memory, language and executive dysfunction

Question 1

what are the stages of memory *

Answer 1

registration - input from senses, and attention and ability into the memory system

encoding - processing and combining the recieved info

storage - holding of that input in the memory system, assimilate with already known info

retrival - recoving stored info from the memory system (if problem at this stage would benefit from prompts/cues)

Question 2

what stage of memory does alzhiemer’s effect *

Answer 2

encoding

prompts dont help

Question 3

theory 2 of memory - duration *

Answer 3

conceptual divisions in memory systems

• sensory - not last long, might not be aware of it at all
• working/short term mem - few seconds - when info processed it is laid down as this
• long term memory - few days

Question 4

describe the model for memory incorporating stages and duration *

Answer 4

info goes into sensory receptors - some info lost, some laid down as short term memory if we focus attention on it; rehearsal means it will stay in short term, if not rehearsed there is a limited capacity so info is lost

info can be stored in long term mem - either from short term or from sensory

info from long term is retrieved (reactivating working mem) - dont know if this is by same architecture as laying down memory eg hippocampi

longterm memory is transferred to neocortex

Question 5

what are the different types of memory *

Answer 5

long term memory is composed of declaritive and non-declaritive

declaritive composed of episodic (problem present that cant remember anything from on holidy for eg), or semantic (acquired knowledge eg capitals)

non-declaritive (w/o consciousness, usually well conserved in lesions) made of procedural (eg driving), priming, conditioning, non-associative learning

Question 6

areas of the brain involved in different aspects of long term memory *

Answer 6

declaritive (explicit) - medial temporal lobe/diencephalon

procedural - striatum

priming - neocortex

simple classical conditioning

• emotional response - amygdala
• skeletal musculature - cerebellum

Question 7

what part of the brain does episodic memory involve *

Answer 7

medial temporal lobe including hippocampus, enterhinal cortex, mammillary bodies, parahippocampal cortex

Question 8

effect on memory of bilateral removal of the temporal lobe *

Answer 8

remove the hippocampus = memory deficits - responsible for learning of declaritive memory - cant remember what just happened

basal ganglia project to prefrontal so might be involved in the problem - retrival deficit

Question 9

what type of memory is the temporal lobe related to *

Answer 9

semantic memory

Question 10

what type of memory is associated with prefrontal cortex *

Answer 10

working memory

retrival

Question 11

what type of memory is the cerebellum associated with *

Answer 11

procedural memory

Question 12

summarise memory disorders *

Answer 12

total amnesia is rare - especially when there is otehrwised preserved cognition

many neuro conditions effect memory with different lesion sites

the various aspects of memory are effected in different ways by different disorders

eg episodic, semantic (primary semantic deficit - semantic dementia), anterograde/retrograde dementia - when people have siezures or epilepsy they might have remote memory problems

implicit memory or learning are often on tact - for example mirror drawing improves each time a person does it, even of they have no declaritive memory of having done it before

Question 13

effect of temporal lobe damage by herpes encephalitis

Answer 13

procedural memory fine

but unable to lay down new memories

Question 14

describe modality of memory *

Answer 14

L hemisphere mainly concerned with verbal information processing

R with non-verbal - ie face processing so prosopregnosia is likely to effect R

Question 15

describe the serial position effect

Answer 15

have primicy effect and recency effect

more likely to remember words at start and end of list

in alzheimer’s the primicy effect is lost - memory already gone because the coding is deficit

Question 16

what alters the probability of remembering words

Answer 16

order

personal salience

number of words

chunking or other encoding strategy - repeat the lsit a few times to see if people can do this - in fronto/fronto-striatal disruption difficulty chunking even with repetition

delay time

distraction

Question 17

clinical implication of the way we remember

Answer 17

give important info at the beginning and end

emphasise and repeat important info at end

make salient - ie link back to initial concerns

chunk info into meaningful categories

avoid overloading with information - working memory is 7+/- 2 items

can use pneumonics

Question 18

summarise language

Answer 18

it is ubiquitous

a system of symbols, rules and structure that enable us to communicate

nio humans found without language

debate whether innate (because universal across cultures) or exposure

both organic and environmental factors are important - there is a critical time frame for language develop, we are designed to develop language but this depends on exposure

Question 19

what is the structure of language

Answer 19

phenome - the smallest uniot of sound in a language that can signal a difference in meaning - humans can express just >100, in english there are 44

morphemes are the smallest units of meaning in a language - typically 1 syllable, combined to make words

words

phrases

sentences

written text and conversational discourse

Question 20

what is syntax

Answer 20

rules that govern teh way morphemes and words are combined to communicate a particular language

theory of universal grammer - under normal conditions humans will develop language with particular properties eg distinguishing nouns from verbs

children of parents who speak pidgin language ie with no grammer, develop languages which are fully gramatical - suggests that there needs to be some exposure but an innnate part of the brain controls syntax

Question 21

describe language development *

Answer 21

1-3months - distinguish speech and nonspeech, prefer speech, undifferentiated crying gives way ot cooing when happy

4-6months - babbling sounds - contain sounds from every language, child vocalises in response to vocalisation from others

7-11months - only phenomes heard in own language, child moves tongue with vocalisations, child discriminates some words without understanding their meaning and begins to initiate word sounds herd from others

12months - firts recognisable words as 1 word utterence

12-18 - increase knowledge of meaning, use single words to express whole phrases, usually nouns

18-24 - vocab extends to 50-100 words, 1st rudumentory sentances usually 2 words, little use of articles, conjunctions, or axillary verbs

2-4yrs - vocab expands rapidly, get larger sentences, grammatically incorrect but express basic syntax, expresses concepts with words and describe imaginary objects and ideas

4-5yrs - child has learnt basic gramatical rules for combining nouns, adjectives, articles, conjugations and verbs into meaningful sentences

Question 22

what happens if children are raised without exposure to language

Answer 22

they are w/o language

even with rehab still incompetent

Question 23

describe the critical period for lanuage gain *

Answer 23

<5yrs

between 5 and puberty it is harder

we know this because of 2nd language acquisition, children with brain injuries at different stages and feral children raised w/o language

exposure to language is required

Question 24

describe hemispheric specialisation for language *

Answer 24

95% of R handed people have L hemisphere dominance

19% of L handed have dominance for R, another 19% have no dominance

therefore post-brain injury dominance may effect recovery

Question 25

effect of lesion to broca’s area *

Answer 25

non-fluent speech

impaired repitition

poor ability of syntax

intact comprehension

effortful expression

this is expressive aphasia

Question 26

where is broca’s area *

Answer 26

l hemisphere, frontal region

Question 27

describe wernick’s aphasia *

Answer 27

receptive aphasia

problem in comprehending speech - input/reception of language

fluent meaningless speech - wouldnt notice the aphasia if you didnt speak their language

paraphasias - errors in producing specific words

semantic paraphasias - substituting words similar in meaning

phonemic paraphasias - substituting words similar in sounds

neologisms - non-words

poor repitition

impairment in writing

can managage aspects of conversation - eg speak at right time but cant respond to specific qns

Question 28

where is wernick’s area *

Answer 28

temporal lobe

Question 29

describe the language circuits*

Answer 29

info about sound is analysed in cortex and sent to wernick’s area

wernick’s area analyses this to see what word was said

this info goes through the arcuate fasiculus to broca’s area

broca’s area forms a motor plan to repeat the word and sends it to motor cortex

motor cortex illicts plan

Question 30

effect of lesion to arcuate fasciculus *

Answer 30

cant repeat word

but can understand because of intact wernick’s

and can speak spontaneously because of intact broca’s

Question 31

what are the different types of aphasia *

Answer 31

global - not fluent, cant comprehend, cant repeat

mixed trasncortical - not fluent, cant comprehend

broca’s - not fluent, cant repeat

transcortical motor - not fluent

wernick’s - cant comprehend or repeat

transcortical sensory aphasia - cant comprehend

conduction- cant speak

anomic - naming deficit - common

Question 32

what conditions are associated with aphasia *

Answer 32

lesions to dominant hemisphere caused by:

stroke

tBI

cerebral tumour

progressive neurodegenerative conditions - primary progressive aphasia

Question 33

what is the new theory of localisation of language *

Answer 33

not just 1 key connective tract - there are many eg uncinate fasciculus, the inferior front-occipital fasciculus, the middle longitudinal fasciculus, inferior longitudinal fasciculus

language is distributed throughout brain - involving frontal, temporal, parietal in middle hemispheres, and the basal ganglia, thalamus and cerebellum

Question 34

what is dysexecutive syndrome *

Answer 34

the disruption of executive function and is closely related to frontal lobe damage

has cognitive, emotional and behavioural symptoms

Question 35

what is executive function *

Answer 35

the mental processes taht allow us to plan, focu attention, remember instructions and juggle multiple tasks

it coordinates response for different things - not just 1 function

involves inhibiting response

Question 36

causes of dysexecutive syndrome (*

Answer 36

head trauma

tumour

degenerative disease

cerebrovascular disease

psychiatric problems

Question 37

what are the 2 possible behavioural and emotional aspects of dysexecutive syndrome *

Answer 37

1

• hyperactivity
• impulsive
• disinhibited
• perseverative
• emotional dysregulation
• socially inappropriate
• rude, crass, prone to swearing

2

• hypoactivity
• lack of drive
• apathetic
• poor initiation of tasks
• lack of spontinuity
• emotional bluntness
• theory of mind difficulties - social cognitive difficulties - dont know whats in other people’s minds
• reduced empathy

get either of these - dependant on discrete brain areas

Question 38

cognitive effects of the dysexecutive syndrome *

Answer 38

attentional and working memory difficulties - prefrontal cortex

poor planning and organisation

difficulty coping with novel situations and unstructured tasks

difficulty switching from task to task

difficulty keeping track of lots of tasks

difficulty with complex/abstract thinking

Question 39

what regions of the frontal lobe are effected in dysexecutive syndrome *

Answer 39

prefrontal cortex - memory

orbito-frontal - impulsivity and disinhibition - behaviour change

medial - loss of spontaneity, initiation - lack of drive, apathy (not depression - report mood as fine), akinetic mutism

dorsolateral - inability to formulate and carry out plans - cognitive problems

Question 40

describe the connections between prefrontal cortex and subcortical structures in dysexecutive syndrome *

Answer 40

it means that conditions look like there is a problem in the frontal cortex, but actually the damage is to subcortical areas

eg movement disorder - parkinsons can develop apathy because of connections, not necessarily direct damage to frontal regions