Delusions(delusions of grandeur, persecutions, control), hallucinations(often auditory), disorganized thought
positive symptoms are present
Negative are effects that are absent
flattened emotions, social withdrawal, poverty of speech, cognitive deficits
when do symptoms(Schiz) typically appear?
typically appear in late adolescence/early adulthood
what causes Schiz.
Genetic factors: related to multiple genes. A person can carry the risk w/o ever developing the disorder. Meaning they can carry it w/o having the actual disorder.
Environmental factors: (schiz)
can be a disruption in the normal development process. It happens greater in the women who experience complications during birth or have a lot of maternal stress. & ppl born in late winter and early spring- Seasonality effects** also the ppl who are born away frm the equator (latitude effect)
Both may be related to winter flu season occuring during the 2nd trimester of pregnancy
structural/ functional alterations
suffer from brain damage. signs: poor control of eye movements, unusual facial expressions and poor pupillary responses. Also Enlarged ventricles, which indicate a loss of brain tissue
Where is tissue lost in Schiz?
prefrontal cortex & temporal lobe. there is also disorganization in the neuron especially in the cortex and the hippocampus.
Schiz. is a developmental disorder. something went wrong early in development that leads alter brain development and schiz.
positive symptoms are related to overactivity of the mesolimbic dopamine pathway
evidence: conventional antipsychotic drugs block neurotransmissions by blocking D2 DA receptors
drugs that increase dopamine can lead to psychotic symptoms
Hypofrontality Hypothesis: Negative symptoms
may be related to loss pf tissue and reduced activation of the pre-frontal cortex, particularly the dorslateral prefrontal cortex
-there is an underactivation, or too little dopamine released in the mesocortical system. This contributes to negative symptoms and cognitive deficits
Schiz. can be related to a reduction in glutamate activity.
-PCP a drug that blocks the NMDA receptor( a receptor activated by the neurotransmitter glutamate) produces both positive and negative symptoms
first pharmacological treatment for Schiz. identified by French neurosurgeon Henri Laborit..this drug blocks the dopaminergic receptors(D2) receptors..produce side effects relapsing, getting back on meds etc. Bc blocking the dopamine affects all of the dopaminergic systems not just the mesolimbic system
characterized by involuntary movements. the drugs lead to an increase in number and sensitivity of dopamine receptors...the system becomes to sensitive to dopamine which is called dopamine supersensitivity
atypical antipsychotic drugs
a newer class of drugs, the atypical antipsychotics (like clozapine) they ultimately reduce activity of the mesolimbic dopaminergic system, without affecting neuronal activity at the nigrostriatal or mesocortical systems. but blocking the serotonin receptors does not affects the mesolimbic system. this allows the drug to reduce dopamine activity in the mesolimbic system and psotive symptoms od Schiz. without the same effects as original antipsychotic drugs.
this is characterized by cycles of mania and depression. The mania typically lasts a couple of weeks, followed by depression that lasts 2-3 times as long. Bipolar disorder affects both males and females with equal frequency.
this is characterized by depression only. The depression can be continuous and unremitting, but more commonly occurs in episodes. Women are 3 times more likely to suffer from unipolar depression compared to men.
-woman are more commonly studied
symptoms of mania and depression
genetic factors: affective disorders run in families. genetic factors interact with environmental factors.
environmental factos: stress & hormones
ppl who are experiencing significant life stressors are more likely to suffer from depression. & individuals who are experiencing their first episode of depression are likely to have just experienced a major life stressor. this can be bc of an overactivity of stress systems. they show an increase in CRF and cortisol
it may be due to the regulation of the HPA axis. When glucocoticoid levels are high, they active the hypothalamus and the hippocampus which tell the HPA axis to slow down
is a chemical that should activate the negative feedback systems and reduce the amounts of CRF release. Depressed individuals fail this test..the feedback is not working well= Feedback resistance
the glucocorticoid cortisol may damage the hippocampus too much cortisol can lead to cell death and damage to the hippocampus. There is a hippocampal size reduction that can be linked to depression
what is happening in the brain of depressed individuals?
reduced hippocampal size(reduced by abput 15% on average)
dysfunction of the prefrontal cortex
dysfunction of the amygdala
these drugs inhibit the action of the monoamine oxidase(MAO) the enzyme that breaks down the monoamine neurotransmitters (serotonin, dopamine, noradrenaline). By blocking the breakdown of the neurotransmitters, the neurotransmitters can be re-packaged and released, so the treatment increases the monoamine neurotransmission. i.e Nardil & Iproniazid
there are certain foods such as cheese, wine & bread that contain pressor amines that resemble the catecholamine neurotransmitters. These are normally broken down by MAO in the blood. if these are not broken down it can activate the sympathetic nervous system= leading to an increase in heart rate and blood pressure. if it gets so severe it can lead to intracranial bleeding or cardiovascular collapse.
block the reuptake of serotonin and noradrenaline
Specific serotonin reuptake inhibitors
Like the tricyclic antideprresant, the SSRIs block the reuptake of neurotransmitters fro the synaptic cleft, except the SSRIs selectively block only serotonin(as the name implies). SSRIs include prozac, paxil and Zoloft
new antidepressant drugs are always being developed and their actions vary from one another. Researchers are trying to manufacture drugs that are more effective with fewer side effects.
* all these drugs increase monoamine neurotransmission they are monamine AGONIST*
depression is due to reduced monoamine neurotransmission. It states that there is underactivation of monoamine neurotransmission (like serotonin and noradrenaline) and this leads to depression.
evidence for the monoamine hypothesis
drug treatment that reduce depression increase monamine neurotransmission
-drugs that reduce monoamine neurotransmission may cause depressive symptoms
-indiv. with suicidal tendencies have reduced serotonin activity
-the tryptophan depletion process will cause depressed ind. who are currently
but how does stress relate to monoamine hypothesis?
it turns out that stress systems and serotonin interact, so increases in glucocoticoids may actually lead to reductions in serotonin
how long do the meds take?
it typically takes a couple of weeks before there is relief from depressive symptoms.
when a antidepressant drug is taken the increased monoamine neurotransmitters in the synaptic cleft also ACTIVATE AUTORECEPTORS. Activation of autorecpetors might initially counteract the effects of the drug
Neurogenesis hypothesis of depression
recent hypothesis is that antidepressant drugs lead to neurogenesis. it takes a couple of weeks for newly generated neurons to mature and establish synaptic connections..this can be the answer to why it takes so long
Electroconvulsive shock treatment
As seen in the video, this is used for cases of suicidal depression
Transcranial magnetic stimulation
electricity is passed through a col and this creates a magnetic field. this field is placed above the scalp and can influence the activity of underlying brain tissue.
total sleep deprivation is fast acting, but short lived
REM sleep deprivation is slower acting but may have longer lasting effects
lithium is a mood stabalizer it is believed to influence 2nd messenger. it is effetctive on 70-80% of indiv. so it was described as the wonder drug. it that soesnt work we can take carbamazepine
some problems thay have with this is compliance.. some ppl miss the feeling of mania and go off the meds so they can expereince the excitemet.. the best thing is to use a combo of drug therapies and psychotherapies. Psychotherapy also influences our physilogy causing changes in brain activity.
Declaritive or Explicit
Episodic: autobiographical memory that pertains to a person's particular history
Semantic: refers to generlaized memory, such as knowing the meaning of a word without knowing where or when you learned it, or knowing that paris is the capital of france.
nondeclarative or implicit (skills and behaviors)
for example, riding your bike playing a piano, classical conditioning, learning a skill or recognizing an object.
non declarative include: perceptual learning, classical conditioning, learning of skills and habits and non-associative learning.
H.M suffered from seizsures that became progressively worse. when we reached young adulthood, his seizsures were out of control. Neurosuregeons decided to remove his MEDIAL TEMPORAL LOBES BILATERALLY(BOTH HEMISPHERES: inc. ). stopped the seizsures but now he had amnesia both retrograde and severe ANTEROGRADE.. HM was unable to form new declarative memories, but was able to
amnesia refers to loss of memory for events that occured before brain damage.
refers to the loss of memory for events that ocurred before the brain damage
amnesia refers to the inability to form NEW memories after brain damage
antergrade amnesia refers to the inability to form NEW memories
which of these brain regions is related to memory deficits
it turns out that the hippocampus and related cortical and limbic structures are important for the consolidation of declarative memories, whereas the amygdala is important for emotional learning.
damage to the hippocampus & amygdala
ind. who have damage to the hippocampus and adjacent cortical tissue are able to develop a conditioned emotional response but not able to describe the relationship btw the CS and US(declarative memory). individuals with damage to the amygdala do not develop a conditioned emotional response but can tell u the realtionsip btw the CS and US. the declarative memory is still intact.
*it turns out that the hippocampus and adjacent cortex are critical for consolidation of declarative memories*
where are long term memories stored?
long-term storage of declarative memories occur in the cortex. Episodic memories memories may be stored in different parts of the cortex from semantic memories
1) hippocampus and adjacent cortex/ limbic system system are important for consolidation of declarative memories
2)declarative memories are stored in the cortex for long-term memory
nondeclarative memories: perceptual
perceptual memory: refers to the ability to recognize stimuli that have been perceived before. This allows us to identify and categorize objects and situations. It takes place in higher sensory cortical areas.
nondec: classical conditioning
emotional conditioning requires the integrity of the amygdala. So if a neutral stimulus is paired with an emotional eliciting stimulus, individuals with amygdala damage fail to develop a conditioned emotional response
*conditioning occurs in the cerebellum*
skills and habits:
memory for skills "knowing how" rather than "knowing what" skills are aquired gradually through repetitive practice-like the mirror tracing task
memory for learning of motor skills, like riding a bicycle, playing tennis, playing th epiano depends on the cerebellum
an example is the weather prediction task. Habit learning involves the BASAL GANGLIA
non-associative learning(aka reflex modification)
reflexes refer to the stimulus response reactions. but reflexes can be modified. Sometimes the responsiveness is reduced following repeated presentations of the stimulus. this is referred to as habituation. in other cases, responsiveness is increased. This is called sensitization. With reflex modification, there are changes in the reflex circuits.
lateralization or hemispheric specialization
functional differences btw the two hemispheres
is more involved in language, analytical processing and sequential processing
involved in spatial processing, processing of patterns, emotional processing, and prosody
our hemispheres communicate through the corpus callosum.
what happens if the corpus callosum is cut(split brain)
the two hemisphers cannot communicate properly, they act independently but over time they adapt so it is less obvious
language is dominant in the left hemis. in over 95% of right handed individuals & 70% of left handed individuals. some are right hemisphere dominant and others are mixed.
*corpus callosum is thicker among left-handed individuals*
Why is the left hemisphere typically in greater control of language?
it may be related to a neuroanatomical difference: the planum temporale an area on the superior (top) surface of the temporal lobe, is larger in the left hemisphere compared to the right hemisphere in over 65% of individuals
primary disturbances in the production or comprehension of speech
Brocas Aphasia (nonfluent aphasia)
Brocas area lies in the left frontal lobe
this is labored, slow and nonfluent speech. They often get frustrated with their speech difficulties
-anomia: they have difficulty finding the word and struggle saying it
-difficulty with articulation:they sometimes will switch letter or mispronounce words, but they say it usually meaningful and can be understood. They often realize their mistake and correct it
agrammaticism: they have problems using and understanding function words. They tend to use content word(open class words) they would have difficulty understanding "the cow kicks the horse"
Wernickes aphasia aka fluent aphasia
superior portion of the temporal lobe
their speech is fluent, just not meaningful, or understandable.
there speech is melodic(prosody) and they us social conventions (taking turns) when speeking with another individual. they have no comprehension of what they are saying. They often seem unaware that they have a deficit
articulate speech: Unlike brocas they have no difficulty articulating words
anomia: Meaningless speech
poor comprhension: even though they dont notice, they do not understand what other are saying
pure word deafness
can not recognize speech sounds. Their recognition of sounds that have rapidly changing components, like word is disrupted. **this is caused by damage to auditory inputs into Wernickes area or to Wernickes area itself
transcortical sensory aphasia
these individuals can not understand speech or produce meaningful speech. The can repeat words.
this is damage to the posterior regions next to wernickes area. the posterior region is an interface btw wernickes area that recognizes speech sounds and the corticol areas that store the meaning of words