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Exam 2 Flashcards

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1
Q

Who (1817-1868) declared that mental disorders were disorders of the brain?

A

Wilhelm Griesinger

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2
Q

Early 1900’s Freud claimed disorders arose from…

A

subconscious mind

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3
Q

What was going on in the 1930’s?

A
  1. Institutions were overflowing with severely mentally ill. Overcrowding.
  2. Rise in severe mentall illness attributed to great depression/WW2
  3. Psychosurgury took root
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4
Q

What was going on in the 1950s and later

A

Psychopharmacology

But sedation not treatment. Zombification, didn’t treat the disorder

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5
Q

Tranquilizing Chair

A

Benjamin Rush. American psychiatry.

Logic: claming and restraining the patient will help. Shock and shake back to sanity

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6
Q

Hydrotherapy and Wet Pack

A

Spray with water to stimulate.

Wrap in wet sheets.

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7
Q

Hot boxes and Lamps

A

Set to 98 degrees
Done to relax patients

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8
Q

How did insulin therapy work?

A

Dangerous and ineffective.
Dr Manfred Sakel

Give insulin to drop blood sugar and induce coma. Convulsive reaction

Wet shock: sweating and drooling
Dry Shock: full brain seziure

Use Glucose to bring out of induced coma
Intravenous injection of metrosol produced grand mal seizures

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9
Q

York Retreat

A

The Retreat opened in 1796 in the countryside outside York. Unlike mental institutions of the time, there were no chains or manacles, and physical punishment was banned. Treatment was based on personalised attention and benevolence, restoring the self-esteem and self-control of residents.

An exception of the time

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10
Q

What happened at July 1935 Second International Neurological Congress in London?

A

Dr. John Fulton showed bilateral resections of prefrontal cortex on chimps reduced aggressiveness (but were also devoid of emotional expression)

Said chimp’s IQ was still fine

Temperament negatively changed. Chimps would sake and kick, pull hair, urinate/defecate, but remoee the whole prefrontal cortex: now docile. Prefrontal cortex is temperament.

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11
Q

Who saw John Fulton at the conference and decided to start lobotomizing people right away?

A

Egas Moniz in 1935

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12
Q

Who nominated Egas Moniz for the nobel prize?

A

Walter Freeman

Prize won by Egas in 1949

Freeman popularized lobotomy in US

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13
Q

What connections did a lobotomy severe?

A

Connections between the prefrontal cortex and thalamus

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14
Q

What else did Freeman do?

A

Brought surgeon James Watts into his operation.

Created transorbital lobotomy

He thought 20-30% rates was good, even if people died. Still a win.
~3000 lobotomies between 1930-1950

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15
Q

Describe a lobotomy

A

Ice pick, shove through nose, break through thin bone, swirl around, severe white matter between prefrontal cortex and thalamus in less than 10 minutes. 25-30 procedures a day.

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16
Q

Rosemary Kennedy in 1941

A

Not successful surgery. Ended up incontinent. Impacted intelligence. Ended up hospitalized the rest of her life.

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17
Q

The fall of Freemen in the 1960s

A

1960’s lobotomy was highly reduced, complications, disappointing results, use of medication, societal shifts.

Medical license stripped, did lobotomy on same person 3x until she died.

Long term follow up of Freeman’s patients with schizophrenia showed 73% hospitalized again.

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18
Q

What does a lobotomized brain look like?

A

Brown discoloration over posterior aspect of right frontal lobe.

Mild bilateral atrophy of frontal gyri

Ablation of frontal white matter

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19
Q

Why did some people actually think lobotomies were humane?

A

Lack of effetive psychopharmacology
Overcrowding and sub-par conditions fo asylums
Social/financial burden of illness
mistreatment of patients

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20
Q

What two things can we take away from lobomoties?

A
  1. Follow up studies in patients are crucial
  2. Randomized controlled trials are gold-standard
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21
Q

Psychosurgury today

A

Not reversible, but viable today for some individuals

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22
Q

ECT today

A

session of ECT viable therapy, success to it. Require patients to have chronic severe drug resistant fail all conventional treatments. Severe depression. In 1 trial, 75% had some benefit.

Decision made by committee of physicians

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23
Q

How is ECT hypothesized to work?

A

Reboot computer, change brain chemistry/blood flow and how regions communicate

Changing syntaptic efficiency. More GABA released that can inhibit negative and perseverative throughts.

Long terms studies suggest memory not significantly affected, but some difficulties. Doesn’t outweigh no function or suicide.

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24
Q

Anterior Cingulotomy

A

Treats OCD

Cuts fibers between dorsal ACC and OFC, amygdala, Hippocampus (HC?)

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25
Q

Anterior Capsulotomy

A

OCD

Cut connection from OFC, subgenual cingulat cortex, caudate to thalamsus

Can be done with gamma knife

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26
Q

Subcaudate Tractotomy

A

Treats anxiety/depression/OCD

Cuts connections between OFC, subgenual cingulate striatum, thalamus, amygala

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27
Q

Limbic Leucotomy

A

Treats OCD/depression/schizoaffective disorder

Combo of cingulotomy and subcaudate tractotomy: affects thalamocortical pathways

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28
Q

Vagal Nerve Stimulation

A

Treats treatment-refractory epilepsy patients

acts via electrode attached to nerve in neck + pulse generators implanted in chest wall. Increases serotonergic and noradrenergic transmission improve limbic system blood flow

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29
Q

Normal vs. Cingulotomy brain looks similar to lobotomy, but what do we have today?

A

MRI tech. You have a sense of brain coordinates so you can avoid language and memory and area for everyday functioning

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30
Q

Deep Brain Stimulation (DBS)

A

Produce inhibition by depolarization blockade and excitatory axonal response to alter activity in neuronal circuits

Instead of destroying tissue, can target where tissue should be stimulated

Lead wire in person’s body, electrode.

Approved for Parkinson’s tremor, dystonia, OCD, ventral capsule/striatal stimulation, epilepsy.

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31
Q

Transcranial Magnetic Stimulation (TMS)

A

Doesn’t require surgury (unlike DBS)

Electrodes on surface of the brain. Stimulate brain. TMS takes this a step further because magnetic signal can reach deeper parts of the brain.

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32
Q

Put these in order of invasivness: DBS, TMS, ECT, VNS

A

TMS –> ECT –> VNS/DBS

TMS doesn’t require surgury. VNS and DBS do.

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33
Q

TMS doesn’t stimluate a [blank] it stimulates a [blank]

A

single cortical site

it stimluates a network

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34
Q

Stimulating one coritical site in TMS stimulates the whole network.

What area is often targeted?

A

Dorsolateral prefrontal cortex. Highly connected with subgenitual cingulate and throughout the brain.

Activates the whole network, motor movement.

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35
Q

Describe TMS use for depression.

A

Approved for treatment of depression, but MODEST effect sizes (15% remission rate, 30% response rate)

By week 6 of TMS, 25% improved vs. 15% on sham procedure for response rate.

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36
Q

Future therapeutic use of TMS

A

Cognitive enhancement:
-recovery of cognitive abilities in stroke/TBI
-slow down cognitive deterioration in dementias
-reduce effects of negative symptoms in schizophrenia
-aid cogntiive therapy in emotional regulation in depression

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37
Q

What did the government approve in 1970?

A

Ketamine approved as anesthetic drug.

Caused dissociation/confusion/deliruim

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38
Q

How did 2019 FDA approve ketamine? What did it do?

A

Esketamine? for treatment resistant depression (intranasally)

Rapid effects and a single dose can last for days (effects begin within hours, dissipate within 2 weeks if not repeated)

NMDAR antagonist- lower doses, leads to greater efficiency of glutamate processing exact mechanisms yet to be worked out.

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39
Q

In depression, this brain area seems to be functionally hyperconnected to other regions, yet structurally, shows cortical thinning:

A

Subgenual anterior cingulate

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40
Q

Prehistory (mid-19th century to 1950s)

A

liberal use of sedatives and hypnotics

Not to treat, but to quiet patients

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41
Q

“Golden Age” 1950s/1960s

A

Chlorpromazine

Drug companies make huge profits

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42
Q

When was the “rise of neuroscience”?

A

Science of the Brain: 1960’s-1980’s

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43
Q

Describe the age of antidepressants (1988-modern day)

A

Newer antidepressants (SSRIs) without the multiple side effects as
older ones

Not covered in paper, but newest discovery: Ketamine

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44
Q

Why SSRIs?

A

Less side effects

Didn’t help everyone, but help a good number of people

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45
Q

Primary location for production of serotonin

A

Raphe Nuclei. Send serotonin throughout centeral nervous system

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46
Q

Why the noreadrenergic system?

A

SSRIs not always targetting serotonergic systems. SNRIS become developed, some SSRIs focus on both

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47
Q

What is the importnat area of the noreadrenergic system?

A

Locus Coeruleus

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48
Q

What does Ketamine work on?

A

The glutamate system

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49
Q

Describe what happens when serotonin is administered via SSRIs in primates and rodents

A

Serotonin levels rise rapidly.

But 2-4 weeks needed to see therapeutic results. Side effects right away, no mood change.

Why? Takes a while to spread in brain. Syanptic transmission rewires itself based on new meds. Takes time to rewire the brain.

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50
Q

Any clues of how serotonin works in humans?

A

Adult Neurogenesis in the dentate gyrus of the hippocampus (one of the few places new neurons form)

SSRI enhance precursors of neural development. We think helps growth factors make more dendrites.

LTP: NMDA receptor opening up, whole series of protein synthesis and growth factor release that helps you grow a new spine on dendrite.

Once you have more spines, you can take up more serotonin.

Sometimes stop taking medication, benefits go away.

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51
Q

What are the problems with the monoamine approach?

A
  1. Many people do not benefit
  2. Takes a long time (2-3 weeks) to notice symptom changes
  3. Focuses on single NT; likely multiple involved
  4. Circuitry of depression may lie in cortical/limbic circuitry where glutamate & GABA, not monoamines, are predominant
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52
Q

How does the whole ketamine blocking NMDA receptor glutamate thing work?

A

NMDA open, allows for efficient synaptic plasticity and connections, yet Ketamine blocks it. Why? How? When more NMDA receptors open and lots of + influx. Leads to more AMPA insertion and more glutatmate. This process has a different process by which more AMPA inserted and more Glutamate despite NMDA blocked.

Blocks NMDA receptors, but blocks them on the GABA neuron (no calcium inflxux, no + ions in) Stops inhibiting glutamate by decreasing release.

Glutamate taken by AMPA receptors. Stablize amount of glutamate being released. NMDA on postsynaptic cell blocked too, but BDNF levels rise. stimulates TrkB receptor, leads to protein synthesis and spine growth. Long term changes related to ketamine treatment.

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53
Q

What do you need for Ketamine usage?

A

Severe symptoms

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54
Q

What are the challenges in ketamine usage?

A
  1. Doesage (0.2 mg/kg subtherapeutic, 0.5 dissociative, 1-4.5 is anesthetic)
  2. Depends on person
  3. Intranasal vs. intravenous or oral. Intravenous has most side effects
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55
Q

How frequently is ketamine administered?

A

2x per week, then tapers off to monthly or less

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56
Q

Long term effects of ketamine are unknown, but what potential problems do we see?

A

Chronic pain and recreational users, sometimes dependence, memory deficits, health problems.

Abuse potential is high (“rave culture”) due to dissociation, derealization, hallucinations

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57
Q

Experience of people who tried ketamine and didn’t like it?

A

Unbalance, disequilibrium, scary, terrifying, blackness, floating away, afraid of what you can’t see, locked in syndrome, body can’t move from panic, no sensation in mouth, feel like throat disappeared.

Afterwards: detached and scared.

Ketamine last ditch effort before surgery. Don’t drive 24 hours later, take addiction history into account.

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58
Q

What did John Crystal, editor of American Journal of Psychiatry who works at Yale-New Haven Hospital have to say about ketamine?

A

There is a risk, experience of losing control could be potentially traumatic experience

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59
Q

Why do we study the genetics of neuropsychiatric disorders?

A

Mental health disorders are complex, etiology is not a single factor

Genetic component to mental health. Must study genetics and interaction with enviornemnt for full understanding of genetic disorders

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60
Q

DNA

A

Stores genetic information and transmits info from one generation to the next.

Made up of nucleotide.

DNA molecule comprises of nucleotides joining to create chains and form long double strands

TCAG

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61
Q

RNA

A

Involved in expressing DNA’s message through translation

UCAG

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62
Q

Synthesis of protein from DNA sequence of a particular gene

Or

the process by which a gene gets turned on in a cell to make a chemical copy (RNA) that may be translated into protein

A

Gene Expression

63
Q

Genotype

A

Genes responsible for trait

refers to combo of alleles (homozygous, heterozygous)

64
Q

Genome Wide Association Study (GWAS)

A

Take those that have disease (ex: schizophrenia) and those that don’t, look at SNP differences

Ideal study results: look at who has a G and who has a T.

Controls. .002, only 1 T
But Schizophrenia group, .03, we see a bunch of T

65
Q

Epigenetics descirbes what?

A

the SHORT TERM MODIFICATION and/or INHERITABLE MODIFICATION of gene expression

NOT: permanent mutation of genetic code in unicellular and multicellular organisms

People with IDENTICAL ALLELES may exhibit DIFFERENT PHENOTYPES

66
Q

We share 99.5% DNA with other humans. What makes people different from each other, and what is it?

A

Single Nucleotide Polymorphism (SNP)

Variation in base pair

If more than 1% population carries same nucleotide at specific position in DNA sequence, this variation is SNP.

10 million SNPs, single base pair substitutions

67
Q

Mutations

A

Permanent chagne in genetic code of unicellular or multicellular organism

68
Q

the same gene has an influence on 2+ seemingly unrelated phenotypes

A

Pleiotropy/Pleiotrophy

Example: same gene deletion in schiozphrenia and autism are observed, but disorders manifest very differently

69
Q

Polygenic Risk Scores

A

Number based on genetic variants present that are associated with risk phenotype; some genetic variants are weighted more heavily and individuals with a greater number of variants have higher risk scores

70
Q

Pharmacogenetics

A

Identifying genetic factors that influence treatment response

71
Q

Endophenotypes

A

Intermediate phenotypes

biological traits that may mediate effects of genes on disorders while having a SIMPLER GENETIC ARCHITECTURE THAN THE DISORDER

72
Q

The extent to which a phenotype (such as a disease) is attiributable to inhertied genetic factors

A

Heritability

73
Q

Segments of DNA that encode proteins

A

Genes

74
Q

____ dictate cell function

A

proteins

Thousands of genes are expressed in particular cell to determine what cell can do.

75
Q

Where are genes located in the cell?

A

Nucleus and mitochondria of cells

76
Q

What are genes made of? What do they look like?

A

Double helix, DNA, goes around histone proteins. Nucleosomes wound up into chromosomes.

Coiled- lots of information in a small space.

77
Q

We have about [blank] genes in each cell

A

20,000

78
Q

Genome

A

a set of 23 chromosomes; one
of the sets inherited
from mother, the other
set inherited from father

Total CHROMOSOMES is 46

79
Q

An organism’s observable characteristics

A

Phenotypes

80
Q

Locations within the human genome where the type of nucleotide is present?

Also what are other facts about them?

A

SNPs

  1. Human genome has millions of SNPs, most which don’t have an effect on health
  2. They are the basis of Genome wide association studies
  3. Allow researchers to determine regions of the
    genome that may be important for disease development
  4. hereditary and shared by individuals of common descent; can be used to track ancestry
81
Q

Manhattan Plot:

x and y axes, what it shows, how to read

A

X axis shows various chromosomes
Y axis is p value (sig of association, (-log10P)

Tall SNP = high association. p value 5x10^-30. Want genome wide result above red line.

82
Q

Genome wide association studies (GWAS) look for individual differences in [blank] that are most strongly associated with the [blank] of interest.

A

SNPs; phenotype

83
Q

Sequence of treatment for refractory depression

A
  1. SSRIs/Psychotherapy
  2. Ketamine (FDA approved in 2019; esketamine)
  3. ECT
  4. Psychosurgury
84
Q

When a genome copied to make a new cell, what happens?

A

Single base pair gets substituted for another one, called SNP

85
Q

Some diseases (Huntington’s) inherited, other diseases (psychiatric) arise from…

A

interactions between multiple alleles at different genetic loci with cues from the environment

86
Q

Even though we can map out the genome, association studies explain very little [blank] in any given disorder.

A

variance

(missing heritability)

87
Q

What is all genetic modifications excluding changes in actual DNA sequence?

What are some of these modifications?

A

Epigenetics

adding molecules (methyl groups), which changes structure/appearance of DNA, alters how that gene can interact with transcribing molecules in cell nucleus

88
Q

Describe the whole endophenotype neuroimaging thing

A

Gene –> phenotype is hard, genes explain little phenotypic variance. Psychiatric disease invovles multiple genes and interactions.

Inhertied genetic variation (BDNF,COMT,Serotonin transporters) –> changes in brain (endophenotype) (structure, function, connectivity) –> phenotype complex behavior (temperament, anxiety, social anxiety disorder)

All these influence by environment.

Endophenotype: biological traits that medicat effects of genes. Simplar genetic architecture than the disorder.

Mediation or interaction analysis

89
Q

A gene is the part of DNA that codes for [blank]. Through a process known as [blank], a copy of the gene is made. Through the process of [blank] mRNA is “read” to form a protein.

A

Protein
TranSCRIPTion (copy of gene)
TransLATION (mRNA is read)

90
Q

Gene expression is synthesis protein from DNA sequence of gene.

Cells have protential to [blank] its functions by adjusting the [blank].

A

Self-regulate

amount and type of protein it manufactures

91
Q

TranSCRIPTion

A

DNA to RNA

92
Q

TranSLAtion

A

RNA to protein

93
Q

Why are genes turned on and off?

A

So expressed at appropriate time

Part of gene expression

94
Q

Persistence of LTP

A
  1. Depends on new protein synthesis
  2. TransCRIPTion in nucleus of cell (DNA copy)
  3. Signaling in nucleus depends on protein kinases (PKA, CaMKIV, Erk-MAPK), which activate transcription factors to promote expression of genes required for maintaining synaptic enhancement
    4.Structural remodeling: groth of new dendritic spines, enlargment of spines, splitting spines

Introns removed

95
Q

Gene transcription in LTP

A

CREB- cAMP response element binding protein

binds to CRE (DNA sequence) to increase or decrease gene transcription.

96
Q

Why are identical twins different?

A

People with IDENTICAL ALLELES may exhibit DIFFERENT PHENOTYPES (identical twins, different because of epigenetics)

97
Q

DNA methylation

A

Most well studied epigenetic modification

Methyl group binds to cytosine in DNA mehtylation

Methyl group= hydrocarbon cluster

Now, other proteins can’t bind to DNA, prevents transcription to RNA. Gene “turned off”

methyl group tags DNA to activate/repress genes

Demethylation: turns on genes

98
Q

Histone Modification

A

Binding of epigenetic factors to histone “tails” which alters the extent to which DNA is wrapped around histones and the availability of genes in the DNA to be activated

Histone tighter, harder to copy, less protein synthesis

Making DNA accessible or inaccessible

99
Q

What are international consortiums like the Psychiatric genomics consortium (PGC) and ENIGMA used for?

A

Gather large amounts of data for SNP. Large samples of PTSD, schizophrenia, bipolar, ADHD, depression, etc.

Polygenetic risk scores: number based on genetic variants present that are associated with risk phenotype; some genetic variants weighted more heavily and individuals with greater number of variants have higher scores

100
Q

Feeling of depression as described by patients

A

Feeling alone, helpless, trapped, everyone else is happy, self-attacking throughts (no matter how outlandish seems credible), nothing brings happiness even when physically active

Self-fullfilling prophecy: little motivation to work or partake in pleasurable activities. No end in sight.

101
Q

How many symptoms of depression do you need?

At least one needs to be which two symptoms?

A

5/9

depressed mood (subjective/observed)

Loss of interest or pleasure

102
Q

Depression symptoms need to be in the same [BLANK] week period and represent a change from what?

A

2 week

change from previous functioning

103
Q

What are the 9 symptoms of depression?

A
  1. Depressed Mood (subjective or observed)
  2. Loss of interest or pleasure
  3. Change in weight or appetite
  4. Isomnia/hypersomnia
  5. Psychomotor retardation or agitation (obsered)
  6. Loss of energy or fatigue
  7. Worthlessness or guilt
  8. Imparied concentration/indecisiveness
  9. Thoughts of death or suicidal ideation or suicide attempt
104
Q

The four additional criteria for depression:

A
  1. Symptoms cause clinically significant distress or impairment in social, occupation, or other important areas of functioning
  2. Episode not attributable to physiological effects of substance or another medical condition
  3. Episode not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schiozphrenia spectrum and other psychotic disorders
  4. No history of manic or hypomaic episode (unless mani was substance induced or attributable to another medical condition).
105
Q

If someone has claimed to be depressed for years

A

Persistent depressive disorder

MDD is change

106
Q

What brain circuits are involved in depression? What might be our approach for getting at them?

A

Multiple circuits and systems involved; Lack of consistency across studies may reflect subtypes of depression, levels of severity of depression, other individual factors that will need to be studied in a precision medicine/RDoC framework

One approach is to examine large scale resting state networks using fMRI to study systems of circuit

107
Q

The [BLANK] gene has been found to be [BLANK] in depression?

A

SLC6A4

Hypermethylated

108
Q

SSRIs and psychotherapy help what % of those with depression?

A

about 60%

109
Q

What are we looking at with an MRI?

A

Not neurons and circuits, doesn’t have spatial resolution (1mm, 1,000 neurons in small space)

Look at large scale networks: regions connected with white matter, big blobs of association areas, more input from all areas of the brain than other local areas

Nodes and connections between nodes

110
Q

Nodes/Hubs

A

Areas critical for integrating information

A certain region or area of the brian

111
Q

Important things to know about collecting MRI data

A

NO METAL
Ear plugs
Not for cluster phobic

You can show stimuli, mouse click, headphones, coil over head to boost signal.

112
Q

What do we mean when we say the MRI and fMRI have 4D data?

A

3 dimensions of brain space across time

113
Q

fMRI: what does it look at? (task vs. resting)

A

FUNCTIONAL changes in the brain

resting state networks or tasked based

Discover DMN when regions coactivate at rest

resting state: just put the guy in the scanner
task based: have them do a task in there (ex: memory, hippocampus and medial temporal lobe)

114
Q

Gray Matter Volumetry

A

Grey matter structure, how big it is

6 layers of neuron

Can see particular areas, intensity of grey vs. white on image. Atlas applied ot brain to get area to measure

115
Q

What do we measure with MRI/Structural MRI?

A

Cortical thickness (on the brain SURFACE), can’t get specifics on 6 layers of neuron.

Shades of grey, dark is grey.

As we age/disease, we lose cortical thickness. Distance between pial surface and white matter.

116
Q

Cortical Thickness

A

Surface of brain, Reflects size, density, and arrangement of neurons, neuroglia, and nerve fibers.

Measured with structural MRI

Doesn’t get a subcortical regions

117
Q

What is good for measuring subcortical regions?

A

Structural Volume (thalamus, basal ganglia, hippocampus, amygdala)

Count up voxels in area of interest, multiply by size of voxel (1mm^3)

Volume = internal structures of brain

Cortical thickness and volume are two different metrics

118
Q

Why use fMRI vs. structural MRI?

A

Complementary types of info

119
Q

Depression patients have smaller what and larger what?

What had less cortical thickness?

A

Small hippocampus large lateral ventricles

Less cortical thickness in anterior cingulate and some regions of prefrontal cortex.

120
Q

Diffusion Tensor Imaging

A

White matter imaging (structural)

Measures axons, not dendrites/cell bodies.
Neurons go through bundles of axons which join into fiber tracts, allow brain area communication.

121
Q

Diffusion Anisotropy

A

Random motion of water molecules except in restricted fibers of the brain.

122
Q

Isotropic diffusion

A

Water moves as it pleases

123
Q

Anisotropic diffusion

A

Like celery stalk. Water only goes one way

Diffuse along longitudinal axis
Elongated oval shape of diffusion.

124
Q

Fractional Atrosophy (FA):

What happens in brain injury?
What about following ECT in depressed patients?

A

Diffuse: FA low, Normal longitundinal: FA high. Injury: FA decreased

Incrased FA (good) after ECT. Suggests ECT helpful in repairing axonal structure.

125
Q

What is fMRI?

A
  • Measures functional activity related to task performance (or at rest)
    • Provides insight into regions/networks involved in a particular function
    • Is a technique for measuring metabolic correlates of neuronal activity (BOLD: blood oxygenation level dependent signal).
126
Q

How does brain get the glucose nutrients and oxygen it needs to fire? What does measuring this give us?

A

Blood

Measuring blood blow gives indirect measure of neural activity

127
Q

Basis of bold signal:

A

Brain uses ~20% body’s engery, but neurons don’t have internal reserves in glucose or oxygen

When activited, provide more energy by ADACENT CAPILLARIES through process called HEMODYNAMIC RESPONSE which supplies them with INCREASED REGIONAL CEREBRAL BLOOD FLOW and incrase in oxygen supply, usually EVEN GREATER than their needs

128
Q

Neurovascular coupling: how does it work

A

How neurons get their energy

Oxygen extracted from blood vessel, processed by astroctye and given to neuron, all tightly coupled

We can measure through fMRI

when neuron works, glutamate released, influx calcium sodium and nitric oxide which sends signal to astrocyte to process blood and oxygen from blood vessel

129
Q

The steps of fMRI and Bold

A
  1. Stimulus leads to neuronal activity
  2. Neurovascular coupling
  3. Haemodynamic response
  4. Detection by MRI scanner
  5. fMRI bold response
130
Q

Normal oxygen extraction vs. when neurons active. How does BOLD use this?

A

Normally, oxygen is extracted from red blood cells within the capillaries resulting in deoxygenated hemoglobin.

When neurons are active, more oxygenated blood is
supplied than needed, decreasing deoxygenated hemoglobin

BOLD measures oxygenated deoxygenated ratio, deoxygenated signal you can pick up, the smaller the amount, the more oxygenated not being picked up.

131
Q

Is the signal we get from fMRI a direct measure of neuronal activity?

A

No. It is a measure of blood flow.

and a ratio because neurons can’t take up all nutrients that is provided to them

132
Q

To image white matter microstructral integrity what type of MRI scan would you use?

A

Diffusion tensor imaging

133
Q

This type of structural MRI metric measures the distance in millimeters of the gray matter situated between cerebrospinal fluid and white matter:

A

Cortical thickness/volume

134
Q

Neurovascular coupling refers to…

A

Cerebral blood blow changes in response to neuronal activity

135
Q

Resting state network: how did this change the game

A

realization that psychiatric disorders are characterized by multiple brain areas involving several distinct brain systems

Studying resting-state networks using fMRI is an important tool for characterizing these functional brain network

1990s- cortical and subcortial regions have synchronized signals in the absence of external input—allows us to study organization of the brain

136
Q

Who discovered motor cortex synchrony?

A

Bharat Biswal

137
Q

Who discovered DMN?

A

Marcus Raichle

138
Q

Why do we look at resting state networks

A

Allows us to view alterations in large scale
networks and their interactions, more closely to
how brain actually works

Resting state networks are more robust, reliable

Easy data to get: short scan times, no task

139
Q

DMN areas and what is related to.

A

Medial PFC, posterior cingulate cortex (PCC)/precuneus, hippocampus,
inferior parietal lobule, lateral temporal cortex

deactive during task, active during rest

Self-generated thought

140
Q

Anterior DMN

A

SELF-REFERENTIAL PROCESSING/EMOTION REGULATION

141
Q

Posterior DMN

A

MEMORY PROCESSING

142
Q

Central Executive network (CEN)

Areas of brain, when active, functions, relationship to DMN

A

Lateral prefrontal cortex (dlPFC), posterior parietal cortex, frontal eyefields, dorsomedial PFC

THIS NETWORK IS MOST ACTIVE DURING TASKS

IMPLICATED IN COGNITIVE FUNCTIONING INCLUDING ATTENTION AND WORKING MEMORY and cognitive control

DMN AND CEN ARE OFTEN SEEN AS OPPOSING NETWORKS

143
Q

Salience Network

Brain areas, activated in response to what, plays a role in what, why is it also called the switching network?

A

Fronto-insular cortex, dorsal anterior cingulate cortex (dACC), amygdala, temporal poles

activated in response to salient stimuli like acute stress

may have role in detecting, integrating and filtering relevant interoceptive autonomic, and emotional information

Switching Network: THOUGHT TO INITIATE SIGNALS THAT ENGAGE CEN (TO MEDIATE ATTENTION, WORKING MEMORY, OTHER COGNITIVE PROCESSES) WHILE DISENGAGING DMN

144
Q

Brain networks are comprised of brain regions aka WHAT and connections aka WHAT that link them

How do alterations in brain network arise?

A

Brain networks comprised of brain regions (nodes) and connections (edges) that link them

Alterations in brain networks can arise from damage to nodes or edges

145
Q

WHAT from damage can propagate to whole network or
subnetworks

A

Aberrant signaling

146
Q

Within Network

A

connectivity among nodes that comprise a single network (e.g., posterior cingulate and medial PFC in the default mode network)

147
Q

Between network:

A

connectivity between nodes of different networks (e.g., posterior cingulate and insula connectivity)

148
Q

DMN in depression

A

Increased connectivity in anterior regions (excessive rumination)

SUBGENUAL ACC APPEARS TO BE
PART OF DMN in depression; highly
connected to it and normalizes with
treatment

INCREASED CONNECTIVITY BETWEEN
THE ANTERIOR DMN AND THE SN

CHANGED CONNECTIVITY BETWEEN
ANTERIOR AND POSTERIOR DMN

DECREASED CONNECTIVITY BETWEEN
THE POSTERIOR DMN AND CEN

149
Q

SSRIs vs. Ketamine

A

SSRIs: block receptors that reuptake serotonin. 2-4 weeks. Synaptic plasticity, LTP, structural change, neurogenesis in dentate gyrus of HC. Protein kinase leads to gene transcription/translation then synatpic growth and dendritic growth. Takes time to rewire the brain.

Ketamine: NMDAR antagonist. Immediate effect. greater efficiency of gluatamate processing via AMPAR upregulartion and synaptic efficiency, NMDAR recprot blocked, BDNF growth factor involved in spinal growth. Then improves growth tht leads to synpatic efficiency for glutamate

150
Q

How is fMRI signal measured and why do we consider it to be a “correlate” of neural activity?

A

BOLD (blood oxygen level dependent contrast) ratio of oxygenated to deoxygenated blood.

Capillaries give glucose and oxygen to neurons so they can work neurons take it up, but the capillaries provide more than they need. higher level of oxygenated blood in that area. When neurons are active, more oxygenated blood is supplied than
needed, decreasing deoxygenated hemoglobin. The fMRI is measuring the difference, the ratio of oxygenated to deoxygenated blood a fMRI is a
technique for measuring metabolic correlates of neuronal activity

It is NOT causal, becuase we don’t know if those nodes/region caused the neuronal activity, we just know that they are associated with it and have increased activity.

151
Q

Advantages of resting state fMRI over task based fMRI?

A

Observe brain that moves together in time and creates basis of a network, how brain connects to other areas.

Networks are more robust and reliable than task based. Decreases amout of time participant needs to be in fMRI. It takes many task based trials to get reliable signal.

152
Q

Describe a resting state network and what is know about it’s function in depression.

A

DMN- rumination/self-generated throught

Anterior (self and emotions)-posterior (memory) dissociation.

Increased connectivity between anterior DMN and salience network.

sgACC part of anterior DMN. Only in depression.

153
Q

Diagnosis Depression

A

Change from previous behavior, same 2 week period, 5/9 symptoms with at least 1 being loss of interest or pleasure or depressed mood.

Other 7: worthlessness/guilt, suicidal ideation, loss of energy/fatigue, imparied concentration/indecicivness, insomnia/hypersomnia, change in weight or appertitle, psychomotor retardation/agitation.

Clinically sig distress
No mania (unless due to drugs or other illness)
No schizophrenia/psychotic related disorders
Not due to substance use or other medical issues

Bio Psych :( (4 decks)

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