Mechanism of Learning, Memory, Addiction and Fear Flashcards
1
Q
What are the major brain structures that make up Anatomy of Memory ?
A
**Cerebral cortex, amygdala, hippocampus make up anatomy of memory **
(also frontal lobes, parietal, occipital and temporal lobes, cerebellum, brain stem and hypothalamus also included)
-Hippocampus- is where memories are first triggered, then consolidated and transferred to long term memory (LTM)
2
Q
Which structures make up the limbic system?
A
Corpus callosum, temporal lobe, cingulate grus, nuclei of thalamus, mammillary body parohippcoampal gyrus, amygdaloid body, and fornix make up limbic system
3
Q
What is Learning? What are three types of Learning?
A
Learning: relatively permanent change in an individual’s behavior or behavior potential (or capability) as a result of experience or practice
Learning types:
1) change in behavior
2) change takes place due to practice or experience
3) Change is relatively permanent
4
Q
What is Memory?
A
Memory: a complex cognitive or mental process that involves encoding, storage and retrieval of information
5
Q
Define the words encoding, storage and retrieval that all relate to memory formation
A
1) Encoding: process of receiving input and transforming it into a form or code, which can be stored.
2) Storage: is process of actually putting coded information into memory
3) Retrieval: process of gaining access to stored coded information when it is needed.
6
Q
Differentiate between word Learning and memory in terms of information
A
Learning is the process of acquiring NEW information
Memory: is the ability to store and retrieve information (the Specific information stored in brain)
7
Q
Describe how informant is stored from sensory memory to long term memory.
A
Sensory memory –> Working Memory– Long-term memory
(Verbal/auditory channel and Visual/pictorial channel will be form of sensory memory that will be transferred to working memory.
Working memory has a limited capacity (of information that can be stored), and is where thinking and processing occurs. Encoding and retrieval occur next as information is stored in Long term memory (Unlimited capcity)
8
Q
Describe the two types of memory that Hebb differentiated between: Short term memory and Long-term memory
A
Hebb (1949) differentiated between two types of memory:
Short-term memory: memory of events that have just occured
Long-term memory- memory of events from Previous times
9
Q
What is consolidation ?
A
Consolidation: process by which short term memories are converted into long-term memories
10
Q
discuss the different types of information present in short term vs long-term memory
A
Short-term memory: IMMEDIATE memory for events, which may or may not be consolidated into long-term memory
Long-term memory: Relatively STABLE memory of events that occurred in more DISTANT past
11
Q
What type of memory are Declarative and non-declarative memories?
Discuss the subtypes of Declarative and non-declarative memories
A
Declarative and Non-declarative memories are forms of LONG TERM memory
-Declarative: things you know that you can tell others (hippocampus dependent) ex: biographical facts, geographical/historical facts
-Nondeclarative (procedural): things you can show by doing (hippocampus Independent) ex; Learn how to ride a bike
Subtypes;
Declarative divide into
1) Episodic: remembering the first day of school (storage in cortex)
2) Semantic : knowing the capital of France (storage in cortex)
Nondeclarative divide into
1) Priming: being more likely to use a word you heard recently (Cortex)
2) Conditioning: salivating when you see a favorite food (cerebellum)
3) Skill learning: knowing how to ride a bicycle (uses basal ganglia, motor cortex, and cerebellum)
12
Q
Differentiate between declarative and non-declarative memory in terms how information is remembered
A
Declarative: EASY to form these memories; EASILY Forgotten
Nondeclarative: require repetition and practice over a long period of time, but LESS likely to be forgotten
(Declarative memory: medial temporal lobe; diencephaplon) cause memory of facts and events
Non declarative memory: Procedural memory; skills and habits (striatum) classical conditioning using skeletal musculature (cerebellum) and Emotional response (amygdala)
13
Q
Describe the anatomical and functional organization of memory
A
A
14
Q
Differentiate between anterograde vs retrograde amnesia
A
Anterograde Amnesia: amnesia for events that occur AFTER trauma
Retrograde amnesia: Amnesia for events that occur just PRIOR to brain trauma
15
Q
What is global amnesia?
A
Global amnesia: when both retrograde amnesia and anterograde amnesia occur
16
Q
What is medial Temporal Lobectomy? Also describes structures involved in anatomy of memory
A
Medial Temporal Lobectomy: Removes tissue to treat seizures
-Result: Remove hippocampus
Anatomy of memory: include frontal lobe, olfactory bulb, temporal lobe, optic chiasm and mammillary body
17
Q
Compared a healthy brain with advanced Alzheimer’s brain
A
normal brain: normal shape and size
-Advanced Alzheimer’s brain: Brain is atrophied.
18
Q
Discuss the differences between Short term memory and Long term memory
A
Differences between STM and LTM:
-Short-term memory has LIMITED capacity; long term memory does not
-Short-term memory fades quickly without rehearsal; Long-term memories persist
-memories from long-term memory can be stimulated with a cue/hint; retrieval of memories lost from STM do NOT benefit from presence of a cue
19
Q
Define the term learning and discuss the non-associative types and associative types of learning
A
Learning (non-associative and associative): is process by which experiences change our nervous system and behavior
Non-assoicative and associative types of learning
-Habituation: decrement in reflexive response due to repeated stimulus presentation (ex: hear a noise, get used to the noise sound)
-Sensitization; INCREASE in reflexive response due to repeated stimulus presentation (ex: due to experiencing fire, when you smell smoke, tend to overreact)
-Classical conditioning: a learning process that occurs through associations between environmental stimulus and naturally occurring stimulus (ex: Pavlov)
-Instrumental conditioning: A learning procedure whereby the effects of a particular behavior in a particular situation increase (reinforce) or decrease (punish) the probably of the behavior (also called OPERANT Conditioning
20
Q
What are the non- associative types of learning and how are they different?
A
Non-assocaitve Learning: a change in behavior over time in response to a single type of stimulus
Two types:
1) Habituation: Learning to ignore a stimulus that lacks meaning
-The response to a repeated stimulus DECREASES
2) Sensitization: a strong sensory stimulus can Intensify your response to all stimuli
- The response to a given stimulus INCREASES
21
Q
Discuss the types of Associative learning and differentiate between them.
A
Associative Leanring: formation of associations between two events
Two types:
1) Classical Conditioning: Associating an effective, response-evoking stimulus with a second, normally ineffective stimulus
-Pavlov’s dogs (salivating to steak; then when bell is rung)
2) Instrumental (operant) conditioning: associating a MOTOR action with a stimulus
-pressing a level produces a food pellet
22
Q
Describe what occurs in memory consolidation
A
Memory consolidation: Sensory information will be transferred through short-term memory. Once in short-term memories, rehearsal of this information will allow for consolidation or transfer of info be converted from short-term memory to Long-term memory
Sensory Info–> STM–> LTM
23
Q
Which important people used Associative Learning ?
A
Classical conditions- I. Pavlov
Instrumental -Operant conditioning: B. Skinner
24
Q
Describe the behaviorism that occurs Classical conditioning with pavlov
A
Classical Conditioning: Pavlov
-A stimulus is presented in order to get a Response
S—R
-S–> US–> UR
A stimulus such as meat becomes an unconditioned stimulus for dogs that will have unconditioned response of salivating when seeing meat
-Then a neutral stimulus (of bell ringing) will initially produce no salivation.
however when unconditioned stimulus (meat) is presented after neutral stimulus (bell), the dog will have unconditioned response (salivation)
-With the neutral stimulus presented alone (bell rings), the dog will produce a conditioned response of salivating. Hence the bell becomes conditioned stimulus.
25
Describe what learner does in classical conditioning vs operant conditioning
Classical conditioning: two stimuli (CS and UCS) are presented at certain times regardless of what learner does
-in operant conditioning; the learner's behavior controls the presentation of reinforcer or punishment.
26
Describe what occurs in operant conditioning. Prvoide an example.
Operant conditioning: by Skinner
-The response is made first, then reinforcement follows.
ex: a pigeon learn how many times to push button to receive reward (Food)
-First pigeon will push button a certain number of times
-Then pigeon will receive food, which will be a reinforcer for pigeon to maintain behavior and keep pushing button
another example; rat enters one arm of maze, and will earn fruit loops to eat as a reinforcement to allow rat to increase responsibility of same response (continue behavior)
-however, if rat is shocked when going through one arm, that will be punisher to stop rat from going through that arm and shift to different response
27
Explain how stimulus and reinforcement stimulus works
Stimulus (ex: sight of lever)--> neural circuit that detects a particular stimulus--> Neural circuit that controls particular behavior--> Behavior (lever press)
-When rat presses lever, it receives food. Food is a reinforcing stimulus that will influence reinforcement system which will then strengthen connection of neural circuit that controls that behavior
28
Differentiate between reinforcers and punishment in operant conditioning
In Operant (instrumental) Conditioning; Responses are followed by reinforcement or punishment that either strengthen or weaken behavior
-Reinforcers- are events that INCREASE the probability that the response will occur again
-Punishment: are events that DECREASE the probably that response will occur again
29
Differentiate between a reinforcing stimulus and Punishing stimulus
Reinforcing stimulus: Appetitive stimulus that follows a particular behavior and thus makes the behavior become more frequent
Punishing stimulus: Aversive stimulus that follows a particular behavior that makes behavior LESS frequent
30
What drives our lives and learning ?
MOTIVATION drives our lives and learning
-
31
Describe how Apylsia California was used as a model for learning. How were Implicit memories used and where are they stored?
Aplysia California: Sea snail used as model for learning
-Implicit memory can be studied through the gill- and siphon withdrawal reflex of the marine invertebrate Apylysia californica (Sea Snail)
-Aplysia is capable o ASSOCIATIVE Learning (including classical conditioning and operant conditioning) and non-Associative learning (habituation and sensitization )
-Aplysia is able to learn very peculiar behaviors that, upon practice, can be consolidated into long term memories
-The animal learns to respond progressively more weakly to repeated innocuous stimuli (ex: light tactile stimulus), a behavior called Habituation, and to Reinforce the response to repeated noxious stimuli (painful electric shock) behavior known as sensitization
These implicit memories are stored in spinal reflex pathways
32
Explain what occurs in the Gill Withdrawal Reflex of Aplysia
Gill Withdrawal Reflex of Apylsia:
-Tactile or electrical stimulation of the siphon or mantle elicits withdrawal of the Gill and siphon into mantle cavity
-Snail contains body with mantle shelf, siphon, gill.
33
How does Habituation occur in Apylsia?
Habituation in Aplysia:
-If the siphon of the animal is stimulated mechanically, the animal withdraws the gill, presumably for protection
- With repeated activation, the stimulus leads to a DECREASE in number of dopamine-containing vesicles that relate their contents onto motor neuron
34
Who Was Eric Richard Kandel and what did he, Arvid Clarssoin and Paul Greengard have in common?
Eric Richard Kandel: Medical doctors from Austria who is known for his work with California Sea slug (aplasia California) aka California sea hare (since it resembled shape of rabbit or hare)
-Sea hares- shell-less sea snale
-He, and Arvid Clarsson (discovered dopamine) , Paul Greengard won Nobel Prize together in 2000 in Physiology for their discoveries conceiving signal transduction in nerve system and dopamine.
35
What causes Habituation?
Motor neuron, receives direct sensory input from the siphon and innervates muscles used for gill withdrawal
-Showed that habituation occurs at the synapse between sensory and motor neuron
-Progressive decrease in the size of excitatory postsynaptic potentials (EPSP's)
-Mechanism:
-Less calcium enters presynaptic terminal
-So fewer transmitter molecules are released
Therefore presynaptic modification
36
Describe the sensitization in Aplysia
REVIEW THIS SLIDE (40)
Sensitization of Gill-Withdrawal Reflex
-Sensory neuron is activated by serotonin
-Sensory neuron is constantly triggered causing sensitization
37
Describe the associative learning that is seen in Aplysia
Associative learning in Aplysia:
-Classical conditioning:
-Unconditioned stimulus= Shock to tail
-Conditioned stimulus= siphon stimulation
-If the two stimuli were paired, subsequent gill withdraw response to siphon stimulation alone was greater
-Uses the same neuron as sensitization, through interneuron
38
Explain the Gill Withdrawal Reflex Sensitization and how it works
Gill Withdrawal Reflex Sensitization
-Shock to the head associated with stimulation of siphon increases gill withdrawal reflex= sensitization
-How does this work?
-Neuron from head synapses on the axon terminal of sensory neuron
-Releases serotonin
-Causes molecular cascade that sensitizes sensory axon terminal
39
What occurs in the sensitization cascade?
Sensitization Cascade
-Serotonin receptor on the sensory axon terminal is a G-protein coupled receptor
-Binding activates adenylyl cyclase enzyme
-Which produces cyclic AMP (2nd messenger)
-which activates protein kinase A (PKA)
-which phosphorylates a protein forming the potassium channel
-Which causes it to close
-Prolonging the presynaptic action potential
-so more calcium enters
-Thus more neurotransmitters are released.
40
What is long-term potentiation (LTP)
Long-term Potentiation (LTP): long-term increase in the excitability of a neuron caused by repeated high-frequency activity of input
41
What is Associative long-term potentiation?
Associative Long-term potentiation:
-LTP in which concurrent stimulation of weak and strong synapse to a given neuron strengthens the weak ones
42
Describe all the features of Long-term potentiation, including where it occurs.
Long Term Potentiation
-A large amount of studies demonstrated that LTP is indeed a valid model of "memory storage"
LTP is observed when postsynaptic neuron is persistently depolarized after a high-frequency burst of presynaptic neural firing
-LTP has a number of properties that make it as suitable as Physiological substrate of memory
-It is ASSOCIATIVE, in that it depends on the co-occurrence of presynaptic activity and postsynaptic depolarization.
LTP occurs prominently in the HIPPOCAMPUS, a structure that is important for memory
-
43
What does the Induction of LTP (long term potentiation) involve?
The Induction of LTP: is known to be mediated postsynaptically and to involve the N-methlyl D-asparteate (NMDA) receptor, which permits the influx of calcium into postsynaptic cell.
44
How is LTP maintained?
LTP is maintained by an increase in the number of alpha-amino-3-hydroxy-5-methyl 4-isoxazolepropionate (AMPA; non-NMDA) receptors in postsynaptic cell and also possibly by increase transmitter release
45
Discuss the differences in synapse before and after long-term potentiation occurs
Before long term potentiation: no change, structures (synaptic vesicles, terminal button, dendritic spine and active zone are normal)
After long-term potentiation: CHANGES in synapse occur
-genearte perforated (hole) synapse
46
How are axons affected after long term potentiation (LTP)? REVIEW
Before LTP: axon normal shape
After LTP: change in axon
47
What is hippocampus structure composed of?
Hippocampus structure:
Schaefer collaterals
-mossy fibers
-Perforant path
-entorhinal cortex, fornix or sensory cortex
48
Describe the connections seen in hippocampus
Connections in Hippocampus:
-entorhinal cortex connects to the hippocampus via axons called Perforant path
-Mossy fibers from the dentate gyrus synapses on CA3
-CA3 cells synapse via Schaffer collateral cells in CA1 region
-Both CA3 and CA1 cells have output fibers to the fornix
49
Where does Long-term Potentiation occur? What kind of receptors are used for excitatory transmission?
Long Term potentiation (LTP) occurs in CA1 when multiple synapses are active at the same time that the CA1 cell is depolarized
-Recall that GLUTAMATE receptors are responsible for Excitatory transmission in hippocampus
50
What is the Mechanism of LTP?
Mechanism of LTP:
- Glutamate is released from synapse
-Na+ ions pass through the AMPA receptor causing EPSPs
-CA1 neurons also have post synaptic N-methyl-D-Aspartate (NMDA) receptors
-These conduct Ca++ ions when cell is depolarized
-Thus Ca++ entering the NMDA receptor indicates that presynaptic and postsynaptic elements are active at the same time.
51
What occurs in the Induction of LTP? how is LTP induction prevented? What causes LTP to be blocked? What will happen after LTP occurs
Induction of LTP;
Rise in postsynaptic CA++ linked to LTP
-LTP induction is prevented if NMDA receptors are INHIBITED
-Rise in Ca++ activates 2 protein kinases:
-Protein Kinase C
-Calcium-calmodulin-dependent protein kinase II (CaMKII)
-Inhibition of either of these kinases Blocks long term potentiation
-Following LTP, a single axon may form multiple new synapses on a single postsynaptic neuron
52
What is Long Term Depression (LTD) ?
Long Term Depression (LTD);
-LTD occurs in CA1 when it is only Weakly depolarized by other inputs
- Inward calcium levels are Lower, activating a different enzymatic response
-Thus, LTP and LTD are two responses of the same system
53
Explain how LTD, LTP and Memory are correlated. What causes a reduction in learning for rats
LTD, LTP and Memory
-LTP and LDP are mechanisms of synaptic plasticity
-They may contribute to formation of Declarative memory
-Recordings from inferotermporal cortex slices from humans shows the Same kind of interplay of LTP and LTD
- Rats with damage to hippocampus show reduced learning in Morris water maze
-Injecting an NMDA-blocker into rats produces the same reduction of learning
54
Describe the model of LTP and LTD. What mediates LTP?
Current model of LTP and LTD:
on The post-synaptic membrane, you will have Glutamate binds to NMDA receptor.
-Calcium will pass through NDMA receptor and either have brief and large excitatory signals when protein kinases ar activated; or have prolonged and moderate excitatory activity when protein phosphates are activated.
LTP mediated by the number of NMDA and AMPA receptors
55
Describe the. Molecular basis of Memory-LTP
What occurs in Pre-LTP, Early LTP, and Late LTP?
Molecular basis of memory-Long Term Potentiation
- Arc Regulation is mediated by NMDA and AMPA receptors
-During synaptic activity, NMDA and AMPA receptors propagate opposing signals that are integrated by sensor and transduced into transcriptional response
-Pre-LTP (basal conditions): the ratio of the activity for NMDA and AMPA receptors are 1:1, with robust transcription of ARC and hence production of ARC protein (transcription ON)
-NMDA receptor activity also initiates signaling pathways that promote the synaptic delivery of AMPA receptors and leads to Early LTP
Early LTP; insertion of early AMPA receptors into the post-synaptic membrane decreases the decreases NMDA:AMPA ratio to 1:3 and INHIBITS ARC transcription (transcription OFF)
- Then ARC promotes removal of synaptic AMPA receptors and another mechanism potentiates NMDA receptor currents
-Late LTP: NMDA:AMPA ratio is RESET to 1:1 which allows synthesis of additional ARC during subsequent rounds of activity (transcription is off) . Synapse becomes stronger, with twice as many AMPA receptors as in pre-LTP stage
*Sensor from nucleus allows for additional AMPA receptor; the number of NMDA or change is receptor is mediated by nuclear function
56
Explain the theory about plasticity linked to activity
Theory: plasticity is linked to correlation of activity
-Neurons that fire together, wire together
-Neurons that fire out of sync, lose their link
57
Explain the regulations that occurs in synaptic plasticity
a high amount neural activity leads to synaptic responses.
However, negative feedback occur when there are a lot of synaptic responses
-a High amount of synaptic responses, will lead to inhibition of neural activity
58
Explain the relationship between synaptic drive and firing rates, and how they are regulated.
Low firing rates INCREASE synaptic drive
-HIGH firing rates REDUCE synaptic drive
-By scaling up and down all synapses, the cell keeps the level of excitation CONSTANT while it preserves the strength of synapses
-it maintains activity without disturbing the "memories"
59
Explain how synapses lead to memory . What is special case of Neural plasticity?
MEMORY is the special case of general biological phenomenon of neural plasticity
-Neurons can show history-dependent activity by responding differently as a function of prior input, and this plasticity of nerve cells and synapses is the basis of memory
-Experience can lead to Structural change at the synapse, including alterations in the strength of existing synapses and alterations in the number of synaptic contacts along specific pathways.
(in presynaptic membrane, glutamate are I vesicles and will cross synaptic cleft; then MG2+ will go through NMDA Receptor, Na+ will go through AMPAR, and calcium will go through VGCC on post-synaptic cell, causing excitation, and leading to transcription in nucleus ; calcium activates knives that causes transcription factor to be activated, making mRNA and translating into proteins) )
60
Differentiate between Normal Brain, Mild Alzheimer's disease and Severe Alzheimer's disease
Normal Brain: cerebral cortex, hippocampus and entorhinal cortex have normal shape and size
Mild Alzheimer's Disease: Cortical Shrinkage, Shrinkage of Hippocampus, and moderately Enlarged vesicles
Severe Alzheimer's disease: Extreme shrinkage of cerebral cortex, Extreme shrinkage of hippocampus, and Severely enlarged ventricles
61
Explain how hippocampus and memory are related. Also discuss our subconscious memory.
Come back to slide 64
Hippocampus is important for memory
-sometimes we learn things unconsciously
-If hippocampus is working, we will know location of platform REVIEW
62
Describe what spatial memories are, and also discuss what a place cell is.
Spatial memories: functional imaging studies have shown that the right hippocampal formation becomes active when a person is remembering or performing a navigational task
Place cell: a neuron that becomes active when the animal is in a particular location in the environment; most typically found in the hippocampal formation
63
Explain how brain cells work to stay alive. What happens when cells need repair?
Repair: staying Alive
-Brain cells can live up to 100 years or longer but in an adult, when neurons die because of disease or injury, they are NOT usually replaced
-To prevent their own death, living neurons constantly maintain and remodel themselves.
(research suggested that Exercise can promote healthy neurons in rats, by causing their neurons to make more protective BDNF ( growth factor that helps neurons survive)
64
Explain the neurogenesis dependent and independent mechanisms that antidepressants can influence .
Antidepressants can influence both Neurogensis dependent mechanisms: Dentate gyrus function (pattern separation and encoding, dentate gyrus excitably) and Neurogenesis Indepenendent mechanisms; Hippocampus, prefrontal cortex, amygdala, Nucleus accumbent and HPA axis )
Both neurogenesis-dependent and independent mechanism all lead to behavioral effects
65
Discuss the pathway of limbic system and how it affects other brain structures.
The limbic system is implicated in adaptation, learning and memory processes, mood and control of the HPA-axis
Pathway:
-Prefronta cortex (planning and control) will divide into emotional aspects controlled by Amydala and Contextual aspects controlled by Hippocampus.
-Both Amygdala and Hippocampus will all be involved in adaptation to stress memory that will lead to PVN--> Pituitary--> Adrenals
66
Explain what occurs in the hypothalamic-Pituitiary-Adrenal Axis (HPA-Axis)
Hypothalamic-Pituitary-Adrenal Axis:
-Corticotropin-releasing factor (CRF) is released in humans in response to almost any type of stress (physiological or psychological).
The hypothalamus secretes CRF, which in turn binds to specific receptors on anterior pituitary cells, which produce adrenocorticotropic hormone (ACTH).
ACTH is then transported to its target of adrenal gland which stimulates production of adrenal hormones
-The Adrenal glands are located on top of the kidneys, which then increase the secretion of cortisol
(Stress--> CRH from Hypothalamus--> Anterior pituitary release ACTH--> Adrenal glands on kidneys to relate Cortisol, causing metabolic effects)
67
What causes Cushing's syndrome? What are the signs of this syndrome?
Cushing's syndrome; which is caused by the excess of cortisol
Signs include:
-Obesity of torso
-Purplish stretch marks
-Round red face;
-High blood pressure;
-Muscle weakness;
-Easy bruisability;
-Acne;
-Diabetes
-Osteoporosis;
-Variety of psychological disturbances; women may develop facial hair.
68
Describe how working memory came about and what it involves. Who proposed this theory of working memory?
Later research has Weakened the distinct between STM and LTM (long-term memory)
-Some memories do Not qualify as distinctly short-term or long-term
Working Memory:
-Proposed by Baddeley and Hitch as an alternative to short-term memory
-Emphasis on temporary storage of information to actively attend to it and work on it for a period of time
69
What are the three major components of Working memory?
There major components of working memory :
1) Phonological Loop- stores auditory input
2) Visuospatial sketchpad- stores visual input
3) Central Excecutive- directs attention and determines which item to store
70
Further explain the role of the central executive in terms of memory . What factors does it control?
central executive:
control phonological loop which is associated with language
-controls episodic buffer- which is short-term episodic memory
- controls Visuo-Spatial sketchpad: controls visual semantics
71
Explain which processes are involved in ability of brain to change its function in response to experience
Learning and Memory
Neuroplastic processes related to the ability of the brain to change its functioning in response to experience
Learning; How experiences changes the brain
Memory: How the changes are stored and later activated
72
Explain the neuropsychology study done with Patient Hm and what it suggested about the importance of the hippocampus
Patient Hm is a famous case study in neuropsychology who had his hippocampus removed to prevent epileptic seizures
-Afterwards, Patient HM had great difficulty forming new long-term memories
-STM or working memory remained intact
-Suggested that the hippocampus is VITAL for the formation of New Long-term memories
73
Define the word amnesic and discuss the differences between retrograde and anterograde amnesia. Also discuss the differences between short term memory and long term memory
Amnesia: any pathological loss of memory
Retrograde amnesia: inability to remember information from the PAST
Anterograde amnesia: inability to remember NEW information; can't form new memories
Short term memory: Storage of new information for a BRIEF time, while a person attends to it.
Long term memory (LTM); storage of New information once the person stops attending to it.
74
Describe the surgery procedure that Patient H.M had and how it affected his memory later on.
Patient H.M (Henry Molasion)
-A patient that had a "bilateral Medial Temporal Lobectomy- as a treatment for his epilepsy
-Removal of medial portions of both temporal lobes; including most of the HIPPOCAMPUS, Amygdala and nearby cortex
-This surgery alleviated most of his seizures, but had a significant impact on his memory
-Much of our understanding of the anatomy of memory derives from studying H.M. and the changes to his memory.
No one since, has had this procedure
75
Describe the amnesia that occurred with H.M
H.M's Amnesia:
-most of his memory from Before the surgery was intact
-With the exception of the 2 years prior to the surgery
-but it was virtually impossible for him to form NEW Long term memories
-As soon as he stopped focus on new information, he forgot it
-He was effectively frozen in time
76
What is Global Amnesia?
Global Amnesia: Amnesia for memory presented in all sensory modalities
77
Discuss how the assessment for H.M's Anterograde Amnesia was made. What kind of tests were performed?
Assessment of H.M. 's Anterograde Amnesia:
-7 eats of his long term memory
1. Digital span + 1 test
2. Block=Tapping Memory-Span test
3. Mirror-Drawing Test
4. Rotary-Pursuit Test
5. Incomplete-Pictures Test
6. Pavlovian Conditioning
78
What is the procedure of the Digital Span + 1 test? What about the Block-Tapping Memory-Span test?
1) Digital Span+ 1 Test:
-Asked to repeat 5 digits that were read to him, then those 5+ a new digit
Normal: 15 digits; HM; failure by 8
2) Block Tapping Memory-Span Test
-Asked to tap a series of blocks on a table in the same order the experimenter did
-Correct at 5 blocks, incapable of 6 blocks.
79
What occurs in the Mirror-Drawing test?
mirror-Drawing test
-Trace a star shape while looking at your hand in the mirror; errors measured
-Repeated many times over a few days
-His performance improved over time, even though he had no memory of having done the task before.
80
Describe what occurred in the Rotary pursuit Test?
Rotary Pursut-Test:
-Maintain contact between a stylus and a target on a rotating disc
-Again, improvement without him remembering the task.
81
What occurred in the Imcomplete-Pictures Test and Pavlov conditioning ?
5) Incomplete-Pictures Test: patient must identify the object in a drawing, with it drawn to different levels of completeness.
-Again, improvement without him remembering the task
6) Pavlovian Conditioning: Eye Blink task
-Tone plays before a puff of air in the eye; eventually the tone alone causes a blink
-HM able to learn this, athough it took longer than usual.
82
Discuss the affects that patient H.M. had regaridng short term and long term memory
H.M. Summary
he had Mild Retrograde Amnesia
-Only 2 years beforesurgery
-Extreme anterograde Amnesia:
-Short term memory was fine
- But long term memory was severely impaired.
-However, tests showed that while he could not consciously remember having done these tasks before, his improvised performance on them, indicates some type of memory was being formed.
83
What were conclusion from studying H.M' Amnesia?
Conclusion from H/M/ "s Amnesia:
-Memory functions seem to be highly dependent on the structures of the Medial TEMPORAL Lobe
-His differential stability to remember things, showed that there were distinctly different types of memory storage
-His specific problem seemed to be with MEMORY CONSOLIDATIOn, the translation of STM to LTM
-Because his performance improved, but he could not remember the task. it was determined that there are 2 categories of LTM (long term memory)
84
What are the two types of LTM?
2 Types of LTM:
1. Explicit memories
-Things you consciously remember
-2 types;
1) Semantic- memories of general facts or information
2) Episodic: memories of events in your life (aka autobiographical memories)
2) Implicat memories: memories that are formed without conscious awareness of them
-Indicated by increased performance over time in tasks such as mirror drawing
85
Discuss what occurs in Amnesia of Korsakoff's syndrome
Amnesia of Korsakoff's syndrome:
Korsakoff's syndrome: is a memory disorder common in chronic alcoholics
-brain damage results from thiamine deficiency
Late stages involve Sensory and motor problems, extreme confusion, personality changes, and potential organ failure.
-Amnesia similar to that of medial temporal lobe amnesia
-Early on, anterograde amnesia for explicit episodic memories is most prominent symptom.
86
What occurs in the Amnesia for Alzheimer's Disease? What may be the cause of this Amnesia?
Amnesia of Alzheimer's Disease
-First symptom of Alzheimer's is the deterioration of memory
-Major anterograde and retrograde deficits in explicit memory
-Often have deficits in STM and some types of implicit memory (verbal and perceptual, not sensorimotor)
- ACETYLCHOLINE Depletion may be the cause of amnesia in Alzheimer's
87
What is the anatomy of reward and addiction? What happens when you lesion VTA (ventral segmental Area) ?
Anatomy of Reward and Addiction:
- gave Dopamine connections through Nucleus accumbent, VTA (ventral Tegmental area) and PFC
-Have opioid peptides that are on Nucleus accumbent, Amygdala, Substantia nigra. LH, ARC, locus correleus and PAG
-Nicotinic receptors are on VTA, Nucleus accumbent and attached to opioid peptide on AMG
-if we lesion VTA, result is apathy (no interest in eating or any behavior; lack of effort to achieve goals)
88
Describe the role of the Medial forebrain bundle.
Medial forebrain bundle (MFB) : fiber bundle that runs through the hypothalamus; electrical stimulation of MFB is reinforcing
89
What is the role of VTA (ventral segmental area)?
Ventral Tegmental Area (VTA); dopaminergic neurons in the midbrain whose axons form the mesolimbic and mesocortical system; plays a role in reinforcement
-
90
What is the Nucleus accumbens?
Nucleus Accumbens:
-Nucleus of the forebrain that receives dopamine secreting terminal buttons from neurons of the VTA; involved in reinforcement
91
Explain the process of Dopamine's Normal Action
Dopamine's Normal Action:
1) after being released into the synapse (the gap between nerve endings and receiver cells), dopamine binds to receptors on the next neuron
2) The dopamine is either quickly reabsorbed or broken down by the enzyme monoamine oxidase (MAO)
92
Describe how drugs like Cocaine, Amphetamines, and Nicotine (cigarettes) affect Dopamine levels
How Drug Affect Dopamine Levels
1) Cocaine; BLOCKS normal absorption of dopamine. As a result, dopamine accumulates in the synapse, where it stimulates the receiver cell
2) Amphetamines: STIMULATE excess release of dopamine, Overwhelming the processes of reuptake and enzyme breakdown
3) Nicotine (seen in cigarettes): STIMULATES the release of dopamine, while another substance in cigarette BLOCKS the action of MAO
93
Explain the Physiology of Addiction
Physiology of Addiction:
-Drug enhances amount of Dopamine in the synapses
-Increased dopamine results in increased feelings of pressure
-Nervous system responds by Reducing the number of dopamine receptor sites
-Addict must take More drugs to produce the same "high"
-So, while addicts begin by taking drugs to feel high, they end up taking them in order not to feel LOW.
94
What occurs during withdrawal?
Withdrawal: physiological response to the lack of drug effects, especially the drug's substitution for naturally produced neurotransmitter
-Withdrawal effects can be intense at first, especially if the drug addict quits abruptly
-Eventually the body's physiology returns to normal, and the person will stop craving the drug
95
what is the DSM IV TR Criteria for Dependence of a drug?
DSM IV TR: Criteria for Dependence
**At least three of the following has occurred in the Same 12-month period:
1) Tolerance
2) Withdrawal
3) Taken in larger amounts than was intended
4) Unsuccessful efforts to cut down
5) Time is spent trying to obtain alcohol
6) Activities given up because of alcohol
7) Continued despite physical or psychological problems.
(A high tolerance or withdrawal predicts a more severe course)
96
What is the DSM IV TR Criteria for Abuse
DSM IV TR: Abuse
-At least ONE of the following has occurred in the same 12-months:
-Role impairment (ex: failed work or home obligations)
-Hazardous use (driving while intoxicated)
-Legal problems related to alcohol use
-Social or interpersonal problems due to alcohol
97
Discuss the affect of drug doses on rats and how they regulated the dosage
rats had an intravenous self- administration of Cocaine.
Rats were implanted with intravenous catheters and trained to self-administer contain with limited access (3 hr/ day) to show stable and regular drug intake.
No tolerance or dependence developed with rates
-Rats had a schedule of Fixed ratio, as one lever press was required to deliver an intravenous infusion of cocaine
Results:
Lowering the dosage of drug per injection caused an increase in the number of Lever presses (self-admistered infusions)
-Increasing the dosage of the drug, decreased the number of lever pressing (less infusions)
(Rats would press lever constantly in response to drug dose to try and achieve a status of well-being from drug)
***However, rates will NOT overdose on cocaine, unless they are being trained**.
98
What mediates the lever pressing?
Lever pressing is mediated by dopamine
-
99
What does medial prefrontal cortex in limbic system comprise of?
Medial Prefrontal Cortex:
-Anterior cingulate (AC), orbitofrontal cortex (OFC), hippocampus (Hippo), central striatum (VS), nucleus accumbent, dorsal striatum (DS), Globus pallidus (GP), Amygdala (AMYG), and thalamus (THAL)
100
Explain what occurs in the cycle addiction that involve different interactions that maintain the drug administration.
The mesolimbic circuit includes the nucleus accumbens, amygdala, and hippocampus that are associated with the REINFORCING effects of a drug, and with memory and conditioned responses that have been linked to CRAVING
-it also likely to be involved in the emotional and motivational changes seen in drug abusers during withdrawal
The mesocortical dopamine circuit; includes the prefrontal cortex, orbitofrontal cortex, and anterior cingulate, which are likely to be evolved in conscious experience of drug intoxication, drug incentive salience, drug expectations/craving and compulsive drug administration.
-also attribution of salience to a given stimulus is a function of the orbitofrontal cortex depends on the value of reinforcer compared to simultaneously available reinforcers, requires knowledge of strength of the reinforcer (function of hippocampus and amygdala)
101
Explain how Fear is processed in our brain and the different types of fear response that occur. Also discuss what Anxiety is.
Fear
-Processing circuits that detect and respond to danger
-Learning is important
Species-typcial fear/defensive responses
-Somatic NS responses (defensive behaviors such as freezing)
-Autonomic NS responses (Heart rate, blood pressure)
-Endocrine Responses (Hormone release)
-Hypoanalgesia (Reduced pain sensitivity)
-Reflexive alterations (Startle)
Anxiety: negative emotion that alerts us to potential threats
-Trait or State
102
Explain the different types of motivational systems with Affective states
What are the different sides of prefrontal cortex and how do they relate to certain emotional states?
Affective State and traits
-Affect correlates with two rudimentary motivational systems
-Approach-Positive (happiness, pleasure)
-Avoid- Negative (fear, disgust)
Motivational/affect and prefrontal cortex
-left prefrontal cortex: happiness and pleasure
-right prefrontal cortex: anxiety and depression
103
Describe the Fear conditions brain areas.
Fear conditioning brain areas
Sensory areas
- Thalamus- Simple representations, fast input
-Cortex- Complex representations, SLOW input
Amygdala
-collection of nuclei
-Fear Relevant areas
-Lateral (LA)- sensory inputs
-Central (CE)- Output
Hippocampus
-Memory and learning
Pre-frontal cortex
-behavioral regulation and control
-Left part_ approach and positive affect
Right part- withdrawal and negative affect
Output areas
-Somatic (voluntary muscles)
-Autonomic (heart, blood vessels, etc)
-Endocrine (hormones)
104
Explain the connections between the different structures in the brain
REVIEW
Sensory information goes to thalamus which will activated sensory cortices to reach hippocampus. Hippocampus will activate pre-frontal cortex or amygdala and amygdala will have areas in Somatic NS, Autonomic NS and endocrine
105
Describe the amygdala and the fear conditions that occurs. What is the role of Lateral Amygdala? What happens if it is damaged?
Amygdala and Fear Conditioning:
-Inactivation of amygdala during learning PREVENTS learning, but inactivation immediately after learning has NO effect
-Memory storage does not necessarily have to be in amygdala
Lateral Amygdala (LA) integrates sensory information from CS and UCS)
-LA receives sensory input from many areas
-Damage to LA ELIMINATES conditioning
-LA cells that respond to tone CS (unit recordings) change responsiveness after paired with US
LTP- responsiveness of neuron changes due to synthesis of proteins (Due to paired activation of pain and CS)
106
What happens in amygdala during Fear conditioning? Describe how Emotional Preservation occurs and how amygdala can affect perception of fear.
Amygdala and Fear in Humans:
-Fear conditioning leads to amygdala activity
- amygdala MORE ACTIVE during FEAR than anger or happiness
-Psychopaths (emotional detachment) show deficits in fear conditioning (but no clear evidence yet of amygdala involvement)
Emotional Preservation:
-Failure of suppressing (extinguishing negative emotions)
-Can occur in depression, anxiety, fear, (post-traumatic stress disorders)
-Amygdala is Overactive (hyper) in these conditions and mPFC (motor prefrontal cortex?) is Under active (Hypo)
-Inverse relation between mPFC and amygdala activity
-Perception of Fear: Amygdala damage leads to deficits in emotional (especially fear) facial and voice perceptions
107
What is post-traumatic stress disorder (PTSD)?
Post traumatic stress disorder (PTSD): is an anxiety disorder that a person may develop after experiencing or witnessing an extreme overwhelming traumatic event during which they felt intense fear, helplessness, or horror.
108
What are the dominant features of PTSD?
Dominant features of post-traumatic stress disorder are emotional numbing (emotional nonresponsiveness), hyperarousal (irritability, on constant alert for danger) and reexperiencing of the trauma (ex: flashbacks, intrusive emotions0
109
What kind of disorder is PTSD?
PTSD is an ANXIETY disorder. Anxiety disorder cover several different forms of abnormal, pathological anxiety, fears, phobias and nervous conditions that may come one suddenly or gradually over a period of several years, and may impair or prevent the pursuing of normal daily routines.
110
what are some of the disorders that must be ruled out when diagnosing PTSD?
Some of disorders to rule out when diagnosing PTSD:
-Acute stress disorder (duration of up to 4 weeks)
-Adjustment disorder (less severe stressor, or different symptom pattern)
-Mood disorder or other anxiety disorder (symptoms of avoidance, numbing or hyperarousal are present before exposure to the stressor)
-Other disorders with intrusive thoughts or perceptual disturbances (obsessive compulsive dissever, schizophrenia, other psychotic disorder )
-substance abuse or dependence disorder
-furthermore, malingerers- that is people who falsely claim to be traumatized- sometimes feign PTSD symptoms in order to win money in court case as compensation for "emotional suffering"
111
What is the criterion for PTSD?
Criterion For PTSD:
-The person has been exposed to a traumatic event in which both of the following have been present:
1) The person has experienced, witnessed , or been confronted with an event or events that involve actual or threatened death or serious injury, or threat to the physical integrity of oneself or others
2) The person's response involved intense fear, helplessness, or horror.
Note: In chidren, it may expressed instead by disorganized or agitated behavior
112
Describe the symptoms of PTSD
Symptoms of PTSD
Intrusive elements:
-Recurrent and intrusive distressing recollections of the event
-Recurrent dreams of the event
-sudden acting or feeling as if the traumatic event were recurring (deja vu)
-intense psychological distress at exposure to things that symbolizes or ensembles an aspect of the trauma, including anniversaries thereof
-Physiological reactivity when exposed to internal or external cues of the event
-At least ONE of these symptoms to be diagnosed with Post traumatic stress disorder.
113
What are avoidance features of PTSD?
Avoidance Features
-Efforts to avoid the thought or feelings associated with the trauma
-efforts to avoid activities, places, people or situations that arouse recollection of the trauma
-inability to recall an important aspect of the trauma (psychological amnesia)
-Markedly diminish interest in significant activities
-feelings of detachment or estrangement form others
-Restricted range of affect-unable to have loving feelings
-sense of foreshortened future- does not expect to have career, marriage, children or normal life span
114
What are the persistent symptoms of increased arousal (not present before trauma) ?
Persistent symptoms of increased arousal (not present before trauma)
-Difficulty falling asleep or staying asleep
-irritability or outburst of anger-irritability can progress to rage
-Difficulty concentration
-Hypervigilence- resembles frank paranoia
-Exaggerated startled response
At lease TWO of these symptoms to be diagnosed with PTSD
115
What are the different types of PTSD.
Types of PTSD
-Acute PTSD- symptoms less than three months
-Chronic PTSD- symptoms more than three months
-although symptoms usually begin within 3 months of exposure, a delayed onset is possible months or even years after the event has occurred.
116
Describe how diagnosis of PTSD occurs. Who does this diagnosis and how is it determined? Can one diagnose themselves for PTSD?
Diagnosis of PTSD
-There are No laboratory tests to detect PTSD.
To diagnose PTSD, a healthcare provider will consider the above symptoms together with the history of trauma.
-He or she will likely also use psychological assessment tools to confirm the diagnosis and involve an appropriately trained specialist
-although it may be tempting to diagnose yourself, the diagnosis should be made by mental health professional. This usually involves a formal evaluation
117
Describe the onset of PTSD. Compare and contrast Immediate vs Delayed onset
Onset of PTSD; symptoms usually begin within the first 3 months after the trauma, although there may be a delay of months, or even years, before symptoms appear.
Immediate onset:
-better response to treatment
-better prognosis (less severe symptoms)
-Fewer associated symptoms or complications
-symptoms are resolved within 6 months
Delayed onset;
-characterized by an onset of symptoms at least 6 months after stressor
-associated symptoms and conditions develop
-condition more likely to become Chronic
-possible repressed memories
-Worse prognosis
118
Explain what occurs during the course of PTSD. How does duration of symptom vary? When can symptom reactivation occur
Course of PTSD
-The symptoms and the relative predominance of re-experiencing, avoidance and increased arousal symptoms may vary over time
-Duration of symptoms also varies: complete recovery occurs within 3 months after trauma in approximately half of the cases. Others can have persisting symptoms for longer than 12 months after the trauma
- Symptom reactivation may occur in response to reminders of original trauma, life stressors, or new traumatic events
119
What are the most important factors that affect chance of developing PTSD? What can influence development of PTSD?
The Severity, duration and proximity of an individual's exposure to a traumatic event are the most important factors affecting the likelihood of developing PTSD
-Social supports, family history, childhood experiences, personality variables and pre-existing mental disorders may influence the development of PTSD
-PTSD can also develop in individuals without any predisposing conditions, particularly if the stressor is extreme
-the disorder may be especially severe or long lasting when the stressor is of human design (torture, rape)
120
eWhat are examples of traumatic events experienced Directly
Examples of Traumatic Events Experienced Directly:
-Military combat
-Violent personal assault (sexual assault, physical attack, robbery, mugging)
-being kidnapped
-being taken hostage
-Terrorist attack
-Torture
-incarceration as a prisoner of war or in a concentration camp
-Natural or manmade disasters
-Severe automobile accidents
-Being diagnosed with a life-threatening illness
121
What are examples of Witnessed Traumatic Events?
Witnessed Traumatic Events:
-Observing the serious injury of unnatural death of another person due to violent assault, accident, war or disaster
-Unexpectedly witnessing a dead body or body parts.
122
What are examples of events experienced by others that are learned about
Examples of Events experienced by others that are learned about
-Learning of a violent personal assault, serious accident, or serious injury experienced by a family member or close friend
-learning of a sudden, unexpected death of a family member or a close friend
-Learning that one's child has a life-threatening disease
123
What is the Estimated Risk for Developing PTSD based on event?
Rape (49%)
Severe beating or physical assault (31.9%)
-other sexual assault (23.7%)
-Serious accident or injury (ex car or train accident) (16.8%)
-Shooting or stabbing (15.4 %)
-Sudden unexpected death of family member or friend (14.3%)
-Child's life-threatening illness (10.4%)
-Witness to killing or serious injury (7.3%)
-Natural Disaster (3.8%)
124
What are the assesment tools used to Diagnose PTSD? What is CAPS?
Assessment Tools:
-Two main categories of PTSD evaluation are structured interviews and self report questionnaires
-Interviews
-Clinican administered PTSD scale (CAPS) developed by National Center for PTSD
-It has a format that requests information about the frequency and intensity of the core PTTSD symptoms and common associated symptoms which may have implications on treatment and recovery. The CAPS-1 yields both continuous and dichotomous scores for current and lifetime PTSD symptoms
125
What other disorders are usually compared to PTSD?
PTSD compared to other disorders:
-While the symptoms of Post traumatic stress disorder (PTSD) may seem similar to other disorders, there are differences
-Acute Stress disorder
-Obsessive Compulsive disorder
126
Explain the similarities and differences between PTSD and obsessive compulsive disorder ?
both PTSD and Obsessive Compulsive Disorder have Recurrent, intrusive thoughts as a symptom, but the TYPES of thoughts are on way to Dinstinguish these disorders.
Thoughts present in Obsessive-compulsive disorders do NOT usually relate to past traumatic event
-With PTSD, thoughts are invariably connected to Past Traumatic Event
127
What are the similarities and differences of PTSD and Adjustment Disorder ?
PTSD symptoms can also seem Similar to adjustment disorder because both are linked with ANXIETY that develops After Exposure to Stressor
-With PTSD, this stressor is a traumatic event.
With adjustment disorder, the stressor does NOT have to be severe or outside the "normal" human experience
128
What are the main treatments used for PTSD?
Treatments:
-Individual therapy
-Group Support (especially for Chronic PTSD)
- Medication
129
Describe the different kinds of treatment used for Acute, Severe acute and Chronic PTSD. Also discuss the preferrerd treatment PTSD in children , adolescents and geriatrics
Treatments:
-Acute PTSD- stress debriefing and psychotherapy
- Severe Acute PTSD- Stress debriefing, medication, group and individual psychotherapy
-Chronic PTSD; stress debriefing, medication, group and individual psychotherapy
-For PTSD in children, adolescents, and geriatrics, the preferred treatment is psychotherapy.
130
What occurs in Exposure Therapy?
Exposure Therapy: Education about common reactions to trauma, breathing retraining, and repeated exposure to the past trauma in graduated doses.
The goal is for the traumatic event to be remembered without anxiety or panic resulting
131
What is cognitive Therapy?
Cognitive Therapy: Separating the intrusive thoughts from the associated anxiety they produce
132
What occurs in Stress inoculation training ?
Stress inoculation training: Variant of exposure training teaches clients to relax. Helps the client relax when thinking about traumatic event exposure by providing client a script
133
What is Cognitive Restructuring? How effective was CBT?
Cognitive Restructuring involved teaching and reinforcing self-monitoring or thoughts and emotions, identifying automatic thoughts that accompany distressing emotions, learning about the different types of cognitive distortions, and working to dispute the distress-enhancing cognitions, with a particular focus on abuse-related cognitions, for which the therapist remained alert during the personal experience work.
In summary for women who did not drop out, CBT treatment was Highly effective for achieving remission of PTSD diagnosis, ameliorating PTSD symptom severity, and reducing trauma-related cognitive distortions, compared with a WL control group.
134
What kind of medications are used to treat PTSD? How do they work?
SSRIs (Selective Serotonin Reuptake Inhibitors)- Sertraline (Zoloft), Paroxetine (Paxil), Escitralorpram (Lexapro), Fluvoxamine (Luvox), Fluxetine (Prozac)
-Affects the Concentration and activity of neuraotransmitter Serotonin
(SSRis block the breakdown and reabsorption of Serotonin; hence increase serotonin levels)
-May reduce depression, intrusive and avoidant symptoms, anger, explosive outbursts, hyperarousal symptoms and numbing
-FDA approved for the treatment of Anxiety Disorders including PTSD
135
Explain how Tricyclic Antipderessants are used as medications for treating PTSD.
Tricyclic Antidepressants- Clomiprimine (Anafranil), Doxepin (Sinequan), Nortripytyline (Aventyl), Amitriptyline (Elavil), Maprotiline (Ludiomil), Desipramine (Norpramin)
-Affects concentration and activity of neurotransmitters serotonin and norepinephrine
- Has been shown to REDUCE insomnia, dream disturbance, anxiety, guild, flashbacks, and depression
136
What kind of treatment is sued in children for depression, OCD? What other forms of treatment are available?
Treatment for Children
-FDA approved Prozac for depression in children
-FDA approved Zoloft for OCD in children
-Cognitive-Behavioral Therapy- Exposure, anxiety management, Cognitive restricting
-Play Therapy
-parental influence and involvement is very important
137
What occurs when PTSD is treatment with medications, therapy and other forms of treatment?
With treatment, symptoms should improve after 3 months.
In Chronic PTSD cases, 1-2 years
