Flashcards
Physio Psychology III
Cards in this deck (144)
- 1Somatosensesskin + body info relaying
- 2Cutaneous Senses1. pressure
2. vibration
3. heating/cooling
4. tissue damage
various signals from the skin - 3Kinesthesiaprovides info about body position and movement;
receptors located in joints, tendons, and muscles - 4Tactile Sensepressure + vibration
"touch" - 5Temperature Perceptionwarmth and cold receptors
react to deviations from baseline (relative)
detected by free nerve endings, "thermoreceptors"
cold receptors are closer to the surface - 6Pain Perceptionassociated with tissue damage
detected by free nerve endings
"nociceptors" - 7Ruffini Endingshairy & glaborous skin
detects skin indentation
Tonic adaptors
found in epidermis - 8Pacinian Corpusclehairy & glaborous ksin
detects high-frequency skin vibration
phasic adaptors
found in dermis - 9Free Nerve Endingshairy & glaborous
detects pain, or changes in temperature
found in epidermis - 10Meissner's Corpuscleglaborous only
detects low frequency vibration
phasic adaptors
found in epidermis - 11Merkel's Disksglaborous only
detects skin indentation (add. sensitivity)
tonic adaptors
found in epidermis - 12Phasic AdaptorsRapid adaptors
respond with burst of firing, but quickly returns to baseline
cease firing when stimulation becomes constant
e.g. Pacinian & Meisner corpuscles - 13Tonic Adaptorsrespond with burst of firing, but slowly returns to just above baseline firing for duration of stimulus
continues to fire even if stimulation is constant
e.g. Ruffini Endings & Merkel's Disks - 14Pacinian Corpuscle mechanismneuron depolarizes when the corpuscle is bent
(carbohydrate chains are linked to ion channel, and mechanical force tugs the chains, thus opening the ion channels)
responds best to vibration - 15Pain detection mechanismvia free nerve endings
involves tissue destruction via thermal stimuli or mechanical force
pain is poorly localized and thus sends info from a large swatch of skin;
and involves an emotional component
respond to: heat, acids, and capsaicin; activated by mechanical/chemical stimulation - 16Dorsal Columnsipsilateral touch
precise touch and kinesthesia
crosses over at medulla! - 17Spinothalamic Trackcontralateral free nerve endings
pain and temperature
crosses over at the spinal level - 18Primary Somatosensory Cortexlocated posterior to primary motor cortex, and superior to primary auditory cortex
also has a homunculus map; feet toward dorsal part of brain - 19Benefits of Gustation- detect acids as foods go bad
- poisons are alkaloids
- salt cravings - 20Bitterpoison
- 21Saltysodium and calcium
- 22Sourspoiled foods
- 23Sweetsafe foods
- 24Gustatory Rectporsare all chemoreceptors!
four different types for each taste - 25Types of Papillae1. Fungiform Papillae
2. Foliate Papillae
3. Circumvallate Papillae - 26Fungiform Papillaeanterior 2/3 of tongue
predominantly sweet
touch, temperature, and pressure
very slow to detect sweet taste; sweets are SAFE, so no need for a fast reaction - 27Foliate Papillaetowards the back of the tongue
predominantly salty and sour
salt: best stimulus is NaCl; Na+ enters receptors, causes EPSP
sour: respond to hydrogen ions preent in acidic solutions; K+ channels are open, but hydrogen closes channels, causing EPSP - 28Circumvallate Papillaeinverted V on the back of tongue
predominantly bitter
since alkaloids are hydrophobic, bitter receptors lay on top of the bumps!
activation sets off reverse parastalsis - 29Taste Perceptionrelates to the density of tastebuds
supertasters: 425/cm2
medium: 184/cm2
nontasters: 96/cm2 - 30Gustatory ProcessingIPSILATERAL!
transmitted through cranial nerves:
7 (anterior tongue) -> 9 (posterior tongue) -> 10 (palate and epiglottis)
then to nucleus of solitary tract (medulla) -> primary gustatory cortex -> amygdala -> hypothalamus - 31Primary Gustatory Cortexlateral frontal; orbitofrontal (right behind the eyes)
brain determines taste by comparing the responses of several kinds of taste neurons; depends on a pattern of responses
tasteotopic: lateral -> medial
salty -> sweet -> sour -> bitter
crave -----------> toxic - 32Olfactionuses chemoreceptors
can discriminate between over 10,000 odors
stimuli are airborne and lipid soluble, so dissolve in mucuous and stimulate olfactory receptors
olfactory receptor info ends up the same place as gustation! - 33Olfactory Receptorsbipolar and respond to specific odors
olfactory epithelium (base of cribiform "perforated" plate; bone at the base of the rostral brain)
100s of diff receptor types; but all include G-Protein stimulation, thus opening Na+ channels -> depolarization - 34Olfactory Receptor Pathwayaxons project from cribiform plate to brain -> ipsilateral olfactory bulb -> contralateral olfactory bulb -> amygdala -> primary olfactory cortex
- 35Primary Olfactory Cortexpiriform and entorhinal corticies of the limbic system, which include:
- hypothalamus (identify mates)
- orbitofrontal cortex (gustatory cortex)
**gives odors an emotional component**
processing takes place mostly in limbic system, so smells elicit strong emotional responses - 36Flexioncontraction of flexor muscle brings limb towards body
- 37Extensioncontraction of extensor muscle brings limb away from body;
it is "anti gravity" - 38Skeletal Muscle Fibers1. Extrafusal
2. Intrafusal - 39Extrafusal Neuronsinnervated by alpha-motor neurons from the spinal cord
EXERTS FORCE - 40Intrafusal Neuronsinnervated by gamma-motor neurons
EXERTS NO FORCE
PROVIDES AFFERENT INFO to brain regarding proprioception
afferent fibers: report length of intrafusal; maintains muscle tone
efferent fibers: contraction adjusts senstivity of afferent neurons - 41Myofibrilsbundles of myofibrils make up each muscle fiber
each myofibril is made up of overlapping strands of actin and myosin
during contraction, myosin move relative to actin filaments, thereby shortening the muscle fiber - 42Neuromuscular Junctionsynapse formed between alpha motor neuron axon and a muscle fiber
neurotranmitter: ACh!
Release of ACh produces large endplate potential, voltage changes open Ca++ channels, Ca++ entry triggers the use of ATP in cytoplasm, and causes myosin-actin interactions
Strength of muscle contraction determined by RATE LAW!!!!! - 43Motor Uniteach axon forms synapses with several muscle fibers;
precision of motor control is related to motor unit size;
- small: precise movements of the hand (1axon:10 muscle fibers)
- large: movements of the leg (1axon:200+ muscle fibers) - 44Smooth Musclecontrolled by autonomic nervous system;
two types:
- multi-unit smooth muscle
- single-unit smooth muscle - 45Multi-Unit Smooth Musclenormally inactive
located in large arteries, around hair follicles, and in the eye (lens adjustment, pupillary dilation)
responds to neural or hormonal stimulation
SYMPATHETIC NERVOUS SYSTEM; mostly activated during high stress - 46Single-Unit Smooth Muscleexhibits rhythmic contraction
found in gastrointestal tract, uterus, small blood vessels - 47Cardiac Muscleresemble striated muscles in appearance, but exhibit rhythmic contractions like single-unit smooth muscle
- 48Spinal Cord Anatomyorganized into dorsal and ventral aspects
- 49Dorsal HornAFFERENT
receives incoming sensory information - 50Ventral HornEFFERENT
issues alpha-motor neurons that innervate extrafusal fibers - 51Monosynaptic Reflexesspinal cord reflex
single synapse between sensory fiber from a muscle and an alpha-motor neuron
activates the alpha motor neuron which contracts muscle fibers;
e.g. patellar reflex (but not in humans, because of interneurons, so not a true monosynaptic reflex) - 52Polysynaptic Reflexinvolve multiple synapses between sensory axons, interneurons, and motor neurons
axons from afferent intracellular muscle synapses:
- alpha motor neuron connected to the agonist muscle
- inhibitory interneuron connected to the antagonist muscle - 53Polysynaptic Reflex (mechanism)intrafusal muscle detects contraction, sends afferent information to dorsal root:
- directly: synapse onto alpha motor neuron of same muscle
- AND inhibitory interneuron, which then stimulates alpha motor neuron for antagonist muscle - 54Types of Motor Movement1. medial and coordinated movements
2. lateral and independent movements - 55Primary Motor Cortexlocated on the precentral gyrus
somatotropically organized
receives input from:
1. premotor cortex -> plans movement
2. supplemental motor area -> plans movement
3. primary somatosensory cortex -> tells you environment and where body is
organizes the "kinesthetic melody" - 56Kinesthetic Melodyknowing how to move the body based on where the body is
- 57Planning of Movementsinvolves premotor cortex and supplemental motor area;
takes info from parietal area (WHERE) and temporal area (WHAT)
helps with event sequencing - 58Cortical Control of Movementparietal = where to move
temporal = what is moving
frontal = plans to move - 59Left (Pre)Frontal Lobe Lesions- ideational apraxia in VERBAL DOMAIN: difficulty expressing/repeating sentence -> "no ifs, ands, or buts"
- M's and N's test in script (cannot write mnmnmnmnmmn)
- Stuttering (inability to plan movements) - 60Right (Pre)Frontal Lobe Lesions- ideational apraxia in SPATIAL DOMAIN
- fail circle, square, triangle test - 61Descending Motor Pathwaysaxons from PMC descend to spinal cord via two groups:
1. lateral group -> independent limb movements; more lateralized
2. ventromedial group -> controls gross or coordinated limb movements that are more medial (i.e. posture, walking) - 62Lateral Groupindependent limb movements
1. corticospinal tract: hand / finger / foot movements
2. corticobulbar tract: face / neck / tongue / eye
3. rubrospinal tract: fore- and hind-limb muscles (crosses over by pons)
lateral on spinal cord - 63Medial Groupcoordinate limb movements
1. vestibulospinal tract: posture
2. tectospinal tract: walking, sneezing, muscle tone
3. ventral corticospinal tract: upper leg/trunk
medial on spinal cord - 64Basal Gangliaincludes: caudate nucleus, putamen, and globus pallidus
- input from: substantia nigra
output: PMC, supplemental motor area, premotor cortex, brainstem motor nuclei - 65Parkinson's Diseasemuscle rigidity, resting tremor, slow movements, postural instability
damage to dpolamine neurons within nigrostriatal bundle
decay of D1, HYPOAROUSAL OF PUTAMEN;
OUTPUT AREAS OF PMC & CEREBELLUM ARE HYPOACTIVATED
treatment: DBS in subthalamic nucleus, bc STN is hyperactivated; DBS turns it off - 66Huntington's Diseaseballistic movements, uncontrollable, jery movements of the limbs and terrible balance
degeneration of caudate nucleus and putamen (loss of GABA-secreting axons) in D2 pathway
hereditary; found on chromosome 4; faulty protein -> huntingtin
OUTPUT AREAS ARE HYPERACTIVATED (PMC & Cerebellum) - 67Apraxiasinability to properly execute a learned skilled movement after brain damage
- 68Sympathetic Apraxiadamage to anterior left hemisphere causes paralysis of right arm and hand
*and vis versa - 69Callosal Apraxiacannot perform movement of left hand to a verbal request;
atnerior callosum interruption prevents info from reaching right hemisphere - 70Left Parietal Apraxiadifficulty in initiating movements to verbal request due to lesion in Wernicke's Area
- 71Constructional Apraxiadifficulty with drawing pictures or assembling objects;
caused by damage to right parietal lobe - 72Measures of Sleep- EMG (electromyography) for muscle tone, eye movements
- Respiration, HR, blood pressure
- EEG (electroencephalogram) for summated brain wave activity - 73Brain Waves (EEG)HIGH AROUSAL: Beta
Alpha
Theta
LOW AROUSAL: Delta - 74Wakefulness (brain waves)Alpha & Beta wave activity
- 75Stage 1 SleepAlpha and Theta waves
- 76Stage 2 SleepAlpha and Theta waves
with sleep spindles (bursts of Beta activation)
& K-Complexes (bursts of Delta activation) - 77Stage 3 Sleep30% Delta, 70% Theta
Synchronized
"Slow Wave Sleep"
Cold, Rational dreams ---> think about things that actually happened! Usually non-emotional in nature. - 78Stage 4 Sleep50% Delta, 50% Theta
Synchronized
"Slow Wave Sleep"
Cold, Rational dreams ---> think about things that actually happened! Usually non-emotional in nature.
nightmares occur during stage 4 sleep - 79REM SleepTheta/Alpha/Beta Activity
"Paradoxical Sleep"
increased respiration and BP
Rapid eye movements
Loss of muscle toe & paralysis
vivid, emotional dreams (irrational) & signs of sexual arousal - 80Sleep Cycles by AgeNewborns spend 50% time in REM sleep, while adults only spend about 20% time
In old age, difficult initiating and maintaining sleep throughout the night; can be due to:
- UTIs
- degeneration of vlPOA - 81Possible Functions of Sleep- adaptive response; indus dolphins sleep even though doing so is dangerous
- brain activity reduced during SWS, may reflect restoration; after intense cerebral activity, need more SWS
- REM sleep may reflect vigilance to environment; facilitation of brain development (infants spend more time in REM sleep) - 82Sleep Deprivation Studies- human sleep deprivation studies indicate that sleep deprivation can impair cognitive function;
- in rats: become ill and die (forced to walk on rotating platform)
- humans with fatal familial insomnia gradually become unable to sleep; lose SWS and die --> damage to thalamus - 83SWS Sleep Benefits- improves consolidation of declarative & explicit memories
e.g. test information - 84REM Sleep Benefits- improves consolidation of nondeclarative / implicit memories
e.g. throwing a ball; things you don't need to try to remember
**no rebound for this type of consolidation** - 85Sleep Reboundcan make up for lost sleep;
50% of REM is made up
70% of SWS is made up - 86Control of Sleep/Wakingnot possible that sleep is controleld solely by blood-borne chemicals;
siamese twins sleep independently, but share circulatory system
bottle nose dolphins' two hemispheres sleep independently
**brain & body never turned off at the same time --> during SWS, brain off, body on; during REM, brain on, body off** - 872 GABA-ergic pathways for Sleepmutual inhibition; "flip flop":
- sleep-promoting region in vlPOA (anterior to optic chiasm)
- arousal systems in brain stem and forebrain, regulated by Ach, NE, 5HT, Histamine - 88NT involved in ARousal1. ACh
2. NE
3. 5HT
4. Histamine
5. orexin - 89Acetylcholine (Arousal)AWAKE
"hindbrain regions"
- activated in ventral pons & basal forebrain regions;
- produces Beta waves! - 90NorepinephrineVIGILANCE
neurons located in dorsal pons
project very diffusely (widespread)
high activation during wakefulness, low activation during sleep, zero during REM - 91Histaminelocated in hypothalamus, synthesized from histadine
diffuse --> affects entire cerebral cortex
produce cortical and behavioral arousal; also associated with mucus production - 925-HTa.k.a. serotonin
stimulation of raphe nuclei (medulla and pons), induces cortical arousal
released most during waking; none during REM
greatest release right after sleeping!
=> release must drive us from REM to awake! - 93Orexinneurons located in lateral hypothalamus
activate all arousal systems;
MOTIVATION TO STAY AWAKE! - 94Other factors affecting sleep- hunger -> suppresses sleep via orexinergic neurons
- satiety -> promotes sleep via inhibition of orexinergic neurons - 95vlPOA in SleepVentral Lateral Pre-Optic Area
anterior to optic chiasm
important for inducing SWS; secretes GABA, suppresses alertness and induces SWS
ADENOSINE INITIATES vlPOA ACTIVITY!!! - 96Adenosineintiates vlPOA activity
during waking hours, adenosine accumulates in your brain, which drives us to sleep;
sleep clears adenosine
found in cerebral cortex; produced by activated neurons and astrocycles lacking glycogen ---> brain is running out of energy!! - 97Biological clock-time of dayaffects (+) LH orexinergic neurons
DAY-NIGHT CYCLE!!
circadian rhythm regulated by suprachiasmatic nucleus (SCN) of the hypothalamus - 98Suprachiasmatic Nucleusreceives information from retina; no role in vision
melanopsin around ganglion cells send info!
traverses retinohypothalamic pathway;
if you lesion out SCN, lose light/dark cycle, but can still sleep
activation inhibits vlPOA, thereby increasing arousal
EXCITE orexinergic neurons - 99Neural Controls of REM SleepPONS!!!!!
PGO (Pons to Geniculate to Occipital) waves are the first indicator of REM Sleep
ACh neurons in peribrachial pons (dorsal) promote sleep
DESCENDING PATHWAY to medulla to inhibit muscle movement - 100Ventral PonsACh
beta arousal
WAKEFULNESS - 101Dorsal PonsACh
beta arousal
REM SLEEP
**think: dorsal = dorm** - 102Insomniadifficult in getting to sleep or remaining asleep;
has many causes
can be situational or drug-induced - 103Sleep Apneaperson stops breathing and is awakened when the blood levels of carbon dioxide stimulate breathing;
people with sleep apnea don't know that they have sleep apnea! - 104Narcolepsygenetic, on chromosome 6, usually includes:
- sleep attack
- cataplexy
- sleep paralysis - 105Sleep Attackurge to sleep during the day, especially during boring times
reduced CSF levels of orexin - 106CataplexyREM paralysis occurs; person is still conscious!
occurs during highly emotional activation!
some problem with the peribrachial pons! - 107Sleep Paralysisinability to move just prior to sleeping, or just after waking;
may sometimes involve REM-like dreams - 108What are emotions?- perturbations of response patterns that are behavioral, autonomic, and hormonal
-as well as feelings that can be negative or positive - 109Why do we have emotions?- elicit autonomic responses to prepare for bodily movement
- motivating (approach or withdrawal)
- persist, and thus help to ensure goal-directed behavior
- enhance social bonding
**negative emotions last longer** - 110Facial Expressionscommon across cultures; may differ in how often you show the emotions, but not HOW the emotions are expressed
- positive emotions: zygomatic muscle (corners of mouth)
- negative emotions: corrugator muscle (forehead) - 111Recognition of Emotionvia visual cues (facial expression, body language) & auditory cues (intonation)
INVOLVES RIGHT HEMISPHERE! --> left-ear and left-visual field advantage for recognition of emotion;
right-hemisphere lesions impair recognition of emotions from facial expressions or hand gestures!
***RIGHT HEMISPHERE -> NEGATIVE EMOTION
LEFT HEMISPHERE -> POSITIVE EMOTION*** - 112James-Lange Theory of Emotion- emotional stimuli evoke physiological reactions, including muscle contraction
sensory feedback -> brain -> generate feelings
- supported by: Sweet's study of reduced emotional sensation to music in man whose sympathetic nerves were transected on one side of body;
& Hohman's study of emotions in persons sustaining accidental cord transduction - 113Cannon-Bard Theory- for evolutionary reasons, brain processes emotions immediately
- emotion is first felt, then action follows the cognitive appraisal
- ALMOST SIMULTANEOUS, perceiver will act
- thalamus and amygdala play central roles in perceiving emotion! - 114Schachter and Singer Theory- experience of emotions involves both physiological and cognitive processes
- exercise increases strength of emotions, especially after a period of time!
- PHYSIOLOGICAL & COGNITIVE!
- emotions driven as a combination of physiology and cognition; feeling & our interpretation of it
---> hot research assistant most attractive 15 mins after work out! there was still arousal, but people attributed it to the research assistant! - 115Facial Feedback Studies (Ekman)- facial features made, perceived, and the rest of the body follows
- different emotional expressions produced different changes in the autonomic NS activity;
- anger: increased HR and skin temperature
- fear: increased HR, but decreased skin temp
-happiness: decreased HR, no change in skin temp
**asked students to place pencil in mouth in two ways!**
CONSISTENT w JAMES-LANGE & SCHACHTER-SINGER - 116Anatomy of the Amygdala- Hypothalamus -> sympathetic
- parabrachial nucleus -> increase respiration
- nucleus accumbens -> reward pathway, motivation
- locus coeruleus -> vigilance
- trigeminal pathway -> facial fear
**damage to amygdala will no longer show preference for remembering emotion-laden events** - 117Input to the Amygdala- hippocampal formation: MEMORY
- periaqueductal gray matter: FREEZING BEHAVIOR
- sensory thalamus: SYMPATHETIC AROUSAL
**not always negative; show pref. for negative, but can also response to positive stimuli** - 118Fear and the Amygdala- threat stimuli inc. neural firing within central nucleus
- lesions of central nucleus diminishes emotional response to fear; red. fear, red. level of stress hormones, red. chance of developing ulcers to stress - 119Conditioning of Emotional Responses- pairing neutral stimulus with painful stimuli, over time, neutral stimulus will elicit an emotional response
- lesions to central nucelus of amygdala will ABOLISH CER
- same with bensodiazepines (GABA agonists) - 120Orbitofrontal Cortex- analysis of social situations;
- inhibitions & self-concern
- lesions -> inhibition of behavior and impair ability to have "appropriate" emotional response - 121Phineas Gagedynamite tamping rod penetrated orbitofrontal cortex;
exhibited reduced inhibitions and self-concern
"changed personality" - 122Ventromedial Prefrontal Cortexlesions impair ability to forsee positive and negative emotional consequences of behavior & inc. in utilitarianism;
trouble planning/following through with future-oriented plans
**patients with lesions shows decreased performance on Iowa Gambling Task**
- no skin conductance, did not experience "bad feelings" about deck - 123Dorsolateral Prefrontal Cortex- damage to LEFT dlPFC -> DEPRESSION
- damage to RIGHT dlPFC -> MANIA
- LEFT -> positive emotional affect
- RIGHT -> negative emotional affect - 124Aggressioninhibited by serotonin
damage to prefrontal 5-HT neurons inc. aggression
aggressive behaviors can be functional:
- gain access to mates
- defend offspring against intruders
also include:
- threatening gestures
- physical attack - 125Predation- NO SYMPATHETIC AROUSAL
- distinct from aggression
- involves an attack of a member of one species on another FOR FOOD! - 126Three Models of Emotion1. Borod Right-Hemisphere Model
2. Tucker Laterialization Model
3. Davidson Lateralization Model - 127The Borod Right-Hemisphere ModelONLY RIGHT HEMISPHERE PROCESSES EMOTIONS
looked mostly at negative emotions
- right cerebrum dominat in the expression and perception of emotion;
- visual stimuli from LVF processed within RH
- Ley and Bryden: when presented with neutral faces to LVF vs RVF, men were quicker and more accurate in identifying valenced faces in the LVF (negatively valenced faces)
- right cerebrum is dominant in emotional expression!!! - 128The Tucker Lateralization Model- Right Hemisphere dominant in negative affect processing;
- right hemisphere damage showed slower response to negative affects in emotion;
- BUT, damage to left hemisphere showed slwoer response to positive affect!!
- left-frontal strokes -> "catastrophic" reactions
- right-frontal strokes -> indifference - 129The Davidson Lateralization Model- left cerebrum is involved in APPROACH behavior
e.g. joy, happiness, positive interest, and ANGER!!
**anger is a NEGATIVE emotion that causes you to engage**
- right cerebrum is involved in WITHDRAW behavior
e.g. sadness, fear, and disgust
- e.g. depression is associated with left-frontal hypoactivation;
Robinson, Starr, and Price's stroke patients
- e.g. approach behavior is reduced in depression!
- e.g. mania associated with damage to right frontal pole! - 130Verbal Behaviors- talking
- understanding speech
- reading
- writing
- ALLOWS FOR SOCIAL INTERACTION!!
- are LATERALIZED!
**LEFT HEMISPHERE DOMINANT**
right hemisphere -> porosody & rhythm - 131Aphasiadeficit in ability to produce or understand language
NOT a result of lack of motivatio, or paralysis
**mostly results from damage to the left hemisphere** - 132Speech Production- just rostral to the mouth area of the motor cortex ==> BROCA'S AREA!
- discovered by Paul Broca, in 1861, after "Tan" stroke patient - 133Broca's Aphasia- slow, laborious speech
- spoken words have meaning, but just slow
- have difficulty with "function words"
- can comprehend the sppech of others
VERY FRUSTRATED!
results from damage to the inferior left frontal lobe;
can observe: aggrammatism, anomia, and difficulty with word articulation - 134Periaqueductal Gray Area- also associated with vocal output
- lesions in frogs produce no "ribbit" sound
- lesions of PGA causes mutism in humans ---> EXPRESSIVE APHASIA! - 135Speech Comprehension- located next to auditory cortex
WERNICKE'S AREA! right where temporal and parietal regions meet
- lesions -> Wernicke's aphasia -> cannot understand spoken or written language, and produced word salads! - 136Wernicke's Aphasia- damage to Wernicke's area (superior left temporal gyrus)
- poor speech comprehension (cannot do non-verbal tasks like, point to XYZ)
- cannot repeat statements made by others
- fluent, but meaningless speech!
- RECEPTIVE DEFICITS
- pure word deafness; can identify other sounds! can also understand PITCH (right lateralized)
- UNAWARE OF DEFICITS so NO FRUSTRATION! - 137Transcortical Sensory Aphasia- damage to posterior language area
- can repeat statements, but do not comprehend them!
- echolalia: enjoy repeating what is said to them;
- Wernicke's allows patients to recognize words; posterior language area allows you to COMPREHEND! - 138Conduction Aphasia- damage at the arcuate fasciculus, which connects Wernicke's area with Broca's area
- meaning gets there, but the sound doesn't!
- can't repeat non-words and complex sentences
- fluent, meaningful speech
THEREFORE, articuate fasciculus must conduct SOUND not meanings!!! - 139Pure Alexia- damage to posterior corpus callosum (splenium)
---> info from left visual field cannot transverse to left hemisphere bc splenium is damaged
- AND damage to left visual cortex
---> can't see from right visual field
therefore, person can write, but cannot read/write what he/she wrote - 140Two Reading Processes1. whole word
**damage here is MUCH MORE debilitating!**
2. phonetic coding - 141Acquired Dyslexiasproduced by brain damage in persons who were able to read;
- phonological dyslexia -> can read using the whole-word method; CAN understand words
**usually left frontal lobe damage, around Broca's**
- surface dyslexia -> deficit in whole-word reading; damage in left lateral/inferior temporal lesion (flexible fusiform area); can sound out words and understand then - 142Two Major types of Agraphia- disability involving writing
1. phonolgoical dysgraphia -> unable to sound out words to write them
2. orthographic dysgraphia -> can only write words by sounding them out! - 143Phonological Dysgraphiacan't sound out words
cannot write prounounceable nonwords
usually damage to Broca's area! - 144Orthographic Dysgraphiacan ONLY sound out!
can write easy words
usually damage to left visual word-form area!