Lecture7 Flashcards
Define Communication; What are some examples of how we communicate?
Behaviours used by one member of a species that convey information to another; Turn-taking, intonation, gesture (body language), eye gaze control, touch
Define language
A communication system that has symbols (e.g. words) and rules for ways to assemble the symbols (grammar)
What is Aphasia?; What is it not?
A loss of language processing ability after brain damage (a neurological disorder); An impairment of intellectual functioning; a psychiatric disturbance; a primary motor or sensory deficit; a developmental disorder
Name the 3 principles underlying classic Aphasia syndromes
Localisation of language processors; damage to a single processor can produce multiple deficits (due to connections between modules); language processor localised because of relationship to primary sensory/motor functions
What are the symptoms of Broca’s Aphasia?; What is the deficit?; Where is the lesion?
Non-fluent expressive speech; major disturbance in speech production & syntactic production; missing function words; telegraphic speech; comprehension intact; Impaired speech planning & production; Posterior portion of inferior frontal cortex
In 1862, Broca concluded that the integrity of which area was responsible & necessary for articulation?; MRI of Tan’s brain showed lesions extending into where?
Left frontal convolution; The deep white matter, including insular cortex & basal ganglia
What are the symptoms of Wernicke’s Aphasia?; What is the deficit?; Where is the lesion?
Major disturbances of auditory comprehension; fluent speech; semantic paraphasia; poor repetition & naming; Impaired representation of sound structure of words; Posterior portion of the superior temporal gyrus
“Der aphasische Symptomenkompleks” documented the localisation of the “storehouse of auditory word forms” in what area of the brain?
In the posterior portion of the left Superior Temporal Gyrus
What are the symptoms of Conduction Aphasia?; What is the deficit?; Where is the lesion?
Disturbance of repetition & spontaneous speech; phonemic paraphasia; Disconnection between sound patterns & speech production mechanisms; Arcuate Fasciculus (white matter tract between Broca’s & Wernicke’s areas - temporal-parietal junction)
What was Lichtheim’s view on word meaning in 1885?; What did his diagram represent?
He didn’t consider the function to be localised in one part of the brain but from the combined action of the whole sensorial sphere; Neural networks - a series of nodes which represent meaning as distributed throughout the entire cortex
According to Lichteim’s House Model, a lesion in the Articulate Speech (motor area) causes what?; A lesion in the Auditory Word Forms (auditory area)?; A lesion between Broca’s & Wernicke’s?
Broca’s Aphasia; Wernicke’s Aphasia; Conduction Aphasia
Transcortical Sensory Aphasia is a disconnection of what?; What are the symptoms?
Auditory & Concept Centres - damage to tracts in posterior Temporo-parietal-occipital junction; Disturbance in single word auditory comprehension & semantic paraphasias, despite fluent grammatical speech, normal recognition of auditorily presented words & intact repetition
Transcortical Motor Aphasia is a disconnection of what?; What are the symptoms?; Where is the lesion?
Concept Centre from motor & auditory language centres - between conceptual word/sentence representations & motor speech production; Severe disturbance in initiating responses & spontaneous speech (aka adynamic aphasia), but intact auditory comprehension & repetition; Deep white matter tracts connecting Broca’s area to parietal lobe
What are some issues with Psycholinguistics & Aphasia?
Classic aphasic syndromes have limitations; poor classification of patients; lesion overlap/variability; little assistance for treatment planning
Rather than viewing language in terms of production & comprehension, what does Psycholinguistics emphasise?; Such as?
Language processing operations; Phonology - sounds that compose language & the rules that govern their combination; semantics - words & their meaning; syntax - methods for combining individual words to convey propositional meaning
According to psycholinguistics, what are the 2 ways to represent sound in speech?
Phonemic - smallest unit of sound that can signal meaning (e.g. b in bat or p in pat); allophones are different representations of the same phoneme (same sounds in different orders; e.g. spill, lisp, lips); & Phonetic - how phonemes are produced in different contexts (e.g difference between cave in English & cavé in French)
In regards to Phonology, what do Broca’s aphasics have difficulty in producing?; What about Wernicke’s aphasics?
The correct allophone of a phoneme; mispronunciation of a phoneme; poor phonetic ability & phonemenic selection/discrimination; They select the wrong phoneme; substitute phonemes (i.e. p for b); poor phonemic selection/discrimination but preserved phonetic ability
What are Broca’s aphasics often referred to as?; Though both production & comprehension are impaired, the deficits are…
Agrammatic Aphasics (a graded impairment); Dissociable
What do we now know that anterior lesions affecting syntax are also associated with?
Comprehension deficits
Lesions resulting in double disassociation of lexical (word form representations) & semantic representations result in what?
Intact semantic knowledge but impaired naming (e.g. tip of the tongue & anomic deficits)
Intact naming but impaired semantics (i.e. semantic dementia; often seen in alzheimer’s) result from lesions in what area?
Anterior Temporal Lobe
Semantic processing can be relatively spared in which aphasics?; Which lesions more often characterise semantic impairments?; When do problems arise for anterior lesioned patients?
Anterior lesioned (Broca’s) aphasics; Posterior (Wernicke’s) lesions; When syntax is important in sentence comprehension (e.g. place the blue circle ON TOP OF THE red square)
What is the classical characterisation of aphasic deficits?; What is the psycholinguistic characterisation?
Production (Broca’s) vs. Comprehension (Wernicke’s); Syntax (Anterior) vs. Semantics (Posterior)
Name & describe two articulatory-motor disorders (which are not language disturbances)
Dysarthria - disturbance of speech musculature in terms of speed, strength, steadiness, coordination, precision, tone & range of motion (e.g.cerebral palsy); corticospinal tract is commonly affected; Apraxia - articulatory errors increasing with increasing word & phrase length; inability to program speech movements; lesion in left insula/operculum
What is Alexia?; What is Agraphia? Can one occur without the other?; Alexia with Agraphia results in the disturbance of what?
Acquired impairment in the ability to read; Acquired impairment in the ability to write; Yes, they are dissociable (can have a problem reading but not writing); Word form recognition (finding optical images for words)
According to Dejerine, where is the visual image centre of words?
Area PC in the left parietal lobe
Explain the dual routes to reading
Phonological route - convert letter strings to sounds (grapheme-to-phoneme conversion); Direct route - printed words are directly linked to meaning in a visual form system (must have mental store for irregular words, e.g. yacht)
What occurs with Surface Alexia patients?; What area is this associated with?; Which route is damaged?
They read by sound (grapheme to phoneme) so have difficulty with irregular words but not regular & non-words; Anterior Temporal Lobe; Direct route
What do patients with Phonological Alexia have difficulty with?; What are they able to do?; What area is this associated with?
Learning new words & pseudowords (both regular & irregular); Read previously learned words via the direct route & extract the meaning directly from the visual form of the word; Lesions to superior temporal lobe & parietal lobe (supramarginal gyrus & angular gyrus)
What kinds of errors do patients with Deep Alexia make?; Which routes are damaged?
Visual errors (e.g. skate & scale); semantic substitutions relating to target word (e.g. hot when they mean cold); abstract words; better with nouns than verbs as they’re imageable; Both Phonological & Direct routes
Explain the subtypes of Agraphia
Central Dysgraphia - problems accessing orthographic information from lexical stores or from applying sound-to-spelling phonological rules (i.e. assembling corresponding sounds); Peripheral Dysgraphia - distortions on written letter formation, oral spelling or typing (motor programs)
Name the two components of Long Term Memory
Declarative (explicit) & Non-declarative (implicit)
What are the two components of Declarative memory & their associations?
Episodic - events; specific personal experiences from a particular time & place; Semantic - facts; world knowledge, object knowledge, language knowledge, conceptual priming
What are the four components of Non-Declarative memory & their associations?
Procedural - skills (motor & cognitive); Perceptual Representation System - perceptual priming; Classical Conditioning - conditioned responses between 2 stimuli; Non-associative Learning - habituation, sensitisation
What is Sensory Memory?; How is it processed?
Sensory memory trace, like an echo lasting just a few milliseconds; Via cranial nerves to primary cortical areas: iconic/visual - retina>primary visual cortex; echoic/auditory - cochlea>primary auditory cortex
Short Term Memory has limited…; It decays quickly without…; What is the average span in the number of items recalled?
Capacity; Rehearsal (cues don’t help); 7 plus or minus 2 items
What can be retained with Long Term Memory?; It persists without constant…; Can be called up with…
Many facts & experiences; Rehearsal; A cue or hint
What results have been found in list-learning tasks?
A gradual increase in performance (i.e. recall); After a distractor/interfering list is presented, performance decreases back to first trial; there’s an increase in following trial but still some decay in memory trace
Explain the Serial Position effects; What effects occur if distracting items are introduced at the end of the list?
Primacy - beginning of list is easier to recall (there’s enough memory capacity to transfer to LTM); recency - end of list items are available in STM as there’s no decay yet; It eliminates recency but not primacy effect
How has evidence supporting the distinction between STM & LTM been weakened?
Some memories are neither short or long term (e.g. where you parked the car this morning or dinner consumed last night); these are too long to be STM but weren’t rehearsed so will fade over hours or days
Describe Working Memory; How can this be tested?; Lesions to what area can impair performance?
The temporary storage of information while we actively attend to or work on it; In the delayed response task (responding to the same stimulus as presented a short time earlier); Prefrontal Cortex
What type of memory was effected when 29 y.o patient H.M underwent surgery which damaged the bilateral medial temporal lobe; What difficulties were demonstrated?; What was still intact?
Declarative Memory; Couldn’t remember meeting people minutes after meeting them, couldn’t form long-term memories, reported age as 27; Biographical knowledge up to the time of surgery & procedural memory
What 5 main findings were generated based on studies of patient H.M?
Memory is a distinct biological function; amnesia spares short-term & working memory; amnesia is an impairment of declarative & episodic memory; hippocampus is a core structure supporting memory; hippocampus supports permanent consolidation of memories
What is Anterograde (going forward) Amnesia?; As well as the hippocampus, what other areas have been observed to be affected?
The inability to form new memories after brain damage has occurred (e.g. H.M); Thalamus, Hypothalamus & Pretectum
In the delayed non-matching-to-sample task, monkeys had to remember the old object, reject it & choose the new one to get more food. How did monkeys with bilateral temporal lesions perform compared to intact monkeys with 90% correct performance?
Performance was ok at short delays but there were increasing decrements with longer delays
When patient N.A suffered a fencing foil to the forebrain, damage was found in the mediodorsal nuclei & mammillary bodies but intact hippocampus formation. What did this result in?; What did his occasional ability to recall something spontaneous demonstrate?
Retrograde Amnesia - initial inability to recall personal or global events for 2 years prior to injury (this shrank in 2 wks); recall of daily events were initially poor; That memories can be accessed unknowingly by cues or triggers in the environment
Describe Retrograde (going backward) Amnesia
Loss of memory for events before the brain damage
Despite patient K.C suffering damage to medial temporal lobe, frontal, parietal & occipital cortices, what normal functions existed?; What type of amnesia did he suffer?; What was still intact?; This suggests….
IQ of 94, normal language, good reasoning & concentration; Retrograde - no recall of personally experienced events, though could recall facts; could learn new info but couldn’t recall how he’d acquired it; Semantic memory for general world knowledge prior to accident; Episodic & semantic memories are dissociable
What are the 3 contemporary classes of theory regarding Semantic memory?
Distributed model - semantic memory is not localised to any particular structure (all connected); distributed-plus-hub model - anterior temporal cortex is a hub in mediating abstract conceptual representations; embodied cognition - the meaning is represented in the same sensory or motor structures that mediate perception & action (somatotopic)
Describe Procedural Memory; When patient H.M performed the Mirror Tracing task, what was found?; What about the Perceptual Priming task (determining objects from fragments)?
Ability to develop motor skills (e.g. riding a bike); Performance improved over 3 days but he couldn’t remember performing the task; Also improvement but no memory of performing the task
Although patient H.M showed intact Pavlovian classical conditioning, attaining & retaining a conditioned eyeblink response to a tone, he showed what?; What does this evidence support?; What is essential for eyeblink conditioning?
No memory of performing the task; The concept of dissociable memory systems; An intact cerebellum
