W2 - Cognitive Neuropsychology

Question 1

Where does cog neuropsych originate from?

Who was the pioneer of early cog neuropsych experiments?

Answer 1

1. 19th century neurology
2. Mid-20th century: Teuber with his psychophysical lab in New York, assessed BD patients from bullet wounds

Question 2

What 5 things were unique and important about Teuber’s approach?

(Considered to be the founder of contemporary neuropsychology)

Answer 2

1. used case studies in experimental neuropsychology
2. Used matched control groups
3. Follow up tests beyond acute stages
4. Used non-verbal tests (in both humans and primates)
5. Studying patients due to overall brain damage not just symptoms

Question 3

How is neuropsych similar to neurology in its aim?

(In Neuropsychologia, neuropsychology was considered to be a particular area of neurology)

Answer 3

1. Neuropsychology aims to study physiological correlates of behaviour, similar to behavioural neurology

Question 4

How was brain damaged treated in the early to mid 20th century?

Answer 4

1. Most clinicians treated brain damage as a unitary phenomenon
   whereby you had or didn’t have brain damage
2. BD was quantified as more or less damage, neglecting the location in the brain or the impact on behavioural symptoms (Lezak)
3. Was considered an organic problem, not a psychiatric problem

Question 5

How did Teuber consider both localisation and lateralisation?

Answer 5

1. Teuber agreed that brain damage from neocortical lesions (lesions to the lobes) could produce localised damage impacting specific functions and general damage depending on the size/extent of the lesion
2. Paid close attention to skeptics of localisation of function, eg., Karl Lashley

Question 6

What was Lashley’s 1st argument regarding lateralisation?

Answer 6

1.One function might be localised in a small brain region, but a second function might be localised in a larger region that includes part of the first brain region

Question 7

How does Lashley argue for partial localization, while other functions are not localised?

Answer 7

1. Some functions are localised, eg,. brightness discrimination is localised to the area striata, but maze learning is not localised, as it can be impaired by damaging any area in the cortex

As 2 functions may be localised in the same region OR the whole cortex

• complex maze spatial orientation is significantly impaired when any 15% of cortex is destroyed
• Simple maze spatial orientation is not affected by lesions even up to 50% of the cortex

the easier task can be kept intact from brain damage compared to the more complex region

Question 8

Imagine brain region R is damaged, performance on task 1 is impaired, but task 2 is intact.

Can you conclude that task 1 is localised to region R?

Answer 8

1. No = task 1 might just be more vulnerable to brain damage, and may performance on task 1 may also be impaired by brain damage to other regions
2. As Task 1 performance has not been assessed in patients with other brain damage, it cannot be localised to brain region R

Alternative explanations
* Task 1 might be localised in a much larger region, including R
* Can’t conclude localisation from single dissociation only

Question 9

Imagine brain region R is damaged, performance on task 1 is impaired, but task 2 is intact.

Can you conclude region R is dedicated to task 1?

Answer 9

1. No = as you have only compared task 1 and task 2, such that brain region R may also be dedicated to other cognitive tasks that haven’t been assessed yet
2. Consider task difficulty: task 2 might unjust be easier to perform well at than task 1, less vulnerable to showing deficits after brain damage

Finding: One-way dissociation of impairments is NOT sufficient to assert region R is dedicated to Task 1

Question 10

What does Teuber argue about localisation?

Answer 10

1. Simple one-way dissociation only supports a case of HIERARCHY of function (for complex vs. simple functioning) rather than a case of localisation
2. Requires evidence for one-way dissociation and reverse/double dissociation

Question 11

Example - What does Teuber argue about dedication/specificity of functions?

Answer 11

1. To demonstrate specificity of the temporal lobes to visual discrimination, we need to do more than show that other kinds of discrimination (eg,. tactile) are unimpaired (this is only a single dissociation)”
2. Single dissociations do not provide sufficient evidence for dedication/specificity, since could argue visual discrimination is more vulnerable to being impacted by temporal lesions than tactile discrimination

Question 12

What is the definition of double dissociation in relation to brain damage? (Teuber)

Answer 12

1. Patient A has a lesion site on R1, showing impaired performance on Task 1 but intact performance on task 2
2. Patient B has a lesion site on R2, showing intact performance on Task 1, impaired performance on Task 2

Question 13

Can you have conclusive proof for localisation with single and double dissociations?

Answer 13

No its only supporting evidence, raising likelihood for one hypothesis over another hypothesis - Task 1 and 2 might be localised to smaller or larger regions within R1 and R2
You can never get conclusive proof in empirical science

Question 14

What might Operated control subjects and control tasks be? (speculative)

Answer 14

1. Operated control subjects = either normal controls, controls with different psychosurgery, animals with psychosurgery, or controls with other neurological problems
2. Control tasks = different cognitive tasks to the cognitive task in question

Question 15

What are the 2 main applications of neuropsychology?

Answer 15

1. Clinical neuropsych assessment
2. Cognitive neuropsychology

Question 16

Lezak: How does neuropsychological assessment differ to traditional neurological examinations?

Answer 16

• studies behaviour to make inferences of brain function
• non-invasive brain examination
• kinship with psych assessment
• differs from psych as uses a different frame of reference, taking brain function as starting point

Question 17

How is neuropsychology a specialisation of clinical psychology?

Answer 17

it is a specialisation within clinical psychology interested in assessment and rehabilitation of people with brain injury

Question 18

What is the aim of COGNITIVE neuropsychology?

Answer 18

learning how the mind works - forming descriptions of the processes of the execution of mental activities such as identifying objects, speaking, planning, memorising…

Question 19

What are the core tools in cognitive neuropsychology?

Answer 19

1. Information is encoded by mental representations
2. Some modules store and maintain mental representations (storing info)
3. Other modules manipulate and utilising mental representations

Question 20

What are the old and new methods used in cognitive neuropsychology?

Answer 20

1. Old = descriptions of mental activities using the information processing approach
   * specific component processes, different series stages for storage, retrieval or combination of information
2. New = experiments with BD and neurologically healthy subjects
   • useful to test a theory’s ability to explain how/why a cognitive ability is impaired in BD patients

Question 21

How does clinical and cognitive neuropsych differ slightly from traditional cognitive psych?

Answer 21

1. Cog neuropsych uses data from BD patients to evaluate theories of normal cognition
2. Clinical uses BD data for treatment/rehab for BD patients
3. Cog neuropsych uses BD data to inform theories of normal cognition.

Question 22

When did cognitive neuropsychology start?

How does clinical NP differ to cognitive NP?

Answer 22

1. In 70s/80s, from cognitive psychology (same theoretical base) and clinical neuropsychology (same methods)
2. Clinical neuropsych is more of an APPLIED science
3. Cog neuropsych and cog psych are THEREOTICAL sciences

Question 23

What are the 2 aims of Cognitive Neuropsychology?

Answer 23

1. To test and evaluate models of normal cognition by exploring performance from BD patients data
   * impair/intact of function is the double dissociation of impairments
   * similar DD definition to Teuber, but do not mention the brain
2. To offer theoretical explanations of what has gone wrong and what is intact in BD patients in the multi- component mental system

Question 24

What was the old assumptions of memory before the findings of HM and KF?

Answer 24

1. Old idea = hierarchical model of memory: from STM (Task 1) and LTM (Task 2), assuming:
   * processes in Task 1 occur before processes in Task 2, and Task 2 needs every process from Task 1 + more
   * If Task 1 (STM) is spared, Task 2 (LTM) could be impaired,
   * but if STM (Task 1) is impaired than LTM (Task 2) will also be impaired

Question 25

How did the findings from HM and KF challenge the old Hierarchical model of memory?

Answer 25

1. Patient HM had impaired LTM, but intact STM, CONSISTENT with the hierarchical model 2. Patient KF had intact LTM, but impaired STM, INCONSISTENT with the hierarchical model (reverse dissociation to HM, from parieto-occipital lesion) 3. Conclusion: this double dissociation allowed researchers to infer that STM and LTM involve relatively independent cognitive systems * Can be damaged either way without affecting the other, STM (task 1) can be impaired while LTM (task 2) can be intact * Some components of LTM are NOT INVOLVED IN STM (task 1), vise versa

Question 26

What was the old assumptions of READING before the DD findings of GR?

Answer 26

1. Previous model argued that reading comprehension was phonologically mediated, 1. You first convert the spelling of the word into the sound form (orthography to phonology - Task 1), 2. then comprehended its meaning (Task 2), ie., Task 2 requires all of info from Task 1 plus more

Question 27

How did GR's pattern of impairment, challenged hierarchical model of READING comprehension?

Answer 27

1. GR made constant errors when asked to read single words aloud (failed at Task 1: could not convert the letter sounds ( orthography) to the spoken sounds (phonology) 2. However, he would say similar words that were SEMANTICALLY RELATED to the actual word, despite NOT A SINGLE PHONEME was pronounced correctly * eg., liberty read as 'freedom', daughter read as 'sister' 3. Challenges hierarchical model as he was failing Task 1 but achieving Task 2 (understood the meaning) 4. Conclusion = a new mode with TWO routes for reading comprehension created - A direct route between orthography to semantic understanding - An indirect route via phonological addresses

Question 28

What are the main 2 assumptions used in cognitive neuropsychology?

Answer 28

1. Assumes that the mind is modular 2. Uses double dissociation o draw conclusions about modular systems of the mind

Question 29

What are the 3 main criticisms of cognitive neuropsychology?

Answer 29

1. Models are often presented in box and arrow diagrams, they tell you what and how they are organised, but neglect: - the format of the box systems representations - The processes that the system carries out - do not explicitly state the proposed mechanisms at work - Not specific enough to be implemented in computer programs - not specific enough to make detailed predictions of cognition

Question 30

Recap: outline the major differences between the 4 branches of cognitive psychology

Answer 30

1. Experimental cognitive psychology * Concerned with cognitive structures and processes, either bottom-up (from stimulus input to higher cognitions) or top-down (influenced by higher order beliefs, expectations) * serial and/or parallel processing * to understand cog. structures by observing cognitive tasks from healthy individuals 2. Cognitive neuroscience * Aims to study cognitive structures and neural bases of behaviour in healthy individuals * Uses MRIs, functioning MRI, ERP, fMRI and MEG * Can locally disrupt functioning with TMS, tDCS 3. Cognitive Neuropsychology * BD patients can inform understanding cognition in healthy individuals * BD impairments can support claims about the modular neural structure of the cognitive system in healthy individuals 4. Computational cognitive science * Uses computational models to replicate/represent human cognition

Question 31

What are the 4 advantages of using a computer model of cognition over traditional cognitive theories?

Answer 31

1. Enhanced precision over box and arrow diagrams or verbal statements 2. Can check if a theory has any imprecise terms or inaccurate assumptions 3. Can make new predictions outside of traditional theories and to be tested later on 4. A computational model of a cognition designed for healthy people can be ‘lesioned’ - and its subsequent performance and predictions can be compared with real BD patients

Question 32

How does clinical neuropsychology differ to other branches of cog psych?

Answer 32

1. It is an applied science interested in brain dysfunction, non invasive methods of studying the brain by studying behavioural consequences, for diagnosis and rehabilitation and research 2. Studying brain activity and organisation - NOT information processing systems 3. Can inform other theories and treatment by studying patients with specific deficits

Question 33

Colheart: What are the different ways of developing cognitive neuropsychological theories?

Answer 33

1. A model of normal cognition comes first, eg., Marr’s 1982 model of normal object recognition for patients with visual agnosia 2. Neuropsych data, which informs the model of normal cognitive functioning = Warrington & Taylor (1978) used data from patients with visual object recognition to develop a cognitive model to explain normal visual object recognition 3. Normal cognitive models and study of BD patients occurs independently, and then converges * eg., Dual-route models for reading and letter recognition developed, independent from studies on patients with reading disorders

Question 34

What unclear relationships does cog NP share with 3 other disciplines?

Answer 34

1. Neurology = studies patients with neurological damage 2. A.I = information processing systems of language and object recognition 3. Linguistics = studies language processing

Question 35

Why have neurology & cog NP remained separate?

Answer 35

1. Cognitive activity is difficult to localise as there are not necessarily any one-to-one relationships between cognition and specific brain regions 2. Remains uncertainty over what cognitive components actually exist in a modular sense, “psychology has to be done before neurology” 3. Brain regions linked to cognitions do not usually activate solely on one cognition, and no evidence of specific cognitions that depend entirely upon one circumscribed cerebral region” 4. Pure neurological data about cognitive processes “must be limited and indirect” - even though it is the main source of data in cognitive neuropsychology

Question 36

Why have AI models & cog NP remained separate?

Answer 36

1.The distinction between what a cognitive program does and how it works has not been taken seriously (Marr) 2. Many studies have tried to mimic cognitive processes over truly understanding them 3. The psychology of the cognitive task has to be known before an AI model can be produced

Question 37

Why have linguistics & cog NP remained separate?

Answer 37

1. It is a more loose relationship; linguistics of the brain seems to “bear no relation, or very little” to the long series of ordered rules in English 2. Clear distinction within linguistics of work that is meant to be psychological and that that is not

Question 38

1955 - What are syndromes and why are they criticised in cognitive NP?

Answer 38

Syndromes are clusters of related symptoms used to describe cognitive disorders and impairments 1. Relationship of symptoms to the syndrome is fuzzy and not sufficient 2. Syndromes assume that every patient should exhibit SOME of the cognitive symptoms but * All of the symptoms should be exhibited by SOME of the patients * Not useful for research, as 2 patients may have completely different sets of symptoms that still fall under the same syndrome * Non-overlapping symptoms entail different etiological explanations for the disorder which lowers research generalisability * Claiming a single model of a cog. system that can offer different interpretations / expressions

Question 39

What are the main differences between an acquired cognitive disorder and a developmental cognitive disorder?

Answer 39

1. An acquired cognitive disorder is an damage to the brain that causes impairment to some cognitive function that was previously intact/normal, 2. A developmental cognitive disorder refers to a failure to ever acquire normal competence to a specific cognitive function *developmental disorders are explained via models of normal cognitive function, eg., models of reading can explain developmental dyslexia

Question 40

Teuber, 1955: What is physiological psychology and what methods does it use?

Answer 40

1. A branch of psychology concerned with all physiological correlates of behaviour, eg., sensory processes, central nervous systems on behaviour 2. 1950s methods like intercurrent cerebral stimulation through implanted electrodes or cerebral ablation, to find physiological correlates to learning by preventing learning

Question 41

1955 - Teuber: What were the findings on sodium deficiency in rats in relation to physiological thresholds for hunger and thirst?

Answer 41

1. Research on rats shows that sodium deficiency increases motivation to consume salt, but not necessarily change taste sensitivity. 2. No difference in gustatory nerve signals (taste sensitivity) between sodium-deficient and normal rats, suggesting two types of thresholds: Absolute physiological threshold – remains unchanged regardless of sodium status Variable preference threshold – influenced by factors like adrenalectomy (salt-deficient)

Question 42

1955 - What were the findings on physiological threshold in rats by Harriman and MacLeod?

Answer 42

1. Trained rats to distinguish between saline and distilled water, gradually lowering the salt concentration and punishing incorrect choices. * Over time, rats improved their gustatory acuity, effectively lowering the discriminative threshold. * The findings suggest that the closer this threshold gets to an optimal level through training, the less additional effect sodium deficiency (or adrenalectomy) has on increasing salt preference.

Question 43

1955 - Teuber: how do physiological adjustments help explain control of drinking in rats?

Answer 43

1. Normal rats can adjust their ingestion of saline/salt, glucose/sugar or fructose depending on how much concentration they are given Giving a rate hypertonic solutions through injections/tubes reduces the rat’s drinking rate of the solution within one minute Conclusion: this control of drinking seems to depend on “post-ingestion factors” OVER taste receptors

Question 44

1955 - How is osmotic balance regulated by a central control mechanism in rats?

Answer 44

1. Osmotic balance seems to be regulated by a central control mechanism, eg., endocrine system or hypothalamus with osmoreceptors 2. Osmo-potentials are recorded in supraoptic nuclei in the hypothalamus in cats given a high hypertonic solution of saline/glucose 3. Osmo-potentials are thought to be like sensory discharges, from a release of neuro-secretions related to posterior pituitary hormones

Question 45

1955 - What 4 examples of physiological damage to certain parts of the brain leads to uncontrolled drinking or eating?

Answer 45

1. Damage to the supraoptic nuclei can produce diabetes insipidus, (excessive urination and excessive drinking) 2. Secretion of the pituitary stalk can alter drinking without abnormal amounts of urination 3. Hypothalamic stimulation or destruction can cause an abnormal level of eating and inability to know when to stop 4. Lesions in hypothalamic ventromedial nuclei can cause overeating and hyperthermia in rats * overheat before and after overeating, seems like lesions cause independent disruptions both to eating and temperature regulation

Question 46

1955 - What is the role of diencephalic regulations in feeding and drinking?

Answer 46

Diencephalic regions include the brain's third ventricle: thalamus, hypothalamus, posterior pituitary, epithalamus, pineal body, and subthalamus 1. Hypothalamic stimulation causes animal to receive misinformation about internal state of being, thus behaviour is a reaction to such misinformation from external stimulation 2. Central and sensory mechanisms in the brain seem to be plurivalent and have multiple degrees of power or capability, including supraoptic nuclei, paraventricular nuclei *can perceive changes in osmotic pressure and hormone secretion

Question 47

1955 - What are the main findings of neural and humoral correlates of emotion?

Answer 47

1. Subcortex seems to be involved in all range of emotional behaviour “from sleeping to diffuse excitement” 2. Hypothalamus arouses the cortex and provides functioning for autonomic systems / involuntary behaviour 3. Levels of skin conductance hoped to correlate the intensity dimension of emotion 4. Differentiation of basic to specific emotions is proposed to be an ONTOGENETIC process relating to the development of an organism from conception to adulthood

Question 48

1955 - What do different rearing of dogs show about ontogenetic processes of emotion?

Answer 48

1. Rearing dogs in RESTRICTIVE upbringings and then showing them emotional stimuli caused them to be only EXCITED 2. Rearing dogs in NORMAL environments and then showing them emotional stimuli caused them to show avoidance and aggression

Question 49

1955 - What is the Klüver-Bucy findings in monkeys with temporal lobectomies?

Answer 49

1. Monkeys with bilateral temporal lobectomies in the temporal neocortex have strong changes to perception and behaviour: * overreact to visual stimuli * strong oral sniffing behaviours * altered diet * hypersexuality, marked emotions * increased tameness and lower anger or fear Other studies find temporal lesions can cause visual problems WITHOUT emotional changes Lesions to the rhinencephalon can produce emotional changes WITHOUT perceptual changes

Question 50

1955 - Hows does on Papez’s theory of emotion try to explain the Klüver-Bucy findings?

Answer 50

1. Papez proposed an anatomical substrate functional ‘circuit’ involving the hippocampus, fornix, mammillary body, to explain for normal emotions and expressions, called “the visceral brain” 2. Criticism = These structures are also activated in somatomotor effects in electrical stimulation, suggest that they are not visceral and may have quite heterogeneous roles

Question 51

1955 - What behavioural changes are observed in an amygdalectomy in animals?

Answer 51

1. Savageness, hypersexuality in cats and monkeys with amygdala lesions, 2. Slower learning about conditioned avoidance responses, eg., aversion for electric shocks - inconsistent results Ultimately unclear and different: Different results might be due to different handling of animals or variations in the lesions, eg., irritative or destructive

Question 52

1955 - What are the two parts of the amygdala and what changes in behaviour are found in stimulating each part in animals? What human neurological condition has similar results?

Answer 52

1. Phylogenetically old amygdala of the amygdala (anterior-medial) * Stimulating produces sniffing, licking, clawing and other autonomic behaviours in animals stimulated with implanted electrodes 2. New amygdala (basolateral) * Stimulating causes bewilderment, fear, angry and fury in animals Fear from new amygdala stimulation is probably from a disorganised brain response resulting in diffuse afterdischarges of behaviour 3. very similar to temporal-lobe epilepsy in people

Question 53

1955 - what 2 methods were used to stimulate the amygdala?

Answer 53

1. implanted electrodes 2. or an application of the excitatory NT acetylcholine

Question 54

1955 - What is the role of the hippocampus and fornix evidence on emotion?

Answer 54

1. Limited or non-significant effects on emotion, lesions on hippocampus do not duplicate results from the amygdala, and fornix section has no effect on behaviour

Question 55

1955 - What are findings on Subcortical / Septal nuclei region of the forebrain?

Answer 55

1. Septal lesions in rats cause savageness, emotional explosive reactions, fighting * reactions/behaviours seem to disappear after 12 days 2. Behavioural changes from stimulation seem to reflect the location of impact * lesions on mediodorsal nucleus leads to irritation *lesions on anterior nuclei = docility * Combining both lesions results in labile behaviour 3. Stimulating septal region of schizophrenics to reduce abnormal electrical activity seems to not work

Question 56

1955 - What does Teuber consider to be the pros and cons of lesion and albation experiments?

Answer 56

1. Pros = good ability to contrast subcortical lesions and ablations to cortical projection zones and compare behaviours 2. Cons = Need sharper categories/symptoms than docility, labile, savageness and more studies on the effects of combined and seriatim (one-by-one) lesions

Question 57

1955 - What is the role of ACTH (adrenocorticotropic hormone) in stress? How is ACTH released?

Answer 57

1. ACTH (adrenocorticotropic hormone) stimulates cortisol production and is part of the stress response. The hypothalamus initiates ACTH release, and ACTH in turn dampens hypothalamic activity, shows how bodily states influence emotional responses.

Question 58

1955 - What are the general findings on ACTH, and where is the hormone secreted from?

Answer 58

1. ACTH (adrenocorticotropic hormone) is secreted from the posterior hypothalamus - as the destruction of this region prevents ACTH to respond to stress. 2. Stimulating the posterior hypothalamus triggers normal ACTH secretion. 4. Injecting ACTH directly leads to reduced hypothalamic electrical activity - negative feedback loop.

Question 59

1955 - a) How can ECS exert effects on behaviour? (rat study)

Answer 59

1. by classical conditioning Pairing an unconditioned stimulus (lever for an aperiodic water reward) with a neutral stimulus (clicking noise) - then after 3 min by a painful shock to the rat’s feet 2. Forms conditioned response with the conditioned stimulus (clicking noise) - After six such trials the animals, on hearing the clicker, stop pressing the lever

Question 60

1955 - What are the findings on the rats given electroconvulsive shocks in relation to conditioning?

Answer 60

1. After one month of 21 ECS per week, the conditioned fear responses goes away, and then returns after 30 days (unless extinction trials or more ECGs are done) 2. ECS conditioning seems to be reversible and long-lasting after conditioned response is established 3. Unsure why CER is maintained with time and wanes over time is unclear

Question 61

1955 - What were the effects of ECS on rats' mood and behaviour?

Answer 61

1. Mood = Heightened irritability and depression 2. Cannot tame wild rats, but can disrupt instinctive behaviour in domesticated rats like nest building 3. Hunger = In malnourished rats ECS led to increased food intake, suggests ECS leds to rats overcompensating for a mild nutritional deficit by overeating

Question 62

What is the limitation of using ECS?

Answer 62

1. Conflicting findings in ECS studies may reflect different feeding schedules which might produce different behaviours

Question 63

What is the limitation of ablation studies (removal of tissue)?

Answer 63

Changes in animal’s performance of a task after ablation may simply reflect changes in motivation rather than changes in the ability to do the task

Question 64

What is the mode of action of ECS?

Answer 64

1. The CONVULSION of ECS is more important than the electrical current, * convulsions without currents mimic ECS effects * as currents without convulsions seem to produce ineffective results * Giving rats electrical shock without convulsion under anesthesia, shows no deficits in behaviours compared with normal ECS * conditioned fear responses remain when ECS under anesthesia

Question 65

1955 - How are primary sensory systems studied?

Answer 65

1. Identify clear sensory deficits caused by lesions 2. Focus on studying functions over just anatomical structures. 3. Infer sensory deficits indirectly through behavioral or perceptual analysis.

Question 66

What's the current understanding of agnosia and scotoma regarding sensory systems?

Answer 66

1. Scotoma = Visual defects often reveal not only localized impairments but also subtle, systematic changes across other areas of the visual field. * mapping a scotoma alone is insufficient to predict full performance impact. 2. Lesions in central visual pathways can lead to complex visual impairments beyond affected areas 3. The nature of agnosia is unclear — it may not reflect a pure dissociation of higher visual functions. * as individuals can exhibit signs of agnosia even without impairment to higher-level visual processing.

Question 67

1955- How did Weinstein test somesthesis (sensory issues) after brain damage?

Answer 67

Patients: 2 BD groups (one with diminished position and light-touch threshold for von-frey hairs ) and BD with no sensory problems) Method = estimate weight of weights on both palms simultaneously or in rapid succession Findings 1. In the sensory group, weights on the affected hand were significantly overestimated In non-sensory group, weights on the opposite side of the lesion were underestimated (contralaterally)

Question 68

1955 - What did Cole & Glees find about somatosensory functions in neocortical lesions in monkeys?

Answer 68

Method = removing postcentral gyrus in monkeys, testing for motor power and dexterity Findings 1. reduced amount of motor power (esp. In contralateral side to lesion), 2. reduced finger dexterity and stereognosis (ability to identify the shape and form of a three-dimensional object) 3. strongly recovered over time

Question 69

1955 - What did Zubek conclude about the first and second sensory area in rats? Rats were peripherally blinded and trained to discriminate between 2 shapes tactilely

Answer 69

Findings 1. Performance was not affected by removing bilateral cortical removals anterior and posterior to somatic areas I and II or Nor (b) by bilateral removal of somatic area I and II, either separately or together Conclusions = somatosensory function seems to be more resilient in organisms further down the ‘phylogenetic tree’, but this may be due to more freedoms/less regulations of research methods in smaller organisms, so this correlation might not be valid

Question 70

How does lesions or ablations affect taste/gustation in animals?

Answer 70

1. Changes in eating habits, in monkeys with brain injuries, might not be related to their sense of taste / or reduced flavour sensitivity but occur of the animal's motivation or behavior is affected 2. Bitemporal lobectomy changed the monkeys' diet from eating plants (herbivorous) to eating both plants and animals (omnivorous). * this did not affect their sensitivity to a bitter substance (quinine), meaning their taste wasn't the problem. 3. Ablation near insula changed sensitivity to bitter quinine, but diet didn't change.

Question 71

1955 - What are the conclusions of primary projection lesions?

Answer 71

1. Lead to complex & circumscribed alterations in sensory functioning 2. Might cause alterations in cognition beyond primary systems 3. Larger lesions might produce specific & general impairments to cognition

Question 72

What is the use of studying anterior and posterior lesions?

Answer 72

1. Studying both effects of anterior and posterior lesions can show double dissociations, indicating specificity of function * Posterior lesions show failures on simple tests like visual discrimination but no delayed responses * Anterior lesions show failures in delayed-response and delayed-alternation tasks

Question 73

1. What skills are affected and intact after anterior lesions? 2. What might be behind deficits from anterior lesions? 3. What is the limitation of these finsings?

Answer 73

1. Delayed responses fall to chance level, but intact visual discriminations 2. Interactions between posture and vision might actually be more important in causing the delayed-response than disruptions to higher cognitions 3. Limitations: Unsure precisely what behaviours are captured in delayed response tasks

Question 74

What 6 factors affect interpreting findings of anterior lesions in monkeys?

Answer 74

1. Environment/internal = changing animal's environment or internal state can make the task either solvable or unsolvable 2. Sedation: Sedating the animal may improve its ability to perform the delayed response task, leading to mixed findings across studies 3. Non/ spatial delayed response: performance is often better when the task is adjusted so the animal's cue is nonspatial (not based on location) * Spatial delayed response = performance is worse when the animal has to remember the location of an item 4. Memory = The problem after brain damage is not memory itself but memory related to LOCATION 5. Chimpanzees: Some BD chimpanzees perform well on delayed response tasks -while earlier studies show severe impairment 6. Frustration and behavior and hypermotility: Chimpanzees react more violently - could affect performance

Question 75

1955 - What is proposed to cause hypermotility, excessive movement after brain lesions in animals?

Answer 75

1. Rat lesions in both frontal poles of the brain can cause hypermotility, not from damage to the dorsal or lateral frontal cortex 2. Damage to the anterior caudate could cause hypermotility, especially if blood vessels are accidentally affected

Question 76

1955 - What are the general findings on posterior lesions in animals? How does task difficulty affect the findings?

Answer 76

1. Near complete ablation in the prestriate (V1, V2, V3, BA 18 & 19) does NOT produce visual discrimination deficits 2. Bilateral temporal lesions DO seem to affect visual discrimination 3. Ablation of the lateral or ventral temporal cortex can cause visual problems, suggests important for visual discrimination 4. Researchers have found the harder the pre-operative task was, the more severe the post-operative deficit

Question 77

1955 - What are the 4 limitations to assessing postoperative damage?

Answer 77

1. No ablations causes disturbances severe enough to be noted in animal’s general behavior, only emerged as deficits in SOME formal testing 2. In ablation cases, primary learning is NOT said to be affected, but rather learning acquisition is effected 3. Generalising postoperative effects of monkeys to humans is hard 4. Task design and difficulty produce different results., eg., colour discrimination can be taught to monkeys if different shades of bread instead of counters

Question 78

Accounting for extraneous factors/explanations

Answer 78

1. Single dissociation ONLY indicates visual discrimination is more vulnerable to temporal lesions than others, like tactile discrimination, really need double dissociation 2. Single dissociations only indicate a hierarchy of function in the brain, 3. Double dissociations can provide evidence to support a localisation of function

Question 79

1955 - What is Teuber's example of a single dissociation?

Answer 79

1. Temporal ablations do NOT impair form discrimination, but parietal ablations DO impair form discrimination 2. Combined ablations cause deficits to become worse, eg., both temporal and parietal are vaguely involved 3. To localise vision to the temporal lobe, would need to have data on both vision and other cognitions, eg., auditory data

Question 80

1955 - What are the main conclusions comparing lesions between anterior and posterior "association” cortex in humans?

Answer 80

1. Anterior cortex (towards the front) is considered to be MORE IMPORTANT than posterior regions 2. The association cortex involves more complex cognitive functions, in the frontal, parietal, & temporal lobes 3. Patients with removal of the anterior regions display more severe psychological deficits than those with removals of the posterior regions - severe cognitive deficits and disinhibited behaviours, eg., motor restlessness, indecent talk (could be a gross oversimplification)

Question 81

1955 - What brain areas are more implicated in complex functions?

Answer 81

1. Differences in findings is most likely to due differences in etiology * tumours might be more cognitively disruptive compared to shot wounds 2. Tumour patients performed worse than controls, but anterior and posterior tumour cases did not differ from each other * but researchers excluded those with "aphasia, agnosia, or apraxia which are severe symptoms are typically associated with posterior lesions

Question 82

1955 - What is the general findings with damage to the parietal lobe?

Answer 82

1. Seems to impact spatial orientation and can last subtly even a decade 2. Worse performance of complex route-finding using maps compared to patients of every other lobe damage and controls, * worse performance observed regardless of whether the maps were presented tactilely or visually, indicating that these deficits do not reflect visual agnosia 3. Worse performance in tasks that “required transfer of information from one sense modality to another” - eg. complex visual to tactile tasks

Question 83

1955 - What are the general findings of temporal lobe stimulation?

Answer 83

1. Temporal lobe direct stimulation can lead to * visual or auditory hallucinations, * complex dreams and memories * convincing experiences of reliving of earlier experiences 2. Disagrees with Penfield’s belief of temporal lobe as a “memory cortex”

Question 84

1955 - Does Teuber argue for a hierarchy of neural importance?

Answer 84

No - While bilateral lesions to the basal brain and diencephalon disrupt cortical activity MORE than neocortical lesions the neocortex should NOT be considered a lesser organ to the diencephalon and upper brain stem

Question 85

1955 - What are Teuber's summary and future directions regarding physiological psychology?

Answer 85

1. Results between primates and humans are more similar than expected 2. Need to compare ECS and electrodes stimulation pre- and post performance 3. Needs to improve vague terms that describe altered behavior, eg., tameness, savageness and visual discrimination deficit 4. Need to improve the uncertainty over localisation via DD to determine if structural areas , eg., primary areas, association cortex, and visceral brain are actually linked to functional systems