Final Flashcards
use it or lose it
cognitive exercise, education, mental acuity, associate with delayed loss of cognition in normal aging and decreased risk of dementia.
Exercise
is any bodily activity that maintains or improves physical fitness health and wellness.
rates
59% Canadian adults are overweight.
15% manage 2.5 hours of activity per week.
26% youth are fat.
cost
- 1 billion for direct health care
6. 5 billion if include loss of productivity.
evidence
math and reading are positively correlated with aerobic fitness.
specific regions, math and reading…
Math: PFC
reading: PFC and posterior cingulate cortex.
Aerobic exercise: network connecting the frontal lobe and parietal lobe is activated.
exercise
it activates the same networks required for math and reading.
criticisms of research
historical and indirect reporting.
meta-analysis
bias; use of a school district with historically poor or high test scores.
exercise; no improvement in;
language fluency, spatial manipulation, object recognition
exercise– improvement
executive function (attention, distinguish relevance, organize, plan) Working memory
what does aerobic exercise do to the brain?
Decreased activation of anterior cingulate cortex (emotional response)
Increased activation of the PFC and parietal cortex (executive function).
*Exercise increased top down control by the PFC.
Mood
running naturally releases endorphins which are associated with improved mood.
Effect
exercise is equal to cognitive therapy, positive effect on depressive symptoms.
Fatigue
associated with neurobiological changes, metabolic disruption affecting the levels of neurotransmitters.
depressed athlete conundrum
constant achievement created stress.
fatigue
**high levels of exercise chronically activate the HPA axis, which is critical in neuropsychiatric disorders.
why is it good
- blood to brain
- neurotransmission; increase concentration, promote communication/
- enhanced neuroplasticity; neurogenesis.
positive effects
due to increases in metabolism, oxygenation and blood flow in the brain.
*Increases neurotransmitter production, particularly serotonin, dopamine, but also GABA, glutamate and norepinephrine.
Memory
exercise increases the volume of the hippocampus.
- Rodents: rich environment leads to increased dendritic complexity.
- For humans increase grey matter volume in frontal and temporal lobes.
Growth factors
- vascular endothelial growth factor (VEGF)
2. Brain-derived neurotrophic factor (BDNF); promotes neurogenesis and axonal growth.
neurogenesis
The new cells are critical for learning and memory.
- reduce anxiety and depression, mice forced swim test, and also mice who exercise are more likely to explore.
- Also resistance to stress, better coping.
mood disorders
psychological disorders characterized by pathological extremes of mood. Bipolar, would be an example of a high and low cycle.
*10% of people.
bipolar
Mania is elevated mood to the point of euphoria or delirium such that it impairs daily functioning.
1-2% population, both sexes equal.
Difference sadness and depression
Sadness is an emotional pain, and a natural consequence of difficult situations which we cannot run away from.
*It becomes pathological depression when we loose sight of its time limited nature, learned helplessness. Untreated it could last 9 months.
MDD
sustained down mood, guilt, worthlessness, anhedonia (loss of interest/enjoyment in everyday activities.)
Effects:
- thought: poor concentration, difficulty making decisions.
- Sleep: insomnia, fatigue
- appetite: increase or decrease
- Libido; decrease
*80-90% experience second episode within 2 years.
depression
most common, but most treatable. 1 in 5 ppl affected. 15% suicide.
CBT
psychotherapy taught to recognize and change thought processes that cause or contribute to deepening symptoms. Positive feedback goes along way to helping.
Cognitive changes from coping. BUT coping is permanent, it is a protective factor.
Monoamine hypothesis
Biological basis is decreased availability of noradrenaline and serotonin.
monoamine hypothesis evidence
- symptoms improved by treatments that increase the synaptic concentration of monoamines.
- Serotonergic and noradrenergic systems regulate emotion, mood, attention, reward processing, cognition, appetite, which are implicated by depression.
Monoamine oxidase
enzyme degrades monoamine neurotransmitters such as dopamine, noradrenaline, serotonin.
MAOI
monoamine oxidase inhibitors; block enzyme MAO from degrading neurotransmitters.
effexor
SNRI
does decreased neurotransmission explain it all?
little evidence that low levels of these neurotransmitters cause depression.
glucocorticoid hypothesis of depression
- dysfunctional HPA axis
- first episode reactive to event, other episodes are endogenous, triggered by minor stressors.
- hypercortisolemia: elevated levels of cortisol even at non-stressful times.
* Impaired negative feedback in the HPA axis. - and reduced hippocampal volume which correlates to length of depression.
Ketamine
fast symptom relief. NMDA receptor antagonist. leads to more Glutamate in the synapse (excitatory).
- Increases density of synapses in PFC, improves cognition.
- Reduces hyperactivity of the amygdala, normalizes emotional response, decreases fear,
- Improves activity in the anterior cingulate cortex, improved motivation and cognitive control.
- Promotes plasticity.
Fear
stress response from immediate danger: emotion.
*SAM axis fight or flight.
anxiety
stress response from your thoughts
- mood arising from expectation that future threat is perceived as uncontrollable.
- cognitive process, chronic, mood state.
Anxiety disorder
When these feelings become so frequent in response to inappropriate events that it takes over life.
anxiety
15-35% pop, share a general proneness to negative affect but differ in the specificity of the threat reacted to.
*Most 50% have multiple anxiety disorders.
Panic Attack
surge of intense fear or discomfort that reach a peak within 10 minutes.
*Activation of sympathetic NS.
panic disorder
panic attacks occur repeatedly without warning or relation to external stimuli.
*fear of future attack, anticipatory anxiety: the fear of having an attack could create an attack.
Phobias
anxiety disorder, panic attacks directed at a specific object or situation.
***Most common, but least disabling…
Amygdala fast response
via thalamus and happens before we even know what it is we are afraid of.
Amygdala slow response
relayed from thalamus to cortex where it is processed allowing you to identify the threat and respond accordingly.
panic regions.
- increase activation cingulate cortex and parahippocampal gyrus (fear learning)
- amygdala is hypersensitive,
- decreased activity in the PFC (confusion, disorientation).
- excessive excitatory neurotransmission may enhance anxiety.
exposure therapy, extinction
stimulus loses its effect as trigger is unlearned.
- habituation
- self-efficacy (belief in one’s ability to manage.
- Emotional processing (attaching new beliefs to fear)
GAD
persistent anxiety, worry, more days than not.
GAD brain,
Not sympathetic NS, increase parasympathetic NS activation, they have increase activity in frontal lobes, Amygdala activates in anticipation of negative image.
Anxiolytics
anti-anxiety properties.
Trauma
personal experience of a severely distressing event.
*more than a month PTSD, intrusive memory etc.
PTSD
learned fear becomes generalized to situations that would normally be considered safe, this results in autonomic hyperarousal in inappropriate situations.
*fear and anxiety
PTSD diagnostic
- recurring and frightening memories
- avoidance of triggers
- heightened arousal
risk PTSD
- women 2x more than…
- genetic component
- choice; there by choice…
- resilience;
brain PTSD
- anterior cingulate cortex, decreased volume,
- hippocampus, reduced volume
- amygdala, increased reactivity.
memory
LTP, electrical stimulation, pre-synaptic, produces increase EPSP post-synaptic, involves glutamate binding to NMDA receptor.
neurons that wire together…
- strong stimulation can depolarize the postsynaptic membrane that the magnesium ion is removed from the NMDA receptor.
- Now glutamate released by weak stiumulation can activate the NMDA receptor to allow Ca influx. this increases the function of AMPA receptors.
Acute stress
cements memory, link trauma and fear, LTP pairs emotional memory and hippocampal memory,
hippocampus
- pattern separation is the recording of events. this in dentate gyrus.
- pattern completion is the ability to recall and complete a memory based on a limited set of sensory inputs.
neurogenesis
birth of new neurons from stem cells.
- subventrucular zone, lateral ventricles.
- Subgranular zone, dentate gyrus of hippocampus.
study
new neurons play a role in encoding and distinguishing among memories that are related but distinct.
hypervigilance
sensitivity to surroundings.
resilience
- capability of a strained body to recover its size and shape after deformation.
- an ability to recover from or adjust easily to misfortune or change.
stress inoculation
good stress; hermetic stress, short term cortisol promote adaption, confidence in coping strategies.
resilience endorphins
touch can stimulate the release of natural opioids, the anterior cingulate cortex is packed with opioid receptors and their activation could create feelings of reward and increase the rational decision making.
resilience oxytocin
oxytocin can reduce emotional responses to frightening images.
this includes reduced activation of amygdala and weaker connections between the amygdala and brainstem.
resilience cingulum
a white matter tract within the cingulate cortex that connects the frontal lobe with the temporal lobe.
**resilient have stronger physical connections between the anterior cingulate cortex and the hippocampus via the cingulum.
neuropeptide Y
hormone released during stress, shuts down the stress response by inhibiting the secretion of ACTH and norepinephrine.
OCD
recurring unwanted thoughts, ideas, which cause the person anxiety and in turn they may try to relieve these feelings by performing compulsions.
Y-BOCS
- time spent
- degree of interference
- subjective distress
- resistance to obsessions
- degree of control one has over them.
**Cortico-striato-thalamo-cortical circuit (CSTC)
Thalamus is hyperactive, leads to hyperactivation of PFC and striatum.
basal ganglia
damage can cause OCD, patients will persist with a habit even if it has a negative consequence. persistence is associated with hyperactivation of caudate nucleus.
ablation
OCD; cingulotomy severing the anterior cinglum have proven useful.
BDD
decreased activity in the visual cortex, extends to non-body and non-face images, visual processing defect.
