Neuro4: Neurobiology Of Mental Illness

Front 1

Phrenology

Back 1

Study of attributing specific experiential functions to the brain

Neglects subcortical structures, anatomy, biology etc

Front 2

Psychiatry

Back 2

Psych: soul (literally last exhalation before death)

-iatry: discipline of treating/healing

Front 3

Body-Mind Dualism

Back 3

Mind structures determine body functoin (automatron, Descartes thought soul in pineal gland)

Front 4

Functional vs Organic

Back 4

Functional - problem has nothing physiologically abnormal which can be found (no apparent lesion)

Organic - IDENTIFIABLE chronic physiological abnormality (lesion)

Front 5

Phantom Limb cause

Back 5

Used to think functional problem due to things like grief

NOW know organic cause is SENSORY cortex that used to process the limb is now being laterally stimulated by the surrounding cortex

Front 6

Wilder Penfield contribution

Back 6

Electrically stimulated epileptic patients' brains to map human cortex

Homonculus, Superior temporal lobe (SOUND of familiar voices, music, memories)

Front 7

Depression electrostim treatment

Back 7

Brodmann's 25

NOT phrenology, anatomy is mapped

Front 8

Diseases that electrostim can treat

Back 8

Parkinson's (STN)
OCD
Depression

Front 9

How to distinguish hysterical pts vs faking with functional explanations

Back 9

fMRI to show lightup in brain

Front 10

What are "therapy" options for psychotherapy

Back 10

give a drug

administer talking therapy

give up and recommend

Front 11

OCD, Presentation, Anatomy change, Pathophysiology, treatment

Back 11

Obsessive-Compulsive Disorder

Presentation: stuck thinking about one thing or only a limited number of things

Anatomy: HYPERACTIVITY in the orbital-frontal cortex, ventral striatum (nucleus accumbens), medial thalamus, and cingulate gyrus

Pathophysiology: Changes in cerebral glucose metabolic rate

Treatment: SSRIs, exposure therapy (normalizes functional changes in brain areas). Exposure therapy just as good as medicine in terms of resolving functional errors in brain

Front 12

Psychiatry vs Phrenology view on functional distribution in brain

Back 12

Phrenology - ONE specific location for each function = wrong

Psychiatry - DISTRIBUTED functional network, no function solely in one part of brain and no one part of brain solely responsible for one function

Front 13

Direct vs Indirect path basal ganglia

Back 13

Direct - Cortex to (+) Striatum (D1 for SNpc) to (-) Medial globus pallidus and SNpr to (-) thalamus to (+) cortex - promotes movement

Indirect - Cortex to (+) Striatum (D2 for SNpc) to (-) Lateral Globus Pallidus to (-) STN to (+) Medial globus pallidus and SNpr to (-) thalamus to (+) cortex - inhibits movement

Front 14

Drugs extracted from plant alkaloids

Back 14

tobacco, coffee, cocaine

Front 15

Serendipity and drug discovery

Back 15

Discovering something by accident that were prepared to discover

ex. iproniazid, TB pts got happy which was a desired effect. usually a drug for something else discovering can be used for a desired therapy

Front 16

Psychosis symptoms often from ?, how do most anti-psychotic drugs work

Back 16

Most symptoms from NMDA receptor blocking (PCP, ketamine, other drugs do this0

MOST drugs are D2 blockers, potency related to ability to occupy receptor at low concentration

Front 17

NMDA receptor structure, blockers, facilitators

Back 17

4 subunits each with 4 transmembrane domains. Domain 2 forms the ion channel

Allows Na and Ca ion pasage

Normally glutamate binds and opens, Mg++ plugs. AMPA co activation (or other cell depolarization) leads to change in membrane potential in depolarization, Mg++ explusion and ion transfer

Blockers: PCP, keatamine, other drugs

Facilitators: glycine

Front 18

Dopamine receptor types

Back 18

D1/D5 - ACTIVATE Adenylate Cyclase

D2/D3/D4 - INHIBIT adenylate cyclase

Front 19

Gross anatomy use in psychiatry

Back 19

NONE, what matters is inter-neuronal organization, what's connected to what and in what way

Front 20

Dopamine supply to forebrain

Back 20

Ventral tegmental area to diencephalon and telencephalon

Front 21

Big Three monoamine neurotransmitters, general role, projection, function

Back 21

Dopamine, Norepinephrine, Serotonin

Generally ACTIVATING - mode/behavior is elevated (but not necessarily good since may be hypervigilant)

Low levels of any lead to lowered level of function

Projections: OVERLAPPING targets, work in concert

Function: "virtually hormonal" - no well-formed post synaptic apparatus but instead NT is exocytosed into interstitum to diffuse around

DIFFUSE effects as opposed to specific information (Glutamate or GABA)

Front 22

VTA and LC projections

Back 22

Ventral Tegmental Area - nucleus accumbens. Also PFC, CPu

Locus Coeruleus - Raphe nuclei, ventral tegmental area

Front 23

Depression body language

Back 23

leaning, head propped, mouth turned down, eyebrows arched

Front 24

Serotonergic system

Back 24

B7 (dorsal raphe) and B9 (ventral raphe) project throughout entire forebrain

Front 25

Addiction hallmark, why do people get addicted, anatomically significant areas

Back 25

NOT physical dependence but OBSESSIVE CONCERN for substance

Replaces normal reinforcers people respond to with a single or narrower range of reinforcers which gain an importance at the expense of other reinforcers

get addicted because good effects are immediate, bad effects are insidious and can be adjusted too at first, then it's too late


Anatomy: VTA, nucleus accumbens, medial prefrontal cortex, function as a group and are interrelated

VTA activity leads to nucleus accumbens Dopamine release implicated in stimulus salience (cue salience - brain more likely to pick out this stimulus above all others)

Front 26

Law of Positive Differential and Drug self-administration

Back 26

People will self-administer a drug if:

a) Bad before, makes them feel better after taking
b) OK before, GREAT after

In both cases feel worse after it wears off than before they started (contrast effect) leading to subsequent drug use

Front 27

Craving and Relapse Drivers, Problems

Back 27

Drivers - Drive, cue, cue salience, secondary reinforcement, urge, discriminative stimulus, incentive motivation, "temptation"

Getting pts to stop is hard, but not relapse is the hardest

Front 28

Occasions of sin

Back 28

catholic catechism

Environments in which a particular sin exists and by merely being in that environment more likely to sin (ie Las Vegas)

Front 29

Cue as a reward, incentive motivation

Back 29

Over time in addiction the cue (predictor) of whatever substance one is addicted to becomes a reward in itself

Actually the amount of release/high is closer to cues predictive value

ie. red light = alcohol, blue light doesnt in mice, mice get high from just the red light after addiction

In humans this cue salience & incentive motivation can come from paraphenalia, advertisements, seeing products, etc.

Front 30

Placebo effect is greatest for which psychiatric disorder

Back 30

DEPRESSION

doctor white coats, stethoscopes, etc are cues to pt that they will be helped. the anticipated effect of a drug has a healing value.

In fMRI same brain areas may light up or decrease with similar functional changes

May not start in same areas but effected areas or downstream areas may all be targeted

Subgenual cingulate is theorized to be tie in location with similar but not identical metabolic effects for drugs and placebo

Front 31

Bipolar disorder difference in wax/wane, Drugs

Back 31

All depression is wax/wane but when bipolar patients feel better they feel great in early clinical course

Drugs:

Lithium - targets GSK 3 (phosphorylates and dephosphorylates stuff)

Anti-convulsants (Carbamazepine)

Front 32

Oxytocin and Affiliation

Back 32

Voles that are monogamous vs promiscuous linked to oxytocin and vacopressin tone in ventral pallidum

HIGH tone = monogamous and social
Low tone = promiscuous and antisocial

SOLELY based on oxytocin, more complicated in humans

There was a molecular switch pre-wired in brain that can be switched on and off