Exam 3 Notes PDF

**Types of learning**   A. Learning is a relatively permanent change in behavior produced by experience. - Changes in the nervous system produced by experiences. - Nervous system changes are physical - Allows us to adapt our behaviors to the environment - Involves...

**Types of learning**   A. Learning is a relatively permanent change in behavior produced by experience. - Changes in the nervous system produced by experiences. - Nervous system changes are physical - Allows us to adapt our behaviors to the environment - Involves interactions among the motor, sensory, and memory systems.     A. Types of learning 1. Stimulus-Response learning -- Learning to perform a particular behavior when a particular stimulus is present - involves connections between brain areas that mediate perception and those that mediate movement - **Classical Conditioning** -- association (pairing) between an unconditioned and conditioned stimulus so that unconditioned response associated with unconditioned stimulus is elicited by conditioned stimulus alone. - Unconditioned Response: reliably provokes a response. - Instinctive - Conditional Response: does not provoke the response. - CS and UCS are paired over many trials. - Test of learning: does the CS alone produce a response? - **Hebb rule** -- if a neuron is repeatedly active at about the same time a post-synaptic neuron fires, changes will take place in the structure and chemistry of the synapse that strengthens it. - Repeated neural activity will produce physical changes in the nervous system. - Strong synapse and weak synapse. The weak synapse will change and get stronger if occurring at the same time as the strong. - Depolarization of Post-Synaptic membrane at the same time as weak synapse activation. - **Operant Conditioning** (instrumental conditioning) -- association between stimulus and response - consequences of behavior determines the probability it will be repeated when same stimulus is present again - reinforcement or punishment causes the stimulus that is present to become a cue to respond or not respond respectively - Reinforcement: Responses that are followed by \"favorable\" consequences (reinforcing stimuli) are more likely to occur in the future. - Reinforcement occurs in the context of a stimulus - That stimulus can elicit the response. - Punishment: Responses that are followed by \"unfavorable\" consequences (punishing stimuli) are less likely to occur in the future.   1. Motor Learning -- learning movements - actually a component of stimulus-response learning - involves changes in motor areas of the brain - but is dependent on and must involve sensory feedback   1. Perceptual Learning -- ability to recognize things perceived before - primary function is to identify and categorize objects - accomplished by changes in sensory association cortex involved in perception - Similar to what Hebb is saying.   1. Relational Learning (no one else uses this term) -- most complex and the learning we do the most and usually think of when we think about learning and memory.   1. many learning situations involve combinations of or all of the above types of learning     **Types of Memory** A. Sensory memory (not really memory) 1. Is the sensory registration of stimulus 2. Lasts milliseconds to a few seconds 3. May or may not be permanently stored   A. Short-term memory or Working memory 1. Is not memory at all (bad name for it) 2. Attention and concentration a. EX: of Digit Span 3. The contents of your focus at the moment 4. May or may not be permanently stored 5. Patients: usually can\'t remember things that happened awhile ago. a. Follow-up on how long it takes them to forget.   A. Long-term memory 1. What we typically think of as memory 2. Information that is consolidated or stored 3. Delayed recall on NP tests is the \"true test of memory\". 4. Types of LTM a. Non-declarative or Implicit memory i. Stimulus-response, Motor & Perceptual learning described above ii. Acquired skills iii. Not factual or contextual b. Declarative or Explicit memory - "Relational learning" described above i. Episodic -- memory for events and contextual memory 1. EX: Knowing what you wore and said in an interview. Interview is context. ii. Semantic -- memory for facts without context 1. EX: Knowing who the first president of US was, but not knowing when you learned.     **Reinforcement** A. Self-stimulation will occur with electrical stimulation in many parts of the brain 1. olfactory bulb, prefrontal cortex, nucleus accumbens, caudate, putamen, thalamus, reticular formation, amygdala, ventral tegmental area, substantia nigra and locus coeruleus. a. Shows that this is a wide ranging action throughout the brain. For now we will focus on the nucleus accumbens.   A. **Medial forebrain bundle** (mfb) is most researched area 1. bundle of axons that travel from midbrain to basal forebrain 2. contains, among others, ascending dopamine, norepinephrine and serotonin axons from midbrain nuclei to forebrain. a. First section of class different pathways for different NT\'s   A. Of these, dopamine plays a primary role in reinforcement 1. dopamine is secreted in several systems; ventral tegmental area important for reinforcement 2. axons project to a wide area of the cortex - axons can have several hundred thousand terminal buttons 3. **Mesolimbic system** projects from the ventral tegmentum thru medial forebrain bundle to limbic structures - amygdala - septum - hippocampus - nucleus accumbens -- located in basal forebrain; most animal research has focused on this area 4. **Mesocortical system** projects from ventral tegmentum to limbic and other cortex - anterior cingulate - prefrontal cortex - hippocampus - association cortex of frontal, temporal and parietal lobes   A. Mesolimbic pathway, especially the projections to the [**nucleus accumbens** (na), is involved in the reinforcing effects of electrical stimulation of the medial forebrain bundle] 1. Animals a. electrical stimulation of ventral tegmental area (where the axons of the dopamine neurons that synapse with na originate) or mfb causes release of dopamine in nucleus accumbens b. injection of amphetamine and cocaine into ventral tegmental area or mfb cause release of dopamine in the na c. presence of water, food or sex stimulates release of dopamine in the na d. Aversive stimuli also stimulate release of dopamine in na indicating this system is involved in stress as well as reinforcement e. Reinforcing and aversive stimuli cause release of dopamine in many areas of the brain in addition to na, so it is not the only reinforcement area of the brain; it's just the one that has received the most research f. Mediates reinforcement involved in addiction. 2. Humans -- functional imaging studies a. Increased na activity when subject\'s expected they would receive money. i. Money considered reinforcer   A. Function of reinforcement 1. Detect the presence of reinforcing stimulus -- sensory fx 2. Strengthen connection between sensory system that detects the discriminative stimulus and the motor system that produces the response. 3. what is reinforcing is very complex, especially in humans and is the product of learning and present circumstances   **Page 415 Figure 13.17 & Table 13.3**   A. VTA responds to [unexpected reinforcement] 1. In animals and humans VTA activated only when reinforcer is unexpected -- or during the learning phase a. When reinforcer is expected or learning has already occurred, VTA active only when discriminative stimulus presented & not during reinforcement 2. VTA active in response to: a. Novelty 1. And information presented in novel contexts learned better than non-novel b. Anticipated reinforcement 1. VTA active when subject's anticipated receiving money 2. And information presented during that time was better remembered   A. VTA and Prefrontal Cortex -- projects to VTA and likely provides increased activation to VTA as actions are coming closer to achieving goals and presumably obtaining reinforcement 1. prefrontal not only provides input into ventral tegmental area to regulate dopamine, but also is a "target" of dopamine activation by way of a. na à gp à thalamus à prefrontal cortex   A. Three elements of synaptic changes in reinforcement 1. discriminative stimulus activates a weak synapse with response neuron because before learning it has weak connection with response 2. circumstances that were present at the time of response activate a strong synapse 3. if reinforcer follows response, dopamine is released a. dopamine activates the response neuron while the weak synapse of the discriminative stimulus is firing thus strengthening the weak synapse 4. study recorded bursts of firing in CA1 of hippocampus which has dopamine neurons a. recorded baseline activity b. administered dopamine, cocaine or saline contingent or non-contingent on bursts of neuronal firing c. rate of firing increased with contingent administration of dopamine or cocaine but not with saline or non-contingent admin. of any d. for all you behaviorists, this is the neural basis of operant conditioning e. Schizophrenia: overactivity of dopamine pathways.   A. Most is more complex than classical conditioning and instrumental learning   A. Involves cognitive processes and associations between numerous different memories from different sensory modalities   Hippocampus   A. Anatomy B. hippocampal afferents 1. entorhinal receives input from: a. amygdala b. various areas of limbic system c. all association areas of brain either directly or indirectly via perirhinal and parahippocampal cortex 1. Mulitmodal sensory association areas. AND prefrontal executive function association area. 2. Modulatory input: NT\'s 2. subcortical input to hippocampus a. subcortical input comes thru fornix b. dopamine input from ventral tegmental area -- mediates reinforcement c. norepinephrine from locus coeruleus -- arousal d. serotonin from raphe\` nucleus -- arousal et al e. acetylcholine from medial septum -- arousal 1. Ach theta waves to the hippocampus 2. Long-term potentiation occurs at peak of wave rather than the trough. 1. Synaptic changes 3. Long-Term Depression occurs at trough: ability to unlearn previous knowledge. f. these subcortical systems regulate the functioning of the hippo   A. hippocampal efferents 1. entorhinal cortex (surrounds hippocampus, part of the temporal cortex) projects to: a. dentate gyrus b. [Cornu Ammonis](https://www.howtopronounce.com/cornu-ammonis/) \[cor-new am-on-nees; Latin for ram's horn\] (CA)3 c. CA1 1. from CA1 and subiculum 2. through entorhinal, perirhinal and parahippocampal cortex 3. to all association areas that hippo received input from d. subiculum à fornix à mammillary bodies à anterior thalamus à cingulate (important for Korsakoff's) B. Hippocampal function -- memory consolidation 1. hippo receives information about "what is going on" from sensory and motor association area, subcortical areas i.e. basal ganglia and amygdala 2. processes the information 3. thru efferents modifies the memories that are consolidated and stored in these areas a. links memories together in way that allows us to remember the relation between the elements e.g. b. order and context of events c. Carlson says without hippo person would have individual isolated memories and it would not be possible to remember episodes and contexts 1. Damage: deficits in memory. Keeps you from making connections through context and the actual storage of the components of it as well. 1. however, patients with hippo are unable to form **[any]** declarative memories. If above were completely accurate, patients with hippo damage would have fragmented, isolated memories and be unable to recall where and when they occurred   A. Episodic and Semantic memory 1. Episodic memory involves context: e.g. when, where, who etc. 2. Semantic memory is factual knowledge without context 3. Hippocampus is required for storage of both a. Pts with hippocampal **damage** have anterograde memory impairment for both episodic and semantic memory 1. Trouble forming new episodic and semantic memories. 4. Semantic memories appear to be stored in [anterolateral temporal lobe] (frontal-temporal dementias) a. Pts with semantic dementia lose semantic knowledge and have initial degeneration in anterolateral temporal lobe. 1. Lose memory of what things are - semantic knowledge. b. TMS inactivation of anterior temporal in controls produced symptoms of semantic dementia   A. Hippocampus: Subgranular Zone & Neurogenesis 1. Stem cells - small cells that can turn into anything. a. Located in subgranular zone b. Have stem cells in your hippocampus. 2. With experience (i.e. learning) stem cells develop into granule cells and migrate to dentate gyrus a. Their dendrites receive connections from the entorhinal cortex b. They project to CA3 in the hippocampus c. Animal studies show increased number of neurons in the dentate gyrus with new learning   **Amnesia** - Failure to remember - Date of onset can be difficult to identify in neurodegenerative diseases. - Can identify date you observed it. - Only produced by bilateral hippocampus damage.   Anterograde - Involves a difficulty in forming new memories for events that occur after brain damage. - Involves inability to learn new information.   Retrograde - Inability to recall events that occurred prior to damage.   Korsakoff's syndrome 1. Severe form of anterograde amnesia associated with chronic alcoholism. 2. results from malnutrition related inadequacy of [thiamine (B1 - a catalyzing enzyme) necessary for metabolism of carbs, fats and amino acids] - can also happen in people who have severe malnutrition without etoh abuse - likely the result of being given glucose without adequate thiamine and resulting buildup of an intermediary metabolite - damages mammillary bodies and dorsal-medial thalamus 3. amnesia: anterograde and retrograde 4. confabulation -- sometimes: unknowingly creates fictitious memories. 5. all sxs not present in all cases   Bilateral medial temporal damage à hippocampus 1. 30 psychotic patients 2. [HM](http://hargreaves.swong.webfactional.com/HM.htm) - for epilepsy \- amnestic after surgery a. No retention of events that occurred post surgery 1953 b. Could recall events that occurred prior to 1953 c. H.M.\'s amnesia was attributed to hippocampal damage. 1. Severe anterograde amnesia follows bilateral damage to the hippocampus. 1. amnesia occurred after some cases of unilateral temporal lobectomy 2. now do WADA/fMRI testing 3. HM died 2008 4. HM and Other Amnesia Patients a. Normal LTM for events prior to brain injury b. Normal Short term memory (attention and working memory) c. Normal Sensory-Response learning d. Normal motor learning e. Normal perceptual learning f. Impairment in transfer from STM to LTM.   Anoxia and Hippocampal Damage - Patient R.B. - case reports of patients with cardiac arrest and anoxia who subsequently were amnestic - First place to get damaged is the hippocampus due to the NMDA and pyramidal cells. - at autopsy CA1 "was gone" - why is CA1 so susceptible to anoxia, seizures, hypoglycemia? - many neurons in hippo have NMDA receptors - metabolic disturbances of various kinds cause release of abnormally high levels of glutamate - this activates NMDA receptors which allow Ca+ to enter neurons - within a few minutes excessive Ca+ destroys neuron - if animals are pretreated with NMDA blockers, anoxia much less likely to produce brain damage - many NMDA neurons makes it easy to establish long-term potentiation - this allows fast learning but also makes the area vulnerable to self-destruction when metabolic disruptions occur   A. Limbic cortex / medial temporal lobe and amnesia (may not be in book) 1. bilateral **damage** to the entorhinal, perirhinal and parahippocampal areas can produce anterograde amnesia or make amnesia associated with hippo damage worse. a. Includes larger section of the hippocampus and medial temporal lobe structures. b. Damage to the areas around the hippocampus - information cannot get to the hippocampus itself.   A. Fornix / mammillary bodies (may not be in text book) 1. projections from hippo (subiculum) thru fornix to mammillary bodies and anterior thalamus 2. case reports indicate bilateral damage anywhere in the fornix, mammillary bodies or anterior thalamus causes amnesia   Hippocampal asymmetry 1. in general, L activated by verbal information a. PET in controls shows subject's with greatest L hippo activation remembered words best. 1. In word list tests the words remembered best showed L hippocampus activation. b. Unilateral L damage produces verbal memory impairment.   1. in general, R activated by spatial / pictorial information a. PET in normals shows photos that had highest hippo activation on initial viewing were best remembered b. R hippo activated in London taxi drivers when describing routes i\. Taxi drivers had larger volume R hippo a. R hippo activated when subject's spatially exploring virtual landscape b. Damage to R parahippocampal area produces inability to learn way around new environments (spatial memory)   Prefrontal lobe and Confabulation (may not be in text book) 1. Korsakoff's case study suggest damage to prefrontal areas causes confabulation - patient who had NP test indication of prefrontal damage and [hypoactivation of medial and orbital prefrontal area] on PET - 4 months later confabulation was gone, no sign of prefrontal dysfunction on NP tests or PET 2. R frontal case study - high rate of false alarms in recognition recall for [related] items ***but not for unrelated items.*** - On word list tests. 3. Pre-frontal lobes thought to help distinguish what is merely familiar from what actually is contextually accurate   ** ** **Retrograde Amnesia** 1. Duration of RA related to the extent of medial temporal lobe damage - damage only to CA1 = no retrograde amnesia - Damage (restricted to) hippocampus including dentate gyrus and subiculum = RA of a few years - Damage to hippo and entorhinal cortex = RA of 1-2 decades - Damage to hippo and much of medial temporal cortex = RA for all except early childhood. - Haven\'t discovered individuals that forget childhood memories. - Loss of episodic memories. - Do you remember when... 2. Spared memories in all RA include: - Semantic information - Memory of personal episodes from childhood - Spatial memory of early home neighborhood   Hippocampus and retrieval of stored memories 1. RA indicates hippocampus is involved not only in storage of memories, but also in retrieval of stored memories for some period of time 2. Page 428, Figure 13.30: Retrograde Amnesia in Patients with Hippocampal Damage. - Study asked amnesia pts (bilateral hippo damage) and controls questions about news events that had happened in past 30 years - Extent of RA for pts was related to how many years before brain injury occurred - Recall was comparable for memories that were **[15 years]** or older 1. 11^th^ edition Page 467, Figure 13.31 - fMRI study of normals memory retrieval showed decreasing activation of hippocampus over time and increased activation of **[right superior frontal gyrus]** until at 9 years both areas were equally activated in recall.   **Implicit Memory** More details of HM / amnesia -- preserved learning ability 1. Stimulus-response learning a. Classical conditioning - eye blink - 2 years reacquired the response in 1/10 the time initially required b. Operant learning -- responses for pennies   1. Motor learning a. mirror drawing b. pressing buttons in sequence with asterisk - 10 step sequence repeated but pts not told - learned as well as normals c. similar to normals, amnesia pts performance improved with practice on "real world tasks" - weaving - tracing figures - operating joy stick - pouring water into jars   1. Perceptual learning a. priming effect with line drawings b. improvement still evident after 4 months delay c. other studies show priming effect in amnestic patients - Korean music - Photos of men accompanied by story of mean / vicious or "nice enough to invite home for dinner" i\. preference still evident at 20 day delay   1. even though amnestic patients can learn these types of tasks, they do not remember that they have done them   A. Declarative / Nondeclarative memory 1. PET study of normals - normal subjects shown list of words - then shown first 3 letters of word - declarative memory - i.e. remember the word that started with these letters -- *[activated hippocampus]* - All more likely to remember the word in this scenario - nondeclarative -- i.e. say the first word that comes to mind -- *[activated visual association cortex and not hippocampus]*   1. 3 patients: shown different colored lights and ship horn sounded after blue light -- (may not be in text book) Blue light paired with ship horn. - B amygdala did not show change in skin resistance when only blue light was shown, but could accurately report the association. - Could not establish a CER - B hippocampal showed change in skin resistance, but did not remember what occurred. - Showed the CER but couldn\'t remember why. - B damage to both showed no change in skin resistance (galvonic stress response) and did not remember what went on   ** Language -- general info** Language: set of symbols used according to rules. A. Primary areas 1. Auditory-verbal comprehension 2. Speech 3. Reading 4. Writing   A. Neurology of Language 1. most comes from patients who have sustained CVA - Strokes usually are lateralized - only affecting one hemisphere of the brain. - these lesions follow vascular distributions that cut across functional areas - thus, a vascular lesion often will affect multiple language areas that mediate different functions - this makes it difficult to precisely determine the unique contribution of separate areas 2. PET / fMRI of normals verifies CVA data - fMRI and Vascular information doesn\'t line up.   A. Lateralization 1. \> 95% of R hand dominant people are L hemisphere dominant for language 2. \~ 85% of ambidextrous people are L hemis dominant for speech 3. \~ 70% of L hand dominant people also are L hemis dominant for language - \~ 15% have R hemis dominance - \~ 15% have bilateral mediation 4. L hemis processes info in a sequential manner and speech is sequential 5. R hemis mediates prosody -- expression and comprehension of emotional aspects of speech   A. Aphasia 1. impairment of language a. Production b. Comprehension 2. not due to simple motor or sensory deficits (e.g., paralysis) 3. Not a result of lack of motivation 4. not all speech impairment is due to aphasia 5. Usually results from damage to the left hemisphere.   **Speech** A. Broca's aphasia -- also Expressive or Non-fluent aphasia 1. characterized by: - slow, labored, nonfluent speech - have difficulty saying function words e.g. a, the, some, in, about - what they produce are content words nouns, verbs, adjectives, adverbs - comprehension relatively intact   1. damage restricted to Broca's area does not produce syndrome - damage must extend to surrounding frontal area and the underlying white matter - damage to basal ganglia, especially head of the caudate also can produce Broca's aphasia     A. Frontal mediation of language 1. speech involves rapid movements of tongue, lips and jaw - it appears Broca's area "contains" the motor programs of these movements - Broca's area is directly connected to the area of primary motor cortex that controls face and mouth movements used for speech. - Broca\'s area is part of the premotor codes for the functional level movement patterns for speech in particular.   Broca\'s as a syndrome: a constellation of symptoms that occur together.   A. Primary types of speech impairments in Broca's 1. agrammatism -- difficulty applying grammatical constructions - rarely use function words, auxiliaries or suffixes that form proper tense - also have impaired comprehension of grammatical formulations 2. anomia -- word finding problems - common to all forms of aphasia 3. word articulation difficulty or speech apraxia - mispronounce words   1. these deficits vary in severity from patient to patient 2. as a general rule Broca's aphasics are aware of their communication problems  3. hierarchy of speech from complex to simple - [grammatical construction] -- word order, word form (i.e. tense, suffix) rules of word use à - Difficulty in comprehension when the meaning is conveyed through the grammatical structure. - [naming] - semantic retrieval and motor programs for individual words à - [articulation] - sequencing individual movements of speech (impairment is apraxia of speech) 4. INSULA: brain mediation of deficits - speech apraxia (i.e. articulation) - all patients in a series with speech apraxia had lesion of insula - none of the patients without speech apraxia had lesion of insula - PET shows activation of L insula when saying words - However, other functional imaging shows Broca's area also activated during speech articulation   1.  Producing Single Words 1. Can produce deficits of just one problem.   **Auditory-verbal comprehension** A. Two primary aspects of auditory-verbal comprehension 1. word recognition 2. comprehension of word meaning 3. word recognition mediated by [middle] & posterior superior temporal gyrus   A. primary characteristics of Wernicke's aphasia -- also Receptive or Fluent aphasia 1. impaired speech comprehension - does not accurately follow simple instructions - does not accurately match heard words to pictures 2. production of meaningless speech - speech is fluent - produces high volume of syllables - intonation generally intact - "appears to be grammatical" i.e. uses function words: the, but - few content words - paraphasias - cannot repeat accurately - expressive deficits make important to test comprehension with non-speech responses i.e. motor responses 3. poor awareness of language deficits - "turn taking" intact 4. neuropsych functioning - auditory association cortex of posterior superior & middle temporal gyrus - i.e. Wernicke's area - recognizes the sounds of words - thought that Wernicke's area is the location of "memories" of sequences of sounds that constitute words   Auditory association area generates a perception for an auditory output. - Recognizes the subset of sounds that form words. - Syndrome comprised of more discrete impairments. - Subjective experience is comprised of speech comprehension and word recognition.   A. Word recognition vs. comprehension 1. word recognition and comprehension are separate and dissociable processes 2. recognition is perceptual a. Mediated by middle and posterior superior temporal gyrus (Wernicke) 3. comprehension involves retrieval of semantic memory - stored all over the brain and cortex regions. a. mediated by different adjacent left temporal / parietal cortical areas   A. Pure word deafness 1. inability to recognize spoken words with no impairment of hearing or understanding word meaning - can understand words perceived by lip reading and reading - can write - can recognize non-speech sounds like dog bark, car horn 2. speech is intact   3. caused by - focal damage to Wernicke's area i.e. L posterior superior & middle temporal gyrus - disruption of input into Wernicke's a. white matter lesion b. bilateral damage to primary auditory cortex   1. PET studies in controls show activation of superior L temporal for perception of words and speech sounds. 2. Series of pts with "deficits in speech comprehension" had overlapping lesions in same area a. However, neither 4 nor 5 is in Wernicke's area 3. L superior temporal processes rapidly changing sounds involved in word discrimination a. i.e. requiring fine grain analysis in time 4. R superior temporal process more slowly changing qualities of melody and intonation that convey emotion and emphasis   1. the key is that Wernicke's area processes rapidly changing sounds and speech happens to be the most prominent example of this   A. Transcortical sensory aphasia 1. Impairment in comprehension of word meaning results from damage to posterior language area surrounding Wernicke's area in the border of the temporal, parietal and occipital lobes 2. damage to posterior language alone (is rare) isolates it from Wernicke's area and produces t.s.a. 3. recognize words as evidenced by accurate repetition of words they hear 4. comprehension of words (heard, repeated or read) is impaired 5. speech is impaired as described before 6. Geschwind's case study - "never said anything meaningful on her own" after brain damage - never gave indication she understood -- e.g. did not follow instructions - repeated what she heard - indicates she didn't just mimic a. not "parrot-like" b. did not mimic accents c. corrected grammar d. completed familiar poems e. learned new songs   A. Word recognition is mediated by a different brain area than word comprehension 1. recognition by Wernicke's area 2. comprehension by posterior language areas 3. Wernicke's aphasia consists of damage to both of these areas producing a combination of pure word deafness and transcortical sensory aphasia   A. Neuropsych of word comprehension 1. word meaning is comprised of the constellation of memories associated with the word 2. these memories -- i.e. word meanings - are stored primarily in the various association areas -- not in the language areas - different categories of memories are stored in different areas of the brain 3. these memories are somehow tied together so that when a word is recognized they are all activated -- hippocampus plays a role in this 4. sequence of word comprehension - sounds are perceived à primary auditory cortex - certain patterns of sounds are recognized as words à Wernicke's area - the word activates the composite of memories associated with it to derive its meaning à posterior language areas connect Wernicke's area to the neural networks that contain the memories (association areas) 5. speech expression essentially is the reverse of this process - idea activates a semantic network in the related association areas - the meaning of this activated semantic network is projected to the posterior language area where the associated word is retrieved - the word is projected to Broca's area which executes the motor movements to say the word 6. evidence that word meaning is stored in various parts of the brain comes from clinical case reports - R hemis damage impaired ability to comprehend words expressing spatial relations - L temporal damage impaired ability to express info about animals whose name he heard but when he saw pictures he could demonstrate full knowledge of the animal and could describe non-animal objects he heard the name of. - Comprehension for category specific - Meaning stored all over cortex so it can be differentially impaired based on where the lesion is. - In controls functional imaging also shows different parts of the frontal and temporal lobes are activated by different categories of words: e.g. tools, animals, furniture etc. - In controls: functional imaging studies indicate interpretation of implication, metaphor and figurative meaning activates R hemisphere. - Related to the spatial nature of it. - This is related to that - spatial.   White matter connections - All connections   **Prosody** A. Rhythm, intonation and emphasis in speech 1. Same as affect   A. Variations in these qualities 1. stress certain elements of what is said 2. distinguishes assertions from questions 3. conveys emotion   A. Posterior lesions usually leave prosody generally intact despite language impairment   A. Broca's lesions disrupt prosody because of the labor and disruption of speech   A. Prosody mediated by R hemis 1. R hemis damaged patients had problems interpreting meaning and discrimination based on intonation - greenhouse vs. green house - discriminating intonation differences of statements vs. questions 2. R hemis also had problems expressing appropriate intonation and emphasis in statements and questions   **Reading** A. reading and writing usually are impaired in the same way and to a greater degree than speech and comprehension 1. Receptive   A. Pure alexia or alexia without agraphia (impaired writing) 1. Can still write, but once written they cannot read it. 2. Auditory processing in tac.   A. Recognition of familiar letter combinations -- i.e. words learned to read 1. mediated by temporal-occipital extrastriate cortex (visual association area) 2. PET study shows activation of this area for words or pronounceable non-words only and not for unpronounceable letter strings 3. alexia not the same as visual agnosia because the two dissociate - pts with alexia can identify and name objects - pts with visual agnosia can read   A. Once words are perceived, meaning is mediated by same area as speech comprehension -- i.e. posterior language surrounding Wernicke's area   A. Two reading paths:   A. Functional imaging and lesion studies show: 1. **[Visual word-form area]** (VWFA): L fusiform gyrus mediates whole word recognition 2. L inferior parietal-superior temporal and L inferior frontal -- including Broca's area -- mediates phonological reading     **Developmental Dyslexia** Involve a reading difficulty in a person of otherwise \"normal intelligence\" (old, no longer preferred definition).   A. Genetic influence 1. 85-100% concordance rate for monozygotic twins a. Chromosome 3, 6, and 15 implicated   A. Phonological deficits common - but not universal 1. Lack of mastery, inefficient learning of the symbol/sound association.   A. Functional imaging findings 1. L occipital-temporal - FFA? 2. L temporal-parietal 3. L fusiform gyrus area when reading.   A. Less common in languages with infrequent irregular phoneme-grapheme associations 1. E.g. Italian and Spanish 2. So many words that have an exception to the regular phoneme-grapheme rules a. Subtle b. F = Ph ** ** **Writing** A. Motor disorders of writing - not related to language. 1. can write letters but not numbers 2. can write upper but not lower case 3. can write cursive but not print   A. In addition to language areas, brain areas involved in writing include 1. Dorsal parietal 2. Premotor cortex   A. "Approaches" to spelling 1. Phonological - sounding out 2. Graphic - recreating a visual image 3. Memorizing letter sequence 4. Motor memory? Typing   A. types of dysgraphia 1. Phonological Dysgraphia - unable to spell by \"sounding out\". a. Lesions in Broca\'s, Ventral Precentral Gyrus, Insula b. Parallel to speech apraxia 2. Orthographic Dysgraphia - can only sound out and have problems spelling words with atypical phoneme-grapheme relation. a. Lesion of VWFA (left fusiform gyrus) a. Word recognition    A. case reports of patients who: 1. can write to dictation but cannot write spontaneously or understand what they write to dictation