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Physio Final Flashcards- Lecture Nov 10
Terms in this set (39)
How did the larynx change 300,000 years ago and what was the impact? Finally, why did this change occur in spite of its associated risk?
The larynx (a hollow sound box), which houses the vocal cords, came to rest atop the trachea (the windpipe). The benefit of this was that more sounds could be made, and the sacrifice was that there was an increased risk of choking as the vocal cords, and thus the trachea, were near the esophagus (which carries food to the stomach). In other words, given this proximity instead of going down the esophagus food can go down the trachea. The evolutionary change happened despite its risks because the advantage of verbal communication outweighed the risks associated with choking.
Explain the overall timeline in which language developed.
-Language emerged over 100,000+ years
-Speech gene evolved by natural selection 100,000 to 200,000 yrs ago
(thus, the speech gene may have predated the emergence of language or coincided with it)
-Gestural origins of all language
-Full language emerged 50,000 years ago; art emerged then as did the memorializing of the dead, which
likely coincided w/the start of spoken language
Which tracts develop when during early brain development?
- at 4 months old Wernicke's area tracts develop
- the corpus callosum comes next after which the frontal lobe develops
- according to medline by 18 months both Wernike's area and Broca's area have fully matured
True or false? Language learning circuits exist throughout the brain.
What was the Wada test and what did it teach us about the lateralization of brain functions?
WADA testing is a procedure that assesses which side of your brain has your language and memory functions. During the test, one side of the brain is put to sleep (anesthetized) by injecting a medication into the carotid artery.
It taught us that language circuits and other serialized tasks are dominant for most persons in the left hemisphere (95%). Meanwhile, the right brain is lateralized for more whole picture learning, including narrative speech, map-reading, prosody
Explain factors that make left handers unique in their biology and perhaps physiology.
1. They might be smarter. Top 0.1% of SAT 2x as likely to be L handed. Higher levels of education.
2. They are over-represented among criminals too.
3. Less brain lateralization among L handers than R handers (only 70% of them). 15% of people who are left handed are lateralized to the right hemisphere whereas 15% of left handers are lateraiized to both hemispheres. This could be related to giftedness for math.
Talk about how speech can be accented non-verbally.
vocalizations/accents and body language are differ across cultures
Where is Broca's area located, what functions is it responsible for, and what are the implications of damage to it in contrast to damage to the basal ganglia.
-location: anterior to primary motor cortex (which is located in the frontal lobe)
-functions: motor memories for speech, articulation, speech production
-implications of damage: u can speak fluently although u can comprehend speech
**note: swears that come out are just vocal ticks
- contrast with basal ganglia damage: basal ganglia damage can mimic this; b/c it controls lip, tongue, palllete movement (e.g., Parkinsons)
Where is Wernicke's area located, what functions is it responsible for, and what are the implications of damage to it in.
location: auditory association cortex
function: memories of the sounds (phonemes) that constitute words, and of their meaning
damage implications: "Gobbledy gook speech" (meaningless) however prosody is maintained (fluidity of sound is associated with an unimpacted broca's area)
Contrast Wernicke's aphasia to other aphasias.
* Anomic Aphasia, Conduction Aphasia & Transcortical Sensory Aphasia (TSA, fluent phasias)
n.b. Aphasia in deaf persons - these are all instances when understandable communication is missing however prosody is still intact
Discuss acquired reading disorders
1) Pure Alexia = Pure word blindness;
Loss of the ability to read or understand the written word (anything written)
2) Alexia without agraphia; can write not read, corresponds with damage to L occipital lobe or R occipital lobe and corpus callosum
3) Dyslexia; post infarct or surgery; can be :
a) Surface Dyslexia, i.e., problem w/whole word reading often resulting from damage to the left temporal lobe, or
b) Phonological Dyslexia, i.e., a problem with phonetic reading, can't sound this out
Contrast phonologic and orthographic dysgraphia
1) Phonological dysgraphia
-Can't write unfamiliar words
-Can't "sound it out"
- Second language problems; do well in class not on exams
2) Orthographic dysgraphia
-Problems spelling irregular words (ph, gh sounds)
-Can only "sound it out"
-Have to see the phonemes in order to write it out (can't pick up on silent phonemes)
Talk about trends in the number of languages in the world.
-6000 languages exist
-80% have not been documented
-90% doomed to extinction in the coming century
-National Geographic Society - one language dies every 14 days, implication cultural loss
We remember what we understand;
we understand only what we pay attention to;
we pay attention to what we want.
Bolles, 1988. Talk about the implications of this quote.
* Everyhitng need to know about learning boiled down. Brings 2gether volition, attention, comprehnesion.
Talk about encoding, consolidation, verses retrieval.
Memory functions comprise three major subprocesses:
Encoding, consolidation, and retrieval
1) Encoding: The perception of a stimulus results in the formation of a new memory trace, which is initially highly susceptible to disturbing influences and decay, i.e., forgetting
- Stm > lgm or storage
- The memory trace from encoding is gradually stabilized thru multiple waves of short and long-term consolidation processes, which serve to strengthen and integrate the memory into preexisting knowledge networks
-The stored memory is accessed and recalled
Talk about HM and the Hippocampus; what was he like and what was the problem before surgery, how did surgery help, and what was he like after it?
1) Prior to surgery
-Suffered from severe, intractable epilepsy
-Seemed to have epileptic foci in both medial temporal lobes
-Bilateral medial temporal lobectomy prescribed for HM
Included removal of hippocampus and amygdala
2) Successful aspects of surgery
-Convulsions reduced in severity and frequency
-IQ increased from 104 to 118 (more than 2 SD)
-Remained emotionally stable with generally superior psychological abilities (DESPTE removal amygdala)
3) consequences: surgery also produced devastating amnesia
Talk about HM 's memory post surgery, what was normal and what showed deficits?
1) Minor retrograde amnesia for events of 2 years preceding surgery (couldn't remember for instance that he moved homes)
2) Normal memory for remote events & short term memory & procedural learning
3) Severe anterograde amnesia b/c he couldn't convert short term memories into long term memories (b/c surgery impacted hippocampus), and create explicit memories including of episodic memories ( of new procedural skills that he had mastered)
Note: Alzheimer's disease & Korsakoff's syndrome (thiamine deficiency) also have poor explicit memory but intact implicit memory
Talk about brain changes in the hippocampus due to mood disorders. Also, talk about what happens in the brain when these diseases remit. And, talk about treatment (psychotherapy and medicine) implications.
- Hippocampal atrophy occurs in depression, PTSD, chronic alcohol use, and BPD
- this is the case irrespective of demographic group and makes sense given comorbidity of many of these disorders
-volume rebounds when symptoms remit.
-implications: SNRI and SSRIs proomote baby neurons maturation;cardio exercise does, perhaps psychothearpies do too
Talk about the relationship b/w aging and depression.
Hippocampal volume decreases w/age as it does w/depression; age related changes in volume could explain elevated rates of depression OR perhaps this occurs because there is a greater opportunity for people to experience depression over their lifetime as they age, thus more people reach old age who have had hippocampal changes resulting from depression earlier in life
What are areas that incubate new neurons in the adult brain? 3 areas
A) Subventricular area. These neurons migrate along cranial nerve 1 (olfatory nerve) in adult brains
2) Dendate gyrus of the hippocampus
3) olfactory bulb
Talk about implicit memory and explicit memory (types of long term memory) verses short term memory and sensory memory (both short acting memories types of different lengths).
Also, talk about the importance of neuroepinephrine for memory.
(A) Long term memory (2 types)
1) Explicit memory
semantic, attend to by studying
episodic, attend to by just living life
2) Implicit memory
procedural - shaving, braiding hair
(B) Short term memory= working memory (< 1 minute)
(C) Sensory memory- takes less than one second. Includes iconic (visual) and echoic (sound). Allows you to to use past exposure to sensory stimuli to make sense of present environment.
**Norepinephrine helps consolidates short term memory so that it becomes long term memory. This hormone's involvement is why we better recall emotional memories
Talk about what Hebb rules says, its implications for learning, classical conditioning, and AI.
The rule: If a synapse repeatedly becomes active at about the same time that a postsynaptic neuron fires, changes (growth process or metabolic changes) will take place in the structure or chemistry of the synapse that will strengthen it
translation: cognition is the movement of charged particles. synaptic changes or growth processes are a result of ongoing molecular changes. When learning happens there are molecular changes. In classical
classical condition implications:
molecular changes occur in a split second at multiple synaptic sites enabling new associations
AI implications: this notion that molecular changes culminate in structural changes has been used as a basis for AI models today.
Talk about long-term potentiation. Explicate how ESPS is involved in ltp. Also, talk about the relationship between ltp and dendritic arborization.
Jessa- I think my notes make sense here but it was a challenge to explain. if you are confused or disagree with my interpretation of the lecture here please look back at your notes and let me know. Thanks!
- ltp is the structure of learning
- Changes in the synaptic space (post synaptic button, dendrites) are where long term potentiation occurs
-a long term increase in firing results in an increase in EPSP in postsynaptic neurons
- this increase in ESPS culminates in structural changes
-dendritic arborization is related to ltp; arborization enables learning at a neuronal, structural level; during this process dendritic spines split when they reach a critical mass of density so that as learning occurs more dendritic surface area can receive signals to do with the type of learning that is occuring.
Discuss how stm becomes lgtm. Also talk about how memories are labile in the context of when they are stored and retrieved.
Talk about the above in relation to EDMR and trauma.
- Takes 5 to 6 hours for transfer data from STM to LTM; Facilitated by NE & E; so transmitters for NE & E area necessary for the learning consolidation process
- storage is labile and not permanente for a few hours to days depending on the content
-retrieval makes memories labile again.
EDMR and trauma: why EMDR works is a mystery . Since memory is the exchange of charged particles along a circuit it doesn't make sense to talk about memories getting unstuck.
What parts of the brain are involved in instrumental, operant conditioning?
What does this tell us about why drugs are reinforcers?
- Nucleus accumbens (NAC) is where reinforcement occurs; dopamine drives reinforcement circuits
-the prefrontal cortex turns on dopamine receptors that act on the NAC, thus the NAC is dependent on the pc for prefrontal learning
-the medial forebrain bundle (midbrain to basal forebrain) is also involved
Drugs as reinforcers; since dopamine is reinforcing, dopaminergic drugs like heroin can help reinforce certain S-R relations. Thus, if you took heroin in the same place many times at the neurological level you might react to the area as if you will find heroin there (so experience a surge in dopamine) even when you don't have it.
Explain similarities and differences of the the nucleus accumbens and basal ganglia.
The Nucluus accumbens like the basal ganglia is a dopaminergic hub for the ventral-tegmental area.
-the nucleus accumbens is unique in that it drives instrumental learning
Talk about the role of ACh in aversive learning.
- aversive learning has special circuits that are cholinergic
-these punishment circuits reside in the Periventricular system, or PVS, which consists of the Hypothalamus, the thalamus and periaqueductal grey matter
- ACh impacts aversive learning; it stimulates the secretion of ACTH adrenocorticotropic hormone, which in turn signals the adrenal glands to release adrenaline
Talk about the relationship between the motor cortex, the basal ganglia, and the cerebral cortex in motoric learning. Also, discuss the implications of this for Parkinson's disease.
- it is expensive metabolically for the motor cortex to be in charge of motor learning, thus the basal ganglia takes on motoric responsibilities
-when learned behaviors get transferred to the basal ganglia it frees the motor cortex to do other things. then, the basal ganglia interfaces with other areas of the cerebral cortex as needed during movement processes
Parkinson's disease implications:
if the basal ganglia is destroyed there is insufficient dopamine, which results in failure to enact learned motor behaviors
Talk about anterorgrade verses retrograde amnesia. What types of memory get compromised?
A) Anterograde- Failure in explicit memory, which is declarative/conscious short term and long term memory. This includes relational learning.
B) Retrograde- Failure in implicit memory, which is Non-declarative.
Note: both anterograde and retrograde amnesia can include consolidation problems and retrieval problems
What are specific neuropathological conditions (3 categories and related subtypes)?
A) Tumors: Malignant or benign; Infiltrating or encapsulating (mestastasizing verses contained)
B) Damage: Compression/ Infiltration/ Momentum
C) Out of control cell division includes:
- Glia cell conditions: Gliomas (including astrocytoma, oligodendrocytoma) and Neurinoma's (Schwann Cells)
- Meninges related conditions,
Talk about factors that are associated with melignancy verses factors that limit it.
Malignancy has to do w/potential for damage
Speed of growth related ease of operation
Delay growth of tumor by delaying the obtaining of nutrition
Possible method for treatent - Nanoskeleton of cell when exposed alternating magnetic current doesn't form functionally, allowing immune system target & kill it
What are the 3 phases of grand mal seizures and how are auras involved?
1) First phase= Tonic phase
- No breathing for approx. 30 seconds
- Massive deploraization > all muscles contract (includes diaphragm)
2) Phase 2 = Clonic phase; Diencephalic inhibition wins out (gabaergic neurons fire in massive waves); also known as thalamic inhibition
3) Phase 3= Post-ictal
-Sleep for 10- 15 minutes
-@ this stage excess gaba gets metabolized
Aura involvement: aura = sensation that relates to part brain where seizure begins; neural firing often shows its first sign with aura; it is not a stage because not everyone who has grand mal seizures experiences this.
Talk about some causes of seizures
-autoimmune disorders (cerebral vasculitis and multiple sclerosis occassionally)
- cerebral edema (eclampsia, hypertensive encephaopathy)
-congenital or developmental abnormalities (includes malformations, genetic disorders, neural migration disorders such as heretopias)
-drugs and toxins- camphor, cocaine, CNS stimlants, lead
-expanding intracranial lesions (hydrocephalus, tumors, hemmorhage)
-hyperprexia (drug toxicity, fever, stroke)
-pressure related (hyperbaric o2 treatments, decompression illness)
-withdrawl symptoms (anesthetics, alcohol, benzos, barbituates)
What are some work arounds for communicating with someone who has Wernicke's aphasia?
- b/c prosody is still there ppl learn to recognize what is being communicated by paying attention to the prosody in context
When you are trying to learn, how is that learning impacted by the stimulation of punishment circuits?
Stimulation of the punishment circuit can inhibit the reward circuit, thus overriding reinforcement (this happens when circuits are simul activated)
Compare partial verses general and simple verses complex seizures
A) Partial vs. generalized - implications for # brain that is seizing
- Partial is Focal (CAN BE COMPLEX OR SIMPLE)
- Generalized involve most of brain (THEY ARE ALWAYS COMPLEX)
B) Simple vs. complex partial seizures (has to do with experience of seizure)
-Simple involves changes in consciousness, stems from seizure occurring in a patch of brain
-Complex involves a complete loss of consciousness
What are absence seizures?
(petit mal); characterized by inattention. Often misdisagnosed as ADHD/LD.
What is Status epilepticus
- Multiple grand mal seizures consecutively, involve excess glutamate release and result in significant hippocampal damage, possibly death
What drugs and toxins can lower the seizure threshold
aminophylline, antideppresants (esp tricyclics), antipsychotics (esp clozapine, busiprone)
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