Final Flashcards
Prosody
- tone, rhythm, etc.
- anything in language that doesn’t have to do with the language itself but the way it’s spoken
- associated with right hemisphere
Posterior language area
At junction of temporal, occipital and parietal lobe
- thought to be central unit that puts together concepts and their language representation
- word comprehension
Wernicke’s area
- in left temporal lobe
- spoken word recognition
Broca’s area
- in left inferior frontal lobe
- associated with motor tasks of language production
Transcortical sensory aphasia
- failure to comprehend meaning of words
- word perception and fluency might be okay but with limited comprehension of what is heard or said
- repeat after ppl
conduction aphasia
- inability to repeat words
- rest of speech and comprehension generally fine
- damage to arcuate fasciculusa
Arcuate fasciculus
- interconnect Wernicke’s and Broca’s areas
- damaged and ppl can look up word in association cortex but can’t say it back (conduction aphasia)
Pure word deafness
- impaired auditory word recognition
- damage to Wernicke’s area
- can hear, interpret non-speech sound, read and write
Wernicke’s aphasia
- aka fluid or receptive aphasia
- combination of pure word deafness and transcortical sensory aphasia
- poor language comprehension, fluid speech with prosody but meaningless
- damage to wernicke’s and posterior language area
Pure alexia
- inability to read or recognize written words but can write
- damage to visual word-form area
Visual word-form area
- in left hemi of fusiform gyrus (opposite to FFA)
Surface dyslexia
- inability to recognize whole words but can read phonetically
phonological dyslexia
- inability to read unfamiliar or non-words, loss of phonetic reading
Broca’s aphasia
- inability to produce speech
- articulation problems
- agrammatism: difficulty using grammar
- anomia: difficulty finding appropriate word
Volitional face paresis
- can express emotions but can’t control muscles to fake them
Emotional face paresis
- can fake emotions but can’t express them naturally
- often seen in ppl w PD
streams of thought vs streams of feeling
cerebral cortex vs limbic system
In what theory of emotion are physiological rxns caused by emotions?
- common-sense view
- dif to study bc damaging brain areas of animals might stop physiological responses but can’t tell whether emotion still present
What theory of emotion involves feedback from PNS responses that gets to the brain to elicit emotions
James-Lange theory
What might a person with an amygdalectomy experience?
Patient S.P.:
- inability to feel fear or identify in other ppl’s faces
- can fake it
Patient S.M.:
- unusual eye movement: didn’t naturally look at other ppl’s eyes
- got better at recognizing emotions after taught to look at eyes
What might you expect of a patient’s brain with a damaged V1 to look like if shown fearful face?
- amygdala will show activity
- person might not be conscious of stimuli but will still mimic fearful face
Suffocation gets fear response even when amygdala is damaged. Why is that?
- regulated by medulla oblongata
Role of vmPFC in emotions
- seems to regulate (down-regulate, inhibitory influence) emotions
- myelination in this area finishes at around 20
- damage to this area causes childish behavior
Atherosclerosis
- buildup of fat and cholesterol obstructing artery
- one of the reasons for strokes
Ischemic stroke
- thrombus: blood clot formed within blood vessel
- embolus: part of tissue dislodged from site of original and occludes artery
Hemorrhagic stroke
- rupture of cerebral blood vessel letting blood out
Malignant vs non-malignant tumor
- malignant has no distinct border so it may invade neighboring tissues and metastasize
- non-malignant encapsulated in clear distinct border so cannot metastasize but may still grow and compress surrounding organs
Causes of seizures
- an imbalance of excitatory/inhibitory neurons
Partial seizures
- localized to one brain area
- simple doesn’t produce loss of consciousness, complex does
Generalized seizures
- involve most of brain
Only infections agent that is just a protein ?
Prion protein
Huntington’s disease
- very clear genetic basis
- causes misfolding of huntington’s protein
- protein highly expressed in basal ganglia
- short life-span, memory loss, uncoordinated movement
Ubiquitin
- protein that breaks down misfolded protein into their amino acids
Parkin
- protein that “marks” misfolded protein to be ubiquitinated
- mutations in parkin gene is one cause of PD
A patient has a neuron degeneration in substantia nigra and reduced dopamine signaling in basal ganglia. What disease do they have?
Parkinson’s disease
Treatments for PD
- no cure
- L-DOPA alleviates motor symptoms because elevates dopamine signaling
- DBS in overactive parts of basal ganglia
Tau protein
- microtubule protein that becomes disfunctional in AD, disrupting intracellular transport
Beta-amyloid
- protein that misfolds in AD due to dysfunctional secretase, accumulating around hippo and neocortex
Secretase
- class of enzymes that cut beta-amyloid precursor protein to be assembled
- cuts it in wrong spot in AD
Negative symptoms of schizophrenia
- social interaction
- doesn’t speak much
- reduced emotional expression
- reduced motivion
Negative symptoms typically emerge first
Cognitive symptoms of schizophrenia
- poor abstract thinking
- disorganized and irrational thinking
- deficits in learning and memory
Positive symptoms of schizo
- delusions and hallucinations
Habituation of the gill withdrawal reflex was related to what change ?
- change in # of vesicles on presynaptic side
- vesicles not being released by sensory neuron towards motor neuron
Endocannabinoids vs nitric oxide
- both retrograde signaling mol
- endo for LTD and nitric oxide for LTP
NMDA receptor
- coincidence detector (b/w glutamate binding and depolarization)
- if glutamate binds and neuron at rest, will open but Mg2+ will clog pore quickly because wants to enter
- If depolarized a little (over -40mV), Mg2+ doesn’t want to enter anymore and will let Ca and Na in
AMPA receptor
- lets in Na ions and causes EPSPs
- mediates “normal” excitatory glutamate signaling
CaMKII
- enzyme controlling amount of AMPA receptors on postsynaptic membrane
- activated by calcium influx through NMDA receptors
Relational learning (stimulus-stimulus)
- explicit memory
- learning relationships among individual stimuli
- basis of episodic and semantic memory
Stimulus-response learning
- pavlovian, classical conditioning
- instrumental, operant conditioning, aka reinforcement learning
Glioma
- example of malignant tumor originating from glia stem cells
grand mal seizure
- generalized seizure
- preceded by aura
- tonic phase (muscle contraction) then clonic phase (rhythmic jerking movements)
Petit mal seizure
- aka absence seizure
- generalized and complex (loss of consciousness)
- type of seizure most children get
Seizure treatment
- benzodiazepines
- increasing inhibitory synapse effectiveness
Multiple sclerosis
- autoimmune disorder that de-myelinate
- prevent APs from propagating
- damage occurs in white matter
Lithium
- very effective way to treat mania
Perinatal Hypoxia
- brief loss of oxygen during birth
- can lead to neural death linked to schizo
Phonagnosia
difficulty recognizing familiar voices
PKU (Phenylketonuria)
Metabolic disorder causing brain damage
Aripiprazole
- partial dopamine D2 receptor agonist
- using in schizo as anti-psychotic
- partial so upregulates activity where too low and downregulates activity when too high
Monoamine theory of depression
- depression is driven by low levels of monamines
- SSRIs take very long to alleviate depressive symptoms which doesn’t support this theory
What would happen if you genetically modify a neuron so that it expresses a lot less K+ leak channels?
- its resting potential would be a lot less negative
- because less K+ would be able to leave cell
What happens if you genetically modify a neuron’s K+ leak channels to be a permeable to Na+ instead?
- resting potential will become positive (around +60mV)
- because Na will enter the cell until electrostatic force = and opposite to force of diffusion
Perceptual and motor learning
- implicit types of memories
Dopamine hypothesis of schizophrenia
- suggests imbalance in dopamine levels b/w nucleus accumbens of stiatum (too much dop) and PFC (too little dop) causes schizophrenia
- high dop levels in nucleus accumbens seem to underlie positive symptoms of schizo and antipsychotics (D2 receptor blockers) work well to alleviate those symptoms but not negative symptoms
- low dop levels in PFC seem to underlie negative symptoms which are similar to those of damaged PFC
- hence the use of aripirazole to treat both negative and positive
Electroconvulsive therapy (ECT)
- very effective in treating MDD and BD
- very common
- works very quickly
- electrically induced seizure that puts brain in “healthy” state, can slow go back to unhealthy depressive state
Abnormally quick brain growth at young age is synonymous with
ASD
Role of sleep in MDD
Ppl with MDD:
- have bad sleep
- start with REM sleep and spend much less time in slow-wave deep sleep
- sleep deprivation helps depressive symptoms but return after a normal night’s sleep
HPA axis
- hypothalamic-pituitary-adrenal gland axis
- refers to hormone signaling cascade that increases glucocorticoid signaling in blood (primarily cortisol) in response to stress
stress stimulates
- the HPA axis
- the sympathetic branch of ANS
What do glucocorticoids do?
- regulate a lot of essential tasks such as heart rate, metabolic and immune function, skeletal growth, reproduction, etc
- prioritize fight or flight by increasing blood-glucose levels as well as blood flow
- deprioritize other functions such as growth and sex hormone signaling, immune functions, etc.
cingulotomy
- cutting of fiber bundle b/w PFC and anterior cingulate
- helps treat severe cases of OCD
