Shared Flashcard Set


Brain and Behavior
Final Exam
Undergraduate 4

Additional Psychology Flashcards




How many forms of learning are there? What kind of forms are they?
4; 3 simple and 1 complex; different types of learning changes different areas of the brain
What are the 3 simple types of learning?
Perceptual, Motor, Stimulus-Response
Perceptual Learning
identifying, organizing, basic information
"I've seen it before"
Change in the brain is only Sensory association cortex (which is most of the cerebral cortex)
Motor Learning
skilled habit that happens to be motor
"learning how to ride a bike as a child is a habit now"
change in the brain is only the motor areas
Stimulus-Response Learning
Classical conditioning and instrumental conditioning, Classical being reflex/response and instrumental being mazes and such
change in both motor and sensory areas
Relational Learning
relations among stimuli in space and time
spatial learning: navigation
episodic learning: aspects of a particular event
observational learning: learn from someone else's mistakes
What are the two motor areas?
As learned behaviors become automatic they transfer to one of the 2 motor areas:
Basal Ganglia
Premotor cortex (in the frontal cortex)
What specific part of the brain is part of stimulus-response learning?
For conditioned emotional response it is part of the lateral amygdala
Most forms also involve the cerebellum (because of motor activity)
there is a different pathway for conditioned stimulus and another pathway for unconditioned stimulus (it converge at neuron for a response)
What is the reinforcement pathway (aversive pathway)?
DA ---> Ventrotegmental Area ---> Lateral hyopthalamus ---> Prefrontal cortex
What is Dopamine's role in the reinforcement aversive pathway?
the action of this neuromodulator (modify) is to act like a neurotransmitter
What is the Ventrotegmental area's role in the reinforcement aversive pathway?
It has input from the amygdala for the emotional aspect
What is the Lateral hypothalamus's role in the reinforcement aversive pathway?
It provides information about the stimulus aspect whether it is an object or person
What is the prefrontal cortex's role in the reinforcement aversive pathway?
The prefrontal cortex provides the cognitive aspect these are areas of the brain that gets animals to not do their action again
What are the 3 brain areas involved in instrumental learning?
Basal ganglia, caudate nucleus, and putamen
the more active the basal ganglia the faster you learn and if the caudate nucleus is very activate that means the animals learn really fast
What is the capacity for Short term memory? How long does it last?
limited capacity 4 +- 1 chunks 4 chunks are translated to 7 digits, 6 letters, or 5 one syllable words
It lasts for seconds
How do you keep information in short term memory?
keep the information by going over it
if you go over it again and again it transfers to long term memory
What is the capacity for long term memory? how long does it last?
Has an unlimited capacity and it is permanent however retrieval and permanency are two different things
What is the process of permanent memory called? What is the most important part?
Memory formation; the first 30 minutes are important for transfer
How was working memory discovered?
STM was too short and we want information that we can discard later
How long does working memory last? Is it part of STM or LTM? What part of the brain is used?
Longest was 30 days; part of STM; and the prefrontal cortex so all of the frontal lobe except the motor areas
What part of the brain takes away irrelevant information and what part of the brain keeps the relevant information?
The left basal ganglia takes away irrelevant information
The right prefrontal cortex keeps the relevant information
What are the two types of long term memory?
Declarative and Non-declarative
What is declarative memory about?
- memories about specific facts, events, and individuals and you can speak about them and manipulate them in your mind and it takes one trial
- need conscious involvement so it is an active process for memorization
- occurs fast
- simultaneously stimuli presented
- You need higher parts of the brain like prefrontal cortex and the hippocampus
What is non-declarative memory about?
- It is rules that govern your behavior
- Most simple forms of learning
- Cognitive habits: riding a bike
- You don't have to be actively working
- It is slow and might take many trials
- It has sequential stimuli so you can make predictions
- No higher levels of the brain
What is the pre-modulatory associative mechanism for Non-declarative?
- the presynaptic and postsynaptic neurons have to be active at the same time
- you have a axoaxonic connection
- Terminal button of the modulatory neuron is synapsing on the terminal button of the presynaptic neuron this is where changes in memory occur
- Interneurons modify the activity of another neuron
- change where memory occurs is when it is presynaptic and post synaptic
What is an example of pre-modulatory associative mechanism for Non-declarative?
Classical conditioning: Ringing the bell, bringing the food, and salivation
- It is the presynaptic neuron that provides the information for the condition stimulus like ringing the bell
- The unconditioned stimulus is provided by the modulatory neuron (bring the food)
- And the postsynaptic neuron provides information about the stimulus response like salivation
What is the classical conditioning level in mammals?
Classical conditioning is at the level of the cerebellum in mammals
• One pathway is ears to pre synaptic neurons
• Another pathway Smell and vision to modulatory neuron
• Post synaptic neuron causes animal to salivate
Behavioral timing equals physiological timing, what does this mean?
There is an optimal time for learning; timing cannot be too close or to far apart and each stimulus is different timing
- two neurons, the pre synaptic and the modulatory neurons, can be active at exactly the same time because the number of synapses (depends on which stimulus)
Which type of memory does LTP and NMDA receptors are involved in?
nondeclarative- in many parts of the brain
declarative- all parts of the brain; if you interfere it you won't form the memory
What is the pre post associative mechanism?
- tells you which two neurons have to be active at the same time
- change or memory occurs in both neurons
- presynaptic and postsynaptic neurons are active the same time
- LTP and NMDA receptors are involved in all locations
Memory formation: Hebb's theory
- in the brain there is a circuit that synapsed on one another
- you keep information you want to remember in the circuit until a change occurred in the neurons where that memory is going to be stored
- it keeps stimulating each other, it keeps reverberating and keeps active until a change occurs
- As this stays active it is sending activity where memory is going to be permanent
- you have different cell assemblies for different things
- how fast you form these cell assemblies is how fast you learn
- Reverberatory circuit: hippocampal formation-not involved in permanent memory
What is the right hippocampal formation?
-Consolidation (forming memories) and retrieval of new (~1 week) declarative memories (episodic, semantic, spatial, relational)
- After first week, changes are not permanent enough for them to be retrieved without use of hippocampal formation which has to be involved for retrieval
- contextual information: helping put individual in his/her proper context
What happens in the right posterior hippocampus?
- Spatial tasks
- Becomes larger when you have to memorize more spatial tasks (taxi drivers)
- Right medial temporal lobe
Relational memories
- Cerebral cortex: final location for relational memories
1) Sleep/stage 3 and 4: transferring declarative memories to LTM in prefrontal cortex: “sharp-wave-ripple complexes” originate in CA1 and CA3 and are propagated to cerebral cortex
2) Medial prefrontal cortex: may be the area that is essential for long-term memory storage and retrieval of information (mice research)
3) For memory-relational underlying mechanism is called long-term potentiation (LTP)
4) Frequent activity of a particular neuron, end result in postsynaptic neuron-increases excitability so next neuron can easily create an AP
5) Block LTP: animal does NOT learn
What is long term depression?
- it is forgetting the opposite results of LTP
- Lower the postsynaptic potential-so you won’t remember what’s happening
What neurotransmitter is involved in LTP?
- Glutamate
 Remember that the reinforcement pathway can speed up memory formation and dopamine is involved so it isn’t surprising that dopamine can enhance LTP but that is only true if a particular enzyme is present
• Enzyme is called PKM-zeta
o You need the production of PKM-zeta for long term memories for long lasting LTP
 So we know its key for a nice long memory
Where does LTP occur?
Hippocampo formation which is in the cerebral cortex
What is LTP?
Give a strong stimulus this axon keeps firing activating the next axon and very strong rapid firing, what will happen the next axon the dentate gyrus it becomes more sensitive it becomes more easily excited and it is going to create a more excitable more excitatory post synaptic potential, more sodium is going to come in more than it normally would, so you get a greater excitatory post synaptic potential (EPSP)
 You can do the opposite you can give a very weak signal and the EPSP is going lower less sodium will be coming in
o If you interfere with LTP, so you haven’t given a chance for that permanent memory, you interfere LTP the memory doesn’t occur
 So we know that it is essential for relational and declarative memories classical conditioning, instrumental conditioning,
What is the basis of forgetting?
 The basis for forgetting is long term compression and that a weak signal is given and because of the infrequent weak signal there is less of an EPSP and that means there is less sodium going in, the ion channel is not going to be open for long unless sodium is going in, so the odds for long term depression you're not going to generally get an AP it is not going to go any further so you are not gonna remember the information.
What is CREB?
A memory molecule
• It gets charged up when a learning signal comes in from other brain cells
• CREB memory molecules sends building blocks back to the point of contact with other cells enough building blocks and the contact point grows locking the connection
- needs an hour to charge
- keep them active with aerobic exercise and using it
What is schizophrenia?
a mental disorder categorized by disorganized thoughts, sometimes delusions, hallucinations, and often bizarre behaviors
What are positive symptoms of schizophrenia?
- rational thinking is gone (some foods are okay to eat)
- disorganized thoughts (answer questions in song titles)
- hallucinations, auditory (a voice tell you to kill yourself)
- delusions
What is the area that is causing the positive symptoms of schizophrenia?
Nucleus accumbens; the reinforcement pathway is disrupted
What are the 3 types of delusions that schizophrenic people have
Persecutions: someone is out to get them
Grandeur: famous person
Control: someone will control them from outer space
What are the negative symptoms?
- flattening emotional response (dont feel anything)
- poverty of speech (dont speak too much)
- lack of initiative and persistence (they don't start anything on their own)
- inability to seek pleasure
- social withdrawl
What is the area that is causing the negative symptoms of schizophrenia?
the prefrontal cortex
What are the cognitive symptoms?
- difficulty sustaining attention
- Low psycho motor speed
- deficits in learning
- poor abstract thinking
- poor problem solving
What is the area that is causing the cognitive symptoms of schizophrenia?
prefrontal cortex
Why is the Negative and cognitive symptoms first and then positive symptoms in schizophrenia?
• Damage in prefrontal cortex first and continues and causes damage in nucleus accumbens-that’s why you get positive symptoms last
• The longer they have schizo the long they more the more brain damage
What is the typical age onset for schizophrenia?
late teens and early 20s
What is the gender differences in schizophrenia?
more common in MEN than women
- women develop later than men
- there is also a better prognosis for women
Heredity for schizophrenia?
Yes it runs in families it is a weak effect also age of the father affects his children
What neurotransmitter is involved in schizophrenia?
- Dopamine is involved in all the symptoms
• Dopamine hypothesis
• Reinforcement pathway is involved-excess dopamine being secreted
• Responsible for the positive symptoms
- Glutamate (hippocampal formation)
• Lower levels of glutamate (noncompetitive binding site on NMDA-prevents opening)
• For the positive symptoms
• If there is too little glutamate the receptors won’t open
• Those non competitive binding sites on the NMDA receptors prevent the opening
• Glutamate cannot attach cause the receptors not opening
• In the hippocampal formations
• The neurons are not lined up in the way it is for the normal individual
• The orientations are all over the place dendrites in all different directions
• Neurons are different in those who suffered from schizophrenia than from those who did
• Disorganized-axons and dendrites go in all different directions

• Dorsolateral prefrontal cortex involved for the negative and cognitive symptoms
• Not active as it should hypofrontality (inactivity in the frontal cortex) Hypo- too low frontality- frontal cortex
• Responsible for the Negative and cognitive symptoms
• Fewer NMDA receptors (glutamate) and DA receptors and more recently that GABA receptors are involved but those are low levels
• Recently wondered about the lower levels of GABA receptors
Other brain information on schizophrenia?
The ventricles get larger and other parts of the brain gets smaller
The loss of the gray matter happens in the temporal and frontal lobe
What is the seasonal effect, environmental factor, stress factor, and substance abuse by mother in schizophrenia?
If you were born Feb-May you might have schizo
If there was vitamin D deficiency you might have schizo
Stress creates toxins that build up during starvation
Especially smoking causes schizophrenia
What is bipolar disorder?
Manic and depression
mania- so much energy
depression- why go on
What is the gender differences in bipolar disorder?
No difference equal for men and women
Is heredity a factor for bipolar disorder?
Yes it runs in families
How long are the phases of bipolar disorder?
Manic phase can be a few days, months, typically weeks and the depression that comes after that will always be 3X longer
What are common characteristic of bipolar disorder?
o Lack of sleep-they will tell you they don’t need sleep
o Increase of activity
o Have feelings of Euphoria
 That they can accomplish everything
o More likely during manic phase to take risks, be impulsive (ie creating a new company)
o Sometimes aggression during manic phase
o Hallucinations are not typical-if they do occur more likely to be visual
 Not disruptive like those from schizo
What is the treatment of bipolar disorder?
Lithium and group therapy
The lithium evens out manic phase
- If they don’t go into manic phase, don’t go into depression phase and Group therapy is to keep them on lithium (many times they will miss feeling of euphoria and some will go off of lithium to have feeling again)
What is Mania?
Only the manic phase
Very rare
Feeling of euphoria
It is a major affect disorder
What are the two types of Major Depressive Disorder?
Reactive depression and Endogenous depression
What is reactive depression?
reacting to a situation or environment and become depressed
o Death of a loved one
o Loss of home
o Solve the problem the depression goes away
o No genetic basis for it
o things get better, time elapsesdepression goes away
o Treatments are same as endogenous with physiological basis
What is endogenous depression?
o Low levels serotonin or low levels or norepinephrine or low in both both
o Serotonin
 (in the prefrontal cortex)
 suicidal individuals
o Norepinephrine
 Assume prefrontal cortex
• Not suicidal
o Women more likely than men
o There is a biological basis for it
What are the 11 treatments for Major Depressive Disorder?
1) MAO inhibitors
2) Tricyclic antidepressants
4) Drugs that inhibit serotonin and norepinephrine these are called SNRI
5) Electro compulsive therapy
6) Transcranial Magnetic Stimulation (TMS)
7) Electrostimulation of the vagus nerve
8) Deep brain stimulation
9) Sleep Deprivation
10) Increase in exercise
11) Cognitive behavioral therapy
What does MAO inhibitors do as a treatment for MDD?
 The enzyme that breaks down serotonin and norepinephrine and any monoamine so dopamine too
 Prevent the breakdown so you get more serotonin and NE in your system
 There are side effects especially If you use it with dairy products
What does tricyclic antidepressants do as a treatment for MDD?
a. They prevent the uptake of serotonin and NE
b. Prevent the uptake of other n.t.
c. A lot of side effects but not as bad as MAO inhibitors
What does SSRI (serotonergic reuptake inhibitors) do as a treatment for MDD?
- Drugs that inhibit the reuptake of serotonin
- Prozac is an example
 Takes 2 to 3 weeks to take an effect
 A combination of SSRI and 5HT1 antagonist
• This combination brought it to 1 week to take effect
 The increase serotonin in the prefrontal cortex
 In taking the SSRIs it is similar to taking many other drugs
• It is like there is more serotonin in the synaptic cleft remember the autoreceptors provide feedback on how much is being released
o Autoreceptors respond by saying there is too much serotonin
 They will decrease their production of serotonin
• What you have to do then is to up the dosage
o You keep doing this until it starts getting bad side effects
 Then you switch to a new drug
• 5HT1 antagonist blocks the autoreceptor and just sits there like the wrong key and lock, so the neuron doesn’t get that feedback that there is more serotonin in the synaptic cleft then what it should be so you don’t get the decrease in the production
• With that combination Increasing the serotonin and blocking the feedback so the neuron keeps producing the same amount of serotonin they have reduced it from 2 weeks to one week
What does SNRI do as a treatment for MDD?
 Newer than SSRIs
 The hope is they have fewer side effects
• Time will tell whether they do or not
 2 to 3 weeks to have effect
What does electro compulsive threapy do as a treatment for MDD?
 For those people where drugs don’t work
 ECT a person is hooked up to electrodes and they fire all the neurons at the same time and it lifts the depression
• Don’t know why it works but it works
 It takes a few days
• It is faster
 The problem is that it might destroy some neurons and it is unpredictable which one
• What they found is the loss of long term memory
• People will lose a memory
 The treatment is typically 3 times a week and usually 6-12 treatments
 Once the depression lifts
• There will be a monthly maintenance
• Once a month they have to come back and have ECT
What does TMS do as a treatment for MDD?
 A more refined of ECT
 Most of the time the magnetic stimulation is circular or oval form
 What they can do is stimulate a more specific region of the brain
 So they can put it over the prefrontal cortex and only affect that area
 Mild side effects
• Headaches
• Discomfort
• Pain to the scalp
• Few had seizures
 Takes a couple weeks to work
 Maintenance is every four months
 The size of the effect is not as great as ECT
• It is not lifting the depression
What does electrostimulation of the vagus nerve do as a treatment for MDD?
 Successful but don’t know why
 Stimulating the vagus nerve they have had a gradual improvement and this is very gradual over months
• They will see a small improvement right away
• Then gradual
 It is indirect
 It is painless
• So no big side effects
• No seizures
What does deep brain stimulation do as a treatment for MDD?
They put in in one of 2 areas both areas have an effect or had success in
 electrodes in 2 different locations
 the subgenual anterior cingulate cortex
 nucleus accumbens
 you see small improvement then gradual improvement overtime
 get gradual improvement (like the vagus nerve stimulation)
 some predicted subgenual anterior cortex = where depression originates
What does sleep deprivation do as a treatment for MDD?
• Does not work for everyone
o Only a specific group of people
• Deprived of sleep for 24 hours
o Then it will lift depression immediately
• The only one where there are immediate effects
• Don’t do it to someone who has bipolar
o Triggers manic phase with someone who has Bipolar
• Works for those individuals that are more depressed in the morning than evening
o Wake up-severest depression
o As day goes on, depression decreases
• For those where it is a constant amount of depression sleep deprivation has no affect
• For those it does work the depression will be lifted
o Must do sleep deprivation once a week to keep it away
o Some just need to change their sleep wake cycle
What does exercise do as a treatment for MDD?
Increase in exercise can help lift depression (not by itself, but in combination with another treatment)
o Exercise can help different disorders
o It increases the creation of neurons (neurogenesis)
What does cognitive behavioral therapy do as a treatment for MDD?
• coupled with therapies 1-8 (must be combined)
• this is the therapy that is most successful
• learning coping techniques
• Look at world differently
• It’s talk therapy
What are some depression theories?
Monoamine hypothesis
Glutatmate hypothesis
Circaidian rhythms
What is the monoamine depression theory?
based on length of 5 HT transporter gene (1 or 2 short alleles)
o Remember serotonin and NE are monoamines
o Lower levels of 5ht or Ne
o How severe it is depends on the 5ht transporter gene
o if you have short allele you are more likely to suffer from depression
o if you have 2 long alleles you are more responsive to treatments and recovery
What is the glutamate depression theory?
if you are depressed, you have more glutamate
o They will have higher levels of glutamate if you are depressed
o Ketamine (vet meds): tried it with patients who are depressed and lifted depression immediately (couple hours) but caused schizo like symptoms
 Bad side effects so severe that it cannot be used as a treatment
o Trying to come up with a drug like ketamine
 But it takes 2 to 3 weeks to take affect
What is the circadian rhythm depression theory?
o when circadian rhythms become uncoupled you see the affective disorder
o for those who are depressed in the morning more than the evening
 they may be creating a depressogenic substance in their body while during the night time
 and then during the day that substance is broken down and it gets better during the day
o 90% depressed people have changes in their sleep patterns
o those suffering from major depressive disorder
 body temp peaks earlier than normal individual
 go into REM sleep faster (sooner)
• this happens to people who are sleep deprived
Interesting facts about MDD?
• leading cause of disability in the west is depression
o before was high blood pressure
• leading cause of disability in the world is back pain
o the second one is depression
• shortening of telomeres-shorter lifespan faster you age
o shorter telomeres are in depressed people
• about 1/3 of depressed people don’t respond to drug treatment
- people with depression produce too much of stress hormone-cortisol
o Stress triggers too much cortisol for too long-toxic for brain
o Makes brain more vulnerable to depression
- Serotonin is low in depression
o Drug allows serotonin to increase in prefrontal cortex
What is the brain abnormalities for MDD?
o Amygdala : high activity
o Prefrontal cortex: low activity
Within that prefrontal cortex that Subgenul anterior cingulated cortex -high activity
**look at to see if this is the possible origin of depression**
What is the most effective way to cure depression?
o Combination of drugs and talk therapy
o Changing synaptic connections-so you process info differently
What is seasonal affective disorder?
o There person depressed in winter months-start during fall
 When the days get shorter it gets bad
• They would lose their jobs
• Things are not fine
 can tell when days starting getting longer-start feeling better
 spring-depression lifts, days longer nights shorter
 springsummer: they are fine
What are the symptoms of SAD?
lethargy (no energy), craving for carbohydrates, sleep disturbances (sleep more than normal)
What part of the brain is associated with SAD?
o problem is with SCN (super chiasmic nucleus)
 needs strong stimulus than what it is receiving
 needs a strong stimulus to reset
o abnormality is that the time between when melatonin is being produced and when they fall asleep is a lot longer
 phase delay between melatonin start to be produced and when they fall asleep
• for them it is later that
Is heredity a factor in SAD?
Yes it runs in families
What is the gender differences in SAD?
women 2-3x more likely than men
 women are not sensitive to artificial light as men are
What is the treatment for SAD?
from sept-Mar (when days are too short) spend a couple hours every morning in front of special lights that have full spectrum (especially blue)
 depression lifts within few days
• and stays away as long as you use the lights
 it looks like a desk lamp
 white florescent lights
What is anxiety disorder?
You have an unrealistic unfounded fear or anxiety there are 2 types
What are the two types of anxiety disorders?
Panic disorder and obsessive compulsive disorder
What are panic disorders?
includes phobias, panic attacks, generalized anxiety disorder, social anxiety disorder
What are the symptoms of panic disorders?
clammy sweat, dizziness, fainting, can’t catch your breath, irregular heartbeat, feelings of unreality and that you’re going to die-nothing outside out of you that is causing panic attack
 Panic attacks can last for a few seconds to a few hours
What is generalized anxiety disorder?
excessive anxiety, worry, not acute behavior as with the panic attacks, difficulty to control anxiety, disrupting daily life
• there is no cause you are anxious but don’t know why
What is social anxiety disorder?
end up not wanting to be in social situations, convinced that everyone is talking about you in a negative way, excessive fear of being exposed to scrutiny of others, when walking into room, fear of everyone paying attention and criticizing you
• this fear is so great that you don’t go to a party or any social event
What is anticipatory anxiety?
anticipate that a panic attack going to happen
• end up developing agoraphobia: fear of open spaces (do not like to leave home)
Is heredity a factor in anxiety disorders?
Yes it runs in families
What are the gender differences in anxiety disorders?
occurs in women 2-3x more likely than men
What is the treatment for anxiety disorders?
cognitive behavioral therapy (desensitization biofeedback/relaxation, exercise)
• you may not have to be on meds for the rest of life they can probably get off their benzodiazepines
• change your views
• learn coping mechanisms so you can handle it-then expose you to it gradually, training you to cope with anxiety in a different way (feel anxious but know you will survive)
• desensitization used to overcome phobias
o exposing them to whatever’s making them anxious little at a time, keeping them relaxed
o virtual reality works as well with computers
• relaxation: train individual to relax, unique techniques
• biofeedback: hook you up to electrodes and tell you to move from one side of the other by producing alpha waves, relaxing (adults) or a train can be hooked up for children
• exercise can help with reducing anxiety
• combined with benzodiazepines-to get anxiety under control so they can work through using cognitive behavioral therapy and reduce it/eliminate it
o many can go off benzodiazepines and just go through cognitive behavioral therapy
What are the neurotransmitters involved in Panic disorder?
o their GABA levels are too low
o they have fewer GABAA receptors
What part of the brain is affected in anxiety disorder particular panic?
o High amygdala activityleads to increase in the severity of symptoms of panic disorder
o Happens in the Prefrontal cortex, cingulated cortex, insular cortex
• for some-use SSRI’s
• for some-use NMDA agonists which attach to glycine-binding site
What is obsessive compulsive disorder?
 obsessions=thoughts
 compulsions=behaviors
 thought pops into mindkeeps coming in with increasing frequencyuntil behavior is done to get rid of thought
 similar to panic disorder-they think that if they do not do behavior, then something terrible will happen
What are the behaviors of OCD?
• counting
o they may have to count to a certain number
• checking
o they may check if the stove is turned off
o is the door locked
o they might do it 40 times in an hour
o it is excessive
• cleaning-fear of germs, excessive cleaning to rid of germs
o cleaning to avoid germs
• avoidance
What is the key to OCD?
What part of the brain is affected by OCD?
• basal ganglia damaged
o end up getting increased activity in caudate nucleus and orbitofrontal cortex
 orbitofrontal cortex is right behind the eyes
• serotonin is too low
• increase serotonin and decrease activity in the caudate nucleus and orbitofrontal cortex
What is the age onset for OCD?
11 years so younger ages
Is it hereditary?
 when genetic (someone else in family has OCD)-as early as 8
• mainly obsessive
• it is heredity
• no gene yet
• when it is 8 just the thoughts just the obsessiveness as they get older compulsion will set in
What is the treatment for OCD?
• adults: cognitive behavioral therapy + SSRI’s (maybe NMDA receptor agonist)
• children and adolescents: start with CBT alone
o keep away from SSRIs
o the SSRI by themselves are the least effective
 CBT is greater that CBT + SSRI’s is more effect than SSRI’s
• Deep brain stimulation of basal ganglia or subthalamic nucleus (this has connection to the basal ganglia
o This reduces OCD symptoms in some individuals
What is the characteristics of Autism?
• Poor or limited social relations
• Sensory overload
o Body just shut down
o Hyper extension of hands
• Lack of touch sensations
• Hard to describe autism there is a wide range (characteristics)
o Poor limited to social relations
 Act as if they are unaware of others
 Occurs younger children
 Ignore people
 If they get hurt they do not seek comfort
• Underdeveloped communicative skills
o During any one-on-one conversation-avoid eye contact (do not realize any value in face)
 They don’t think that there is anything to gain from the facial expression
- repetitive behaviors
- lack of imagination
o Differential sensitivity to sensory stimuli, fascination with aspects of objects
 Cannot filter out sounds
 Sensory stimuli will be more sensitive than normal individual-loud sounds/bright light can hurt them
 Love to manipulate objects
• Take something apart
• Put it back together
What is the typical age onset of Autism?
• May times present at birth
o But obvious by age 3
What is the gender differences in Autism?
o 4 times more likely in males
What parts of the brain effects Autism?
• Brain malformation
o 20-24 days after conception
o area between medulla oblongata and pons shorter
o no superior olive (audition and hearing)
o facial nucleus (muscles of facial expression) is smaller
• Other brain stuff
o fewer neurons in amygdala
 no social interactions
 no emotions
 can’t read social expression
They have low levels of oxytocin
What is the cause of autism?
o for some it is genetic, for others exposure to toxic chemicals during embryonic development could be the underlying cause
What is the treatment of Autism?
o medications don’t help the core characteristics of autism (e.g., social and intellectual functions)
 does reduce repetitive, stereotyped behaviors
o most treatments
 are behavioral, using behavioral modification technique (no punishment nor aversive stimulus)
• great success but hard
• only positive reinforcement
o Structure is important
 Simple structures
• Reading in one location
• Math in another location
• Using these same locations helps
 education stressing positive discipline, structure, skills, visual cues
• reinforcements for social behaviors or basic language
What are the characteristics of ADHD?
• remaining still is hard
• concentration is hard
• childhood-most common disorder
o typically found in classroom
 this child is more active than the others
• delay reinforcement gradient is steeper than normal
o when steeper must give reinforcement faster
What is the gender differences in ADHD?
o prevalent in males more than females
Is heredity a factor?
Yes it runs in families?
What neurotransmitters are involved in ADHD?
o low DA (there are more transporters than normal to take up the DA )
• common treatment: medication to inhibit reuptake, inhibit transporters-Ritalin
o more normal level of DA
What causes ADHD?
possibly low NE along with low DA
- Air pollution when mother is pregnant
The more pollute the more likely to suffer from ADHD
o Increase of external activities
What area of the brain effects ADHD?
o less activity in prefrontal cortex and caudate nucleus
o cerebral cortex grows slower as a child
 by adult, size would be the same
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