NEUR 1202 > Final > Flashcards

Final Flashcards

(52 cards)

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1
Q

ADHD

A

Attention-Deficit Hyperactive Disorder. Developmental disorders diagnosed typically as inattentive, hyperactive, and combined. Manifestations of the disorder must appear across multiple settings. Academic performance suffers and social rejection, motor/speech/language delay tends to present. Elevated in first-degree biological relatives of people with ADHD.

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2
Q

Gene-environment interactions in ADHD

A

Children with DAT1 mutations whose mothers smoke during pregnancy are more likely to develop ADHD. Perinatal hypoxia is also linked to ADHD.

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3
Q

ADHD and clinical tasks

A

Perform more errors of omission/commission in Go/NoGo tasks, pick from risky deck in Iowa Gambling Task

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4
Q

Behavioural markers of ADHD

A

Rewards have apparently have less influence over behaviours of children with ADHD

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5
Q

Alerting network

A

Frontal, parietal cortex and thalamus

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6
Q

Frontostriatal circuit

A

Affective/cognitive components of executive control.

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7
Q

Psychostimulant treatment

A

Mainstream pharmacological treatment for ADHD: methylphenidate, amphetamine, d-amphetamine. Long-acting, slow release versions.

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8
Q

ASD

A

Autism Spectrum Disorder, a neurological/developmental disorder that is chronic throughout the lifespan. Graded from 1 (low support needs) to 3 (high support needs). Typically appears in early childhood. Normal development until 12 months, then startling decline. Three major areas of difficulty: impaired communication, social interactions & restricted behaviour, interests, and activities.

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9
Q

Impaired communication in ASD

A

Echolalia, overly literal understanding, odd combination of verbal abilities

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10
Q

Impaired social interaction

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Lack of affective social competence or sense of emotion

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11
Q

Restricted behaviour

A

Stereotypies/stimming, preference for status quo, ritualistic behaviours

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12
Q

Social cognition

A

How you think about yourself/the world, tested by theory of mind

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13
Q

Theory of mind

A

Ability to attribute mental states to others. Low functioning ASD patients never develop theory of mind.

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14
Q

Etiology of ASD

A

Highly heritable: MZ concordance rate of 36-91%

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15
Q

ASD environmental risk factors

A

Maternal diet/smoking, air pollutant exposure, poor socioeconomic status, low maternal education level, advanced maternal/paternal age, folic acid status

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16
Q

Medical comorbidities in ASD

A

Immune dysregulation and gastrointestinal disturbances

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17
Q

Neurobiology of ASD

A

Results from overall brain disorganization (not one focal region).

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18
Q

Extreme male brain theory

A

Autism is linked to extreme profile of male brain function: prenatal testosterone reduces performance on emotion-reading tasks.

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19
Q

Mirror neuron system

A

Respond to understanding of an action. Deficits observed in autism are controlled by mirror neurons.

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20
Q

How do antipsychotics work?

A

By blocking D2 dopamine receptors (D2 antagonists)

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21
Q

Perinatal factors in schizophrenia

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A

Influenza/viral exposure, prenatal stress, pregnancy/delivery complications

22
Q

Prodromal stage

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A

1-2 year period preceding first episode, subdued symptoms begin to appear

23
Q

Physiological basis of schizophrenia

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A

Enlarged lateral ventricles imply that other parts of the brain are less developed/atrophied. Reduced dendritic spine density in prefrontal cortex. Reduced size of hippocampus due to degradation.

24
Q

Striatum

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A

Dorsal involved in habit learning, motor and action planning, ventral involved in reward learning, motivation

25
Hypofrontality
Understimulation of D1 receptors in prefrontal cortex, can explain why people with schizophrenia struggle with planning, problem-solving and high-level reasoning
26
Reward
Stimuli that are positive and can affect behaviour
27
Mesocorticolimbic dopamine system
Ventral tagmental area (TVA), contains neurons that produce dopamine. These neurons project to/release dopamine in the nucleus accumbens (esp in addictive drugs), hippocampus and prefrontal cortex
28
Genetic component of depressive disorders
First-degree relatives 2-3x concordance
29
Monoamine hypothesis of depression
Depression thought to be strictly due to limited release of monoamine (monoamine signaling). MAOIs are effective antidepressants.
30
How do SSRIs work?
Post-release, excess serotonin is broken down by MAO and cleared by serotonin reuptake transporters. SSRIs block SRTs, increasing serotonin in the synapse
31
Evidence against MA hypothesis
SSRIs don't help everyone, long lag time between treatment and reduction of symptoms, little evidence that low lvls of these NTs cause depression
32
Glucocorticoid hypothesis of depression
Dysfunctional regulation of HPA axis stress response contributes to depression
33
HPA axis dysregulation in depression
Hypocortisolemia occurs in severe depression, causing unnecessarily high cortisol levels in blood, which impairs HPA axis response. Normally, cortisol binds to glucocorticoid receptors in hippocampus to activate the negative feedback response and shut down stress response.
34
Depression and the hippocampus
Longer the depression, further the damage. Hippocampal cell density reduced/neurons shrunken, overall reductions in hippocampal volume. Antidepressants reverse damage by increasing neurogenesis in the hippocampus.
35
Estrogen and the HPA axis
Levels vary over menstrual cycle, but E itself is protective against stress and depression - SSRIs work better when combined with estrogen
36
Psilocybin
Is converted to psilocin when absorbed (hallucinogenic effects) - which is an agonist to 5HT2A (structurally similar to 5HT), may reduce depressive symptoms
37
Characteristics of anxiety disorders
High rate of suicidality, comorbidity
38
Anxiety
Apprehension related to the future, related to real or perceived worries/threats (GAD)
39
Fear
Emotional and physiological response to real or perceived threats (panic disorder)
40
GAD neurobiology
SNS less responsive to stressors, worry increases PNS response. Increased activation in frontal lobe during stressful stimuli. Greater amygdala response in anticipation of negative stimuli. Increased PFC activity.
41
Panic disorder neurobiology
Sudden panic attacks. PFC activity decreases. SNS and limbic system increase.
42
Panic attack neurobiology
Resembles fear response, but unprovoked. Amygdala activates in response to anxiety-inducing stimuli. Amygdala can also by hyposensitive under certain conditions. COMT gene clearly linked to PD.
43
Anxiolytics
Drugs that treat anxiety - benzos are agonists to GABA receptors, increase inhibitory signalling. Beta blockers treat autonomic symptoms.
44
OCD psychological loop
Stimulus triggers obsession + distress/anxiety, which triggers compulsions + temp. relief
45
Neurobiology of OCD
Several genes related to glutamate/GABA, CSTC. Serotonin, dopamine, glutamate.
46
PTSD
Trauma exposure, intrusion, avoidance, cognitive, arousal reactivity for 1+ months.
47
Fear circuitry
Medial PfC appraises threat, if threat, HPA axis/amygdala signals. Amygdala to hippocampus and hypothalamus. In PTSD, amygdala is rendered hypersensitive, PFC activity is reduced, resulting in hypervigilance, arousal, etc
48
Anatomical findings in PTSD
Significant volume reduction in hippocampus and ventral medial portion of PfC
49
Neurobiological differences in PTSD
PTSD patients show enhanced stress activity in SAM and HPA axis pathways, altered adrenaline, cortisol and noradrenaline level (n is biomarker)
50
Pharmacological treatment of PTSD
Propanolol administration within a couple hours of traumatic event prevents noradrenaline binding and reduces chance of PTSD developing. CBD can reduce symptoms.
51
Endogenous cannabinoid system
Activated in times of stress: helps to regulate and return to baseline using endogenous ligands (AEA and 2-AG). 2 main receptors CB1 (brain) and CB2 (immune)
52
THC in the brain
THC mimics shape of endogenous ligands and binds in axon terminals
NEUR 1202
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