Neuroscience and Clinical 2 Flashcards

(286 cards)

1
Q

what is congenital brain injury

A

brain injury from genetic factors, pre-natal or birth related trauma

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2
Q

what is acquired brain injury

A

things we do to ourselves
traumatic or non-traumatic

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3
Q

what is non traumatic brain injury

A

stroke
infections
tumours
hypoxia / anoxia

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4
Q

what are the types of strokes

A

cerebral haemorrhage
cerebral ischaemia

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5
Q

what happens in a cerebral haemorrhage stroke

A

aneurism causes blood to enter brain
blood is toxic to neural tissue

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6
Q

how to prevent a haemorrhagic stroke

A

maintain low blood pressure
avoid strenuous activity

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7
Q

what is a cerebral ischaemia

A

where there is an interruption of blood supply to the brain due to a blockage of a vessel
leads to lack of oxygen / glucose leads to neuronal cell death

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8
Q

what can cause a blockage

A

thrombus
emboli
cardiovascular disease - athersclerosis

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9
Q

what is the goal of treatment for a ischaemic stroke

A

rescue penumbra by reopening blocked blood vessel

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10
Q

what is a traumatic brain injury

A

intracranial injury
involves closed / open head injury

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11
Q

what is a closed head injury

A

where there is no penetration of skull

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12
Q

what is dementia pugilistica

A

punch drunk syndrome
repeated powerful blows to head
cumulative structural damage results in dementia symptoms

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13
Q

what is an open head injury

A

where the skull doesn’t remain intact
damage to the skull where brain fragments damage the tissue

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14
Q

what is alzheimer’s

A

a disease that causes dementia, with selective decline in memory
mostly cognitive symptoms in early stages

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15
Q

what is parkinson’s

A

neurodegenerative disease with predominantly motor related symptoms

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16
Q

what causes alzheimer’s

A

abnormal build up of amyloid protein and tau (neurofibrillary tangles)

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17
Q

what is alzheimer’s associated with (neurotransmitter)

A

loss of acetylcholine

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18
Q

what causes parkinson’s

A

lack of dopamine in a particular pathway
excessive inhibitory output from basal ganglia causes symptoms

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19
Q

what is dementia

A

chronic or persistent disorder of the mental processes caused by brain disease or injury
marked by memory disorders, personality changes and impaired reasoning

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20
Q

what are the symptoms of parkinson’s

A

bradykinesia - slow movement
akinesia - no movement
increased muscle tone - rigidity
resting tremour
shuffling gait, flexed posture
impaired balance

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21
Q

what treatments are there for parkinsons

A

replace lost doapmine
surgical intervention

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22
Q

what surgical intervention is there for parkinson

A

electrical stimulation of basal ganglia - deep brain stimuli
replace lost DA cells

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23
Q

what are the treatments for alzheimer’s

A

target loss of neurones that produce / release the neurotransmitter acetylcholine

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24
Q

what is cholinesterase (AchE)

A

enzyme that breaks down the neurotransmitter acetylcholine
(alzheimers)

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25
what other brain diseases are there with neurodegenerative component
cerebrovascular disease cancer epilepsy infections other movement disorders psychiatric
26
what is a fertilised egg calledd
zygote
27
what is the zygote called on day 4
morula
28
when does the morula become a blastocyst
day 5
29
what are the two layers of the cell on day 5
inner cell mass - embryo encompassing sac - trophoblast / placenta
30
what are the two layers inside the embryo - day 5
epiblast (embryo) hypoblast (gut)
31
what does the encompassing sac do
cells secrete fluid creating a cavity
32
what happens between day 13 - 19 with the zygote
gastrulation
33
what is gastrulation
formation of a groove / primitive streak
34
what is the name of the cell at day 13-19
gastrula
35
what are the three cell layers in the gastrula
ectoderm mesoderm endoderrm
36
where does the nervous system start develop
ectoderm thickens to form neural plate neuroectoderm in front of primitive streak
37
what happens on day 20
uneven rates of cell division form neural groove - midline of embryo
38
what day does neuralation happen
day 20
39
what is neuralation
where it becomes a neurula bulge on either side of ectoderm come together to form neural tube interior becomes fluid filled vesicles of brain and central canal of spinal cord
40
what are the three major divisions of the brain
presencephalon (fore) mesencephalon (mid) rhombencephalon (hind(
41
what is in the presencephalon
telencephalon diencephalon
42
what is in the rhombencephalon
metencephalon myelencephalon
43
what happens at 3-4 weeks
the telecephalic tube grows over the rest of the the brain to make cerebral cortex forms the occipital and temporal lobe
44
when are neural precursor cells developed
in gastrulation receive a chemical signal from notochord
45
what happens to precursor cells after neurulation
divide into either primitive neuron (neuroblast) or glial cell (glioblast)
46
how does the axon develop
immature neurons produce a number of small extensions - neurites one side becomes axon, other becomes dendrite
47
how do neurons find target location
using growth cones receptors in filopodia sense attractant or repellant chemical cues in the environment
48
what are diffusible agents
chemoattractants , chemorepellants
49
what are non diffusible agents
contact attractants contact repellants
50
when are the majority of neurons that make the adult brain created
7th pre-natal month
51
what happens to cerebral development post natal
severe dilation of lateral ventricles postnatal hydrochephalus
52
what is postnatal hydrocephalus
build up of CSF fluid within brain magendie's foramen
53
what is the main visual pathway in humans
geniculostriate system
54
what can post natal wiring of the brain be influenced by
experience
55
what is a critical period
specific time during early development when the brain is particularly sensitive to environmental stimuli
56
how is distribution of cortical neurons affected
based on stimulation of both eyes in early years
57
what is monocular deprivation
blinding one eye
58
what does monocular deprivation cause
width of ocular dominance columns in the visual cortex - normal eye wider than normal affects axonal branching in the visual cortex
59
what is the critical period for cat eyes
first 3 month
60
what is the critical period for monkey's eyes
6 months
61
can neuroplasticity occur in adults
yes
62
examples of neurplasticity in adults
london taxi drivers have bigger posterior hippocampi visual cortex responds to braille in late-blind individuals
63
what is the mechanism for adult neurogenesis
new neurons and glial cells generated in two regions of the adult brain
64
which two regions generate neuron and glial cells in the brain
olfactory bulb hippocampus
65
where is the olfactory bulb
adjacent to lateral ventricles
66
what does the olfactory bulb do
provides neuroblasts that later form neurons in the olfactory bulb
67
what does hippocampus do
produces cells in the area of dentate gyrus called sub-granular zone
68
what contacts the newly generatdd granule cell in the adult hippocampus
GABAergic synapses
69
what disease is epilepsy
acquired traumatic brain disease
70
what is epilepsy
chronic medical condition produced by temporary changes in the electrical function of the brain, causing seizures which affect awareness, movement or sensation
71
what are the types of epilepsy
partial epilepsy auras generalised epilepsy
72
what are the types of partial seizures
simple partial seizures complex partial seizures
73
what are the types of generalised seizures
grand mal seizures petit mal seizures
74
what is a simple partial seizure
localised seizure to a specific area - usually sensory or motor
75
what is a focal motor seizure
type of simple partial seizure localised jerking and progressing to clonic movements of entire arm
76
what is the jacksonian march
progression of seizure up the arm produced by eplepticform activity in motor cortex
77
what is a complex partial seizure
localised to a specific area due to common localisation
78
what is complex partial seizure also known as
focal onset awareness or temporal lobe epilepsy
79
what is complex partial seizures associated with
coordinated / ordered but inappropriate motor behaviour
80
what are the symptoms of a complex partial seizure
running, chewing, buttoning absent lasts a few minutes often no memory of episode
81
what is an aura
symptoms that happen before a partial seizure
82
what causes aura
abnormal electrical activity originating from seizure focus
83
what are the signs of aura
sense of fear rising feeling in abdomen strange tastes / odours metallic visual sensations akin to hallucinations
84
what is a grand mal seizure
can involve entire brain patient loses consciousness and has a tonic-clonic seizure
85
what is the tonic phase
rigidly extend all limbs
86
what is the clonic phase
jerking in all extremities
87
what is a petit mal seizure
entire brain briefly absent / disrupted consciousness
88
can partial seizures generalise
yes
89
what can be used to identify epilepsy
electroencephalography
90
what can an EEG do
detect synchronised activity of many neurones
91
what are we interested in on an EEG to help diagnose epilepsy
signal over time frequency components of the signal (how fast the waves are oscillating)
92
what EEG sign is assocaited with petit mal generalised seizures
spike and wave
93
what are the medical treatments of epilepsy
carbamazepine, phenobarbital, phenytoin (dilantin), valproic acid
94
what do the drugs for epilepsy do
target GABA / NA+ channels dapens excessive neural firing - via increasing release of inhibitory neurotransmitter GABA
95
what other treatments are there for epilepsy
surgery - in severe . drug resistant causes
96
what is neuroplasticity
changes to brain structure, connectivity and function over time in response to changing environment
97
what are the three principles of neuroplasticity
neurodegeneration neural regeneration neural reorganisation
98
when does neurodegeneration happen
when there is a disruption of homeostatic environment in and surrounding the neuron
99
what leads to neuronal death
disruption of neurotransmitter function loss of fuel supply attack from infections, toxins or immune system faulty genetic signalling physical injury
100
what is necrosis
death due to cellular ill health
101
what is apoptosis
cellular self destruct adaptive
102
where in the nervous system has clear capacity for regrowth / regeneration
peripheral nervous system
103
what is the peripheral nervous system
everything but brain and spinal cord
104
what are the two systems within PNS
somatic nervous system - external environment autonomic nervous system - unconscious, automatic interacts and regulates body's internal environment
105
what does regeneration depend on
tissue environment whether the cause of degeneration has been removedd
106
what cell is critical for regeneration and regrowth of PNS neurons
schwann cells - guide the wiring
107
what are the myelination cells of CNS
oligodendrocytes
108
which neurons are difficult to regenerate
spinal cord neurons central nervous system
109
what is the treatment
focus on guiding regrowth and enhancing tissue environment
110
what is neural reorganisation
where the map of the brain needs to be reconfigured
111
what does neural reorganisation require
isolated activation of a single muscle connected areas expanding to take over tissue that receives no input
112
why do problems like phantom limb pain occue
the neural system loses input but cell / structures remain the same involves loss of peripheral input
113
what is a neurocognitive disorder
experiences, environment, genes can give rise to problematic thoughts and behaviours
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what are the common causes of neurocognitive disorders
dementia stroke traumatic brain injury
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what are the cognitive impairments in NCD
memory attention language visuospatial skill learning perception executive function motor
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what happens with a memory impairment
amnesia - retro and antero damage to the hippocampus or broader temporal lobe injury
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what does attention impairment indicate
earliest indication of onset of degenerative NCD
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what does a lack of attention stem from (brain region)
frontal and parietal regions networks extend to subcortical structures
119
what aphasia's are there
broca's aphasia wernicke's aphasia conduction aphasia
120
what is broca's aphasia
difficulty initiating speech or producing complex words hard to produce speech non fluent speech
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what is anomia
poor word retrieval
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what is agrammatism
difficulty word ordering, selection and inflection
123
what is wernicke's aphasia
production of incoherent jumbled speech deficit in understanding written / spoken language structurally intact speech rate unaware of impairment
124
what happens to speech rate and fluency in wernicke's aphasia
maintained but meaning lost
125
what is conduction aphasia
difficulty repeating speech
126
what agnosia are there
prospagnosia amusia akinetopsia
127
what happens when we lose visuospatial skill
unable to process sensory info unable to recognise objects or people independent of memory loss
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what is prospagnosia
face blindness loss of familiarity of known faces but understand components
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what causes prospagnosia
right hemisphere stroke
130
what is amusia
music processing problems
131
what is akinetopsia
loss of fluid motion perception vision becomes stroboscopic
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what part of the brain is damaged when learning is affected
hippocampus or broader temporal lobe injury
133
what happens when EF is impaired
poor judgement, inappropriate behaviour, erratic mood swings
134
what is damaged if EF is impaired
frontal lobe
135
what is apraxia
loss of ability to execute learned movements
136
what is motor apraxia caused by
lesion or degeneration of posterior parietal lobe
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what is limb apraxia
affects ability to perform gestures or interact with objects
138
what is speech apraxia
deficit in planning, sequencing required movements to produce sounds in speech
139
what are key features of NCD in DSM-5
primary clinical deficit in cognitive function acquired rather than development decline from a previous level of function
140
what are the specific causes of NCD
alzheimers vascular disease NCD due to parkinson's NCD due to TBI NCD due to HIV NCD due to prion disease NCD due to huntington's frontotemporal NCD
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what is a mild NCD
neuroinflammation acquired NCD after neural insult effects of repeated minor brain injuries
142
why are psychologists relevant for NCD
diagnosis assessment rehabilitation supporting caregiver research
143
how is an NCD diagnosis made
basis of neuropsychological testing for cognitive / behavioural impairments EEG, fMRI, PET, biomarker assessments, historical contexts
144
what is needed to determine specific causes
nature of deficits, location of neural insult onset, type, severity and progression of symptoms
145
why is it difficult to diagnose NCD
there is a lot of overlap with other disorders, with crossover in both psychological and neurocognitive disorders
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what is a major NCD
significant deterioration in at least one of the cognitive domains cognitive function, or performance documented via standard testing cognitive deterioration interferes with self reliance in every day activities
147
what is used to assess NCDs
Wechsler Adult Intelligence Scale - IV Montreal Cognitive Assessment
148
what is the WAIS-IV
aggregate measure used to provide scores on broad indices of ability: verbal comprehension perceptual organisation wokring memory information processing speed
149
what are some sources of deficits
alcohol abuse alzheimers stroke
150
what is the montreal cognitive assessment
high sensitivity tool to diagnose mild NCD
151
what are some examples in the montreal cognitive assessment
trail making tests - processing speed, integration of visuomotor functions clock drawing - visual neglect simple word lists - comprehension, WM
152
what is the cognitive rehabilitation programme used for
improving cognitive function basic training procedures extended practice at task
153
what can be used to help aid memory deficiit
every day memory promptss, pager / diary to recall daily events label cupboards and rooms visual imagery mnemonics prompt recall of known events
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what is used to treat attentional deficits
attention process training shifts of attention based on previous info, listening to tape that contains target that must be distinguished
155
what does EF treatment look like
interventions similar for memory and attention more specific for problem solving, planning and goal directed behaviourss
156
what can be used to combat prospagnosia
focus on voice, body shape, gait to assist recognition
157
what treatment can be used for apraxia
gestural training demonstrate use of common object and mimic observed gesture associated with reduction in errors during everyday tasks
158
what can be used to help with language impairment
speech therapy - to help with production and comprehension of speech
159
what can be done to help aphasia
constraint induced movement therapy mass practice of verbal responses when unable to gesture
160
what is group communication treatment (aphasia)
increasing communication and info exchange through any possible route not limited to speech
161
what do emotions help us do
build connections, connect with others, avoid certain situations, help us communicate physiological reactions -> increase in heart rate etc.
162
what is the james-lange theory
emotion induced sensory stimuli triggers change in organs and muscles autonomic and somatic responses trigger experience of emotion in brain
163
what is the cannon-bard theory
emotional stimuli hass two independent excitatory effects excited both feeling of emotion in brain and expression of emotion in nervous system parallel process that has no direct causal relation
164
what is the two factor (modern day) theory
three principal factors in emotional response perception of emotion inducing stimuli, autonomic and somatic response to stimuli experience of emotion
165
what emotion is the easiest to infer behaviour in most species
fear
166
why is fear an important function
adaptive function, motivating avoidance of threatening situations
167
what does an instinctual reaction to fear do
instinctual survival response
168
what is involved in fear conditioning in the brain
amygdala
169
what is the amygdala believed to hold
emotional significance of sensory signals - where it is stored and retained
170
how do we get a behavioural response to fear (pathway)
pathway via peracqueductal gray (PAG) of midbrain - defensive response
171
how do we get a sympathetci response to fear (pathway)
through lateral hypothalamus
172
what is the Kluver-Bucy syndrome
decreased emotional reaction seen when anterior temporal lobes of monkeys removed
173
what did Urbach-Wiethe disease cause
bilateral amygdala destruction
174
What did Papez suggest about the limbic system
emotion states expressed through action of other structures of the circuit on the hypothalamus and experienced through action on their cortex
175
where are the sites of emotion
medial portions of prefrontal lobes
176
what role does hippocampus have in emotion
remembering experiences influences how we behave and respond in the future
177
what cortex is involved in output of emotion
motor
178
what is the Right-Hemisphere model
where the R hemisphere is specialised for all aspects of emotional processing
179
what is the valence model
where the R hemisphere is specialised for negative emotions L hemisphere is specialised for processing positive emotion
180
what is the current model of emotion
emotional situation causes widespread increase in cerebral activity - not just amygdala and prefrontal cortex
181
what is stress
mental, physical, emotional and behavioural reactions to any perceived demands or threats significant unusual demand in physical, personal and social
182
what is the short term stress response
activation of anterior-pituitary adrenal-cortex system
183
what is the product of the anterior pituitary adrenal-cortex system
glucocorticoids
184
what happens when we are stressed biologically
activation of sympathetic nervous system SNS - adrenal medulla - noreadrenaline and adrenaline causes increased heart rate, breathing, sweating, dilating pupils
185
what are the types of stress
positive tolerable toxic long term stress
186
what is the adaptive immune system
slower reaction, specific to antigen
187
what is the innate immune system
fast response, not specific to antigen, responds to all sorts of foreign material
188
what does the sympatheic division do
arousal pupils dilate, decrease salivation perspire increase respiration etc.
189
what does the parasympathetic division do
calming effects
190
what are the differences between stress, fear and anxiety
stress - physiological and psychological demands fear - emotional response to threat anxiety - anticipatory response to unknown threat
191
what is a specific phobia
marked fear or anxiety confined to a specific object or situation
192
what are the 5 subgroups of phobias
animal natural environment blood - injection - injury situational otherr
193
what is the DSM diagnosis of phobia
disproportionate fear to specific object or situation that is actively avoided significant distress in important areas of functioning cannot be explained for at least 6 months
194
what are the psychoanalytic accounts of phobia
freud say phobias as a defense against anxiety produced by repressed ID impulses the phobia becomes associated with external events that have symbollic relevance to ID impulse
195
what are the limitations of the psychoanalytic account
not all phobias are linked to a traumatic experience, and not everyone acquires a phobia doesn't take into account incubation
196
what is the biological account for phobias
biological preparedness seligman proposed that we are prewired to acquire certain phobias
197
what is the evolutionary perspective of phobia
biological predisposition to associate fear with stimuli that have been hazardous for our ancestors
198
what is the cognitive theory for phobia
attentional bias acquired by cognitive bias or maladaptive thinking we pay more attention to words/pictures associated with phobia in comparison to neutral words
199
what is the way phobias are acquired
multiple pathways
200
what is the treatment for phobias
exposure therapy address phobic beliefs that sufferer holds about phobic event/stimuli
201
what is post traumatic stress disorder
direct experience, or via family member, witness to traumatic event, repeatedd exposure to details
202
what are the symptoms of PTSD
intrusive symptoms - dreams /flashbacks direct exposure negative changes in mood / cognition increasedd arousal and reactivity symptomss can't be explained by other disorders
203
what conditioning is associated with PTSD
classical conditioning
204
what is dual representiation theory
we have two memory stores verbally accessible memory situationally accessible memory
205
what is verbally accessible memory
easily accessible info memory of trauma consciously processed at the time integrated with biographical memories
206
what is situationally accessible memory
perception based info received from sensory channels records info that isn't consciously processed
207
what are the interventions for PTSD
graded exposure psychological debriefing cognitive restructuring
208
what is obsessive compulsive disorder
trio of intrusive thoughts, obsessions and compulsions
209
what are intrusive thoughts
thoughts and actions that are repeated often, result in distressing disabling life
210
what are obsessions
intrusive and recurring thoughts that individual finds disturbing and uncontrollable
211
what are compulsions
represent repetitive or ritualised behaviour patterns that individual feels driven to perform in order to prevent some negative outcome from happenig
212
what are the types of OCD
checking contamination symmetry and ordering rumination / intrusive thoughts
213
how is OCD diagnosed
presence of obsessions and compulsions individual belief that behaviour will prevent a catastrophic event
214
is there evidence of inherited component for OCD
yes, twins have high concordance for monozygotic twins compared to dizygotic twins
215
what are psychological factors of OCD
doubting clinical construct inflated responsibility thought action fusion mental contamination thought supression pervasion and role of mood
216
what is clinical construct in OCD
purpose is to link thoughts, beliefs and cognitive processes to subsequent symptoms
217
what is inflated responsibility
sufferers tend to have inflated conceptions of their own responsibility for preventing harm. believe they have the power to prevent negative outcome
218
what is thought action fusion
OCD sufferers believe that their thoughts influence events in the world
219
what is mental contamination
feeling of dirtiness provoked without any physical contact with a contaminant caused by images, thoughts and memories
220
what are interventions for OCD
graded exposure ritual prevention CBT pharmacological - SSRI neurosurgery (last resort)
221
what is generalised anxiety
disporportionate fear relating different asspects of your life feeling of anxiety accompanied by symptoms of restlessness, agitation, muscle tension
222
what factors are there for generalised anxiety disorder
Genetic /biological element - GAD show hyper-response in amygdala environmental cognitive biases
223
what medications are there for GAD, panic and social anxiety
benzodiazepine B blockers SSRI
224
what other interventions are there for GAD, panic and social anxiety
CBT
225
what are the two sides of panic disorder
unexpected panic - spontaneous - essential to diagnose panic dissorder situationally bound - anticipation, immediately on exposure to trigger
226
what are the signs of panic disorder
hyperventilation heart palpitations nausea chills/hot flashes sweating trembling / shaking numbness / tingling dizziness
227
what do we need to diagnose panic disorder
spontaneous, unpredictable panic attacks recurrent worry about further panic attacks rule out other diagnoses
228
what is the cognitive model for Panic disordeer
perceived threat body sensation interpretation of sensation as catastrophic back to beginning
229
what is social anxiety disorder
social interaction triggers anciety avoided or experienced with intense fear lasts more than 6 months
230
what is cognitive bias in social anxiety
we focus on all negative aspects of a social situation struggle to process anything positive
231
what are the symptoms of depression
cognitive - difficulty concentrating, making decisions behavioural - social withdrawal, agitation somatic - insomnia or hypersomnia affective - depressed mood, feelings of worthlessness
232
DSM 5 for dementia
five of the following depressed mood most of the time less interest or enjoyment significant weight change insomnia / excessive sleep substantial fatigue / lack of energy feelings of worthlessness/guilt lack of concetration recurrent thoughts of death, suicide and suicide attempts
233
what are the subtypes of depression
reactive depression endogenous depression unipolar affective disorder bipolar affective disorder
234
what is reactive depression
triggered by a negative experience
235
what is endogenous depression
no apparent negative life event
236
what is unipolar affective disorder
depression
237
what is bipolar affective disorder
depression with periods of mania (energetic, impulsive, positive, confident)
238
what is the diathesis stress model
if genetic risk factor and environment risk factor combined, more likely to be depressed
239
bipolar genetics
92% concordance in identical twins compared to 23% in fraternal twins
240
what are the main pharmacological treatments of depression
MOA inhibitors tricyclic antidepressants
241
what does MOA stand for
mono amine oxidase
242
what does MOA do
breaks down monamine neurotransmitters
243
what does monoamine make
serotonin
244
an example of a MOA inhibitor
iproniazid
245
what is the path to producing norephinephrine from MOA
monoamines -> catecholamines -> dopamine, epinephrine, norephinephrine
246
how to make serotonin from MOA
moa indolaminess serotonin
247
what are tricyclic antidepressants
chemical structure that include three ring chains they block reuptake, leaving more transmitter in the synapse
248
what are examples of antidepressants
Prozac - blocks reuptake MDMA - reverses reuptake transporter and blocks reuptake
249
what is used to treat bipolar disorder
lithium
250
what is the monoamine theory of depression
depression caused by deficit of monoamine neurotransmitter
251
what is becks' triad
negative views about the world -> future -> oneself loop
252
what is seligman's attributional model
attributions of negative events in 3 dimensions internal vs external global vs specific stable vs unstable internal + global + stable = depression
253
what does sleep follow
a circadian rhythm
254
what is a zeitgeber
external timing cuue
255
what is sleep defined as
reduced motor activity reduced response to stimulation
256
EEG high frequency (15-30 hz) is called
beta activity
257
EEG medium frequency (8-12 hz) is called
alpha activity
258
EEG lower frequency (3.5-7.5) is called
theta activity
259
high amplitude activity of less than 3.5 hz is called a
slow-wave sleep delta activity
260
what activity is the first stage of sleep
theta activity
261
what do sleep stages 3 and 4 consist mainly of
delta activity
262
when can sleep talking / walking occur
delta activity
263
what is stage 1 of sleep
transition between wakefulness and sleep - muscles still active, eyes show slow gentle rolling movement
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what is stage 2 and 3 of sleep
sleep gets deeper eeg gets lower in frequency, higher in amplitude
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what is stage 4 of sleep
deepest stage of sleep, reached in less than an hour relatively high amplitude (delta) EEG activity
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what does REM sleep look like on EEG
looks awake and active EMG quiet
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when do story like dreams occur
REM sleep
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non-rem sleep dreams cause
isolated experiences like falling
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what did freud say about dreams
dreams triggered by unacceptable repressed wishes manifest dreams - what we experience latent dreams - underlying meaning
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what is activation synthesis theory for dreams
modern theory dream due to cortex attempting to make sense of random braina ctivity
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what physiological activity can be measured using electrical recordings
muscle movement - electropmyography eye movement - electro-oculography brain activity - EEG
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what are the minor effects of sleep deprivation
impairment in: logical deduction critical thinking physical strength motor performance
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what are the larger effects of sleep deprivation
EF - prefrontal cortex assimilating changing info updating plans and strategies innovative, lateral, insightful thinking reference memory
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what is the effect of 3-4 hours of deprivation
increased sleepiness disturbances displayed on written tests of mood poor performance in vigilance
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what is the effect of 2-3 days
microsleeps - naps of 2-3 seconds
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what can sleep deprivation increase
sleep efficacy stage 4 and SWS increases short sleepers get same amount of SWS as long sleepers
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what is the recuperation theory
sleep is needed to restore homeostasis wakefulness causes deviation from homeostasis
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what happens if REM sleep deprivation
proceed more rapidly into REM as deprivation increases suffer REM rebound - more time spent in REM afterwards
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what is the adaptation theory
sleep is result of internal timing mechanism sleep evolved to protect us from dangers of the night
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what is REM's purpose
processing explicit memories, maybe brain development difficult to remain in nREM sleep
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what region is involved in timing of sleep
hypothalamus is involved in control of body temp, hunger, thirst and circadian cycles
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what structure in the hypothalamus acts as the major internal clock of medial hypothalamus
superchiasmatic nucleus (SCN)
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what is responsible for basic rest-activity cycle (Brax), cycles of REM sleep and slow-wave sleep
pons
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what is reticular formation
set of interconnected nuclei located throughout brainstem
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what is pontine reticular formation
brain region without clearly defined borders in the center of the pons - which can be stimulated to awaken people
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what does brainstem reticular formulation stimulation do
produce change in cortical state