Neuropsychology 2307 Midterm#1 Flashcards

Question

Fritsch and Hitzig

Answer 1

Electrically stimulated dog's brains to identify what is now the area called the primary motor cortex

Answer 2

* record electrical activity in muscles and nerves * Heart - ECG * Eye - electroretinogram * Brain - electroencephalogram Challenge: slow to respond

Answer 3

Developed an amplifier to be able to better record small electrical signals

Answer 4

shows how signal voltages vary as a funciton of time

Answer 5

Natural Selection * structural and functional characteristics that allow an organism to reproduce more successfully are passed on to offspring * characteristics the become more prevalent in species

Answer 6

Localize where and understand how the DNA of a genome gives rise to normal and abnormal neural tissues

Answer 7

* Behavioral - learning / experience * Physical - trauma * Surgical - remove tissue * Chemical - drugs, alcohol, chemicals * Electrical - electroshock, TMS

Answer 8

Used electrical stimulation to map the cortical functions of awake epilepsy patients during a craniotomy "Montreal Procedure"

Answer 9

Must be humane and worthwhile; need "ethical approval" from the American Psychological Association (e.g.)

Answer 10

Signals within neurons are mainly electrical Signals between neurons are mostly chemical

Answer 11

* Within cells: specialization of cellular organelles * Between cells: specialization of cell groups * Among multicellular organisms: society, civilization

Answer 12

Plant and animal cells Selectively permeable plasma membrane Different ionic concentrations of cytosol and ECM or interstitium

Answer 13

Ability to sense the environment through muscles, glands and neurons and create electrical signals which convert to the release of neurotransmitters to respond to the information

Answer 14

Done through the Dendrites, Soma and Axon

Answer 15

Sensory, Motor, Interneuron

Answer 16

1. Diffusion: ions and molecules move from area of higher to lower concentration 2. Facilitated Diffusion: Proteins embed in plasma membrane and are "gated" by ligands, mechanical force or voltage 3. Active Transport: proteins use ATP to pump the ions through the plasma membrane (sodium/potassium pumps) - every cell has one

Answer 17

* ATP pumps ion through the membrane * Each cycle pumps 2 + potassium ions in and 3 + sodium ions out so net charge is negative voltage across membrane * 100's and millions of these pumps along membrane * -50 to -70 mv inside cell (resting potential)

Answer 18

* Cells float in this * It is outside the cell * Help coordinate how the cells all relate to each other

Answer 19

* Astrocytes can make, store and relese glycogen * When Glucose molecule oxydizes it makes ATP * ATP proveds the energy for the neuron * Neurons use 3x as much ATP as other eukaryotes

Answer 20

* Voltage difference across the cell membrane * typically about -70mV * Neurons **change the voltage difference** to be able to signal by adding or subracting ions * (Change the **ionic permeability** of the plasma membrane)

Answer 21

**Depolarization**: * change the ionic concentration to a "less negative number" - i.e. more towards zero * as it heads towards zero it is likely to produce an Action Potential and be an Excitatory Post Synaptic Potential (EPSP)

Answer 22

Concentration across post synaptic membrane to a more negative number (further away from zero) * inhibits Action Potentials

Answer 23

* Spikes of electrical signals along axons that starts at the axon hillock and can contiue over a long distance * It is how neurons send messages; in the resting state not information is being sent, not communicating * **Less subject to degradation** * **All or none** ballistic process and stays same (same shape, same amplitude); only the rate of production changes

Answer 24

* Can be either excitatory or inhibatory * Signal amplitude is proportional to the stimulus intensity * Used mostly for grey matter or for signals that do not have to travel a long distance * Are more subject to **degradation** * Message will become distorted if long axon

Answer 25

* changes the electrical properties of the receiving neuron (post-synaptic potential PSP) * changes the permeability of the Post. Syn. Membr. * bind to receptors that are gated

Answer 26

* Receiving neuron **integrates** received signals in dendritic tree (from all arbors) * If IPSP and EPSP add to 0 then no net result * Has to exceed the "threshold of excitation" to force open enough voltage gated channels to depolarize a membrane (usually about -55mV)

Answer 27

* Voltage gated channels change the membrane potential * Voltage gated sodium channels open first * Potassium channels open next to allow potassium out * Returns to resting * Voltage gated calcium channels are activated by signals along the membrane; once the channels are activated they cause the NT's to migrate to the pre-synaptic membrane

Answer 28

* Signals are chemical, chemicals called neurotransmitters

Answer 29

* chemical synthesized in transmitting neuron * able to bind to receptors on receiving neuron * able to decompose in synaptic cleft (enzymatic) * able to bind to receptors on presynaptic membrane, causing the NT release * NT's can also bind with autoreceptors in the pre-synaptic membrane (to shut off the dumping of NT's into the cleft) - usually G protein receptors

Answer 30

Only way Action Potentials can be used for signalling is to vary the **number produced** over time (because all same shape and size)

Answer 31

number of action potentials produced per period unit time "Spike" - single Action Potential

Answer 32

At the synaptic bouton the process begins It is a chemical process between neurons

Answer 33

* Last place in the neuron that electrical activity is able to have any influence * millions of synapses within a cubic millimetre * Any synapse will be excitatory or inhibatory

Answer 34

1. NT is synthesized from precursors 2. NT are stored in vesicles 3. Those NT that leak from vesicle are destroyed by enzymes in cytosol then recycled 4. AP causes teh vesicles to fuse with the pre-synaptic membrane & release NT into synaptic cleft 5. Released NT's bind with receptors on post-synaptic membrane 6. Signal is created via the binding process 7. Deactivate any NT's that don't bind (reuptake, enzymatic degradation)

Answer 35

* Ions flow into cytosol of receiving neuron on to the dendritic tree * Each signal (either an EPSP or IPSP) is a local graded post-synaptic potential, which are then all integrated at the hillock * Can have both IPSP and EPSP signals and sum will determine whether there is hyperpolarization or depolarization * If net sum is more towards zero then more likely to result in an AP being produced * If no binding, no transmission, no flow information

Answer 36

* Found in terminal boutons * Spheres * Hollow * Contain NT molecules * Don't live long - hours * Constantly being recycle

Answer 37

* Pre-syanptic zone * Omega figure on the membrane * interior of the presynaptic membrane to which synaptic vesicles attach to relase their NT's into the synaptic cleft

Answer 38

A receptor molecule in the post-synaptic membrane of a synapse that contains a binding site for a neurotransmitter

Answer 39

Ion channel that opens when a molecule of a neurotransmitter binds with a postsynaptic receptor

Answer 40

1. Ionotropic Receptor: contains a binding site for an NT and and ion channel that opens when a molecule of the NT attaches to the binding site (DIRECT) 2. Metabotropic Receptor: binding site for the NT activates an enzyme that produces a chemical reaction (via G Protein) causing an ion channel elsewhere in the membrane to open when the molecule of the NT binds to the site (INDIRECT) Note: the shape of the transmitter matches the shape of the receptor

Answer 41

1. Monoamines - dopaine, epinephrine, serotonin, melatonin, etc. 2. Amino acids - gluamate, aspartate, GABA 3. Peptide NT's - cholecystokinin, somatostatin, etc. 4. Gases (act as NT's) - Nitris oxide, carbon monoxide some of these in sufficient quantities are toxic

Answer 42

convey the chemical messages that activate the enzymes that open the ion channels Note: a second messenger (chemical produced when the G protein activates the enzyme) carries the signal that opens the ion channel

Answer 43

Reentry of a NT once released by the terminal bouton (comes back through the membrane, terminating its postsynaptic potential)

Answer 44

Destruction of a NT by enzyme after it has been released into the cleft (e.g. breaks down the NT) Important that they be destroyed if they do not bind so they don't migrate and bind elsewhere

Answer 45

* Receptor molecule located on the **pre-synaptic** membrane of a neuron that bind to its own NT * shuts down the release of NT in the presynaptic neuron (negative feedback) Why? * regulate the internal cell processes * regulate synthesis of NT and release of NT * Basically: inhibit the activity of a transmitter

Answer 46

* Circuits that produce cyclical activity * Called "reverbatory" circuits * circuits can be complex (cortex) or simple (spinal cord) * signal passes through a series of neurons then back to originator * not really aware of the present due to the delay in neural transmission ("now" is 100 milliseconds old)

Answer 47

Process where there are only ESPS's caused by excitatory NT's: would have a seizure or convulsion Can't control behavior, thought, sensation

Answer 48

Most neurons elicit 5-10 spikes / second which is just noise but NOT information (does this in resting state)

Answer 49

* Neurons that can integrate EPSP's and IPSP's * Sparse coding saves energy * Can NOT integrate AP's but they can be propogated down axon to AP's on other axons * The inhibitory and excitatory PSPs summate and control the firing rate in the neuron * If EPSPs too far apart: 1st one dies away * If EPSPs close: sum together and exceed threshold needed to create AP

Answer 50

* Spatial: Sum of PSP's (e.g. EPSP's) from multiple neurons (may be enough to push it over the threshold and create an AP) * Temporal: many EPSP's generated at the same synapse

Answer 51

How much information a neuron can carry within a unit of time The dynamic range will be limited by the neuron's ability to create AP's Neuron has a max production rate of 100 spikes / second (resting 5 spikes / sec)

Answer 52

AP production is a function of the SUM of ALL actions from all receptors on post synaptic membrane **(taken over a limited time interval AND limited spatial region)**

Answer 53

* Anything capable of changing the physiological condition of the processes of neural communication (typically a chemical or drug) * typically "dose dependent"

Answer 54

* Functional relationship between the dose level of a drug and the drug's effect on the nervous system and/or other tissues * ED50 = effective dose * TD50 = dose at which 50% sample show toxicity * LD - lethal dose

Answer 55

* Therapeutic effects: intended consequences on NS of a NS agent * Side Effects: effects not related to the purpose of taking the drug * Contraindications: negative side effects * Placebo effect: psych response that can enhance the therapeutic effect (esp wrt pain), stronger when intervention more invsie so tease part the therapeutic effect from placebo effect for eff. dose

Answer 56

* Narcotic analgesic: act on sigma and mu receptors in body to DECREASE perception of pain * Non-narcotic analgesic: reduce level of prostaglandin synthesis to DECREASE inflammatory response * Cholinergic: increasing or decreasing amts of available acetylcholine or acetylcholinesterase * Adrenergic: affects Sympath. NS - promotes or depresses alpha and/or beta responses

Answer 57

* CNS stimulants: INCREASE available amt NT norepinephrine to INCREASE AP production * Anti-convulsant: increases sodium ion evactuation or prevent its entry into cell, elevates GABA or DECREASES acetylcholine levels * Sedatives/hypnotics: reduce activity in thalamus and cortex so can gate the info out; reduce arousal level * Anti-depressants: either 1)increase norepinephrine &seratonin in brain or 2) inhibit prod. of MAO which breaks down the NT's - SSRI's -inhibit reuptake so more of it is still in the synapse, increasing potency

Answer 58

* Antipsychotics: block dopamine receptor (D4) sites in brain or decrease responsiveness of medulla * Anxiolytics: alter responses in limbic center OR increase GABA levels * Psychedelic: alter cognition and perception (typically as seratonin receptor agonist)

Answer 59

1. Agonists: drugs that increase the rate of synaptic communication via NT - increase the likelihood of an Action Potential 2. Antagonists: drugs that decrease rate of synaptic communication via NT - decrease the likelihood of an Action Potential

Answer 60

2 Types: 1. Direct binding: bind to postsynaptic receptors. (Dopamine, apomorphine, nicotine) 2. Indirect-binding: enhance NT actions by stimulating NT release (cocaine)

Answer 61

2 Types 1. Direct-acting: block NT from binding to the receptors (**Atropine**) 2. Indirect-acting: inhibit release or production of NT (**Reserpine**) So: less NT in cleft and less chance of an ESP and less chance therefore of an AP

Answer 62

1. _Drug substitues for precursor involved in production_ of NT dopamine, norepin., epin. (in **terminal bouton**) where NT is synthesized - **AGONIST / L-DOPA** 2. _Drug inhibits prod. of NT_ by precursor chemical (**ANTAGONIST - in presynaptic processes) Fenclonine or PCPA** - inhibits tryptophan (prouces serotonin) - overdose perm inable to produce serat.

Answer 63

3. _Drug prevents storage of NT in vesicle:_ **ANTAGONIST, in presyn. processes in cytoplasm (Reserpine),** blocks moanamine transporter _4. Drug stimulates release of NT in vesicle:_ **AGONIST, presyn. membrane (Latrotoxin)** - too much, convulse 5. _Drug inhibits release of NT:_ **ANTAGONIST, presyn. processes leading to NT prod. (Botulinum toxin)** blocks nerve impulses, causes paralysis of muscles, no excit. pot on post-syn. membrane

Answer 64

6. _Drug stimulates postsynaptic receptors_: **AGONIST,** **postsynaptic receptors, (Nicotine)** increase effectiveness levels of the NT's 7. _Drug blocks postsynaptic receptors:_ **ANTAGONIST, acetylcholine receptors on postsynaptic membrane, Curare and Belladonna** - no receptor to receive it so no ionic change 8. _Drug stimulates autoreceptor action:_ **ANTAGONIST; presynaptic processes leading to NT prod. (apomorphine)** inhibits prod. so reduces effect

Answer 65

9. _Drug blocks autoreceptor action:_ **AGONIST, presynaptic processes leading to NT prod., Clonidine** increase sysnthesis of NT (e.g. adrenaline) 10. _Drug blocks reuptake of NT in synapse:_ **AGONSIT, synapse, (Cocaine)** leaves more dop, serot and nor in cleft to bind to recept of postsynap. so more potent signal 11. _Drug inactivates acetylcholinesterase (enzyme):_ **AGONIST, synapse (Physostigmine)** enzyme can't break down acetylcholine, more left in cleft, greater excitatory effect

Answer 66

* Orally (convenient, safe) * Injection in to nervous tissue (most effective) * Intramuscular inj. * Inhalation (cocaine) - fewer barriers on way to brain * transdermal patch (nicotine, fentanyl) * I.V. infection / Intrathecal inj. * Anal suppository MUST cross the blood-brain barrier to be effective!!!

Answer 67

* in meninges junctions of endothelial cells (astrocytes) that make brain capilleries are tight so only allow small, non-ionized molecules to pass thru capillery wall * need Active transport (ATP, sodium/pot. pump) can convey larger molecules (glucose, amino acids, etc.)

Answer 68

Pharmacy Industry * billion $ to create a drug by time get FDA approval * 10-15 yrs. to do, so want investment protected once patented so drugs expensive * OHIP drugs are vetted, assessed as well so $$ * compare that to: STREET DRUG - wholesaler buys drug, dilutes it with "something", no regulation, no research, no scientific rigor. * not all PHARME drugs perfect - sampling error

Answer 69

* need to determine therapeutic and toxic dose of drug (typically done with experimental animals) * need to determine the operational definition of what is a "toxic dose" - ideally want a large ratio of therapeutic to toxic side effect (lg buffer) * Example of small ratio drug? Chemotherapy, alcohol * Diazepam small - 100 (toxic) to 1 (therapeutic) * the smaller the toxic index (TI) more careful have to be

Answer 70

gradual increase in the effective dose of a drug * with repeated exposure the effective dose of a drug creeps up towards the toxic dose (TI shrinks) * once TI so small, tiny change dose can result death (e.g. heroin) * if give schiz. patient much antagonist and inhibit dopamine too much can get Parkinson's symptoms) * Goldilocks principle: get dose "just right"

Answer 71

* invented to treat stomach cramps from Aspirin * acetelated the acid in Aspirin a made ASA (buffers) * so...started acetelating other things like morphine * (had "heroic effect" - Heroine) * used treat TB (suppressed coughs) * used in baby colick remedies BUT ppl saw had to keep taking more (become "tolerant") so needed to buy more so collected scarp metal for $ (term "junkie")

Answer 72

Agonist used by opthamologists * freezes eye, dialte pupil * (nightshade has Atropine in it) * used as cosmetic to drop near eye - dilated pupils thought to be sexually attractive * now air brush models to have larger pupils

Answer 73

* Molecules produced by glands and sent into the bloodstream or the air * **Broadcast** versus narrowcast (don't know exact location of receiver * effects orgnans that have receptors the hormones can bind to)

Answer 74

* Endocrine: hormones secreted directly into bloodst. thorugh fenestrated capilleries * Exocrine - hormones secreted via ducts * Paracrine - hormones diffused through E.C. Matrix to close (fluid in E.C.M. barely moves) target tissues * Pheromone - hormones "broadcast" into environm.(typically into air; \* capable of inter-NS commun.)

Answer 75

1. Biosynthesis of hormone in a tissue 2. Hormonal storage and secretion 3. Transport of hormone to target cell 4. Recognition of hormone by assoc. cell membrane or receptor 5. Relay and amplification of received signal through transduction or binding 6. Breakdown of hormone ## Footnote **KNOW FOR EXAM**

Answer 76

* Stimulation or inhibition of growth * Regulation of circadian shythms * Mood * Programmed apoptosis (cell death) * activation or inhibit. of immune system * regulation of metablolism * Prep body for mating, fighting, metamorph(insects) * reproduction * hunger regulation * sexual arousal

Answer 77

* Hormones can signal over longer distances * Homonal signals are "omnibus" (travel all over) / NT's are restricted to axonal tracts * Neural signals are MUCH faster (milliseconds) * NT is "all or none" (binds or not) vs hormonal - continuously variable and dependent on concentration (which increases prob. of binding)

Answer 78

1. Sensory - (light/touch eg) - produces neurohormones in hypothalamus that enters pituitary (hypophysis) 2. Pituitary gland secretes scondary hormones into circulatory system - travel thru body 3. Circulating hormones act on target organs in body and brain structures (feedback for more release like reuptake/feedback loop in synapse for NT's)

Answer 79

* **Steroid:** (testost, cortisol) - fat soluble, synthes. from cholesterol; affects DNA in target cell * **Peptide:** (insulin, endorph.) - manufactured by cell DNA; binds to metab. receptors on cell membrane generating G Protein which sends out 2nd messeng. to affect permeability

Answer 80

* regulate physiological systems (hypothalamus) - e.g. digestion, circadian shythms, core body temp which is imp. for ATP production * **Melatonin:** (hormone) - secreted by pineal gland - regulates other hormones, circadian rhythm

Answer 81

* Estrogen: primary female sex hormone (regulation and devp reprod. system, 2nd sex charac.) * Testosterone: gender develop / expression * Progesterone: steroid - menstural cycle, embryogenesis of humans

Answer 82

* secretion of glucocorticoids - carb & protein metab., blood sugar levels - F or Fl. 2 WAYS: * FAST: Hypothalaums to Spinal Cord to activate Symp. Auton. NS - stimulate Adrenal, relase epineph into bloodstream (hormonal response) - activate endocrine * SLOWER: Hypothalamus release of Corticotrophin into pituitary which releases Adreno-Cortico-Trophic (ACTH) into adrenal gland - release cortisol (easily measured in saliva) into blood which THEN activates endocrine

Answer 83

* Hippocampus regulates prod. of cortisol vis negative feedback loop - lots cortisol receptors then inhib. at hyptothalamus * prolonged stress: prolonged exposure of hippocampal neurons to cortisol (destroy or less functional) - reduce brain's ability to shut off cortisol (chronic state arousal - linked to PTSD)

Answer 84

* any brain damage - not unusual for there to be an associated visual symptom (why? neural infrastructure all over brain) * most tissues react to visual stimulation

Answer 85

* Optometry: anterior part eye ball, eye's optics * Ophthalmology: docs who diagnose and treat diseases of eye * Neuro-opthalmology: docs who treat diseases affect neural part of periph. visual system, central disorders * Neuropsychology - e.g. visual agnosias (can recognize location of object and interact but can't name it) - damage in inferotemporal lobe

Answer 86

* neuropsychol studies higher level losses in visual perception (i.e. higher than regino-geniculo-cortical pathway)

Answer 87

1. Central vision 2. Whole field sensitivity 3. Higher level visual perception (attention, visual search, object recognition, visually guided reaching and manipulating)

Answer 88

* might have caused some evolution (eg see fruit ripe, reach for it...etc.) * deficiencies: (test for) - Muscular Distrophy, Hemophelia located same region) * **Perimetric field tester**: find visual field defect which is key as test might indicate where a lesion is in brain on occipital cortex so **typical neurological psych test** * NOT JUST VISION / NO VISION - whole variety of functions

Answer 89

Info into occipital pole then forms 2 streams: 1. Vetral Stream: object perception and recognition; disorder: Agnosias (inability to name an object)' confrontation test: describe object spec. & generally 2. Dorsal Stream: object manipulation and visually-guided reaching; disorder: Apraxias (name "cup" but can't manipulate it)

Answer 90

1. Apperceptive: can't perceive whole when presented with the parts 2. Simultagnosia: can't perceive more than one object at a time; bilateral damage to occipital lobes 3. Asociative: can't link perception to knowledgebase (e.g. prior experiences) 4. Prosopagnosia - can't identify faces (normal perception is "orientation specific" so looking at something upside down can throw you off) 5. Landmark: can't use environment for "wayfinding"

Answer 91

* failure to report, respond or attend to stimuli or events in the hemifield contralateral to a brain injury * patient often unaware of the deficit * 4 tests: * Line Bisection * Cancellation * Spontaneous drawing or copying * Mental Imagery (memory colour neglect)

Answer 92

* inability to name colours and/or to sort into grps of same colour * "central" colour blindness: complete loss of colour perception * colour anomia: can't name colours but can answer a verbal question re a colour * specif-colour aphasia: can't answer the verbal quesitons about colour * Colour Neglect: see colour only on one side

Answer 93

* inaccurate visually-guided reaching (can't grasp things) * inaccurate visually-guided fixation - can't pick something out of larger field of vision (i.e. crowd) * difficulty walking on uneven ground * difficulty switching between two visual tasks * bumping into obstacles when talking while walking (and you are NOT looking down at the time)

Answer 94

* Williams Syndrome - poor performance on visuo-spatial and constructional tasks * deletion on Chromosome 7 * hemiplegia (loss of use of legs) * autism * developmental dyslexia * fragile X

Answer 95

* damage to white matter connections between brain parts * hard to perform complex functions like guy who could write something down but not read it back from the page

Answer 96

* electrical responses from diggerent generators within visual system * even though recorded through scalp, get rapid signals so better than fMRI which is slower * caused by visual stimuls (like checkerboard with alternating color swap) - light stimulus * read from an EEG * commonly used to test for MS * looks at visual pathway from eye, along optic nerve to the brain * used more for central vision function and to detect any damange on afferent visual pathway

Answer 97

* damage to retinohypothalamic tract which is involved in circadian rhythms of mammals * daily delays in sleep onset and wake times * common in people who are totally blind *

Answer 98

* audiology: hearing testing, hearing aids * otolaryngology: conductive and sensorineural nearing losses * Speech therapist: develop. hearing issues that affect the ability to acquire and use speech * Neuropsych: auditory neglect (e.g.) and other higher level auditory dysfunctions

Answer 99

* outer, inner and middle ear: ENT or audiologist * cochlear implants: surgical ENT * nerual: neuropsych (for high level losses in auditory perception in concert with other issues) and speech therapy

Answer 100

1. Peripheral Auditory System Function (typically threshold tests) - psychophysical method 2. Sound localization and lateralization 3. Higher level auditory perception tests

Answer 101

* checks the minimum energy necessary to detect the presence of a sound (psychophysical method), requires patient participation * plainly: test ability to hear sounds * Pure Tone Audiometry(PTA) test hearing of both ears (detect tone in headphones and tap corresp. ear) *

Answer 102

* used to measure loudness and pitch * vertical axis (decibels) is quiet (up at zero) and loud (as numbers get higher closer to x ahoriz. axis) * horiz. axis is pitch (herz) from low (left) to high (right) * normal hearing - soft sounds at -10 to +20 db, severe loss is between 71db and -95 db., profound loss is greater than -95db *

Answer 103

* used to diagnose cause of hearing losses and to test patients who may not be able to perform behavioural rests (babies) * tests for nervous system disorders as well * detects electrical activity in the cochlea and in the auditory pathways in the brain

Answer 104

* Conductive Hearing Loss: anything that affects conduction of sound to the cochlea (can even be wax in ears) * Sensorineural Hearing Loss: factors affecting transduction of acoustic energy to neural response in cochlea (so root cause lies in inner ear or cochlea or vestibulocochlear nerve - cranial nerve VIII or other neural part)

Answer 105

* factors affect receipt and coding of sound and interpretation of signals from auditory nerve * Auditory Agnosia: unable to recognize or identify sounds despite normal peripheral hearing test * Aud./Verbal Agnosia: pure word deafness * Receptive amusia * Cnetral Aud. Process. Disorder - disconnect between what is heard and what is understood; can interpret sounds differently esp. if room noisy or complex information - language-learning impairment

Answer 106

* somc devices can restore partial hearing for profound hearing loss (can't use hearing aid) * device is implanted in the inner ear or auditory cortex and activated by device worn outside ear * cochlear: $40 - $60,000 (adults eligible for one, babies for 2) * uses around 24 electrodes so okay for speech improvement but not sensitive enough for music appreciation

Answer 107

* For humans, touch is critical * if not touched can lead to psychosis and other emotional disorders * 2 types of skin: Hairy skin and Glabrous skin * Hairy Skin: more sensistive to pressure * Glabrous skin: on palms, soles of feet; no hair follicles

Answer 108

* WAY more receptors in tip tongue, fingers, than all of skin * greatest density of mechanoreceptors is in mouth, hands, lips, cheek, nose as compared to other areas of skin

Answer 109

* sensory receptors that are triggered in response to movement, stretch, pressure or vibration

Answer 110

somatosensory receptors that convey information about temperature

Answer 111

somatosensory receptors that convey information about pain in response to tissue damage

Answer 112

aspect of somatosensation that monitors the position and movement of the parts of one's own body

Answer 113

somatosensory receptors embedded in the muscle that sense the length of the muscle and prevent the muscle from being overstretched

Answer 114

* somatosensory receptor embedded in tendon that connects the muscle to the bone, and senses changes in muscle tension * prevents tension or force from damaging muscle

Neuropsychology 2307 Midterm#1 Flashcards

(138 cards)