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Neuropsychology week 1 > Neuropsychology week 3 > Flashcards

Neuropsychology week 3 Flashcards

1
Q

What is aphasia?

A

Acquired impairments of speech production

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2
Q

What is the first thing to determine when you are presented with a patient with speech problems

A

Ensure they do not have any developmental conditions which impact there speech. E.g. issues with hearing.

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3
Q

What psychiatric condition can have symptom overlap with aphasia

A

Schizophrenia

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4
Q

What are vascular presentations of aphasia

A

Patients who have had a stroke and have their speech impaired because of it

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5
Q

What are the areas believed to be implicated for each of the two aphasia in the original theories by Broca and Wernicke

A

Broca’s area- BA44,BA45 (dominant hemisphere) required for motor speech representations. (key for speech output)
Wernicke’s area- Superior temporal lobe
Luria’s hypothesis (deficit to acoustic analysis)
Wernicke’s hypothesis (impairments to phonological representations)

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6
Q

Localisation

A

Some thought that symptoms are determined by the area of damage injured whilst some thought it is determined by damage to whole brain.

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7
Q

What is name of Broca’s original patient and what symptoms did he present with?

A

TAN.
Severely non fluent
Poor articulation (slurred) (dysarthria)
Poor melodic line (flat) (dysprosody) (can sound like a foreign accent)
Poor grammar
poor speech volume (hypophonia) (Strained, low)
Can start swearing a lot. (lexical vs non lexical route)
Often see neologisms (that ARE RELATED to phonological words)

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8
Q

Which pathway is implicated in Broca’s aphasia

A

Lexical/ventral.

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9
Q

What is the reconstructive cognitive process

A

Selection of words happens in real time. stringing together the phenomes which make up the word. pieces of the puzzle are not retrieved in real time.

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10
Q

When assisting Broca’s patient do you want to give them conceptual information or phonological? Why?

A

Phonological. they know what they are trying to say (semantically) just don’t know hot to say it.

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11
Q

Does Broca’s aphasia affect intelligence

A

no

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12
Q

What are the characteristics of Wernicke’s aphasia

A

Severe Auditory comprehension deficits
Speech output is rapid (fluent) but often meaningless.
Phonemic, semantic and neologism.
(stool to pool) (stool to chair) (stool to gwool)

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13
Q

Why does Tree say Wernicke’s aphasia mimics brit abroad?

A

They don’t realise what they are saying is non sensical. think raising their voice and speaking slower will fix the problem. Some hypothesis it is a malfunctioning of the system which monitors speech production.

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14
Q

Is Wernicke’s aphasia a malfunctioning of the language system? Why?

A

NO. because if you ask a patient to say a word and ask them again in 2 weeks they will make different errors.

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15
Q

What is the name of the white matter connecting speech input region and speech output. (input to output route)

A

Arcuate fasciculus (issues in this reason is responsible for conduction aphasia)

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16
Q

What are the different clinical classifications of aphasia.

A

Broca’s aphasia, Wernicke aphasia (Non fluent vs fluent)
Conduction aphasia (Fluent, good comprehension poor repetition)
Anomia (fluent, good comprehension, poor naming)
Global aphasia (Non fluent, poor comprehension/ repetition)
Transcortical motor aphasia
Transcortical sensory aphasia (Fluent but empty speech, repetition good, comprehension and naming poor)

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17
Q

What are two ways one could develop Aphasia?

A

Stroke (haemorrhages/infractions)
Trauma (Closed head injury) and tumours

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18
Q

Transcortical motor aphasia symptoms

A

Affects speech production
Impaired motoric transmission of information from brain to mouth
Coordination of speech from automatic thoughts
Good at repetition struggle generating speech for themselves

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19
Q

Transcortical sensory aphasia symptoms

A

Issues in coordinating heard speech into understanding or accessing conceptual representations
Good repetition
impaired comprehension
Sometimes miss out some letters of words

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20
Q

Problems with syndromes

A

1.Distinguishing criteria quite general
2.Syndrome depends on symptoms being present or absent but impairments are a matter of degree of impairment
3.collection of symptoms that tend to co-occur( modal presentation) not always the case
4.Behavioural deficits and lesion correlations sometimes violated.
5.Symptoms not always stable over time. two syndromes can sometimes blend to each other.
6. Gerstmann syndrome (weird syndrome where symptoms cluster together that have nothing to do with each other)

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21
Q

Issue with making causal inferences based on structural lesions?

A

“To locate the damage which destroys speech and to locate speech are two different things”
Essentially lesions do not mean that the implicated brain region is solely responsible for an impairment. Need to be careful about making causal inferences around lesion location and function disorder.

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22
Q

Does Cognitive neuropsychology emphasise grouping or looking at differences in case studies?

A

Single case studies.

23
Q

What is anomia?

A

Permanent state of tip of the tongue.
loss of naming ability.
Able to reject incorrect options (thus not a semantic problem)
system implicated: Phonological output processing.

24
Q

Confrontational naming task

A

Used to tests for the type of errors in anomia. errors can be semantic, circumlocution(dog-woof), phonological, neologisms

25
Q

What 3 components can be involved in naming impairment

A

Visual processing (object agnosia)
Semantic/ conceptual processing (what an object is)
Phonological output processing (speech sound access)
syndrome approach would group all these impairments in the same bucket

26
Q

What is dysphasia

A

Disorder of repetition

27
Q

What are the 3 processes involved in name repetition

A

recognition (auditory), conceptual representation (semantic), name retrieval (output lexicon).
2 routes (lexical/ventral and non lexical/ dorsal)

28
Q

Non lexical/ dorsal route

A

sound to meaning. Projects from SGT to boundary between parietal/temporal regions. articulatory route. (translate auditory information into speech)

29
Q

Non lexical (dorsal) vs Lexical (ventral)

A

automatic (Words broken down into smaller sounds and chunked together to create a word) vs way of meaning (box for auditory representations and box for semantic information)
then speech produced through output lexicon.

30
Q

What is the route of conduction aphasia?

A

Go from superior temporal lobe to SPT to output region. This argues that the cortical region (SPT) is implicated in conduction non word repetition. (NOT just arcuate fasciculus)

31
Q

Buchsbaum et al 2011 study

A

85 % of conduction aphasia patients (n=14). had lesions in SPT. Nearly 50% of controls showed activation of SPT in phonological memory tasks.

32
Q

STG

A

“initial input for auditory information”. area of input of auditory information. in the dorsal region and responsible for articulation
Damage to STG bilaterally lead to pure word deafness
Damage to dorsal projections= conduction aphasia- damage to auditory input speech output mappings.
Damage to ventral projections= transcortical sensory aphasia. disruption to auditory input conceptual meanings.
Damage to both ventral and dorsal regions- Wernicke’s aphasia.- negative symptoms of both conduction aphasia and transcortical motor aphasia.

33
Q

SPT

A

Key interface between superior temporal lobes and Broca’s area. (similar idea to arcuate fasciculus). in the ventral region responsible for meaning

34
Q

Wernicke’s aphasia as a dual process impairment.

A

Robson et al 2012. found that WA patients are impaired on both nonverbal and verbal comprehension. Semantic impairment (lexical/ventral) and output issues (non words, sub lexical/dorsal)

35
Q

How do we know that reading and writing are dissociable in the brain

A

MR C can write perfectly well but cant write. Dejerine found patient that can write but cant read.

36
Q

What is acquired Alexia/ Dyslexia

A

disorder of reading

37
Q

What is acquired agraphia/ dysgraphia

A

disorder of writing/ spelling

38
Q

What are the different types of dyslexia

A

Developmental (from childhood)
acquired (were able to read but cant anymore)
Peripheral (impairment due to some other deficit e.g. attention)
Central (specific reading or writing problem)
Surface dyslexia
phonological dyslexia
deep dyslexia

39
Q

Acquired central phonological dyslexia

A

normal reading/spelling of familiar words.
impairment in reading or spelling unfamiliar and non words.
suggests dorsal/non lexical route implicated

40
Q

acquired central Surface dyslexia

A

struggle with irregular words. (ventral route implicated)
Overgeneralisations- cant access semantics of how word should sound.

41
Q

Acquired central deep dyslexia

A

Make semantic errors in how reading/ spelling) (e.g. priest to imam)
can occur due to impairment in connection between semantic memory and output

42
Q

Peripheral dyslexia types

A

Attentional dyslexia- cant identify letters but can read (problems with focused attention)
Neglect dyslexia- Ignore half of word (opposite side of hemifield)
Pure alexia without agraphia- letter by letter reader. can use tactile kinaesthetic feedback as activates premotor cortex rather than superior temporal lobe, Longcamp et al 2005)

43
Q

Dual route model of reading.

A

Similar to repetition. Lexical and non lexical route. recognition, retrieval, output.
Phonological lexicon- how words are pronounced
orthographical lexicon- recognising what to read.

44
Q

Name 3 clinical tests for Aphaisa

A

Western aphasia battery
PALPA (Psycholinguistic assessments of language processing in APHASIA)
Pyramids and palms test

45
Q

Western APHASIA battery

A

Testing of speech (fluency), comprehension, repetition, naming, reading.
Generates an aphasia quotient
syndrome approach
requires alot of training

46
Q

PALPA

A

Testing of repetition, naming, reading, spelling (these tests can manipulate a number of psycholinguistic variables)
Testing of semantic memory
Testing of phonology (homophone, rhyme judgement, segmentation, blending)
This battery uses a cognitive neuropsychological approach
require training and there’s an intimidating number of assessments that are theoretically driven to choose from and administer

47
Q

Therapy approaches for Aphasia

A

Reactivation/ relearning- aims to activate impaired language processing/ knowledge reacquired through learning
Brain organisation/ cognitive relay- Encouraging alternative parts of brain to take over impaired function.
Compensation- using an alternative prosthesis to promote communication. maximise language function without focusing on impaired function.

48
Q

Three C’s for clinically aware therapy

A

Collaboration- occupational therapist, working with others(holistic approach)
Combination- therapy approach can be used with one another
coordination- client plays an active part in there treatment.

49
Q

Acquired dyslexia therapies. (pure alexia)

A

Lexical decisions therapy.
Involves rebuilding visual system.
tactile kinaesthetic therapy. Can use different modalities (Nicklas et al, 2010) uses sound.

50
Q

Acquired dyslexia therapies (attentional)

A

Use a carboard window that surrounds text to help them focus their attention. Shyimer et al 2009.
very low tech

51
Q

Surface dyslexia

A

input subtype- flashcard + mnemonic aid
output subtype- relearning words with auditory presentation. (ellis et al 2000)
semantic subtype- sentence completion task to learn via context. the lady made cream teas vs tease

52
Q

Interventions for aphasia

A
  • Errorless learning for anomic cases (enhances reinforcement mechanisms) (provide correct feedback over and over again, regardless of their reply)
  • Successful repetition exercise paired with donepezil (cholinesterase inhibitor)- successful in treating conduction aphasia (Berthier et al 2004)
  • IMITATE (computer assisted aphasia therapy). Combines audiovisual presentation of words and phrases with oral repetition of same stimuli shown to improve language function (Lee et al. 2010) (Allows work form home, reduces travel of patient, also reduces white coat effect) (although some individuals prefer the social interaction of face to face intervention)
  • Melodic intonation therapy- modulates intonation and rhythm through repetition- can improve production task performance in Broca’s APHASIC cases. May even be linked to remodelling of the right arcuate fasciculus. (increasing number of fibres, lengths and volume (Schlaug et al, 2009) (changes measurable volumetrically in brain of patients) (highlights the difference between lexical and sub lexical route)
53
Q

Treatment of comprehension disorder

A
  • Identification of categorical loss
  • Targeted semantic therapy using category members. (birds). (birdy birds vs non birdy birds) how related to the category should be the items taught. Do I teach them penguins or pigeons? Depends on the category of impairment. If semantic dementia better to provide items that are typical of that category to reinforce their knowledge, whereas with stroke patients more beneficial to provide items of low typicality (enabling patients to relearn the boundaries of a particular category)
  • Word/Pix matching. Y/N questions- PIX categorisations
  • Methods include:
    o Word priming
    o Word/ picture matching
    o Spoken definition
    o Reading and repetition

Neuropsychology week 1 (6 decks)

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