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Year 2 Semester 2 > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

metabolic comorbidities of obesity: (9 points)

A
  • asthma
  • NAFLD
  • gallstones
  • infertility
  • cancers
  • cardiovascular disease
  • type 2 diabetes
  • thrombosis
  • gout
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2
Q

mechanical comorbidities of obesity: (5 points)

A
  • impaired physical functioning
  • urinary incontinence
  • arthrosis
  • sleep apnoea
  • chronic back pain
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3
Q

what are the 3 parts of the appetite control system

A
  • Sensory INPUT
    Sight, smell, sound, taste, touch
    Nutrient signals generated from pre-ingestion to oxidation
  • Neural INTEGRATION
    Bottom-up and top-down
  • Appetitive OUTPUT
    Behavioural (motor)
    Autonomic & endocrine
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4
Q

the 2 elements of the energy balance equation (EBE)

A

intake:
-hunger & satiety
-hedonics
-nutrient absorption

expenditure:
-metabolic rate
-thermogenesis
-activity

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5
Q

the 5 components of appetite

A

Hunger:
-the drive to consume

Wanting (craving):
-motivation to consume a specific food

Liking (hedonic):
-sensory pleasure elicited from contact with food

Satiation:
-negative feedback, leading to meal termination (within-meal inhibition)

Satiety:
-end state of satisfaction (between-meal inhibition)

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6
Q

hormones that control energy balance

A

-insulin
-leptin
-ghrelin

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7
Q

Hormones: stomach

A
  • Release of Ghrelin the hunger hormone suppressed by carbohydrate, fat and protein
  • gastrin - produced in the stomach when it is stretched.
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8
Q

Hormones: duodenum

A

Cholecystokinin (CCK) released in response to protein and free fatty acids
(duodenal brake)

CCK stimulates the gallbladder to contract and release stored bile into the intestine

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9
Q

Hormones: ileum

A

GLP-1 released in response to carbohydrate and fats and influenced by fibres
(Ileal brake)

It has the ability to decrease blood sugar levels by stimulating insulin secretion and inhibiting glucagon secretion

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10
Q

Hormones: colon

A

Peptide YY (PYY) released in response to carbohydrate and fat and influenced by fibres

PYY acts on NPY receptors and inhibits gastric motility, increases water and electrolyte absorption in the colon, and may suppress pancreatic secretion

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11
Q

How does stored energy feedback to the CNS to alter subsequent eating behaviour, and maintain weight / energy balance?

A

Leptin (leptos -‘thin’) - protein produced by adipose tissue (the body’s fat stores) when ‘full’.

Leptin is a potent reducer of food intake and Leptin appears act as a natural adiposity (body fat) signal

leptin binds to ‘leptin receptors’ in the hypothalamus, which:
- suppresses appetite
- increases the metabolic rate
- stimulates thermogenesis

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12
Q

what was the finding of the study on obese mice?

A

Obese mice (ob/ob) could not produce leptin because they were born without required gene code. Once the leptin producing gene was identified is was termed the ob-gene.

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13
Q

Congenital Leptin Deficiency

A

In humans there is a rare condition in which, due to a single gene defect, leptin cannot be produced.

Children demonstrate excessive weight gain and various appetites.

Administration of recombinant leptin completely reverses this condition

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14
Q

what was Eliot Stelar’s dual centre theory? (1950s)

A

lateral hypothalamus (LHA) as ‘hunger centre’

ventromedial hypothalamus (VMN) as ‘satiety centre’
activity influenced by circulating glucose & lipids etc

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15
Q

What do new CNS Integrations of Appetite Control
theories focus on

A

neuropeptides, produced & released by arcuate (ARC) regulate other hypothalamic & extra-hypothalamic areas
and
are themselves regulated by a host of peripheral feedback signals (CCK, GLP-1, Leptin

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16
Q

CNS structures involved in appetite regulation

A

-Arcuate Nucleus (ARC)

-Ventro Medial Hypothalamus (VMH)

-Lateral Hypothalamus (LH).

-Paraventricular Nucleus (PVN).

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17
Q

The arcuate nuceus (ARC) is the source of two major neuropeptide systems involved in appetite regulation

A

Neuropeptide Y system (NPY) – appetite stimulation (Orexigenic)
Melanocortin system (αMSH) – appetite inhibition (Anorexigenic)

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18
Q

what is Orlistat?

A

pancreatic lipase inhibitor that reduces fat absorption from gut produces modest weight loss, (unpleasant GI side-effects, only effective with high fat diets…)

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19
Q

what does ‘Bupropion and Naltrexone’ do?

A

Bupropion stimulates the release of the MC4R agonist αMSH from the POMC neurons in the PVN

Naltrexone preventsinhibition of POMC neurons by blocking the action of β-endorphin potentiating Bupropion effects

improves control over eating

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20
Q

what does Liraglutide and Semaglutide do?

A

GLP-1 analogues enhance satiety and reduce energy intake

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21
Q

6 biological changes in aging:

A
  • Immune system: Increase susceptibility to infection.
  • Cardiovascular system: Inc size and weight of heart, inc collagen in blood vessels, hardening of the blood vessels and change in blood pressure.
  • Respiratory system: Decrease lung capacity – alveoli decrease in efficiency
  • Musculoskeletal system: Reduction in muscle mass and strength, loss of bone matrix.
  • Gastrointestinal system: Decreased blood flow to gut and liver and decreased absorption of GI tract.
  • Integument: Graying of hair, wrinkling of skin, decrease in melanin.
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22
Q

what is corneal flattening?

A

In the aging eye the corneal surface flattens, admitting less light into the eyeball. This change reduces the transmitted light into the elderly eye by one third.

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23
Q

what happens to the lens with age? and how does this affect vision?

A

The transparency of the lens actually diminishes with aging which weakens available light to receive colors with short wavelengths such as blue and violet. When new lens fibers naturally multiply at the edge of the lens, older fibers move to the center to create a dense center of the lens.

Over time, the lens accumulates yellow substances which filter out the blue part of the color spectrum. Blue actually appears more green. Warmer colors like reds and oranges, seem stronger in comparison.

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24
Q

how is the retina affected with age? and how does this affect vision?

A

The most sensitive part of the retina gradually functions less well with age due to decreased blood supply and the cumulative effects of radiation damage.

The result is decreased spatial discrimination, black and white contrast, and flicker sensitivity.
You become less able to tolerate glare and have more trouble adapting to darkness or bright light.

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25
Q

how is the elasticity of the lens affected with age? and what does this cause?

A

Over time the lens of the becomes less elastic which diminishes the focusing power of the eye and causes a decline in visual acuity.

This changes can start as early as 30 years old but is usually first noticed around age 40 and is called presbyopia.

As presbyopia becomes more pronounced, people hold reading materials further away from their eyes. Some get headaches or “tired eyes” while reading or doing other close work.

By age 55, most people require glasses for reading at least part of the time. Those who already wear glasses may need bifocals.

Fortunately, only 5% become unable to read and about 20% have enough visual impairment to prevent driving.

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26
Q

what is macular degeneration?

A

The macula (region of the retina) may lose effectiveness or thins over time. sometimes deposits (Drusen) also collect causing a loss in central vision.

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27
Q

what is a cataract? and what can be done to treat it?

A

Cataract is a clouding of the lens and it is like looking through a fogged up window. It is also a normal part of aging but can be caused by steroid treatment or diabetes.

This, in fact is one of the most common surgeries performed on the NHS and replacement of the lens is a relatively straight forward procedure.

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28
Q

what is glaucoma?

what causes it?

how can it be improved?

A

Glaucoma is a disease of the optic nerve and when this is damaged blind spots occur in peripheral vision.

It can be hard to detect as blind spots are naturally filled in by the brain.

This damage to the optic nerve is caused by blood pressure changes that primary restrict the outer fibres of the optic nerve leading to the outer part of the visual field being affected.

This issue can in some cases be improved by reducing blood pressure and releasing the nerve fibres from that pressure.

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29
Q

what happens to the ear with age?

A

A number of age-related changes occur in the ear.
- Membranes in the middle ear, including the eardrum, become less flexible with age. - the small bones in the middle ear, the ossicles, become stiffer.

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30
Q

For younger people the frequency range of normal hearing is ………… cycles per second, while for older adults the range is from ……… cycles per second. Normal speech requires a frequency range of ……… cycles per second.

A
  1. 30 to 20,000
  2. 250 to 8,000
  3. 500 to 2,000
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31
Q

Changes in the middle ear with advancing age also contribute to a weakening sense of …..

A

balance.

The vestibular apparatus begins to degenerate with age in a similar way to the hearing apparatus

Equilibrium becomes compromised and older individuals may complain of dizziness and find it difficult to move quickly without losing their balance.

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32
Q

what is presbycusis?

A

literally “old man’s hearing”– is the most common form of hearing loss with aging. It is characterized by a decrease in perception of higher frequency tones and a decrease in speech discrimination.

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33
Q

age’s effects on the brain? (5 points)

A
  • atrophy (especially in the PFC)
  • decreased neurogenesis
  • ventricular enlargement (gaps in the brain)
  • decreased cerebral blood flow - which results in a decrease in neurotransmitters and nutrients going to the brain
  • Increase in “senile plaques” and neurofibrillary tangles
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34
Q

what are senile plaques? what causes them?

A
  • decaying nerve terminals around the amyloid Beta core found in grey matter.

-

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35
Q

what are neurofibrillary tangles? what do they consist of?

A
  • are insoluble twisted fibres that are not longer functioning, found inside the brain’s cells
  • Thesetanglesconsist primarily of a protein called tau, which forms part of a structure called a microtubule. The microtubule helps transport nutrients and other important substances from one part of the nerve cell to another.
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36
Q

what are the 3 main lines of evidence for suggesting aging is governed by genes?

A
  • It has been found that the siblings of centenarians tend to live longer and have a reduced probability of Alzheimer’s (Perl et al (2002).
  • Studies have found monozygotic twin pairs show more similar patterns of cognitive decline than dizygotic twins (Swan et al, 1992).
  • Identification of genes in fruit flies that affect the duration of life. (Rera et al, 2011 in Cell Metabolism, 14(5):623-634).
37
Q

how did scientists increase the life span of a fruit fly?

A

manipulating PGC-1 gene. By making this gene more active (which is a gene also found in mammals) increases activity in the mitochondria of cells specifically in the intestines.
They found that by doing this they would increase the fly’s life span by up to 50%.

38
Q

which 2 forms of intelligence/ability tend to be maintained with age?

A
  • Numeric ability such as solving Maths equations and
  • verbal ability in use of language and tends to be maintained in older adulthood.
39
Q

The cognitive functions commonly associated with cognitive decline in aging are

A
  • Decrease in attention
  • Working memory deficits
  • Increased forgetfulness
  • Increase in learning time
  • Slowing of problem solving
  • Increase in reaction times
40
Q

which part of the brain controls bottom-up attention and which part does top-down attention?

A
  • parietal lobe
  • PFC
41
Q

what were the findings of Li et al.’s (2013) study on attention in the ageing brain?

A

No difference in pop-out (bottom-up attention), but significant decline in accuracy in visual search (top-down attention) in older adults

42
Q

what were the findings of Stevens et al.’s (2008) study looking into the affects of age on forgetting?

A
  • 12 younger and 12 older adults were put in an fMRI scanner and did a face recognition task (old/new) and confidence rating.
  • Same number of faces recognised in both YA and OA.
  • OA showed increased activity in auditory cortex (loud noise produced by fMRI scanner) and left PFC for forgotten faces. With left HPP active for remembered faces in both YA and OA
43
Q

what are the effects of aging on memory?

A
  • non-declarative memory such as learning motor skills and priming is maintained.
  • Episodic memory clearly peaks in young adults before declining
44
Q

impaired memory in normal aging (episodic and short-term memory) can be attributed to several changes in the cortex:

A

(1) smaller neural networks (due to decrease in neurons) (2) loss of synaptic innervations,
(3) decrease in the storage capacity of single neurons

45
Q

brain areas that reduce in volume with age:

A
  • Caudate Nucleus
  • Prefrontal Cortex
  • Cerebellar Hemispheres
  • Hippocampus
46
Q

brain regions with minimal reduction or stable volume with age:

A
  • Primary Visual Cortex
  • Entorhinal Cortex
47
Q

what is Park and Reuter-Lorenz’s (2009) Scaffolding Theory of Ageing and Cognition or (STAC)

A

They propose a way that the brain can alter and compensate for these challenges in terms of scaffolding such as:

  • engaging in new learning, exercise and cognitive training to enhance the function and how our brains can recruit extra regions such as the PFC and activate more bilateral brain areas and also regenerate to help compensate for these issues.
    These both work together to maintain a good level of cognitive function.
48
Q

what were the findings of Gutchess’ (2014) study on plasticity?

A

This study basically found that artificially inducing plasticity, using a transcranial direct current stimulation (tDCS), in the prefrontal cortex of the brain reduces the amount of errors made in attention and memory tasks.

49
Q

what is the difference between a free and a bound morpheme?

A

A free morpheme is a morpheme that can stand alone as a word and convey meaning on its own.

A bound morpheme is a morpheme that cannot stand alone as a word and must be attached to a free morpheme or another bound morpheme to convey meaning.

50
Q

what is an inflectional and a derivational morpheme?

A

they are 2 types of bound morphemes

Inflectional morphemes are bound morphemes that are added to words to indicate grammatical relationships such as tense, number, aspect, mood, or case.
e.g. (-s, -ed, -ing)

Derivational morphemes are bound morphemes that are added to words to create new words or to change their core meaning, part of speech, or semantic category.
e.g. (un-, -ness, -ize, re-)

51
Q

what method do fMRI studies use to identify differentially active cerebral regions?

A

they use the subtraction method
in which they take a control reading and subtract that from the active reading

52
Q

what is aphasia?

A

language deficit caused by damage to the brain

53
Q

what is a cerebrovascular accident?

A

CVA – stroke; i.e., sudden damage or death of cells in a localised area of the brain, due to inadequate blood flow

54
Q

what are the 3 main causes of CVAs

A
  • Embolism
  • Thrombosis (most common cause)
  • Haemorrhage
55
Q

for language deficits, which artery is ‘damaged’?

A

Middle Cerebral Artery (MCA)

56
Q

what are the main arteries of the brain?

A
  • internal carotid arteries
    -middle cerebral artery
    -anterior cerebral artery
  • vertebral arteries
    -basilar arteries e.g. posterior cerebral artery
  • circle of willis
    -at base brain
57
Q

what did Paul (Pierre) Broca (1824-1880) discover in his patient, Monsieur Leborgne (known as “Tan”) who had trouble with speech production

and what did Broca argue

A

Post-mortem examination showed a lesion in the LH at the Pars Opercularis, Lower Motor Cortex, and Insula

Broca argued that the production site of language is in the left hemisphere in the area around the Posterior part of the Inferior Frontal Gyrus (Broca’s area)

58
Q

what is Broca’s Aphasia or Non-fluent Aphasia characterised by?

A
  • Effortful speech production; speech is halting, slow
  • Speech timing is disturbed (dysprosody)
  • Telegraphic speech: loss of function words (e.g. determiners, prepositions, conjunctions)
  • Bound morphemes tend to be missing, specifically, inflectional affixes.
  • Phonemic paraphasias
  • But relatively spared comprehension
  • Most Broca’s aphasics are painfully aware of their mistakes
59
Q

what did Karl Wernicke (1848-1905) discover in 1874?

A

Patient had suffered a stroke; able to speak, his hearing unimpaired, but could barely understand what was said to him. Nor could he understand written words

Post-mortem examination revealed a lesion in the Posterior Temporal/Parietal region in left hemisphere (Wernicke’s area)

Wernicke concluded that this region, which is close to the auditory region of the brain, was involved in speech comprehension

60
Q

what is Wernicke’s Aphasia or Fluent Aphasia characterised by?

A
  • Poor auditory comprehension
  • Semantic paraphasias (“chair” for “table”)
  • Phonemic paraphasias (“plick” for “clip”)
  • Neologisms (creation of new words)
  • Written language may be impaired in similar ways
  • Repetition is paraphasic
  • But intonation and grammar are preserved but language production is gibberish (Jargonaphasia)
  • Wernicke’s aphasics are unaware of deficit, produce word salad
61
Q

where are the language systems localised in the brain?

A
  • in the left hemisphere around the Sylvian Fissure, in Perisylvian regions
  • Posterior and Anterior language areas are assumed to be connected with the Arcuate Fasciculus
62
Q

A lesion in the Arcuate Fasciculus results in…

A

..Conduction Aphasia (impaired repetition)

63
Q

damage in the right hemisphere causes abnormalities in what area of language? This is backed up by which study?

A

in the interpretation of lexical items which have alternate meanings, and an inability to revise an initial interpretation

this is supported by Winner & Gardner’s (1977) study in which they tested participants with damage in their LH and RH and NC using metaphorical lanaguage
Participants with damage in the RH took metaphors literally

64
Q

what is a PET scan and what does it measure?

A

a short-lived radioactive tracer isotope is injected into the subject; PET scans are increasingly read alongside CT or (MRI) scans, the combination giving both anatomic and metabolic information
(measures glucose levels)

65
Q

what are Event Related Potentials (ERPs)?

A
  • ERP refers to the brain’s electrophysiological response to specific events, such as sensory stimuli, cognitive tasks, or motor actions.
  • ERP is extracted from EEG data by averaging EEG segments time-locked to the occurrence of the event of interest.
66
Q

Characteristics of ERP components:

A
  • Polarity (positive (P) or negative (N))
  • Latency (How long after stimulus presentation does it
    peak? (e.g. 100ms - P100)
  • Functional Significance (What cognitive (or perceptual) activity is it
    sensitive to?
    What makes it bigger or smaller?)
67
Q

what is an EEG?

A
  • EEG is a non-invasive neuroimaging technique that records electrical activity generated by the brain using electrodes placed on the scalp.
  • EEG measures the summation of the postsynaptic potentials of cortical neurons, providing a temporal record of brain activity with high temporal resolution (milliseconds).
68
Q

what do P300, N400 and P600 readings signify in language ERPs?

A
  • P300 component
    Elicited by surprising events
    Related to updating model of
    world in memory
  • N400 component
    Elicited by meaningful stimuli
    Measures processing difficulty
  • P600 component
    Elicited by ungrammatical stimuli
    Related to P300 component
69
Q

give an evolutionary explanation of why language is lateralised

A
  • Lateralisation of language function may have evolved to avoid the problem of coordinating activity in the two hemispheres to produce the precisely timed sequences of movements used in speech.
  • Probably preceded by lateralisation of hand control to allow specialisation in the use of the two hands (handedness).
  • The ability to execute coordinated rapid movements (e.g., throwing a spear) is highly lateralised. Language is (usually) in the same hemisphere that controls the dominant hand.
70
Q

what is laterality?

A

the idea that the two cerebral hemispheres have separate functions

71
Q

In the 1860’s, John Hughlings-Jackson and Pierre Gratiolet first observed what?

A
  • that the cortical convolutions on the Left Hemisphere-LH mature more rapidly than those on the Right Hemisphere-RH
  • Observations largely ignored until the 1960’s when Norman Geschwind and Walter Levitsky renewed interest
72
Q

To date, eight major anatomical differences, assuming to reflect functional asymmetries, between the two cerebral hemispheres have been confirmed:

A
  1. RH slightly larger and heavier than LH, but LH has more gray matter
    2.Marked structural asymmetry between the temporal lobes
    3.Asymmetry in the cortex of temporal lobes correlated with midbrain asymmetry in the thalamus
    4.Slope of Lateral Fissure gentler in LH; thus, temporoparietal cortex lying ventral to lateral fissure appears larger on RH
    5.Frontal Operculum (Broca’s area) organised differently in LH and RH; area visible on the surface about 1/3 larger on the RH, while area buried in the sulci larger in LH
    6.RH extends farther anteriorly, LH extends farther posteriorly; five times more likely that the occipital horns of the lateral ventricles are longer on the RH
    7.Distribution of various neurotransmitters asymmetrical both in cortical and subcortical regions
    8.Details of anatomical asymmetry affected both by sex and handedness
73
Q

what is double dissociation

A

two areas of the neocortex are functionally dissociated by two behavioural tests, each test being affected by a lesion in one area but not the other.

74
Q

who pioneered the Carotid Sodium Amobarbital Injection and what does it do?

A
  • Juhn Wada pioneered the technique of injecting sodium amobarbital into the carotid artery to produce a brief period of anaesthesia of the ipsilateral hemisphere; the Wada test (1949)
  • Typically used before surgery in epileptic patients to establish the language dominant hemisphere; short lived effects (about 10 min)
    Left carotid injected  LH anaesthetised  patient cannot speak, move right arm, see on the Right Visual Field-RVF
75
Q

in the 1940s, what would they do to epileptic patients?

A

cut the Corpus Callosum and sometimes the Anterior Commissure to relieve patients from intractable epileptic seizures. No severe deficits observed in those patients.

76
Q

what is the function of the Corpus Callosum? (explain Sperry’s study)

A
  • In the 1950’s, Sperry did experiments with cats and monkeys to study split-brain; they severed the Corpus Callosum, the Anterior Commissure and the Optic Chiasm.
  • Taught animals Visual Discrimination and tested them with one eye closed; found that information never crossed to the other hemisphere. Also experimented with somatosensory information teaching animals to touch a surface with one paw.
  • So, Corpus Callosum allows cortical areas from one hemisphere to communicate with cortical areas of the other hemisphere.
77
Q

In the 1960s Sperry moved to CalTech to study patients; Gazzaniga was his student.
explain their study that used tachistoscopic presentation

A

Flash the word BANANA to the RVF/LH, split-brain patients can say the word
But, flash the word BANANA to the LVF/RH, split-brain patient not able to say the word!
However, able to collect the right object using the left hand!
So, LH is responsible for language; RH cannot produce language, but has reasonable comprehension ability for simple things

78
Q

explain Sperry’s study looking into spatial organisation skills of split brain patients

A

Flash a 3D line drawing of a CUBE to the RVF/LH, right hand of right-handed split-brain patient cannot reproduce the drawing
But, flash the 3D line drawing of a CUBE to the LVF/RH, left hand of right-handed split-brain patient able to reproduce the drawing!
So, RH is responsible for spatial organization

79
Q

explain the finding’s of the ‘perception studies’ of split brain patiemts

A
  • Both hemispheres can “see” whether the illusory rectangles are fat (a) or thin (b)
  • But when outlines are added, only the RH can still tell the difference (c and d)
80
Q

explain the findings of the ‘synthesis studies’ of split brain patients

A
  • RH flashed “bow”, LH saw “arrow.” Patient drew a bow and arrow; erroneous assumption that LH and RH were still able to communicate and had integrated the words into a meaningful composite.
  • RH flashed “sky”, LH “scraper”. Resulting image revealed patient was not synthesizing: sky atop a comb-like scraper drawn, not a tall building. RH/left hand drew what it had seen, then LH/right hand drew its word.
  • So, no synthesis across hemispheres.
  • RH flashed “fire”, then “arm”. Left hand drew rifle rather than arm on fire
  • So, clear that each hemisphere is capable of synthesis.
81
Q

what are Asymmetries in the Visual System? using tachistoscopic presentation

A
  • LH/RVF advantage for words
  • RH/LVF advantage for faces and other visuospatial stimuli
82
Q

Asymmetry in the Auditory System using dichotic listening:

A
  • LH/Right-Ear advantage for words, digits, morse code, difficult rhythms, tone used in linguistic decisions
  • RH/Left-Ear advantage for melodies, musical chords, environmental sounds, tones independent of linguistics
    No Ear Advantage for vowels, rhythms, nonmelodic hums
83
Q

Summary of Data on Cerebral Lateralization
Function – Left Hemisphere – Right Hemisphere

  • visual
  • auditory
  • somatosensory
  • movement
  • memory
  • language
  • spatial processes
A

Visual system:
LH - Letters, words
RH - Complex geometric patterns, faces

Auditory system:
LH - Language-related sound
RH - non-language environmental sounds, music

Somatosensory system:
LH - ?
RH - Tactile recognition of complex patterns, Braille

Movement:
LH - Complex voluntary movement
RH - Movements in spatial patterns

Memory:
LH - Verbal memory
RH - Nonverbal memory

Language:
LH - Speech, reading, writing, arithmetic
RH - Prosody

Spatial processes:
LH - ?
RH - Geometry, sense of direction, mental rotation

84
Q

what is the difference between specialisation theories and interaction theories?

A

specialization theories propose unique functions for each hemisphere, while interaction theories propose cooperation between the hemispheres

85
Q

what are specialisation models?

A
  • Unilateral specialization models state that only one hemisphere facilitates a given psychological process
  • LH operates in a more logical, analytical fashion, analyzing input sequentially, abstracting relevant details and attaching verbal labels
  • RH is primarily a synthesizer, more concerned with the overall stimulus configuration, organizing and processing information as gestalts or wholes
86
Q

what are interaction models?

A

Both hemispheres have the capacity to perform all functions but they do not; three versions exist
1. The two hemispheres function simultaneously but work on different aspects of processing
2. Although both hemispheres have the capacity to perform a given function, they inhibit or suppress each other’s activity (e.g., LH suppresses the RH’s language processing)
3. The two hemispheres receive information preferentially and thus perform different analyses simultaneously;
or some mechanism enables each hemisphere to “pay attention” to specific types of information, thus leading to different hemispheric analyses

86
Q
A
87
Q
A

Year 2 Semester 2 (5 decks)

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