Design the folded-cascode circuit of Fig. 12.9 to provide voltage gain of 80 dB and a unity-gain frequency of 10 MHz when CL = 10 pF. Design for IB = I, and operate all devices at the same . Utilize transistors with 1-m channel length for which is specified to be 20 V. Find the required overdrive voltages and bias currents. What slew rate is achieved? Also, for = 2.5 = 200 specify the required width of each of the 11 transistors used.
Exam 2 Study Guide Hormones Gradual, slow, long distance, diffuse, can depend on time, graded effect Usually temporary effect, but not always Cushing’s disease- from excess glucocorticoids (from steroids) Endocrine pathway 1) Hypothalamus (secretes releasing hormone/TRH) 2) Pituitary (anterior secretes tropic hormones/TSH) o Posterior – Vasopressin and oxytocin/Anterior- All other hormones 3) Thyroid (secretes thyroid hormone) a. Act on target cells or 1 or 2 to inhibit (negative feedback) b. Thyroid medicine increased thyroid hormone i. Body compensates TSH to opposite of thyroid level 1. High serum thyroid = low TSH c. Needs iodine i. Goiter – swollen gland from iodine deficiency d. Thyroid deficiency at birth can cause microcephaly Gender Not a dichotomy, a continuum 7 levels of determination o 1) Chromosomal sex (SRY on Y chrom. makes testes) o 2) Gonadal sex (whether you have testes or not) o 3/4) Internal and external organs o 5) Brain sex (brain structures) Women have a larger corpus callosum (cognitive skills) Women have greater gray matter % in dorsolateral prefrontal cortex (planning behavior) and superior temporal gyrus (language) Males have greater asymmetry than females Thicker/larger R hemisphere Males are better connected front-to-back (focusing) Women are better connected left-to-right (multitasking) o 6/7) Gender identity; gender preference Organizing effects – occur prenatally or shortly after birth (testosterone) Activating effects – occur at any time; reversible Behavior differences – mostly overlap Sexual orientation Biological hypothesis (involves early changes, birth order, genetic and hormonal influence) o Gay and straight males have the same testosterone levels but prenatal exposure to testosterone may have an effect Brain involvement o Women and gay men (vs heterosexual men) have a… Larger anterior commissure (white matter – communication between L and R hemispheres) – related to visual/spatial ability Smaller INH3 (may be testosterone related) Larger suprachiasmatic nucleus (SCN) Sex Involves hormonal control and specific brain areas Necessary for species but not individual survival Estrogen pulsatile secretions relates to female sexuality Testosterone is necessary for male copulation Almost all men have the same sexual response curves; women’s vary Brain areas o Male Mostly VTA (addiction) Oxytocin release Sexually dimorphic nucleus (in MPOA = INH3) o Female Entire brain involvement (some activation/some inhibition) Activates deep cerebellar nuclei Inhibits orbitofrontal cortex (decreased judgement) No VTA activation Ventromedial hypothalamus (hunger and receptivity to advances) o Both - medial amygdala (dimorphic) NT o Dopamine – excitatory (activates MPOA/INH3) o Serotonin – inhibitory Homeostatic systems Use negative feedback; defend a set point Thirst Hypovolemic o Loss of volume (water and salt) dec. BP (detected by baroreceptors) renin from kidneys inc. in angiotensin II constriction of vessels (by vasopressin raised BP), reduced flow to bladder, and thirst (by triggering subfornical organs) Pituitary adenoma – too much vasopressin Diabetes – no vasopressin, too much flow to bladder chronic thirst Osmotic o High salt concentration (osmolarity) sensed by mechanoreceptors osmosensory neurons in OVLT (hypothalamus) shrink and open sodium channels release of antidiuretic hormone by the pituitary Hunger Glucose (principal fuel) – stored as glycogen (short-term) or lipids (long-term) Hunger involves multiple signals which are integrated to decide hunger or not o Involves external factors (emotions, food desirability, environment, etc.) Pro-hunger o Ghrelin- made by stomach cells o Cortisol o NPY/AgRP neurons in arcuate nucleus (hypothalamus) Make neuropeptide Y and agouti-related peptide Anti-hunger o Leptin – made by fat cells; measured by hypothalamus; blocks AgRP o Glucose, insulin, norepinephrine o PMC/CART neurons in arcuate nucleus Make pro-opiomelanocortin and cocaine- and amphetamine-related transcript (CART) Hypothalamus o Hunger control center o Lateral hypothalamus (LH): pro-eating, helps control set point o Ventromedial hypothalamus (VMH): anti-eating, helps control set point o PVN (periventricular nucleus) integrates signals from LH and VMH o Arcuate nucleus (in hypothalamus) contains 2 sets of opposing neurons (NPY/AgRP vs PMC/CART) Eating disorders Anorexia o Continually lowering set point o Have a larger insula (disgust) and orbitofrontal cortex (tells you when to stop eating) o Commonly occurs with other psychiatric disorders Bulimia o Different than anorexia; recurrent binge eating and compensatory behavior Obesity o Brain disorder – derangement in homeostasis o Occurs with Prader-Willi syndrome (elevated ghrelin) o Strenuous/frequent exercise o Treat as an addiction Obese people have fewer dopamine receptors and lower prefrontal lobe metabolism o Gastric bypass reduces ghrelin Metabolism BMR (basal metabolic rate) = energy required to fuel brain/body/maintain temp BMR falls starting a diet to prevent weight loss 40% decided by heredity Increased by activity and drugs Emotions Emotion = a change in physiological activity accompanied by related feelings Studied using fMRIs Model - 2 axes (X: avoidance vs approach behavior; Y: Intensity of emotion) o Only 8 main emotions but variations in intensity Stimulus cognitive appraisal effects (autonomic and somatic) o Feedback – effects change emotional feelings which change cognitive appraisal Culture o Emotions are pan-cultural (biological) Culture regulates end result (how you express an emotion based on what is “appropriate” to that culture/situation) Facial expression impairment limits social interaction o Moebius syndrome facial paralysis/ Bell’s palsy half of face paralyzed Facial feedback o Facial expressions tell the brain how to feel Fake smile real happiness Sad face – makes pain seem more intense Can’t frown (botox) – have less amygdala activity = less anger Brain areas – control the intensity of the emotion Locus coeruleus – site of norepinephrine synthesis (moderate pleasure/content) VTA/substantia nigra - dopamine (extreme pleasure/exhilaration) Orbitofrontal cortex (“controller”) (=prefrontal/frontal lobe) o Activated by laughter and “shock value” (cursing) o Inhibits raw emotion from the amygdala o Case: Damage can’t feel emotions o Last place before action (judges consequences) May suppress laughter in church, etc. o When damaged can understand social rules but can’t apply them o Abnormalities associated with aggression, depression, and schizophrenia Limbic system (“integrator”)- Integrates info to make decision Hypothalamus - ANS reactions (heart rate, pupils, etc.) Amygdala – fear and aggression o Memory formation and recognition of fear in other people o Amygdala damage overly trusting people o Anxiety-reducing drugs act on the amygdala Hippocampus- memory (emotional, spatial) o Experience determines the severity of the situation Cingulate gyrus (= anterior cingulate cortex/empathetic nervous system) o Pain processing and empathy o Combines all information in a conscious emotional experience Pathway o Stimulus (sensory organs) activate thalamus, sensory cortex, and hippocampus amygdala hormones and hypothalamus (ANS and emotional behavior) o The amygdala is the link between the hippocampus and emotional behavior (hypothalamus) Aggression Intended to harm; not always physical Can activate reward/addiction areas (amygdala and striatum/nucleus accumbens) Reactive aggression - emotional and unplanned (ex: road rage, murderers) o Lower activity in prefrontal cortex Less gray matter in prefrontal cortex is associated with antisocial personality disorder o Reckless, overreact, sexually promiscuous Proactive aggression is premeditated, unprovoked, emotionless (ex: planned killings) o Associated with psychopathy (no remorse) o Less autonomic response to stress o Impaired amygdala function Hormones o High testosterone levels associated with aggression/criminality Aggression and competition (winning) increase testosterone Testosterone increases dopamine (addictive) Brain areas o Murderers have higher activity of the amygdala and hypothalamus o Tumors in amygdala, hypothalamus or septal area can cause aggression o Seizure activity in the amygdala increases aggression Stress Responses o Activates autonomic nervous system (ANS) high cortisol (adrenal cortex), low testosterone, and high epinephrine and norepinephrine (adrenal medulla) o Hypothalamus activates sympathetic nervous system (part of ANS) inc. heart rate, blood flow, breathing Acute stress o Hypothalamus and pituitary stimulate adrenals to release epinephrine and norepinephrine (increases output from the heart and glucose) and cortisol (increases energy) o Beneficial - boosts immune system and brain builds new neurons o Harmful- can lead to heart attacks Chronic stress o Negatively impacts many areas; compromises the immune system (noradrenaline) o PTSD – involves the limbic system (amygdala- fear) Symptoms include re-experiencing, avoiding triggers, hyperarousal Low success rate for treatment (20%) Behavioural desensitization – repeatedly exposing to triggers; stressful Propranolol – may help block memory of event Ecstasy – similar to SSRI but much more potent Damages (reduced volume) the… o Frontal cortex (executive function) Can lead to inappropriate behavior (abuse, cycle of abuse, etc) o Hippocampus, cortical tissue, amygdala (enlarges then atrophies) o Damage due to stress is caused by cortisol Other emotions Pleasure/happiness - Related to craving and addiction o Involves medial forebrain bundle – contacts midbrain, hypothalamus, locus coeruleus, VTA, and nucleus accumbens Surprises - involves the nucleus accumbens (NAC) – addiction o Unexpected surprises more activation Klüver–Bucy syndrome - lesions in temporal lobe o Removal of temporal lobes socially unacceptable behavior Failure to recognize other’s emotions o Studies showed that the amygdala is important in fear Disgust and guilt activate the insula Romantic love o New love activates nucleus accumbens and VTA (“lust”) o Old love – lust areas do not activate o Septal nucleus (limbic system) - pleasure, sexual fantasies, and arousal Physiological basis of personality Introverts (social anxiety) have higher norepinephrine (NE) - blocks immune system Person with higher activity in the L hemisphere had a better response to the flu shot Two hemispheres Left side of the face (R hemisphere) is more expressive R brain - more emotional Right hemisphere identifies tone of voice Left hemisphere processes words/meaning of vocal message Left frontal lobe o Activated behavioral approach More active during positive emotions Damage to the left hemisphere anxiety and sadness o Regulates anger and joy Right frontal lobe o Activation behavioral withdrawal More active during negative emotions o Regulates fear and sadness o Damaged patients more likely to be unbothered or euphoric Sensory processing Stimulus to receptor produces a graded potential (EPSP) o If big enough action potential o Not big enough sensory receptor still feels it even though the brain didn’t Processing intensity Both light touch and pain signal an action potential (all the same) 3 strategies; brain can know intensity based on… o 1) How fast it fires A single neuron increases the frequency with increased intensity o 2) How many fire Multiple neurons fire together (more neurons with inc. intensity) o 3) Which neurons fire Different neurons respond to different ranges Range fractionation - “specialized neurons” Different neurons fire based on intensity; brain knows how intense based on which neurons fire Neurons limited in intensity because of refractory periods Pathways of processing Any sensory input goes to the thalamus primary sensory cortex non-primary (on both sides) to process signals 2 systems o Dorsal for touch and vibration (do NOT use free nerve endings; use 4 other) o Spinothalamic for pain and temp (use free nerve endings) Skin spinal cord PAG thalamus cingulate cortex and somatosensory cortex PAG (periaqueductal gray) – midbrain; has opioid receptors (endorphins); can block pain transmission if necessary Cingulate cortex/gyrus – Branch off pathway from skin to somatosensory cortex Part of limbic system - emotional memory (of pain) Opioids take away the emotional quality of pain not the actual pain Increasing pain: spinal cord thalamus Decreasing pain: limbic and hypothalamus PAG Somatosensory system Detects touch and pain (different/independent systems) Dorsal root ganglion –involved in all sensation o Cell bodies of the sensory neurons throughout the human body Somatosensory cortex – “the homunculus” o Analyzes all sensory info in the postcentral sulcus/gyrus o Postcentral sulcus – divided into regions – one for each part of body (cortical map); smaller receptive fields = bigger area in cortex o After extremity is amputated, the other areas take over 4 receptor classes- pain and touch (epidermis); vibration and stretch (deeper) 5 types of receptors o 1) Free nerve endings – sample extracellular fluid (pain and temp) o 2/3) Merkel’s disc and Meissner’s corpuscle – very precise o 4/5) Pacinian corpuscle (vibration) and Ruffini’s ending (stretch)- less precise Temperature (pain pathway) o Temperature receptors (free nerve endings) Cold receptor – CMR1, warm receptor – TRPV1, hot receptor – TRP2 o Pain pathway uses 2 types of neurons Small unmyelinated C fibers- dull pain; most common; cold/warm Dull because not myelinated (conducts slowly) Signal from spinal cord through dorsal to thalamus Capsaicin (chili pepper) activates via TRVP1 and kills fibers Larger myelinated A-delta fibers- sharp pain; hot Injury is a “2 phase” response: A-delta fibers then C fibers Vibration o Oldest/simplest receptors; unipolar o Vibration stretches skin – opens sodium channels system fires Touch – 2 parallel systems (early or later touch) st o 1 phasic then tonic o Phasic receptors – Burst of intense/fast firing to grab the brain’s attention Adapt quickly by decreased frequency o Tonic receptors – Fire from onset, keep firing after phasic stop Slow or no decline in action potential frequency Pain o Involves sensation and other effects; multisystem reaction o Free nerve endings (pain receptors) fire action potential to spinal cord which transmits info to brain where pain processing occurs o Cognitive system – involves frontal cortex o Motivation-affective – leads to motor response Can block pain signals o Sensory-discriminative – brain identifies characteristics (change in pain/which side hurts) o Peripheral mediation (other effects) Trauma chemical release Histamine swelling Substance P- transmits pain Serotonin- signals C fibers to fire o Disorders Congenital insensitivity – mutated Na+ channel in pain fibers Congenital hypersensitivity (“man on fire”); gain of function mutation in Na+ channel o Mild pain prevents bedsores & losing feeling in an area from lack of blood flow o Gate control theory Blocking pain by deep pressure – activates A-beta fibers which closes the gate from c fibers to spinal cord TENS – electrical nerve stimulation; activates A fibers o Chronic pain – pain after injury has healed because pain signals remain active Has emotional effects 2 kinds: neurogenic (nerve damage) and psychogenic (no damage) o Neurogenic pain = reflex sympathetic dystrophy Stage 1 (normal) –pain from injury Stage 2 (abnormal/chronic) – pain; swelling; muscle wasting Mechanism Injury released chemicals to CNS to trigger the sympathetic nervous system which releases the same chemicals back to injured area for inflammatory response and more pain o Cycle: more signaling to SNS more signaling back Occurs over months More likely to happen in young females (higher activation of sympathetic nervous system) Treatments Antidepressants, cut sympathetic nerve to injured area Anti-inflammatory to block chemical release o Chronic pain remodels the spinal cord and brain The spinal cord learns to be in pain (= inappropriate pain signaling) This causes neurogenic pain Spinal cord neurons take up substance P (released during pain) and remodel their dendrites Non-pain and painful dendrites become cross-wired – what stimulates touch (non-pain) receptors also stimulate the pain receptors Dorsal horn neurons (light touch) become hyper-excitable Somatosensory cortex is rewired in chronic pain (over- active) What makes it go away Spinal cord/brain remodel themselves after a while Pain becomes an emotion in the cingulate cortex (activates when somatosensory cortex reaches max activity) Receptive field The part of the world a sensory neuron responds to Smaller in areas that are more precise (hands/tongue) Touch receptive fields “on center, off surround” o Touch in center of field = max firing; excitatory o Touch in surrounding area = dec. firing; inhibitory o Touch far away = no effect (out of receptive field) Sensory integration disorder Most common in children; continuum- all people have it 1) Hypersensitivity to touch (stimulus avoiders) o Light touch activates the pain pathway o SID is part of autism but not enough for a diagnosis of autism 2) Hyposensitivity to touch (stimulus seekers) o Less common o Ranges from tapping foot to banging head and biting/hurting kids o Correlated with hyperactivity Synesthesia- stimulus creates sensation in wrong modality Cross linkage between sensory systems (any 2, not all) Causes: LSD, posterior temporal lobe seizure, blindness/deafness, spontaneous Basics of sound Sound is vibrating air that the brain can detect Amplitude = Intensity/loudness; measured in decibels (dB) Frequency = pitch; cycles per second; measured in hertz (Hz) o Cats hear higher frequencies o Elephants hear low frequencies because of large ears – hear footsteps o Mothers hear higher frequencies than other people o Humans hear about 20 Hz – 20K Hz Conversation range is 2000Hz or less Speech evolved to be in the best range for hearing Pure tone - single frequency of vibration; electronic; not interesting to brain Musical tone – modulated pure tones with repetition (rhythm); involves a pattern Noise – random sounds; un-patterned; most sounds Fourier analysis o Complex sound = sine waves added together o Brain breaks sounds down to individual waves o More waves (hundreds) = probably noise Parts of the ear Outer ear: The external ear and ear canal - collect low frequency sound waves Middle ear: Up to tympanic membrane (= ear drum) Inner ear: cochlea (including oval window which is in cochlea “membrane”) Two muscles in the middle ear protect hearing o When activated too much, they stiffen/retract so that they don’t vibrate the oval window even when sound is coming in to the eardrums o Protection because loud sounds kill hair cells which cannot be repaired Auditory hair cells o Inner – “transducers”; used in understanding speech Die over time with age o Outer- “amplifiers”; hearing support (not as important) Adjust the volume by increasing the volume of the signal and noise Makes it difficult to distinguish sounds o Neurons run to the ear from the brain and back (feedback) o Hair cells do not have axons - no action potentials (graded only) Hearing pathway Air molecules vibrate and come through the ear canal which vibrates the ear drum Ear drum vibrates bones which causes the oval window to vibrate Causes basilar membrane in the cochlea to vibrate which causes the stereocilia on hair cells to bend o Hair cells are stuck in the tectorial membrane so that when the basilar membrane moves, they bend Stereocilia bending causes ion channels to be mechanically pulled open by tip links that connect all the stereocilia on a hair cell to one another Causes ions to come in = depolarization and calcium influx glutamate release From ear to brain: o Auditory nerve cochlea cochlear nucleus superior olivary (SO) nuclei inferior colliculus medial geniculate nucleus (in the thalamus) auditory cortex SO nuclei is the first place with bilateral input Most right ear sounds are processed by the left hemisphere but the process is bilateral Auditory cortex Processes sounds- distinguish noise from patterned sound then Fourier analysis Auditory cortex cells each have a ‘preferred frequency’ (receptive field) o Some cells are less picky than others – larger receptive field Trying to pick up any sound Good at detecting whether sounds are changing Auditory neurons have tonotopic organization (arranged by tone) Cells that detect high frequency are on the inside, in the back Low frequency sounds are processed by the anterior auditory cortex Neurons next to each other are similar frequencies Auditory cell’s receptive field can shift if needed (plasticity) Auditory cortex analyzes complex sounds in two streams o Dorsal stream (frontoparietal lobe) – used in sound location o Ventral stream (temporal lobe)- analyzes “what is it” Speech is analyzed much more than random noise Left hemisphere processes sounds that you know; R processes sounds you don’t Two ways that we hear pitch (frequency) 1) Frequency coding - encodes pitch by the firing rate o Only works for lower pitches because there’s a max rate o Volley principle Each fiber only fires at a certain point in the cycle but does not respond to each cycle – all together = “complete transcript” 2) Place coding - Brain knows frequency by which part of the basilar membrane vibrated o Not as accurate as frequency coding o The cochlear apex is shaped like a triangle; skinny end = high pitch Different thickness of string = different frequency Place and volley mechanisms act together 1. Low frequencies - frequency coding 2. High frequencies - place coding 3. Intermediate frequencies (1000-5000 Hz) use both Detecting sound location Binaural cues detect sound location Compare the ears in intensity (which is loudest) and latency (which got here first) o Mainly uses superior olive (SO) High frequency - intensity differences in the lateral SO (lateral compares loudness) o Travel too fast to tell difference in arrival times Low frequency - latency differences in the medial SO (medial compares meeting times) o Notes where the input from the left ear and right ear meet in the MSO o If the sound is from the far right side, right ear is farther along in processing so sounds meet closer to left Unconscious hearing Involves three systems: sleep, limbic system, and hypothalamus Separate pathway than conscious hearing Hearing loss Central deafness - rare; hardest to treat o Caused by problems (lesions, injuries) in the brain o Associated with neurologic disorders (multiple sclerosis, tumors) o Involves CNS (cortex, brainstem, or ascending auditory pathways) o 1) Cortical deafness Pure word deafness Can speak normally and identify nonverbal sounds Can’t understand speech Auditory agnosia Can only hear pure tones Cannot recognize verbal or nonverbal sounds o 2) Auditory hallucinations Hearing things that aren’t there Common in schizophrenia, injury to secondary auditory cortex, or during a temporal lobe seizure More common than visual hallucinations in schizophrenia Usually negative towards themselves (danger or insults) Can be caused by damage to brainstem structures (like SO) Conduction deafness o Disorders of outer or middle ear - sounds don’t reach cochlea o Causes- otitis Media (swelling of the eardrum), TM Perforation, or ossicular arthritis (small bones can’t move/conduct properly) Sensorineural deafness = SNHL (sensorineural hearing loss) o Problem with cochlea, auditory nerve, or hair cells o May cause loud voice (can’t hear themselves) o High frequency loss common speech sounds distorted o Can be caused by viral infections (measles/CMV) that kill developing hair cells Other hearing problems NIHL (noise induced hearing loss) - #1 preventable cause of deafness o Can be sudden or gradual (accumulated damage over time) Presbycusis o Gradual onset hearing loss; starts at age 30 o As age increases, higher frequencies have to be louder Tinnitus o Ranges from moderate to severe (suicidal) o Damage to cochlea initiates tinnitus, CNS maintains chronic tinnitus o Brain problem, not a hearing problem (maladaptive memory) = an auditory hallucination All languages have similar basic elements Phonemes – basic speech sounds Semantics – meanings of words or sentences Syntax – grammatical rules for constructing phrases and sentences Learned or innate From birth, babies can distinguish phonemes in any language Language dev. depends on experience during a sensitive period (first few years) Basic disorders of language Dysphasia/aphasia– any language disorder; impaired language ability Dysarthria – inability to speak clearly (muscle control problem) o “Speaking with marbles in your mouth” Dyspraxia – inability to sequence a complex motor act o Intrusion error – trying to say one phoneme and another comes out Dysgraphia – inability to write Dyslexia – inability to read Types of aphasia Paraphasia – substitution for a word by an incorrect, unintended word o "The Lord is a shoving leopard“ Neologism - an entirely novel word (person can’t recall the correct word) Broca’s (non-fluent) aphasia o Most common type of aphasia Can understand other people’s speech May occur with anomia Continuum; ranges from moderate to severe Affected area = Broca’s area (right next to motor cortex) CQ: A stroke in Broca’s area causes… Non-fluent aphasia Ex: Severe case “Tono” aphasia Can say the numbers 1-10 but everything else is “tono” Intonation is normal Caused by a left hemisphere stroke – can’t move right hand Can understand what someone is saying but can’t understand his own speech Ex: Less severe case Patient can hear himself, knows that his speech is messed up and is trying to fix it but can’t Ex: CQ Woman is asked where her son is She answers “Car..home..yes” in response She has a less severe case of Broca’s aphasia Wernicke’s (fluent) aphasia Complex verbal output with many paraphasias AKA – “word salad” Ex: “Train flogging into my question, are you why is it thirty letters down under peanut butter, what is it” Patients cannot understand what they read or hear Left brain problem - affects Wernicke’s area (temporal area) Can tell that someone asked a question because they can hear the intonation but don’t understand the question Global aphasia = Broca’s + Wernicke’s Total inability to understand or produce language Large left-hemisphere lesions, affecting all speech zones Prognosis is poor Caused by horrible trauma Conduction aphasia Impaired repetition of words only Lesions of arcuate fasciculus axons produce conduction aphasia Arcuate fasciculus – axons connecting Wernicke’s area to Broca’s area Supports Wernicke-Geschwind model that damage to connections (axons) causes language impairment Anomia Cannot name a seen object or speak a written word Naming a seen object requires transfer of visual information to the angular gyrus Lesions disconnect visual and auditory systems Patients can speak and understand, but can’t read aloud Lectures 15 and 16: Language and Cognition All languages have similar basic elements Phonemes – basic speech sounds Semantics – meanings of words or sentences Syntax – grammatical rules for constructing phrases and sentences Learned or innate From birth, babies can distinguish phonemes in any language Language development depends on experience during a sensitive period (first few years) o Japanese babies can understand the distinction between R and L but raised in Japan with no exposure to English they lose this ability Basic disorders of language Dysphasia /aphasia– any language disorder; impaired language ability Dysarthria – inability to speak clearly o Muscle control problem – “speaking with marbles in your mouth” Dyspraxia – inability to sequence a complex motor act o Intrusion error – trying to say one phoneme and another comes out Dysgraphia – inability to write Dyslexia – inability to read Types of aphasia Paraphasia – substitution for a word by an incorrect, unintended word o "The Lord is a shoving leopard“/“The light at end of the candle” o Common to occur every now and then but in the case of paraphasia it’s functionally impairing Neologism an entirely novel word o Affected person has to make up words because they can’t recall the correct word Broca’s (nonfluent) aphasia o Most common type of aphasia o Can understand other people’s speech o May occur with anomia o Continuum; ranges from moderate to severe o Affected area = Broca’s area (right next to motor cortex) o CQ: A stroke in Broca’s area causes… Nonfluent aphasia o Ex: Severe case “Tono” aphasia Can say the numbers 110 but everything else is “tono” Intonation is normal Caused by a left hemisphere stroke – can’t move right hand Can understand what someone is saying but can’t understand his own speech o Ex: Less severe case Patient can hear himself, knows that his speech is messed up and is trying to fix it but can’t o Ex: CQ Woman is asked where her son is She answers “Car..home..yes” in response She has a less severe case of Broca’s aphasia Wernicke’s (fluent) aphasia o Complex verbal output with many paraphasias AKA – “word salad” Ex: “Train flogging into my question, are you why is it thirty letters down under peanut butter, what is it” o Patients cannot understand what they read or hear o Left brain problem affects Wernicke’s area (temporal area) o Can tell that someone asked a question because they can hear the intonation but don’t understand the question Global aphasia = Broca’s + Wernicke’s o Total inability to understand or produce language o Large lefthemisphere lesions, affecting all speech zones o Prognosis is poor o Caused by horrible trauma Conduction aphasia o Impaired repetition of words only o Lesions of arcuate fasciculus axons produce conduction aphasia Arcuate fasciculus – axons connecting Wernicke’s area to Broca’s area o Supports WernickeGeschwind model that damage to connections (axons) causes language impairment Anomia o Cannot name a seen object or speak a written word o Naming a seen object requires transfer of visual information to the angular gyrus o Lesions disconnect visual and auditory systems o Patients can speak and understand, but can’t read aloud Anatomy of Aphasia • WernickeGeschwind model = disconnection theory • Language impairment from loss of connections among brain regions involved in language • Explains most clinical aphasias Recovery from aphasia If injury to left hemisphere occurs early in life, the right hemisphere can take over language o Can have completely normal recovery If damage occurs later, language control is more likely to shift into bordering areas in the left hemisphere o Right hemisphere won’t take over; the brain has to rely on what is remaining in the left hemisphere but can still get some recovery o Plasticity is severely diminished later in life Ability of other areas to take over language functions (either right or bordering areas depending on age of injury) may be due to their normal participation in language o Indicates that the right hemisphere may be more involved in language than previously thought Melodic intonation therapy (MIT) for aphasia uses the fact that singing is often intact after a left hemisphere stroke o Intact because music is processed by the right hemisphere o In therapy, they try to use music to incorporate language ASL Uses the same brain mechanisms as spoken language o Lesions that cause aphasia in normal speakers also cause impairment of ASL use in the deaf fMRI studies show that signers and normal speakers have similar activation in language tasks but signers have extra activation in the right hemisphere Mirror neurons May be critical to develop language Active during imitation of others’ actions, not experience of themselves speaking o Babies learn speech by watching others speak Overlap Broca and Wernicke areas Brain looks at whole words – not every letter As long as the first and last letter of a word are the same, you can read a sentence where every middle letter is rearranged Bilingualism If a second language is learned before age 11, the same brain regions (angular gyrus) are used for both languages o Angular gyrus is the “dictionary” of the brain If learned after age 11, different regions are used o Angular gyrus used for the first language and the insula for the second Language acquisition is more difficult in adulthood, reflecting diminished plasticity Easier to learn a language earlier in life but may be beneficial to learn it later – if a stroke wipes out the angular gyrus you can still speak Identifying words via tactile ASL Can use braille; but they’re feeling someone’s hands as they’re signing Regions involved in vision become used for tactile stimulation in a blind person The brain activates more with real speech More active with real word than real sounding word than random letters than characters Brains use two language systems to read Learned because of dyslexia One focuses on sounds of letters, the other on meanings of words Dyslexia Visual AND auditory processing disorder Surface dyslexia errors in reading restricted to details and sounds of letters o Pretty read as “PRItee” Deep dyslexia errors in reading one word as another o The words are related in meaning o They substitute a word for a synonym that’s easier to say o Caused by extensive damage to lefthemisphere language areas Dyslexics have distortions among cells in the cerebral cortex o In the planum temporale there is micropolygyria (excessive cortical folding) and ectopias (clusters of extra cells) o CQ: some dyslexic brains have… Too many neurons along the surface of the brain Dyslexic brain uses more of the right hemisphere than a normal brain to read Dyslexia improves with training and brain changes occur o Before remedy, there is little activation in Wernicke’s and Broca’s area o After remedy, there is a lot of activation in both Cerebral lateralization* Left face is more expressive because emotional expression is in the right hemisphere Arithmetic – left cortex even though it’s not language (but it’s a language of sorts) Geometry (not a language) is in the right hemisphere Fourier transformations (for dissecting sounds) are in the left hemisphere Corpus callosotomy Cutting corpus callosum (connection between the hemispheres) to prevent seizures from spreading Allows study of each hemisphere independently (=splitbrain patients) Hemispheres of splitbrain patients function independently Left hemisphere can tell what it sees Right hemisphere can show what it sees In splitbrain patients: o Present a picture to the right visual field (stimulate left brain) Left hemisphere can tell you what it was Right hand (left hemisphere) can show you, left hand can’t o Present a picture to the left visual field (stimulate right brain) Subject will report they do not know what it was Right brain can’t tell you what it is Left hand (right hemisphere) can show you what it was, right hand can’t Right brain can only show you Another way to test the hemispheres independently Dichotic listening – presents different sounds to each ear at a different or same time Sound into left ear has to go across the left to the right hemisphere then back to the left Sound into right ear goes across right straight to left hemisphere o = More efficient; right ear advantage Shows that the left hemisphere is dominant for language If you play both at same time – you’ll only hear the right ear because it’s more efficient and thus overtakes the left ear Righthanders identify verbal stimuli delivered to the right ear more easily Some lefthanders have leftear advantage o This implies some lefthanders have language in their right hemisphere Wada test Injection of amobarbital into the carotid artery briefly sedates that hemisphere Righthanders: Language restricted to the left hemisphere in 95% of patients Lefthanders: only 70% have left lateralization, 15% have right lateralization (right dominant) and 15% mixed dominance Structural asymmetry of the planum temporale Generally larger on the left Asymmetry is present by week 30 in gestation Support for innate language o Innate verbal specialization of the left hemisphere for language Chimpanzees also have this but people can’t get them to talk so maybe support against innate hypothesis Music and the right hemisphere Auditory areas of the right hemisphere play a major role in perception of music Musical perception is impaired by damage in the right hemisphere Music activates the right hemisphere more than the left (some activation on left) However, simple tones and perfect pitch involve the left hemisphere Cognition Human cortex is divided into 4 lobes: frontal, parietal, temporal, and occipital lobe o Lobes are named for bones not for function; it just so happens that the division of lobes based on the bones also matches with division of function The little man inside the guy’s head is called a homunculus – meaning “little man” Two functional types of cortex Primary cortex (pink): First cortical area processing sensory input or motor output o Processes the simple question: What is it o Evolved first so it represents all of the primary cortices (primary visual, auditory etc.) o Motor cortex – once association cortex decides what to do, it carries out the function Association cortex (blue): Multimodal cortex (most of cortex covers more area) o Association areas – visual association area, etc. o Processes complex question: what does it mean o Acts as commander: What do I do now Info starts in primary (what is it) then travels to association (what does it mean/what do I do) and then back to primary (do it involves motor cortex) The areas are not 100% accurate which can lead to hallucinations or illusions The brain changes information based on genetics, experiences, etc. Frontal Lobes: Anatomy Everything in front of the central sulcus 1) Motor cortex (blue) 2) Premotor cortex (green) 3) Prefrontal cortex (purple) o Makes decisions o Divided into 2 partitions Dorsolateral – logical/reasoningtype thinking Not connected to amygdala so no role in emotion Inferior prefrontal cortex = orbitofrontal Located really close to the amygdala = more emotional Frontal lobe damage Phineas Gage railroad worker Explosion drove a tamping rod up through left cheek and out the top of his head o Serious left eye damage but most people injured by a tamping rod don’t survive Damaged orbitofrontal cortex bilaterally ( trouble regulating emotions) Prior to accident, Gage was a sober, serious workman; afterward, he was moody and uninhibited Abuse/stress cortisol frontal cortex damage w/o trauma Symptoms of frontal lesions Children (5 year olds etc.) whose frontal lobes have not yet developed also have frontal lobe issues (similar to trauma patients) Perseverative errors Failures of planning o Like a 5 year old; impulsive; like ADD Reduced pain reactivity o Prefrontal cortex connects pain perception and sensation o Children can break their arm, cry and then be fine 10 seconds later because they have reduced pair sensation Inappropriate social behavior o A child asks a stranger why they’re fat Attention and memory problems, though little change in IQ score o Prefrontal cortex is not responsible for “smart” Dorsolateral damage poor judgment and selfcare, motor programming problems o Damage doesn’t affect emotion o Involved in guilt o People drink alcohol affects inner monologue because it directly affects the frontal lobe which leads to less anxiety Orbitofrontal damage environmental dependence, poor social insight, emotional damage All cortexes talk to the frontal cortex Parietal lobe organizes space Parietal lobe injuries produce diverse impairments – it touches all three other major lobes Touches all other lobes, so it’s logical that it integrates/is involved in sensory integration o Ex: body’s position in space, body image, phantom limb The least is known about the parietal lobe Injury to postcentral gyrus (somatosensory cortex) results in tactile deficits on the opposite side – but not anesthesia Astereognosis – inability to recognize objects by touching and feeling them – mostly right hemisphere o People could tell what an object is by feeling it without looking at it because they create a map of the object and put it together in their head Hemispatial neglect Damage to right parietal lobe results in neglect of the left side of the body and space Diagnosis – patient tries to copy picture and only draws the right side o If you ask them where the left side of the picture is, they’ll say “it’s right there” because they know it’s supposed to be there o It doesn’t make sense to them why it’s not there in their drawing when their experience tells them it should be there Prosopagnosia People fail to recognize familiar faces, even theirs Recognizing faces is a learned behavior o Involves the visual parietal cortex Ex: Man couldn’t tell if his wife was a wife or a hat until she started talking because they have roughly the same shape Bilateral damage to fusiform gyrus causes prosopagnosia o Fusiform gyri is specific for human faces Often accompanied by other forms of agnosia (inability to identify items) Case Man felt ‘someone’s leg’ in the bed Tried to throw it out of bed but he came after it and it was now attached to him Tried to pull it off Someone told him it’s his own leg and he didn’t believe it They asked “if it’s not yours then where is your left leg” He said it had disappeared Always happens to the left leg because it’s caused by damage to the right parietal lobe o Left parietal stroke/damage – not much change o Right parietal lobe is involved in emotion, body map, and spatial reconstruction Lecture: Attention Why don’t we always know where our tongue is in our mouth We don’t notice until asked Your brain’s job is to constantly scan the environment to answer 3 questions: o Will it kill me Can I eat it Can I have sex with it Attention is how we filter out unimportant details All the incoming stimuli is more than you can process so the brain has to choose what to pay attention to A decision has to be made very fast – brain immediately goes through the 3 questions 2 systems decide what to pay attention to Topdown (left side on picture) Dorsolateral frontal cortex = dorsal frontoparietal system = dorsal stream o Connected by axons to parietal o Parietal – special awareness/frontal – makes decisions AKA voluntary attention The dorsal network allocates attention under goaldirected control A decision is made (rules set) before you experience the stimuli – “I’m going to pay attention in class today because the test is next week” o This screens out all the other information and you only pay attention to what will be useful for the test o Uses prior knowledge – have to know what will be useful Higherorder cognitive processes exclude unattended information before any perceptual processing has occurred o Higher analysis controls what you take in Problem – what if you pick the wrong rule o Ex: You listen for “test” and miss parts when he says “exam Example: not hearing your girlfriend when the Cowboys are firstandgoal o Dorsal says pay attention to auditory and visual channel and ignore touch stimulus so you don’t notice when your girlfriend is tapping you on the shoulder o Problem – maybe your brain made the wrong decision in putting the game above your girlfriend Bottomup (right side on picture) Temporoparietal system = ventral stream AKA involuntary attention No decision made Process everything at a shallow level and then decide what to pay more attention to based on change This system is activated by novel or unexpected stimuli The more ventral network responds to stimulus demands Useful in situations where you don’t know the “rules” o Ex: first day of college – you don’t know what’s important for the test You try to take in everything but you can’t a decision still has to be made o So, the brain looks for novelty (change) Ex: if you have chronic pain, feeling pain is not helpful but if it’s a new pain it’s worth paying attention to Ex: paying attention when your girlfriend pours your beer on your head o That’s unexpected enough that you notice o But your girlfriend taps on your shoulder all the time Ex: child throwing a tantrum over a new bike they want – trying to talk/reason isn’t helpful because you talk all the time – instead “hey look santa claus” is enough to distract them – or picking them up by the heels and carrying them upside down – when you put them down they’ve forgotten all about the bike Ex: commercials constantly change the image ever 150 milliseconds to keep people’s attention Our brain guesses what it sees we see what we expect to see Why have 2 systems Topdown is more efficient/faster o Tries to make it even faster by guessing what it sees What you expect to see changes how you process the stimulation o Biases effect how you see, smell, feel things Topdown processing is a “shortcut” in which early visual inputs are sent, partially analyzed, from early visual cortex to prefrontal cortex (PFC) An interpretation of the crude visual input is generated in PFC and then sent to inferotemporal cortex (IT), subsequently influencing the slower, bottomup process This shortcut minimizes the number of object representations required for matching, thereby speeding object recognition, but is errorprone People with PFC injury have slower response times, due to only bottomup processing Ex: Scorpion in boot one day. Next day there’s a brown leaf in the boot. They freak out thinking it’s a scorpion because the brain filled in the blanks with a scorpion o The brain’s primary job is to protect you not represent reality 100% accurately ADD/ADHD: major symptoms Common Everyone has it, but some have it worse than others Situationdependent The problem isn’t that you aren’t paying attention but that you’re not paying attention to what you want to; you’re paying attention to too much Bottomup system is dominant and topdown is weak Medications for ADD help all 3, but some medications target only one Inattention easily distracted and doesn't listen fails to finish – doesn't stick with an activity o More important than impulsivity in class situations Impulsivity doesn't wait for turn acts without thinking – can’t organize work speaks out loudly in class o More important in social situations Hyperactivity can't sit still fidgets bothers classmates o Does not imply inattention o Hyperactivity is a way of increasing focus o Because it’s a pattern/predictable, it blocks out other stimuli Consciousness Attention is part of (a defining feature of) consciousness Consciousness involves awareness, attention, and a sense of self (something that distinguishes you from the world) To check for consciousness – you tap (stimulus) and look for a response o If they respond to stimulus they must be conscious Altered states of awareness There are more states than just wake or sleep Arousal – the intensity of response to a stimulus Brain dead – no awareness and no arousal (at intersection of bottom left) Coma not deep sleep; “hibernation state”; o Unarousable and unresponsive to stimulation o By definition, is a short term process (12 week process) o After short term – you either die or transition to a vegetative state Vegetative state o Almost no awareness May respond to a stimulus by a change in heart rate (reflexive response) No voluntary interaction In some cases they’re more responsive than we think o Still has arousal – a sleep/wake cycle o Can transition to minimally conscious and in some cases back to normal Ex: 15% recover from drug exposure that causes a vegetative state Minimally conscious o Some voluntary response but can’t communicate reliably Lockedin syndrome o Full consciousness, but mostly uncommunicative because of paralysis (brainstem lesions) o Can’t move anything but their eyes (because different part of brainstem) Sleep o With increased awareness and arousal – deep sleep then light then drowsiness then conscious wakefulness REM sleep (dream sleep) o Same (low) arousal as deep sleep but more aware Lucid dreaming o Same (low) arousal as deep sleep and REM sleep but increased awareness More states: hypnosis, trance, dreams, meditation, intoxicatio Where is consciousness Consciousness involves a widely distributed network o The whole brain is involved Prefrontal cortex o Active when you become aware of a relationship between objects o Acts as a commander – it makes a decision o Organizes things but not the site of consciousness If it’s cut out people are still conscious Parietal lobes o Its ability to locate objects in space is needed to combine an object’s