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Neuropsychology 2307 Midterm#1 > Neuropsychology 2307 Midterm#1 > Flashcards

Neuropsychology 2307 Midterm#1 Flashcards

1
Q

Human Neuropsychology

A
  • The scientific study of the brain-behavior relationship with an emphasis on humans
  • employed by hospitals, rehabs, governm. etc.
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2
Q

Goal of Neuropsychology

A
  • how the nervous system functions lead to the emergnece of experience and behaviour
  • functional / anatomical relationship between different brain structures
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3
Q

Clinical Neuropsychology

A

Brain behaviour studies applied to diagnosis, rehab and long-term prognosis of abnormal brain-behavior relationships

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4
Q

Goal Clinical Neuropsychology

A
  • differential diagnosis of pathology
  • assess for dementia and associated conditions
  • affect TBI on cognition / behavior
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5
Q

Experimental Psychology

A
  • Assessment of CNS function using testing procedures requiring behavioural responses
  • Standardized testing
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6
Q

Valuable Skills to study Neuropsychology

A
  • scientific research
  • computer literacy
  • applications for testing
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7
Q

neurolinguistics

A

the neural mechanisms in the brain that control the comprehension, production, and acquisition of language

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8
Q

alexia

A

loss in the ability to read

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9
Q

agraphia

A

loss in ability to communicate through writing

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10
Q

la belle indifference

A

inappropriate lack of concern for the perceptions by others of one’s disability, usually seen in persons with conversion disorder

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11
Q

maximum number of items hold in short term memory

A

7

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12
Q

conversion disorder

A

(neurological) symptoms that can’t be explained by a neurological disease or other medical condition.

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13
Q

in vivo Neuroimaging Techniques

A
  • see structure and function of neuronal tissues
  • CT, MRI, PET, fMRI, SPECT
  • CT can show blood vessels and therefore show if there is an aneurysm or sub-arachnoid hemorrage
  • non-invasive / non-destructive
  • dTI (e.g. MRI) Tracks flow of water:

Measures direction and get picture of region of brain where water flow signal is large

travels on large tracs, axonal fibres

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14
Q

Tractography

A

Traces axon bundles through the brain in 3D

Mapping connection amongst brain areas

  1. Long connections - one lobe to another
  2. Relatively short connections - one part of lobe to another part same lobe
  3. Interhemisphereic connections: homotopic points (in “typcial” brain) and heterotopic points (in patients with Agenisis of Corpus Collosum AgCC) - missing part of CC
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15
Q

Connectional methods to link brain and behaviour

A

Connections to and from neurons or a given region of the brain using tracer substances (maps - non invasive)

MRI, fMRI, Diffusion Tensor Imaging

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16
Q

Correlational Methods

A
  • Make observations of brain activity while an individual performs a behaviour
  • Identify pathway and region whose activity correlates wtih the behaviour

Note: need to back up correlational study with causational study

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17
Q

Lesion Method

A
  • Study the effects of brain lesions
  • TBI, Stroke, Tumor, Infection, Degenerative disease
  • MRI maps out the lesions

Note: lesions can sprawl and include structures that are not involved

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18
Q

Stimulation Method

A
  • Stimulate the brain region or neural circuit and observe effects on cognition and behaviour
  • Transcranial magnetic stimulation
  • Transcranial direct current stimulation

Risk: can spread beyond target site

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19
Q

Franz Joseph Gall

A
  • Founded phrenology
  • Link between mental faculties and specific brain locations
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20
Q

Paul Broca

A

Broca’s area

Region in frontal lobe (usually left) with functions linked to speech production

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21
Q

Locating Cognitive Functions

Gunshot Wound Neurology / Mental Chronometry

A
  • Gunshot Wound: looked at functional loss associated with damage to that area
  • Chronometry: break down human tasks to see stages of information processing during timed task
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22
Q

Brain Metabolism for localization

A

measure relationship between function and structure by monitoring changes in brain metabolism

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23
Q

Golgi’s Stain

A
  • Used silver nitrate to stain slices of the cerebral cortex to see cellular level in the tissues
  • prove nervous system made up of individual cells
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24
Q

Cajal

A

Used Golgi’s method to show individual neurons

Neuron Doctrine; billions of discrete cells that communicate with each other

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25
Q

Fritsch and Hitzig

A

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

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26
Q

Galvanometer

A
  • record electrical activity in muscles and nerves
  • Heart - ECG
  • Eye - electroretinogram
  • Brain - electroencephalogram

Challenge: slow to respond

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27
Q

Lee Deforest

Audion

A

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

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28
Q

Oscilloscope

Hodgkin and Huxley’s observations of giant axon in squid

A

shows how signal voltages vary as a funciton of time

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29
Q

Darwin’s Theory of Evolution

A

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
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30
Q

Molecular Biology

A

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

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31
Q

Intervention in Brain Function

A
  • Behavioral - learning / experience
  • Physical - trauma
  • Surgical - remove tissue
  • Chemical - drugs, alcohol, chemicals
  • Electrical - electroshock, TMS
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32
Q

Wilder Penfield

A

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

“Montreal Procedure”

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33
Q

Ethics of Research on Humans and Animals

A

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

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34
Q

Signals in the Neuron

A

Signals within neurons are mainly electrical

Signals between neurons are mostly chemical

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35
Q

Biological Information Processing

A
  • Within cells: specialization of cellular organelles
  • Between cells: specialization of cell groups
  • Among multicellular organisms: society, civilization
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36
Q

Eukaryokes

A

Plant and animal cells

Selectively permeable plasma membrane

Different ionic concentrations of cytosol and ECM or interstitium

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37
Q

Transduction

A

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

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38
Q

Iinformation Processing from Within the Neuron

A

Done through the Dendrites, Soma and Axon

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39
Q

3 Main types of Neurons

A

Sensory, Motor, Interneuron

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40
Q

3 Ways Eukaryotes transfer ions across plasma membrane

A
  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
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41
Q

Active Transport

A
  • 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)
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42
Q

Interstitium / Extra cellular Matrix

A
  • Cells float in this
  • It is outside the cell
  • Help coordinate how the cells all relate to each other
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43
Q

Neuron-Astrocyte Cooperation

A
  • 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
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44
Q

Transmembranal Potential

A
  • 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)
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45
Q

Depolarization

A

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)
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46
Q

Hyperpolarization

A

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

  • inhibits Action Potentials
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47
Q

Action Potential

A
  • 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
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48
Q

Graded Potential

A
  • 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
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49
Q

Synaptic Transmission

A
  • 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
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50
Q

Integration of Signals

A
  • 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)
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51
Q

Channels

A
  • 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
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52
Q

Signals Between Neurons

A
  • Signals are chemical, chemicals called neurotransmitters
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53
Q

Neurotransmitters

A
  • 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
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54
Q

Rate Law

A

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

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55
Q

Action Potential Rate

A

number of action potentials produced per period unit time

“Spike” - single Action Potential

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56
Q

Where does the process begin to signal between neurons

A

At the synaptic bouton the process begins

It is a chemical process between neurons

57
Q

Synapse

A
  • 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
58
Q

Neurotransmission

A
  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)
59
Q

Binding Process

A
  • 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
60
Q

Synaptic Vesicles

A
  • Found in terminal boutons
  • Spheres
  • Hollow
  • Contain NT molecules
  • Don’t live long - hours
  • Constantly being recycle
61
Q

Release Zone

A
  • 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
62
Q

Post-synaptic receptor

A

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

63
Q

Neurotransmitter-dependent ion channel

A

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

64
Q

Types of Receptors

A
  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

65
Q

Types of Neurotransmitters

A
  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

66
Q

G Proteins

A

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

67
Q

Reuptake

A

Reentry of a NT once released by the terminal bouton

(comes back through the membrane, terminating its postsynaptic potential)

68
Q

Enzymatic Deactivation

A

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

69
Q

Autoreceptor

A
  • 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
70
Q

Neural Circuit Process

A
  • 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)
71
Q

Runaway Excitatory Process

A

Process where there are only ESPS’s caused by excitatory NT’s: would have a seizure or convulsion

Can’t control behavior, thought, sensation

72
Q

Spontaneous Action Potentials

A

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

73
Q

Neural Coding

A
  • 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
74
Q

Spatial Summation

Temporal Summation

A
  • 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
75
Q

Dynamic Range of a Neuron

A

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)

76
Q

Neuronal Integration

A

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)

77
Q

Nervous System Agent

A
  • Anything capable of changing the physiological condition of the processes of neural communication (typically a chemical or drug)
  • typically “dose dependent”
78
Q

Dose Response

A
  • 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
79
Q

Effects of NS Agents

A
  • 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
80
Q

Types of CNS Agents

A
  • 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
81
Q

Types of CNS Agents (cont.)

A
  • 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
82
Q

Types of CNS Agents (cont.)

A
  • 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)
83
Q

Agonists / Antagonists

A
  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
84
Q

Agonist

A

2 Types:

  1. Direct binding: bind to postsynaptic receptors. (Dopamine, apomorphine, nicotine)
  2. Indirect-binding: enhance NT actions by stimulating NT release (cocaine)
85
Q

Antagonists

A

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

86
Q

11 Ways NS AGents affect Neurotransmission

A
  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.
87
Q

11 Ways (cont.)

A
  1. 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

  1. 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
88
Q

11 Ways (cont.)

A
  1. Drug stimulates postsynaptic receptors: AGONIST, postsynaptic receptors, (Nicotine) increase effectiveness levels of the NT’s
  2. Drug blocks postsynaptic receptors: ANTAGONIST, acetylcholine receptors on postsynaptic membrane, Curare and Belladonna - no receptor to receive it so no ionic change
  3. Drug stimulates autoreceptor action: ANTAGONIST; presynaptic processes leading to NT prod. (apomorphine) inhibits prod. so reduces effect
89
Q

11 Ways (cont.)

A
  1. Drug blocks autoreceptor action: AGONIST, presynaptic processes leading to NT prod., Clonidine increase sysnthesis of NT (e.g. adrenaline)
  2. 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
  3. Drug inactivates acetylcholinesterase (enzyme): AGONIST, synapse (Physostigmine) enzyme can’t break down acetylcholine, more left in cleft, greater excitatory effect
90
Q

Delivery of NS Agents

A
  • 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!!!

91
Q

All CNS Agents MUST cross Blood-Brain Barrier

A
  • 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.)
92
Q

PHARME

A

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
93
Q

Drug Therapeutic Index

A
  • 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
94
Q

Drug Tolerance

A

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”
95
Q

development of (ASA)

A
  • 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”)
96
Q

Atropine

A

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
97
Q

Hormones def’n

A
  • 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)
98
Q

Hormonal Secretion

A
  • 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.)
99
Q

6 Steps Hormonal Signaling

A
  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

KNOW FOR EXAM

100
Q

Effect of Hormones on Body

A
  • 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
101
Q

Hormones VERSUS NT’s

A
  • 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)
102
Q

3 Stage hierarchical control by hormones

A
  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)
103
Q

Classes / Functions of Hormones

A
  • 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
104
Q

Homeostasis

A
  • 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
105
Q

Reproduction and hormones

A
  • Estrogen: primary female sex hormone (regulation and devp reprod. system, 2nd sex charac.)
  • Testosterone: gender develop / expression
  • Progesterone: steroid - menstural cycle, embryogenesis of humans
106
Q

Hormones and Stress Response

A
  • 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
107
Q

Stopping Stress Response

A
  • 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)
108
Q

Visual System and brain damage

A
  • 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
109
Q

Specialists

A
  • 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
110
Q

Treatment of Vision Loss

A
  • neuropsychol studies higher level losses in visual perception (i.e. higher than regino-geniculo-cortical pathway)
111
Q

3 Categories Function Tests

A
  1. Central vision
  2. Whole field sensitivity
  3. Higher level visual perception (attention, visual search, object recognition, visually guided reaching and manipulating)
112
Q

Color vision

A
  • 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
113
Q

Cortical Visual Streams

A

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)
114
Q

Types of Visual Agnosia

A
  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”
115
Q

Spatial Neglect

A
  • 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)
116
Q

Colour Agnosia

A
  • 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
117
Q

Dorsal Stream Deficits

A
  • 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)
118
Q

Dorsal Stream Vulnerability

A
  • 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
119
Q

Disconnection Syndromes

A
  • 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
120
Q

Visually Evoked Potentials (VEP’s)

A
  • 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
121
Q

Non 24 Circadian Rhythm Disorder

A
  • 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
    *
122
Q

Specialists for auditory system

A
  • 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
123
Q

Hearing Loss

A
  • 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
124
Q

Tests for hearing function

A
  1. Peripheral Auditory System Function (typically threshold tests) - psychophysical method
  2. Sound localization and lateralization
  3. Higher level auditory perception tests
125
Q

Audiometry

A
  • 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)
    *
126
Q

Audiogram

A
  • 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
    *
127
Q

Auditory-evoked Potentials (AEPs)

A
  • 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
128
Q

Causes Hearing Loss

A
  • 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)
129
Q

Central Hearing Losses

A
  • 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
130
Q

Electronic Implants / Cochlear Implants

A
  • 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
131
Q

Touch

A
  • 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
132
Q

Receptors in Skin versus other

A
  • 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
133
Q

mechanoreceptor

A
  • sensory receptors that are triggered in response to movement, stretch, pressure or vibration
134
Q

thermoreceptor

A

somatosensory receptors that convey information about temperature

135
Q

nocireceptor

A

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

136
Q

Proprioception

A

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

137
Q

muscle spindles

A

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

138
Q

golgi tendon organ

A
  • 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 (1 decks)

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