Neuropsychology Flashcards
what does neuropsychology study?
studies the link between brain and behaviour. fundamentally about studying impairments in individuals who have suffered brain damage
what is the aim of clinical neuropsychology?
understanding the condition (diagnoses, assess)
what is the aim of cognitive neuropsychology?
understand normal functions in the brain by studying patterns of impairment after brain damage
what is the difference between ‘strong’ and ‘weak’ cognitive neuropsychology?
strong= use patient data to construct a theory
weak= use patient data to refine a theory
list seven causes of brain damage:
-traumatic injury
-stroke
-lack of oxygen (hypoxia)
-tumours
-brain infections or inflammation
-nutritional deficiencies
-chronic alcohol abuse
-surgery
Name the four assumptions in neuropsychology:
1- universality
2- modularity
3- fractionation
4- transparency
Explain the assumption ‘universality’ and how justified it is:
-cognitive processes are the same in all individuals. there is still scope for differences but average group of individuals is reflection of any individual in wider population
-everyone has the same structure of the brain but there are little differences in individual gross anatomy. brains are not symmetrical and some brains show different proportions of matter in different places
Explain the assumption ‘modularity’ and how justified it is:
complex cognitive processes can be broken down into simpler processing units
-there is very little actual evidence because it is difficult to prove
Explain the assumption ‘fractionation’ and how justified it is:
brain damage can result in the selective impairment of a particular process
-there is an abundance of evidence
Explain the assumption ‘transparency’ and how justified it is:
the cognitive system of brain damaged patient is fundamentally the same as that of a normal subject except for a local modification of the system- all other processes are in tact
-there can often be disruption to other cognitive processes, behavioural compensation, and natural re organisation
how do split brain patients complicate neuropsychology assumptions?
surgery is done in some epilepsy patients where they cut connection between the two hemispheres which stops the connections involved in epilepsy. for these split brain patients, once the fibre is cut the brain is deemed as acting ‘normal’ which means their original brain was abnormal. is it a fair assumption that their brain is representative of everyone?
What post morbid damage was found in patient HM that was resulted from surgery?
there was evidence of an undetected stroke as a result of brain trauma from the surgery, also there were metal chips left in the brain which had corroded over time and began to damage tissue around them
What is the group study approach?
patient group vs control group. inferences are drawn from between group comparisons, looking for associations of common deficits or common sites of damage
what are some problems with the group study method ?
-relies on the assumption of universality
-similar behavioural symptoms may arise from different underlying patterns of damage
-similar sites of damage may be associated with very different symptoms
-specific behavioural impairments within a syndrome may vary
-it is time consuming to find patients
-there is a risk of over interpreting associations
what is the Case Study approach?
looking for specific single deficits in a patient. mainly concerning dissociations between behaviour patients can or can’t do
Explain Single and Double dissociations:
Single Dissociation: if patient can do A but not B, A and B are likely to be independent processes in the brain and may involve different brain regions
Double Dissociation: one patient can do A but not B, another can do B but not A. strong evidence of involving different cognitive processes and brain regions
What is an alternative explanation for a single dissociation?
may simply be that B is harder than A, so damage to the process that controls A and B results in a more noticeable problem in B than in A
How was double dissociation used to distinguish Broca’s and Wernicke’s aphasias?
patient had spared word order and meaning (A), but impaired fluency (B).
other patients had impaired word order and meaning (A), but spared fluency of speech (B)
= different lesion sites for the aphasias
Why are double dissociations difficult to replicate?
it is difficult to find patients with purely damage to one cognitive process, and that are complementary to each other
what are the methods in Cognitive Neuropsychology?
-studies of individuals with localised brain damage
-studies of individuals who have been surgically operated on
-behavioural studies of healthy individuals
-imaging studies of both healthy and brain damaged individuals
-inducing temporary lesions in healthy patients
how can neuropsychologists confirm links from functions to structure?
-post mortem; confirm deficits in anatomy after death
-imaging techniques
Name four functional imaging techniques and a disadvantage of them:
-fMRI; slow time course
-PET; involves radioactive materials
-EEG; bad spatial resolution
-MEG; few machines in the world
What is a famous example of fMRI potential for error?
Emotional processing of faces by dead salmon
Explain fMRI:
-measures changes in oxygenation levels in the blood supply to the brain, not brain activity
-compares activity during task to a control group for tasks vs rest groups or difference between tasks
Explain TMS:
-Transcranial Magnetic Stimulation
-temporary damage to the brain to understand the link between structure and function
-sends electric pulse to temporarily disrupt activity in a localised function
Who established the term ‘Agnosia’?
Freud, 1891
What is visual object agnosia sensitive to?
specific to visual modality but can also be category specific e.g. recognising man made objects or natural things
how would a person with associative agnosia perform in the Matching by Appearance Task?
they could tell if the tow object items are the same, but they could not explain what the object is
Describe apperceptive agnosia:
can tell things about an object such as colour, shiny ness etc. but cannot understand how the individual components fit to make one object
how would a person with associative agnosia perform in a matching by function task?
they could make a match based on what object has the closest three dimensional structure
How much of a three dimensional understanding do associative agnosia patients have?
they can piece together pieces into three dimensional understanding of an object but they can’t name it
describe how associative and apperceptive agnosia patients perform when they are told to copy a drawing:
associative: can copy drawing but don’t know what they’re drawing
apperceptive: struggle to copy a drawing but can produce some of the correct elements
describe how associative and apperceptive agnosia patients perform when drawing from memory:
associative: could not draw from memory
apperceptive: could draw an object from memory
what are the damage sites of patients with associative and apperceptive agnosia?
apperceptive: unilateral right hemisphere damage in the right inferior parietal lobe
associative: usually bilateral. crucial area thought to be left hemisphere, more ventral than apperceptive
According to Warrington’s anatomical model, how does normal visual processing happen?
initial visual processing in occipital lobes, info passed to right hemisphere where perceptual categorisation happens, once the three dimensional model is complete info is passed to left hemisphere where semantic processing happens
How is perceptual categorisation disrupted according to Warrington’s Anatomical Model?
the three dimensional model can’t be made and the information cannot be passed on to semantic categorisation. but if they can access semantic categorisation by memory individually, info can be accessed.
In associative agnosia what part of the anatomical model is damaged?
semantic categorisation
What did progressive cerebral atrophy suggest about there being two distinctive types of agnosia?
there may be a continuum of agnosia with apperceptive on a more severe end than associative (De Renzi 1986)
describe pareidolia:
our facial recognition is so powerful that we can even see faces in cars, inanimate objects, food etc.
What might severe prosopagnosia look like?
patients can’t tell what is a face and what isn’t i.e. may think a clock is a person
What strategies can people with prosopagnosia use?
they can recognise people on the basis of other features like hair colour and clothing
What damage is associated with specific failure of face recognition?
damage to right fusiform gyrus
True or False: imaging face and object processing are the same process?
false, they are different processes
what is the inversion effect?
happens to recognition abilities when things are turned upside down.
why are faces harder to recognise when turned upside down?
inversion effect. we use the fact eyes are above nose and mouth, and also spacing between them. turning faces upside down upsets that configuration.
how do patients with prosopagnosia perform better in upside down face recognition?
inverted images release the pressure of the process of estimating nose and mouth spacing, and patients can use the other characteristics such as hair colour instead
how did patient WJ recognise his sheep after three strokes resulting in prosopagnosia?
found that he was able to recognise his sheep really well. categories of stimuli other than faces are in tact
what happened to Patient RM after he suffered an aneurism and was unable to recognise faces?
he was a car enthusiast and although he couldn’t recognise faces he was exceptionally able to recognise different cars
is right fusiform gyrus key for recognising and processing faces?
no, some patients have other damage. right fusiform gyrus also shows activity for non face stimuli and so is not specifically tuned to human faces
how does the right fusiform gyrus work for patients with congenital prosopagnosia?
there is brain activity when looking at faces like normal
how did dog breeders perform in the dog inversion tasks?
found dogs much harder to recognise upside down
how was Greeble Inversion consistent with ‘expertise’ recognition bias?
by the end of a special ‘training’ on made up creatures the participants started to show inversion effect but less so than for faces
why is expertise recognition probably untrue?
if right fusiform gyrus is process for recognising expertise, people with damage to this should not be able to become experts on recognising anything that’s new. this is not true i.e. farmer able to recognise sheep again after time
Why did Henry Molaison (patient HM) need surgery after being knocked down by a bike age 7?
he suffered from severe epilepsy
What was a negative unanticipated consequence of patient HM epilepsy surgery?
he had immediate and profound memory impairments
How did Patient HM provide evidence towards localised brain functions?
Pattern of memory deficits revealed new insights into memory processes and suggested localised memory function in the brain
What type of memory impairments did patient HM suffer from?
severe anterograde amnesia (ability to form new memories), mild retrograde amnesia (for three years prior to surgery)
what lesion resulted in patient HM memory problems?
bilateral hippocampal lesion
Which famous faces was HM unable to recognise?
people who became famous after his surgery
What happened to patient HM’s semantic memories?
his new semantic memories were severely impaired, as shown by word and famous name tests. but in all experiments performance for 1950s stimuli was above chance which is evidence that some new semantic memory must have been laid down
What happened to patient HM working memory and short term memory?
he had a normal working memory and could maintain a conversation but if someone left and came back he wouldn’t remember
What happened to patient HM motor memory, what did this suggest?
remained intact, suggests distinction between motor learning and other memory systems
describe the dot priming task:
*Show target pattern to join dots and
ask participant to copy this onto dot
pattern
* Distractor task
* Then given dots and asked to join
them in any way they want to
* Look at how frequently they
produce the target patterns
How did HM preform in Gollin’s incomplete picture task?
he performed better on the retest but did not remember doing the test before
Describe declarative memory:
conscious knowledge of facts and events
Describe non declarative memory:
skill learning, motor learning, perceptual learning, priming. develops gradually but with little ability to report what is being learned
are declarative and nondeclarative memory the same system?
Distinct memory systems with distinct anatomical localisation
what memory system did patient HM help identify?
a medial temporal lobe memory system: key role in laying down new memories, not the site of memory storage and not central to accessing stored memories.
Why couldn’t patient HM have an MRI?
due to worries about clips left in his brain after surgery
What was found in patient HM’s brain in a post mortem?
he suffered from sever cerebellar atrophy due to anti seizure drugs. there was also a 5cm medial temporal lobe lesion
How did patient HM help identify a distinction between remote semantic and autobiographical memory?
early reports suggested intact memories for life up to three years pre surgery but autobiographical memory was quite impaired when examined- impaired autobiographical, spared semantic
What happened to patient HM’s brain in later life?
damage found in 1998 had progressed by 2003. various white matter lesions were found in 2003, more than typical for healthy ageing. cortical thinning found in 2003.
How did patient HM react to himself in the mirror?
he was unaware of his own age and appearance but not confused when looking in a mirror
What is Wernicke-Korsakoff syndrome?
-anterograde and retrograde amnesia as a result of chronic alcoholism. episodic and some aspect of semantic memory formation is impaired. the effects vary between individuals.
-severity of retrograde and anterograde amnesia are not always correlated
-procedural memory is spared but working memory may be impaired
Why may the working memory be impaired in some Wernicke-Korsakoff patients but not all?
it is linked to the extent of frontal lobe damage
What is the biological causation behind Wernicke-Korsakoff syndrome?
consequence of thiamine deficiency
What happened to patient CW after contracting Herpes viral encephalitis?
he suffered brain damage to hippocampus, temporal lobes, and prefrontal cortex
what problems were caused by patient CW brain damage?
severe anterograde and retrograde amnesia. his memory was restricted to 30 seconds. also had object recognition difficulties for living things
What skills did CW manage to keep after injury?
preserved IQ, normal range on perceptual tests, fluent reading
Why did patient CW get frustrated by his diary entries?
he refuses to believe he wrote the previous entries
In what ways did Angie lead a successful life after brain damage?
she married, had three step children, and a successful career.
what strategies did Angie use to minimise the impact of her brain damage on her life?
-simplified complex problems into smaller tasks
-made lists to tick off tasks
What damage did Angie have?
closed head injury resulting in severe anterograde amnesia and right sided motor weakness
Which area of the brain is involved in motor issues like Parkinson’s, Huntington’s, and Tourettes?
The Basal Ganglia
Which area of the brain is affected in ataxia?
Cerebellum
Which part of the brain is affected in apraxia?
the cortex
What is the striatum made up of?
caudate nucleus and the putamen
the striatum, pallidum, subthalamic nucleus, and substantia nigra are all major regions within the what?
the basal ganglia
Explain the nature of the symptoms in Parkinson’s disease:
Three categories:
-Cognitive
-Positive: tremor, rigidity, involuntary movements
-Negative: akinesia/bradykinesia, posture/action initiation, locomotion, speech
What happens to dopamine in people with parkinson’s?
degeneration of dopamine producing neurons in substantial nigra causing reduced levels of dopamine in the brain
What drugs are used to treat Parkinson’s?
L-dopa (levodopa) and dopamine agonists
How effective is long term levodopa use in Parkinson’s patients?
-some patients might deteriorate as use continues long term
-symptoms like dyskenesias in long term
What is the primary target for surgical treatment (i.e. Electrical stimulation) in Parkinson’s?
sub thalamic nucleus
True or False: Huntington’s disease is genetic
true
What is the nature of symptoms in Huntington’s disease?
there are motor and non motor symptoms that worsen as HD progresses.
motor symptoms progress to hyperkinesias (excessive uncontrollable movements) in late stages/
What structural areas of the brain are effected in Hungtinton’s disease and what changes for the dopamine?
damage to striatum reducing inhibitory connections. also changes in dopamine from high dopamine in early stages to low dopamine in later stages
Describe the brake accelerator model for Huntington’s disease:
overactivity leading to excessive production of motor programmes
Describe the brake accelerator model for Parkinsons disease:
overactivity leading to excessive inhibition of motor programmes
What is the DSM IV criteria for Tourette’s Syndrome?
-two or more motor ticks
-one or more vocal ticks
Vocal ticks can be inarticulate or articulate (coprolalia, echolalia, palilalia)
What are dopaminergic problems in Tourette’s Syndrome?
excess dopamine activity or increased sensitivity to dopamine activity
What Basal Ganglia issue is involved in Tourette’s Syndrome?
problem with suppression of unwanted actions
What is ataxia associated with?
damage to cerebellum
What are symptoms of cerebellar ataxia?
ipsilateral control, initiation and termination problems for action, jerky/inaccurate movements
Which functions are associated with the following parts of the cerebellum; medial, intermediate, lateral?
-medial; stance, initiation
-intermediate; limb movement control
-lateral; adjusting movements in novel contexts
what can explain many observed deficits in ataxia?
issues in timing
describe testing the timing hypothesis:
TMS in healthy brains while participants paced finger tapping. compared different stimulation sites.
-Specific impairment in variability when stimulated medial cerebellum
what are the motor roles of the cerebellum and basal ganglia?
classic idea of basal ganglia for selection and inhibition of motor plans, cerebellum for timing/refinement of selected plans. recent suggestions of basal ganglia for reinforced learning and cerebellum for supervised learning.
describe apraxia symptoms:
-specific difficulty with previously learned, skilled, purposeful movements.
-no sensorimotor problems or comprehension difficulties
-often more impaired on transitive (tool use) than intransitive (gestures) movements
what are the main subtypes of apraxia?
three major subtypes found to also have different sites of damage
-Limb-Kinetic
-Ideomotor
-Ideational
Describe Limb-Kinetic apraxia:
-clumsy arm or leg movements
-often unilateral deficit (contralateral to damaged hemisphere)
-both voluntary and automatic actions
-problems during object use, pantomiming and mimicking
Describe ideomotor apraxia:
-problems producing actions on demand
-problems mimicking another or pantomiming object use
-con produce actions spontaneously and typically described as able to use objects spontaneously
-may show same impairments in actual object use
- problems of knowing how to produce specific actions
Describe ideational apraxia:
-co occurs with aphasia
-can mimic object use
-can identify the objects but cannot demonstrate sequence of actions to complete task
-conceptual misuse of objects i.e. stirring bottle opener in empty glass
-problems of correct sequencing i.e. performing actions in wrong order for task
-problem knowing what to do to complete the task
What damage is associated with apraxia?
-often left hemisphere damage for ideational and ideomotor apraxia
^suggests dominant role for left hemisphere in purposeful movements
-more posterior parietal for ideational compared to more anterior parietal for ideomotor
-can be either hemisphere for limb-
kinetic apraxia, premotor cortex, impairment is seen in limb contralateral to damage
Describe Liepmann’s model of motor control:
Movement Formula: Memories that guide
purposeful movement - i.e. knowing what to do
Innervatory Patterns: How to execute the
purposeful movement - i.e. how to do it
What are treatment options for Apraxia?
-gesture production exercises
-strategy training
-direct training (carrying out everyday activities with help for therapist to reduce errors)
-exploratory training (infer object use from its structure)
why are biomarkers useful?
they are objective markers that may indicate conditions that are hard to identify. they can indicate risk of conditions that develop during life span. easily administered, non invasive indicators of disorders.
Diagnostic Markers Need to be able to:
1) distinguish condition from healthy controls
AND
2) distinguish this condition from other conditions
Name a potential biomarker?
they eyes
What is the role of the retina?
translates the light energy into electrical signals in the brain
When are cones and rods used?
Rods- night
Cones- day
Why do we move our eyes?
When staring at a picture or scene we only focus on a very small part in detail, perception is blurrier as we move more to the peripheral. we move our eyes to be able to focus on detail in different areas
Describe a saccade eye movement:
very fast movement of the eyes from one position to other as quickly as possible. period where vision is disrupted because things are blurry is over and sone with extremely quickly
What allows us to compensate for saccades and keep the image on the retina still between saccades?
-Vestibular Ocular Reflex (VOR)
-smooth pursuit
Describe Vestibular Ocular Reflex (VOR):
when you move your head or body we rotate our eyes to offset what the head is doing and keep our image clear
what does smooth pursuit allow eyes to do?
keep focus image stationary on the retina, keep moving target in focus
Do smooth pursuit and VOR mechanism work together?
No, in order to initiate smooth pursuit the VOR must be turned off
Why might eye movements be clinically relevant?
They are a useful objective measure with well characterised brain circuity and motor behaviours. reproduceable and lawful set of movements
What happens to eye movements in psychiatric disorders?
eye movements can be disrupted
Describe eye movement in someone with end stage syphilis:
problems maintaining fixation and making saccades between movements
Describe eye movements in shizophrenia
lots of jumps, unable to do smooth pursuit but normal saccade movement
what are potential eye movement markers?
-problems with fixations
-problems with saccades
-problems with smooth pursuit
-problems with scanning
what types of instability may be present in patients with fixation problems?
-drift
-nystagmus (unable to hold eyes in a fixed position)
-saccadic intrusions (involuntary conjugate saccades that interrupt fixation)
what conditions may entail problems with eye fixation?
-cerebellar disease, multiple sclerosis, schizophrenia, progressive Supranuclear palsy
Describe problems with saccades:
-timing (delayed initiation in Huntington’s disease, slowed movement eg. some ataxias)
-accuracy (shifts too small, shifts too big)
Describe hypometry and hypermetria:
problems with the accuracy of saccades. hypometry falls short, hypermetria goes too far/overshoots
Hypometry or Hypermetria may be present in what conditions?
Parkinsons Disease, Multiple Sclerosis, Cerbellar lesions
Which conditions have impairments associated with smooth pursuit?
neurological diseases, schizophrenia, amblyopia (lazy eye), dyslexia
Describe some problems with pursuit:
Velocity gain where movements are too fast or slow. Catch up and backup saccades (saccadic intrusions).
What conditions may include problems with scanning?
-Hemispatial neglect
-Schizophrenia
-Autism
What is hemispatial neglect?
failure to search on left. frequent re fixations on right, barely look at left. failure to keep track of search locations
why is hemispatial neglect hard to diagnose?
because patients are unaware that they are not seeing anything on their left
Describe scanning problems in autism:
-impaired/restricted scanning of faces when freely viewing or trying to identify emotions
-lack of eye contact
What biomarker can be used as a diagnostic marker of autism?
scanning impairments which show problems with social information
What model showed good ability to predict diagnosis of autism?
objective and quantitative eye tracking via two eye-movement based measures
what was a problem with the eye tracking model as a diagnostic biomarker for autism
it could differentiate between neurodivergent and neurotypical, however not between autism other conditions
Describe disruptions in face scanning in Schizophrenia:
patients have impaired scanning and judgements of facial emotion. scan paths can be restricted.. for sad faces scan paths and judgements were less impaired.
Why was Schizophrenia not fully a diagnostic biomarker?
schizophrenia and bipolar eye movements differed from controls, however there was no distinguishing between the two conditions
How can Schizophrenia eye movements differ from bipolar and does this make it a diagnostic biomarker?
spatial distributions were different between the conditions. However this can only distinguish Schizophrenia from one other condition
Describe a probabilistic neural network model built for schizophrenia:
-promising network made by combined data from pursuit, free viewing of images, and fixation task
-98% accuracy to distinguish from healthy controls
How can biomarkers be used in predicting risk of developing/inheriting neurological conditions?
-eye movement abnormalities in relatives of those with autism
-smooth pursuit abnormalities in first degree relative of those with Schizophrenia
what are current limits in using biomarkers to make diagnosis?
-Individual differences: autism face viewing not always found to be different to controls
-Co morbidity
-medication induced effects
-motivation and mental state
How are autism and alexithymia hard to distinguish by biomarkers?
it might not be the autistic traits that correlate with whether people look at eyes, it could be alexithymic traits as alexithymia is present in 50% of individuals with autism
What other factor could be causing impairments in smooth pursuits of those with schizophrenia?
-long term anti psychotic use.
-causing caution in interpreting smooth pursuits deficits as being illness related
When may healthy controls may show Schizophrenia like smooth pursuit?
unmotivation: when they are distracted, tired, or bored
What did Risperidone and Haloperidol do to eye movements in people with Schizophrenia?
Risperidone treated patients show more looks to eyes than Haloperidol treated patients
How does vestibular stimulation treat hemispatial neglect?
cold water to left ear canal making people look more to the left side, helping overcome left side neglect in eye movements
What is an old ‘treatment’ in therapy for those with autism, that is now proven wrong?
people believed if you could make an autistic person learn to look into people’s eyes their autism could be ‘cured’
Why can’t correcting eye movements cure conditions associated with abnormal eye movements?
correcting eye movement does not mean successful treatment
How has eye movement therapy used to help stroke patients, how successful was this?
-eye movement based training to help people make large saccades and search tasks
-improvements in ADL for some patients after the training
