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Termin 2 > Biologisk och emotionell psykologi > Flashcards

Biologisk och emotionell psykologi Flashcards

1
Q

Mesencephalon:

A

Midbrain

Dopamin:
Ventral tegmental area(VTA)
Substantia nigra

Serotonin:
Dorsal raphe nuclei

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2
Q

Diencephalon

A

Betweenbrain

Hypothalamus: Regulates circadian rhythm aswell as melatonin production in the epithalamus(tallkottkörteln). Serotonin is a precursor to melatonin. Epithalamus is also involved in emotion and memory.
Regulates the pituitary gland and connects it to the nervous system.
Regulates stress.

Thalamus. Receptor of signals, and transmitter of signals. Relay station between cortex and the rest of the brain.
Reconnecting loops.

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3
Q

Cerebrum - Telencephalon

A

Cortex, basal ganglia, limbic system

Subcortical systems “allocortex”
Limbic system/Allocortex:
- Amygdala
- Hippocampus: Fornix - White mass that interconnects hippocampus with e.g hypothalamus.
- Bed nucleus of stria terminalis
- Orbitofrontal cortex
- Cingulum, anterior cingulate cortex ACC
- Insular cortex

Basal ganglia:
- Striatum:
Dorsal striatum - Putamen Caudatus
Ventral striatum: Nucleus Accumbens
-Globus pallidus : Ventral pallidum

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4
Q

Myelencephalon

A

Medulla:
Regulates heart frequency
Breath. Sensors detect blood PH. Too high or low can be fatal. Hyperventilation causes medulla to stop breath - this can exacerbate panic attack. Common with panic attacks where you exhale too much CO2.
Transfers afferent sensory information from organs.
Cranial nerves

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5
Q

Metencephalon

A

Pons: Sleep regulation: REM-sleep, sleep paralysis
attention, breath, bladder controll, posture
Transfers motor signals from cerebrum to cerebellum - important for motorics. Only place these two brain regions are connected.
Coordinates eye movement.

Cerebellum: Fine adjustment of motorics
3.6 times more neurons than cerebrum. Same ratio for all mammals. Indicates that neocortex didn’t develop after cerebellum, but that they’ve grown together.
Can be likened to a data center. Not an interaction of signals, they are fed forward.
Receives info from few cells, processes this info using many neurons, then feeds it to progressively fewer and fewer neurons that ultimately deliver the result of the processing.

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6
Q

Mesencephalon:

A

Midbrain:
Substantia nigra
Ventral Tegmental(Täcke) Area - Dopamin cell nucleus reward system.
Red nucleus: When we reach for something.

Tectum(tak)

Superior collicululus:
2D eye maps for movement and localization
Distraction - lower pre-frontal input leads to easier distraction. Important implication for ADHD.

Rostral raphe-group:
Dorsal raphe:
Cell nucleus of serotonin system.

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7
Q

Limbic system

A

Allocortex
- Amygdala
- Hippocampus: Fornix - White mass that interconnects hippocampus with e.g hypothalamus.
- Bed nucleus of stria terminalis
- Orbitofrontal cortex
- Cingulum, anterior cingulate cortex ACC
- Insular cortex

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8
Q

Amygdala

A

Creates emotional memories. Fear memories.
HPA-activation
Nucleus Accumbens - important for motivation and reward. Important for approach/avoidance-conflicts

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9
Q

Hippocampus

A
  • Episodic and spatial memories. Episodic memories goes to ACC.
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10
Q

Orbitofrontal cortex

A

Part of pre-frontal cortex.
Bodily changes because of emotions such as nervosity. Damages to this leads to increased risk behavior.

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11
Q

Anterior cingulate-cortex

A

Info from OFC about different scenarios (reward or non reward)

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12
Q

Basal ganglia

A

Motivation(addiction)
Voluntary movement - Prepares and coordinates movement. Keeps track of parts of complex movements. Fine-tunes strength of movements. Important for movement learning. Procedural memory is possible thanks to basal ganglia.
Habits
Learning
Dopamin-system

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13
Q

Striatum

A

Dopamin-governed system
Dorsal striatum:
Voluntary movement in coordination with cerebellum and motor cortex. Involved in cognition aswell. Cognitive and motoric complications with Parkinson disease.

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14
Q

Globus pallidus

A

Part of the basal ganglia and adjusts voluntary movement. Does so through the inhibitory control loops exerted on the thalamus. Damage to the basal ganglia, and thus the globus pallidus leads to absence of control on the output of the thalamus. This is evident in Parkinsons Disease where regulation of movement is unsuccessful.

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15
Q

Ventral pallidum

A

Forms part of the brain’s reward system, aswell as with ventral striatum (primarily nucleus accumbens)

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16
Q

Nocioception

A

Perception av smärta och temperaturändring

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17
Q

Hapsis

A

Förmåga att skilja objekt med hjälp av beröring, olika receptorer för vibration, beröring, reaktion på tryck osv

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18
Q

Proprioception

A

Uppfattning av kroppens, huvudets och lemmars position och rörelse.

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19
Q

Fast adapting receptors

A

Active briefly, in beginning and end of stimulus. Eg. ruffini corpuscles - vibration

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20
Q

Slow-adapting receptors

A

Active during whole period of stimulus. Eg. hair receptors, Merkel’s receptors.

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21
Q

Dorsal-root ganglion neurons

A

Responsible for carrying signals from receptors, along the system. Their axions vary in diameter and level of myeliniation. Deliver signals from receptors to spinal cord along to the brain for further processing.

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22
Q

Vestibular system and balance

A

A sensory system in the inner ear that helps us maintain balance and posture. Provides information about head orientation and movement in space. Allows for us to know where we are in relation to gravity. It is an integrated system that interacts with our eyes and our proprioception. When our head is moving, the vestibular system controls eye movement to allow objects to remain in visual focus. This allows for a coordinated, stable and integrated sense of movement.

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23
Q

Hypokinesia

A

Absence of spontaneous movements (akinesia) or difficulity performing movement at all.
Tremor

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24
Q

Hyperkinesia

A

Chorea - Involuntary spasmic movements characteristic of Huntingson syndrome or Tourettes.
Atetos - Twisting uncontrollable movements in eg. cerebral pares.

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25
Q

Pyramidal system

A

Pathway for voluntary movement. Goes from primary motor cortex directly to muscles via the corticospinal tract. This is responsible for skilled and dexterious movements that are precise and voluntary.
Some fibers cross to contralateral side of the medulla.

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26
Q

Extrapyramidal system

A

Pathways for control/postural movements aswell as reflexive movement. Originates in brainstem aswell as basal ganglia. Cortex can influence this system via inputs to brain stem. This system and its pathways are responsible for automatic, rhythmic and involuntary movements such as oral movement during speech and chewing aswell as breathing.

Fibers do not cross.

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27
Q

Dorsal visual pathway

A

Dorsal way: Goes directly to motoric cortex without passing consciousness and without analyzing spatial characteristics. This is for quick processing and general comprehension. Localize objects, where? Damaged area leads to not being able to reach for objects or identify where they are.

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28
Q

Ventral visual pathway

A

Ventral way: Analyses och identifies characteristics such as colour, shape and object recognition.
Good at recognizing places, faces and bodies.

Damaged ventral pathway leads to not being able to identify objects.

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29
Q

Sensation(Sensory)

A

Process where stimuli is received by sensory organs and converted to phy

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30
Q

Intersex

A

Atypical internal and external anatomical sex characteristics. Mixed androgyn characteristics. XX-chromosomes with a high testosterone level leads to androgyne appearance in genitalia. Testosterone should be decomposed but it does not thus this leads to too much and this causes androgyne feutuses.

XY-chromosomes with too little testosterone or faulty test receptors.

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31
Q

Östradiol

A

Steroidhormon viktigt för kvinnlig utveckling men även skelettbildning. Män konverterar testosteron till östradiol. Nödvändigt för sexuella funktioner.

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32
Q

Estrogen

A

Affects cell health. Affects CNS aswell as effect and concentration of serotonin etc.

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33
Q

Progesteron

A

Affects GABA signaling. Affects CNS activity. Affects neurotransmitter activity. Affects balance and mood.

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34
Q

Testosterone

A

Affects myelinisation. Connected to sexual drive in both women and men. Testosterone lowers when men are in a stable relationship aswell as when caring for children. Men with high T are more prone to divorce and cheating. T levels are affected by competetive activities more than by bond-maintenance activites.

Some studies show ambiguous results amongst women.

High levels of T connected to criminality and aggression. Not with youth criminals.

Not just aggression and competetiveness. Encourages just and fair division in economical games.

Testosterone varies with age and hour of the day. Hard to interpret results.

Testosterone leads to increased muscle mass and oxygen uptake capacity.

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35
Q

Challenge hypothesis

A

T drives aggression when it is favorable eg. reproduction, rivality, social instability.

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36
Q

Dual hormone hypothesis

A

T is connected to aggression but not always. Cortisole needs to moderate this relationship in order for aggression to arise.

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37
Q

Evolutionary Neuroandrogenic Theory

A

Evolutionary pressure, people with historically higher T leads to possession of more resources, leads them to be in a favorable position. Thus this leads to biological changes, higher production of androgenes. Gives rise to manifestation of competitive behavior and victimization. Increases both brute behavior such as war and aggression but also sophisticated behavior, such as inventions and achievements that help society.

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38
Q

Gender differences in mental health

A

MDD and PDD double as high for women as men.

GAD higher for women as well as more comorbidity.
Phobias, PD, SAD women double as high.

Suicide:
Double as high with men. No difference in young age, higher with older group.

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39
Q

Gender differences in neuropsychiatric disability

A

AST: 80% boys, girls underdiagnosed?
Schizofrenia: More men some studies, no difference others ambiguous.
ADHD: More boys, girls more inattentive
Dyslexia: More boys, bigger variation?
Tourettes syndrome: More boys.

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40
Q

Structural gender differences

A

Biggest difference in hypothalamus; which regulates hormone production. Aswell as reproductive behavior.

Men bigger heads.
Women more neurons.
Men more myeline, due to higher T level.
Women have bigger Orbital Frontal Cortex.
Men have bigger cerebellum.

Women better at face processing where anatomy is connected to ability/function.

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41
Q

Behavioral gender differences

A

Girls better at communication and language early on.
Boys better at spatial abilites - mental rotation etc.
Same level of aggression. Girls more relational aggression.
Boys more instrumentally aggressive.
Cultural variation is evident.

Differences caused by parents, biology and environment.
Genus conscious parents raise kids with less gender differences.
Boys with higher prenatal concentration of testosterone are better at spatial tasks in some studies.

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42
Q

Biological gender differences

A

Big difference of hormonal exposure between men and women. Aswell as function because of differing receptors.

Reproductive behavior is different and that’s what is connected to biological and anatomical differences. Hard to separate biological and social causal factors.

Hormone levels affect behavior.
Behavior affects hormone levels.

Early interests greatly affects future. Infant toys predict play preferences in preschool.

Toys in childhood predicts future education and profession.

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43
Q

Gender differences in play

A

Fantasy play leads to higher executive functioning.
Construction play leads to STEM(science, technology, engineering and mathematics)
Kids play and interests plays a big role in development:

  • Psychological
  • Rough, and fine motorics
  • Social interaction
  • Practice their roles
  • Act their future selves.

Affected by parents (modelling)
Girls and boys play with different toys. Inherent or social factors?

Socialization does not occur in a vacuum and neither does biology. They interact.

Parents are affected by child’s biological temperament in their choices for their child. This affects the social contexts in which the child find themselves.

Biology is affected by environment. Epigenetic expression due to social circumstances, some genes are activated in certain contexts. Aswell as neurological and neuropharmaceutical factors that affect biology later on in life.

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44
Q

Neurotrophic factor

A

Proteins that contribute to neuron survival, synapse genesis and the forming of long term memories.

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45
Q

Long term potentiation

A

Long-term potentiation (LTP) is a persistent increase in synaptic strength resulting from specific patterns of neuronal activity, which is thought to underlie certain forms of learning and memory. LTP is considered one of the most long-lasting and widely studied forms of synaptic plasticity, the mechanism by which the strength of the connections between neurons can change in response to their activity. The phenomenon of LTP has been extensively studied in the hippocampus, a region of the brain involved in learning and memory.

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46
Q

Dopamine projection

A

The dopamine projections to the striatum refer to the neurons that originate in the substantia nigra and project to the striatum which is the main input nuclei in the basal ganglia (caudate nucleus and putamen), releasing the neurotransmitter dopamine in the process. These projections play a key role in regulating movement, motivation, and reinforcement, and are also involved in the brain’s reward system.

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47
Q

Long term depression

A

Long-term depression (LTD) is a phenomenon in which the strength of synaptic connections between neurons decreases over time, lasting much longer than short-term synaptic plasticity. LTD is thought to play a role in memory formation and synaptic scaling, where the overall strength of synapses is globally adjusted to maintain a balance between excitation and inhibition. Unlike long-term potentiation (LTP), which is a long-lasting increase in synaptic strength, LTD is a decrease in synaptic strength and is considered a form of synaptic plasticity.

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48
Q

Non-associative memories

A

Changes in behavior in the form of conditioning where there is no association between a stimulus and a specific outcome or event after the stimulus.
e.g: sensitization and habituation.

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49
Q

Tulving model

A

Psychological model that proposes that our memory is constructed of semantic and episodic memory. The different systems involved in memory are phylogenetically and ontogenetically differing in age.

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50
Q

Retrograde amnesia

A

Affects memories that were encoded before the amnesia arose.

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51
Q

Anterograde amnesia

A

Affects memories that are encoded after the amnesia arose. LTM is affected as we can’t form new memories but we can remember old ones. Spatial memory is affected aswell.
Episodic and partially semantic memory are affected.
WM is intact.

Procedural memory and thus implicit memory formation is still possible.

Some associative memory formation is possible.

Priming/perceptual memory is possible aswell.

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52
Q

Rutnätsceller

A

Aktiveras i funktionella moduler - sexkantigt rutnät - när man rör sig i rummet.

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53
Q

Huvudriktningsceller

A

Aktiveras då huvudet vrids åt ett visst håll.

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54
Q

Gränsceller

A

Aktiveras i yttre gränszoner (väggen)

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55
Q

Kognitiv karta

A

Entorhina cortex och hippocampus celler tsm bildar kognitiv karta om var man är samt för att navigera sig.

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56
Q

Standard model of consolidation

A

Episodic memories become independent of hippocampus after consolidation.

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57
Q

Multiple trace theory

A

Episodic memories are always dependent on hippocampus. Semantic memories can be independent though.
Multiple Trace Theory is a model of memory that proposes that memories are not stored in a single, unified location in the brain, but instead exist as multiple, distributed traces across various neural networks. According to this theory, each time a memory is retrieved, a new trace is created, strengthening the overall memory representation and increasing the chances of future recall. These multiple traces can interact with each other and are thought to contribute to the persistence, stability, and malleability of memories over time.

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58
Q

Episodic memory encoding and retrieval

A

Interaction between prefrontal cortex and hippocampus. Encoding: FFA left frontal lobe and hippocampus.

Retrieval: FFA right frontal lobe.

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59
Q

Alzheimer disease

A

Senile placks that are buildup of protein that are called beta amyloid that prevent nerve signals. Protein gets tangled up and affect neurofibrils. This causes nutrients to not reach cells. These neurons die and over time the brain volume shrinks due to loss of neurons.

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59
Q

Alzheimer disease

A

Senile placks that are buildup of protein that are called beta amyloid that prevent nerve signals. Protein gets tangled up and affect neurofibrils. This causes nutrients to not reach cells. These neurons die and over time the brain volume shrinks due to loss of neurons.

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60
Q

Dorsomediala hypothalamus

A

Äta, dricka och dygnsrytm. Output till preoptic nucleus

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61
Q

Preoptic nucleus

A

GABA-signalering till stora delar av (A)RAS. Initierar icke-REM-sömn. Dvs aktiveras kraftigt vid insomnande. Trött av bensodiazepiner.

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62
Q

Paraventricular nucleus

A

Viktigast för aktivering av det autonoma nervsystemet. Mer kopplat till stress än dygnsrytm.

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63
Q

Inititation of REM-sleep

A

Pons has pontine REM-on and REM-off neurons that interplay to regulate REM sleep.

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64
Q

Laterala hypothalamus

A

Producerar orexin(hypocretin). Brist på detta finns vid narkolepsi typ 1. Autoimmun reaktion som dödar orexinproducerande celler. Finns bara 20 000 såna här celler.

Samlar info kring nuvarande sömnbehov och vår nuvarande sömnskuld. Exciterar många olika system som ökar vår vakenhetsgrad.

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65
Q

Posterior hypothalamus

A

Hög densitet av histaminreceptorer. Binder histamin där leder det till högre grad av vakenhet.
Antihistamin kan leda till trötthet.
GABA-aktivitet från preoptic nucleus ökar non-REM sömn.

66
Q

Hypothalamus centrala roll

A

Hypothalamus reglerar sömn genom att den kommunicerar med olika hjärnområden som är involverade i sömnreglering. Den får input från dels retinala ganglionceller gällande blåljus-exponering och vidareberfodrar informationen till tallkortskörteln som responderar med minskad melatoninproduktion. Hypothalamus producerar även hormoner och neurotransmittorer som reglerar sömn, dels orexin som stimulerar vakenhet genom att agera på hypothalamus och basala förhjärnan som ansvarar för vakenhet och inhiberar hjärndelar som bidrar till sömnighet som t.ex ventrolaterala preoptiska nucleus.

67
Q

Beta-vågor

A

Vakna och aktiva, samt vid REM. Liknar vakenhet för det är livliga drömmar.

68
Q

Alpha

A

Reflektiv, vilande.

69
Q

Theta

A

Groggig och trött.

70
Q

Delta

A

Sömn, drömmar.

71
Q

REM-sömn

A

Ponto-geniculo-occipitial waves: Fasiska(plötsliga) vågor av neuronaktiveringar under REM-sömn. Kan vara viktiga för att konsolidera minnen från dagen.

Signalering med acetylkolin i pons är extra viktigt under REM-sömn.
Signalering med monoaminer (t.ex serotonin) i pons minskar kraftigt. Vid närvaro av serotonin aktiveras inte REM-sömn. SSRI-behandling kan leda till minskad REM-sömn pga förhöjda serotonin-nivåer.
Signalering med GABA i pons minskar REM-sömn. Därför kanske bensodiazepiner leder till minskad REM?

72
Q

Sömndeprivation på sikt

A

Högt blodtryck, hjärtinfarkt, stroke.

Övervikt - ökar problem med sömnapne.

Diabetes
Ångest- depression
Sova 5h jämfört med 7h = 15% ökad “all cause” death risk
Räcker inte att sova ikapp på helger.

73
Q

Insomni & stress

A

Stress (HPA-aktivering)- ofta ökade problem, alltså att man har fler problem än vanligt i livet. Upplevelse av hot leder till mer stress. Leder till mer stress pga sömnbrist. Sämre problemlösningsförmåga vid insomni. Ökad irritabilitet. Depression och ångest står för 35% av insomni.
Högre nivåer av ACTH-nivåer och kortisolnivåer.

74
Q

Insomni orsaker

A

Olämlig sovmiljö. Ljusföroreningar, LED-lampor som ser vita ut men är egentligen mer blå.

Oregelbunden livsstil, skiftesarbete samt JET-lag.

Brist på rörelse under dagen.

Största två riskfaktorerna för insomni är att vara gammal och kvinna.

75
Q

ACTH

A

Hormone that regulates production of cortisol.

76
Q

Sömnapne

A

Långa andningsuppehåll under natten.
Lider till trötthet under dagen samt ofrivilliga tupplurar.
Orsakas av övervikt men även av neurologiska orsaker.

77
Q

Narkolepsi

A

Misstänker autoimmun sjukdom som angriper orexinceller.

78
Q

Kataplexi

A

Plötslig förlust av muskelkontroll, särskilt vid upprymdhet och skratt.

79
Q

Sömnparalys

A

Pons stoppar rörelse för att man inte ska leva ut sin REM-sömn men man är vaken ändå, därför kan man inte röra sig men man hallucinerar ändå.

80
Q

Behandling av sömproblem.

A

Effektiv behandlingsterapi som hjälper 70-80%.
Sömnhygien.

Utmaningar:
Variation i behandlares kunskap om effektiva behandlingar.
Patientens motvilja att följa råden.

81
Q

Bensodiazepinliknande preparat

A

Snabbare insomning och längre sömn. Ökar GABA-signalering. Cl- kanaler öppnas oftare.
Zopiklon
Beroendeframkallande, ihållande trötthet och ostadighet.

82
Q

Bensodiapeziner

A

Går ur kroppen långsammare än efterliknande preparat. Men tiden påverkas inte av ålder, därav förskrivs det till äldre.

Oxazepam.

83
Q

Melatonin

A

Bäst för jet-lag, återställer dygnsrytm.
Förskrivs åt äldre, 55 år+ pga sänkt seratonin/melatonin nivå.
Cirkadin, Melatan.

84
Q

Antihistaminer

A

Inte beroendeframkallande, kan användas vid alkoholberoende. Påverkas (A)RAS.

85
Q

Serotonin antagonist och reuptake-inhibtors (SARI)

A

Work as sedatives and cause drowsiness.

86
Q

Snabb emotionell respons

A

Stimuli via synen → thalamus → Amygdala → Emotionell respons

87
Q

Långsam emotionell respons

A

Stimuli via synen → thalamus → Hjärnbarken(sensorisk cortex)→ Amygdala → Emotionell respons

88
Q

Spontan återhämtning vid utsläckt ångest

A

Rädslan återkommer en tid efter behandlingen är avsultad och patienten är problemfri.

89
Q

Renewal vid utsläckt ångest

A

När något i kontext ändras, varesig det är inre eller yttre kontext så kan detta resultera i ångest.

90
Q

Hedonic regulation

A

Increase pleasure/Decrease pain.

91
Q

Instrumental regulation

A

Increase expected benefits. Use regulation as a tool to reach goals.

92
Q

Processmodell emotion

A

Situation - Går i mörk skog
Attention - Upptäcker mörk skugga, hör ljud.
Appraisal - Utvärderar huruvida det är farligt, man kan uppfatta det som att det är en björn.
Response - Vi blir rädda och försöker ta oss därifrån.

93
Q

Emotionsregleringsstrategier Situation - Precaution

A

Undvika situationer där jobbiga situationer kan uppstå. Kanske gå i skogen under dagen och i mer öppna platser för att undvika jobbiga känslan att vara rädd för björnar.

94
Q

Emotionsregleringsstrategier Situation - Modification - ändra situationen

A

Ta med sig en kompis för stöd och hjälp i situationen.

95
Q

Emotionsregleringsstrategier Attention

A

Styr uppmärksamhet mot något annat.

96
Q

Emotionsregleringsstrategier Appraisal

A

Ändra värderingen av situationen, är det verkligen en så farlig situation?

97
Q

Emotionsregleringsstrategier Response

A

Reglera vår emotion, stävja rädslouttryck som skrika och springa, istället gå lugnt därifrån när man möter en björn.

98
Q

Produktion av dopamin

A

I ventrala tegmentala regionen samt i substantia nigra. Huvudsaklingen i axonterminalerna eller påväg mot axonterminalerna som det produceras dopamin.

99
Q

Synthesis of serotonin

A

In Raphe Nuclei in the midline of the brainstem.

100
Q

Raphe nuclei

A

A cluster of neurons in the brainstem along the midline of the brainstem that produce serotonin aswell as regulate the release of it. These nuclei are found in the pons aswell as the medulla.

101
Q

Complexity of serotonin

A

We do not know exactly how and in what direction serotonin affects our well-being. Is it an excess or deficit that causes issues? The synthesis, release, reception, binding, reuptake and reuse of the serotonin is also a complex matter wherein we have 15 different receptors solely for serotonin.

102
Q

Critique against the serotonin hypothesis

A

There is no clear evidence to low concentrations of 5HT causing depression. 5HT-autoreceptors decrease synthesis, we do not see an increased activity of these autoreceptors during depression.

We’ve actually seen a decrease in transporter binding and therefore more serotonin the cleft with people with social anxiety.

103
Q

Autoreceptor

A

An autoreceptor sits on the same neuron that produces and releases neurotransmitters. It modulates the concentration of the neurotransmitter in the synaptic cleft, reducing synthesis and release when a high concentration has been reached and the opposite is true for low concentrations. Autoreceptors are important for the maintenance of homeostasis in the synaptic cleft.

104
Q

Nucleus accumbens

A

A region that is part of the basal ganglia. It is located in the ventral straitum, near the basal forebrain and is connected to other important brain regions such as the prefrontal cortex, amygdala and hippocampus.

It plays an important role in the brain’s reward and motivation aswell as reinforcement system and is activated by pleasureable stimuli such as food, sex, drugs etc.

It is also a part of decision making and emotional regulation.

105
Q

Emotional regulation

A

Flexibility in our regulation and response. Not every situation elicits the same reaction. Executive functions are involved in emotional regulation, therefore children and people with ADHD might have difficulty regulation emotion.

106
Q

Damages to Orbitofrontal cortex

A

Personality change.
Difficulty regulating emotion.
Bad judgement.
Bad impulse control.
Difficulty identifying and interpreting emotional information and their potential consequences.

Prefrontal and orbitofrontal cortex play a part in regulating emotion and supressing inappropriate emotional responses.

107
Q

Damages to the peripheral somatosensory system can be

A

Loss or reduction of sensation and touch in the affected area.
Muscle weakness and paralysis.
Loss of reflexes
Muscle atrophy.
Tingling, burning or numbing sensation.

108
Q

Damages to the central somatosensory system

A

Loss of perception of where body parts may be.
Problems with deafferentiation pain, absence of stimulus from body parts may lead to phantom pain where the limb would have been.
Sensory loss, hypoesthesia. Or increased pain sensitivity: hyperalgesia.
Sensory ataxia, affects coordination and balance.
Difficulty in locating sensations.
Changes in perception of body image such as size and shape and ownership of body parts.

109
Q

How does the vestibular system help with motorics?

A

4 ways.

  1. Balance and posture. The vestibular system provides us with information about our body and head position in relation to the surroundings. This is important for maintaining balance and posture during movement.
  2. Eye movements: The vestibular system controls eye movements when we move our bodies or our surroundings move, this is so that we can hold an object in focus visually.
  3. Movement coordination: An integration of proprioception, visual information and orientation of the body information results in us being able to coordinate movements smoothly and in a stable manner.
  4. Reorientation: The fluids in the inner ear react in relation to the heads orientation and this allows us to get a sense of where we are in relation to gravity. This allows us to compensate for change and remain upright aswell as reorient our sense of where we are.
110
Q

Hierarchy of the sensomotoric system.

A
  1. Sensomotoric cortex in the brain: Plans, controls and inhibits movement. Outer layer of the brain responsible for higher-level processing of sensomotoric information and plans voluntary movement.
  2. Basal ganglia: Group of nuclei in the brain that play a role in voluntary, involuntary movement and posture. Finely adjusts movement.
  3. Cerebellum: Allows for skillful movement. Coordinates movement and balance.
  4. Thalamus: Receives information from the brainstem and relays it to the cortex for further processing.
  5. Brainstem: Receives information from the spinal cord and transmits it to the thalamus aswell as cerebellum.
  6. Spinal cord: Part of the CNS, receives sensory signals from the PNS aswell as sends motor signals to the muscles through the PNS.
  7. Peripheral nervous system: Receives sensory signals from the receptors that is sent to the spinal cord. Receives motor signals from the spinal cord and sends it to muscles for movement activation.
  8. Receptors: Mechanoreceptors, thermoceptors, etc that send signals to the PNS.
111
Q

Convertion of sound to nerve signals

A
  1. Sound waves: Sound waves hit our ears causing mechanical vibration.
  2. Ear mechanics: These vibrations are transmitted by the eardrum to the inner ear where they cause the inner ear fluids to vibrate causing waves in the fluids.
  3. Cochlea: The fluid waves pass through the cochlea which is a spiral-shaped organ in the inner ear which contains hair cells. These hair cells are mechanoreceptors responsible for converting the fluid waves to electrical signals.
  4. Auditory nerve: These electrical signals then are passed along to the auditory nerve which is a part of the PNS, that sends the signal to the auditory cortex.
  5. Auditory cortex: Electrical signals are sent to the auditory cortex that interprets the signals created by the cochlea and the hair cells that determine what signals to send depending on frequency of the waves.
112
Q

Utricle

A

Detects movement and acceleration in linear plane. Has hair cells that react to acceleration because fluids in the inner ear start to produce waves. These waves produce electrical signals by the hair cells that are relayed to the thalamus through the vestibular nerve. This helps us compensate for the change in acceleration in order to maintain balance and posture.

113
Q

Saccule

A

Detects movement and acceleration in vertical plan.

114
Q

Planning and initiation of motor movements.

A

Happens in the primary motor cortex, located in the frontal lobe. Plans movements here then sends signals through the corticospinal tract that goes from the brain through the spinal cord to the muscles.

115
Q

Inhibitory control loops of basal ganglia

A

The basal ganglia orchestrate inhibitory control loops to make sure that movement is coordinated, correctly tuned in terms of strength and appropriateness. It does this by receiving information from the motor cortex, then prepares the movement and then relays this information to the thalamus that then sends information to the motor cortex again. The inhibition is exerted by the basal ganglia through release of GABA on the thalamus, which inhibits thalamus’ output to the motor cortex.

116
Q

Cerebellum

A

Programs movements. Coordinates movements. Assists in learning of new skills. A clock that regulates the rhythm of movement. Also center for predictions, predictive control in movement.

117
Q

General adaptation syndrome(GAS)

A

Consists of three phases, alarm, resistance and exhaustion.

Sudden activation of the sympathetic nervous system triggers the alarm phase.

Resistance is when the body’s resources are mobilized during a prolonged time. Stress hormones are continually secreted. There is a limit to how long this can be sustained.

Exhaustion occurs when the body’s immune system is too weak, and vulnerability to disease is very high. Can lead to collapse, sickness or death.

Critique against GAS theory:

Unspecific and general.

Are rats and humans really able to be compared when rats were tortured?

What is stress? The stimulus or response?
Is it the emotional interpretation of signals?
Everything threathens homeostasis, is everything a stressor?

118
Q

Riskfaktorer för stress

A

Otrygg anknytning.
Bristande socialt stöd.
Dåliga sömnvanor, samt oregelbunden livsstil.
Dålig self-efficacy
Dålig coping.

119
Q

Aktivering av stressrespons

A

Binjuren utsöndrar kortisol, adrenalin och noradrenalin. Höjer blodsockerhalt, blodtryck samt puls. Mer energi åt musklerna, blodet koagulerar snabbare och nedsatt nocioception, mer syretillförsel till musklerna.

120
Q

Slow-acting stress pathway

A

Activated by the hypothalamus when a stressor or dangerous stimulus is detected by the thalamus that asks the hypothalamus for evaluation. This leads to an release of corticotropin hormone that stimulates the pituitary gland that releases adrenicorticotropin-hormone into the bloodstream. This further stimulates the adrenal glands to release adrenaline and cortisol. This elevates blood pressure, increases glucose concentration in the blood stream and elevates pulse to prepare us for a fight or flight. The hypothalamus receives input from the HPA-axis to regulate the activation of said axis. We only want so much cortisol and adrenaline coarsing through our veins. When the stressor is eliminated, the HPA-axis is deactivated and vitals are returned to base level. This repairs stress-related damage aswell.

121
Q

Long term consequences of stress response activation

A

With the repeated activation of the stress response, the chronical presence of adrenaline and cortisol can produce long term effects on the immune, cardiovascular and nervous system causing different issues such as heart disease, cardiovascular issues, depression, anxiety and other chronic conditions. It can also affect the hippocampus causing cell degeneration, this is seen with PTSD patients who suffer memory loss. The hippocampus is involved in shutting off the stress response as it communicates with the hypothalamic HPA-axis. Thus a dysfunctional hippocampus leads to a prolonged stress reaction that leads to further stress. Hippocampus detects cortisol levels in blood and elicits a negative feedback loop that results in the HPA-axis shuts off. Hippocampal neurons are damaged by excess cortisol.

122
Q

Fast-acting pathway of stress

A
  1. Stressor detected by the body.
  2. Signaling from brain that sends signal to adrenal medulla through the sympathetic nervous system.
  3. Release of neurotransmitters such as adrenaline and noradrenaline into the blood stream.
  4. Physiological changes occur to prepare to fend off and deal with stressor.
  5. Post-stressor deactivation of stress response. Physiological regression to base line.
123
Q

Beroende innebär

A

Eskalering av bruk.
Tvångsmässigt intag
Återfall efter försök att sluta.

124
Q

Riskfaktorer för beroendeutveckling

A

Adverse Childhood Experiences ACE
Kvinnor, delvis pga kroppsvikt men även hormonella faktorer

125
Q

Wanting-Liking

A

Produced by different brain regions.

Wanting - Striving, effect increases after escalation of use. Sensitivization increases because of learning.

Liking - Liking the effects. This effect decreases with abuse.
Tolerance increases.

126
Q

Sensitivization of the mesolimbic dopamin circuit

A

Mesolimbic dopamin circuit connects the ventral tegmental area and the nucleus accumbens.

In summary, sensitization in the mesolimbic dopamine circuit plays a crucial role in the development of drug abuse and addiction by increasing both wanting (craving) and liking (pleasure) associated with drug use.

127
Q

Alkohols beroendeeffekter

A

Ökar GABA
Blcokerar glutamatreceptorn NMDA, som är excitatorisk(Påverkar inlärning negativt)
Ökar dopaminfrisättning
Ventral tegmental area - dopamin till prefrontala kortex, därför får vi inhiberad impulskontroll.
Alkohol inhiberar VTA = lever ut impulser i ökad grad.
Högt långvarigt bruk mycket skadligt.

128
Q

Bensodiazepiner beroendeeffekter

A

Ökar GABA.
Lugnande effekt beteendemässigt
Tillvänjningseffekt kräver ökad dos, men platå uppnås oftast.
Ska utsättas långsamt.
Oförtjänt dåligt rykte. Ibland är det det bästa alternativet. Sällan dödliga överdoser, dock ökar dödlighet i kombination med alkohol och opiater.

129
Q

Lustgas N2O

A

Lugnande, sövande, smärtlindrande med inslag av eufori. Utvidgar blodkärl i lungorna.

Enkel molekyl. Ökar GABA signalering.
Inhiberar NMDA (glutamatreceptorer)
Ökar mesolimbisk dopaminsignalering från VTA till limbiska systemet samt nucleus accumbens/ventrala striatum.
Verkar också genom opioidsystemet.

Inte ofarlig vid hög användning.
Blodförändringar som kan ge arrytmier.
Genförändring vid djurstudier.
Akut vitaminbrist med nervstörningar.

130
Q

Cannabis

A

Huvudsaklig aktiv substans: THC
Fettlöslig, lagras i hjärnan.

Aktiverar cannabinoidreceptorer.

Beteendeeffekter:

Eufori
Försämrat korttidsminne
Ökad aptit
Hallucinationer
Ångest
Paranoia
Psykos

131
Q

Amefetamin och Metamfetamin

A

“Drunken uncle” : Kommer in i neuronet och vänder upp och ner på möblerna.
Stoppar domain(amfet) och serotonin (metamfet.) Stoppar upptag till vesiklarna som skulle fylls med neurotransmittorer.
Vänder på transportörens flöde och spottar ut monoaminer i synapsen.

Beteende:
Eufori
Ökad puls
Ökad kroppstemperatur
Ökad vakenhet
Beroende
Aggressivitet
Anorexi
Psykos
Depression
Sömnstörningar/epilepsi
Torr mun, LOL

132
Q

MDMA

A

Blockerar återupptag av serotonin, vänder transportörens riktning och ökar frisättning.
Ökar också noradrenalinfrisättning.
Vissa SSRI kan blockera effekten, men man kan även få serotonergt syndrom.

Beteende: Milda hallucinationer
Eufori
En känsla av infre frid
Förhöjd känslighet
Förhöjd känsla av intimitet

Sker forskning på MDMA som medicin för behandlingsresistent PTSD och depression.

133
Q

Psilocin (Psilocybin)

A

Stimulerar serotoninreceptor 2A.

Hallucinogen
Nya stjärnan på psykofarmahimlen.
Främst för behandlingsresistent PTSD och depression.
Trippar i lugn miljö med guider närvarande. Lugn musik. Ögonbindel pga ljuskänslighet???
Oklart vad den terapeutiska mekanismen är.

134
Q

Ketamin

A

Smärtlindrande, sövande. Minskar suicidalitet snabbt, SSRI fördröjt.

135
Q

Opiater

A

Smärtstillande
Ångestlindrande
Frisättning av dopamin(inhibierar GABA-neuron) och Histaminer

Typer:
Morfin
Heroin - Snabb ökning av mikroreceptorer ger tolerans
Fentanyl - Superdödligt
Endorfin(Kroppsegen opiat)

136
Q

Selektiv uppmärksamhet

A

Förmågan att välja ut de uttryck värda vidare bearbetning. Styrs av top-down och bottom-up processer.

137
Q

Fokuserad uppmärksamhet

A

Förmågan att ignorera irrelevant intryck.

138
Q

Delad uppmärksamhet

A

Förmågan att uppmärksamma två intryck samtidigt.

139
Q

Faktorer som påverkar uppmärksamhetsförmågan

A

Vakenhetsgrad: Viktig för uppmärksamhet och arbetsminne. Optimal vakenhetsgrad, inte för aktiv.
Stimulusdriven uppmärksamhet: Den typ av uppmärksamhet som dras till salient stimuli. Men även tankar som dyker upp i vårt huvud som ej går att släppa.
Kontrollerad uppmärksamhet: Den typ av uppmärksamhet som vi använder när vi väljer att fokusera på en specifik sak. Då ignorerar vi även irrelevant input.

140
Q

Stimulus-styrd uppmärksamhet

A

Nyheter, plötslig förändring, rörelser, yttre stimuli

141
Q

Självkontrollerad uppmärksamhet

A

Anstränga sig för att fokusera
Ta sin tid
Hålla saker i minnet

142
Q

Uppmärksamhetens neurala bas

A

A(RAS) - Vakenhet
Superior colliculus - styr ögonen
Thalamus - pulvinarkärnan
Cingulate cortex, innanför prefontala cortex
Parietalloberna, orientera i rummet
Frontalloberna, framför allt prefrontala cortex

143
Q

Pulvinarkärnan

A

Kopplad till ventrala visuella strömmen
Input från superior colliculus: 2D-karta över synfältet
Styr eller speglar uppmärksamhet?? Återkopplingsloop med cortex

144
Q

Lateral genicular nucleus

A

Sitter i Thalamus, tar emot och filtrerar input från synnerven.
Ponto-geniculo-occipital waves??

145
Q

Ponto-geniculo-occipital waves

A

Ponto-geniculo-occipital (PGO) waves are electrical waves that occur in the brain during the transition from wakefulness to sleep. They originate in the pons, a part of the brainstem, and then travel to the lateral geniculate nucleus in the thalamus before finally reaching the occipital cortex, which is responsible for processing visual information.

PGO waves are thought to play a role in the regulation of sleep and the consolidation of memory. They have been observed in various animals, including cats, rats, and humans, and their pattern and frequency can change depending on the stage of sleep.

Ponto-Geniculo-Occipital (PGO) waves are electrical brain wave patterns that occur during rapid eye movement (REM) sleep. They are characterized by bursts of electrical activity in the brainstem regions known as the pons, lateral geniculate nucleus, and occipital cortex. PGO waves are believed to be involved in the generation of REM sleep, as well as in the processing of visual information during dreaming. Research has also suggested that PGO waves may be disrupted in certain neurological disorders, such as Parkinson’s disease and schizophrenia.

146
Q

Emotion’s effect on attention

A

Motivation:
Nucleus accumbens
Ventral pallidum
Anterior cingulate cortex, ACC

Emotional memories:
Amygdala
Stria terminalis
Hippocampus
ACC

147
Q

Exekutiva funktioner

A

Bibehållen uppmärksamhet
Reflektion
Organisation
Självreglering
Självuppskattning
Social kognition
Medgörlighet
Arbetsminne
Koordination av rörelse

148
Q

Vid ADHD gällande exekutiva funktioner

A

Koncentrationssvårigheter
Impulsivitet
Hyperaktivitet
Planeringssvårigheter
Oflexibel
Dålig självkänsla
Nedsatt social kompetens
Trotsigt beteende
Disträ
Motoriska svårigheter

149
Q

Första reaktionen vid stress och vad som händer om vi inte lyckas lösa stressoren

A

Storhjärnan jobbar för att lösa problemet. En avancerad hantering av påfrestningar som gör att vi lyckats utvecklas så långt som vi gjort som art. Vi använder vår analytiska förmåga för att komma undan faran. Vi använder rationella bemästringsstrategier. Endast när detta misslyckas använder vi oss av mer primitiva biologiska metoder. Om inte våra kognitiva/emotionella coping-strategier fungerar triggas fight or flight.

150
Q

Neuroplasticity

A

Hippocampus can be rebuilt and stem cells can regenerate to a certain extent. It might take time. Activities that help regeneration:

Peace and quiet.
Physical activity
Stimulation of the soul, nature and culture.

151
Q

Congenital adrenal hyperplasia

A

XX-chromosome feutus exposed to too much testosterone. Leads to external parts of genitalia developing in masculine direction.

152
Q

Hypogonadism

A

XY-chromosome not being exposed to enough testosterone. Leads to development of breast, but not body hair nor testicles nor ovaries.

153
Q

Neurobiological differences between men and women in adults

A

Synthesis and reception of neurotransmitters differ between the two groups.

Varies in women in relation to menstrual cycle.

154
Q

Suprachiasmatic nucleus

A

24h-klocka som koordinerar olika hjärndelar för att uppnå synkronisering av cirkadiska rytmen. Får input från intergeniculate leaflet i thalamus om både visuell men även icke-visuell sensorisk input från andra delar i genikularkroppen.

155
Q

Melanopsin

A

Pigment i ögat som aktiveras av kortvågigt blått ljus. Skickar signaler om huruvida melatonin bör produceras.

156
Q

Lateral thalamus

A

Collects information about current sleep debt. Excites many systems that regulate wakefulness.

157
Q

Dorsomediala hypothalamus

A

Äta, dricka och dygnsrytm. Output till Pos nucleus

158
Q

Distributed network theory

A

This theory proposes that long-term memories are stored in a distributed network of neurons throughout the brain, rather than in a single, specific location. According to this theory, each memory is represented by the activity patterns of a large number of neurons that are distributed across multiple brain regions.

159
Q

Engram theory

A

This theory proposes that the changes in the structure and biochemistry of neurons otherwise known as engrams underlie long-term memories.

160
Q

Synaptic plasticity

A

Refers to the changes in strength of the synapses between neurons. It is this change that underlies the long-term memories. New experiences affect the synapses’ strength and this modification affects the memories.

161
Q

Standard model of consolidation - Squiremodellen

A

Episodic memories become independent of hippocampus after consolidation.

162
Q

Acetylcholine

A

Important for attentional functions. Sustained and selective attention seems to be affected by low acetylcholine levels.

Increase in acetylcholine leads to heightened wakefulness. Levels decrease when we enter sleep and increase when we wake up.

Termin 2 (6 decks)

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