characteristics, and
are classified into 3 types depending on how many action potentials they produce ‘at rest’ (i.e. when there is
no sound). High spontaneous rate axons (20-50 spikes per second in quiet) will respond to low intensity
sounds, but they saturate (i.e. can’t fire any faster) once sound level reaches ~ 40 dB SPL. Medium (< 18
spikes/s at rest) and Low (< 1 spike/s) spontaneous rate axons will not increase their firing rates with sound
level until it reaches 20-30 dB SPL, and they continue increasing firing until sound level increases to 80 dB
SLP or more. Thus, individual axons have different response gains – some respond better to low sound
levels and others high sound levels: this differential activity may contribute to our perception of loudness over
such a wide range.
All of this is quite suggestive of the importance of a place code for signalling sound frequency. However,
reliable temporal information is also available to the brain…
D) Describe the path of air vibrations that are perceived as sounds.
Vibrations are channelled by the outer ear (pinna and meatus) to the ear drum (tympanic membrane).
The air pressure differences between the two sides of the ear drum cause it to move in and out with the sound.
The next step is the complex ossicular chain of the
middle ear: the malleus, incus and stapes. The Malleus
is attached to the ear drum, with the stapes interfaces
with the oval window of the cochlea. This complex
chain of bones serves to act as an impedance
matching device. This is needed because the cochlea
is filled with fluid (perilymph) that has a much higher
impedance than air. By analogy, if you shout to a friend
swimming underwater, they are unlikely to hear because
the majority of the sound energy would bounce off the
surface of the water due to the water’s higher
impedance. So it is with the cochlea – if the ossicles are
damaged – sounds need to be very loud for a person to
have any chance of hearing them. The area of the ear
drum is much larger than the face of the stapes, meaning
that the ossicles concentrate the same force over a
much smaller area (think of it like a drawing pin – you
can push these into a hard wall because the point of the
pin is very small in relation to the area you push with your
thumb). The hinge-like ossicular chain also provides a
degree of leverage to further amplify the movement of
the stapes. This arrangement is quite complex, because
muscles interfacing with the ossicles allow a reflex to
partially disengage the stapes during loud sounds (the
acoustic reflex). This reflex is rather slow (it won’t
protect your ears from sudden loud sounds), but it can
help reduce damage to the cochlea in high sound
pressure environments. It also disengages when we
speak – probably accounting for why recordings of our
own voices sometimes sound odd.
A) Repetition suppression
B) Visual word form area
C) Dysexecutive syndrome
D) The limbic system
