Module 3 Flashcards
What was the surgery that was performed on H.M and why
medial portions of his temporal lobe removed to treat epilepsy
- called a bilateral medial temporal lobectomy
what structures specifically were removed in the case of HM
most of the hippocampus, amygdala, and adjacent cortex
what is the difference between a lobectomy and lobotomy
ectomy = fully removed botomy = connections to other areas severed
what were the successful aspects of HM’s surgery (3)
- generalized seizures eliminated
- partial seizures down from several per day to at most 2, even tho he was taking less anticonvulsants
- his IQ increased
what were the unsuccessful aspects of HM’s surgery?
- mild retrograde amnesia for events within 2 years before his surgery
- short term memory was fairly normal (digit span was nearly normal)
- long term memory anterograde amnesia was entirely removed, once something left his short term memory, it was gone
what is retrograde amnesia
backward acting, loss of memories derived from experiences before the onset
what is anterograde amnesia
forward acting, loss of memories derived after the onset
what are the two mechanisms of anterograde amnesia
short term memory problems - can’t hold things in short term
long term - can’t encode short term mems for long term storage
What is the Digist span +1 test and what does it diagnose? How did HM perform?
tests verbal long term memory
repeat 5 digits at 1 second intervals, if good, add one on the next trial
normal is 15 digits after 25 trials
he got 8
what is the Block-tapping memory-span test and what does it diagnose? how did HM perform?
Tests for Global amnesia (as opposed to the verbal digit test) - same procedure but taps blocks in order.
had a normal span of 5, but could never learn 6
what is the mirror drawing test, what does it measure, and how did HM perform/
Tests implicit memory storage, in which HM performed just fine (improved each time) despite not recalling ever having taken it before. thought that it was purely sensorimotor learning that he could do…
what is the incomplete picture test, what does it measure and how did HM pervform
Nonsensorimotor test that employs sets of fragmented drawings where you try and identify it at most fragmented, then less and so on until correct.
again, HM got better with time without recalling performing the task
Could HM learn through pavlovian conditioning?
yes, but slower than is typical
what are the three major scientific contributions of HM’s case?
- demonstrating the importance of the medial temporal loves in memory, challenging the view that memory function was distributed throughout the whole brain - spawned research aimed at understanding the mnemonic role of the hippo etc.
- Separated memory into short term, long term and remote, and introduced the concept of memory consolidation (short term to long term) which HM struggled with
- Differentiated between implicit and explicit memories, the second of which HM had trouble with
what is medial temporal lobe amnesia?
the profile of mnemonic deficits similar to those of HM that present with preserved intellectual functioning and evidence of medial temporal damage
maintenance of the ability to form implicit long term memories, but not explicit
what do we call tests that measure implicit memory capacities? describe them
repetition priming tests, ex the incomplete pictures test, but most often using words (A___H__E, even those with explicit amnesia perform about as well as controls)
what is the evolutionary explanation for the distinction between the implicit and explicit memory systems?
Implicit probably arose first (simpler), so we must as why do we have conscious memories at all?
What do experiments suggest is the reason for the conscious (explicit) memory system?
describe the studies that looked at this
flexibility!
1. patients with amnesia
2. monkeys with medial temporal lobe lesions
both learned implicit tasks as well as controls, but if they were asked to use this knowledge in a new, but similarly engaged, context, they failed to do so.
- so, it looks like it arose to allow us to generalize learning to broad situations
are most people with medial temporal lobe amnesia as incapable of forming explicit memories as HM?
no, most struggle with episodic rather than semantic memories
what are episodic memories
explicit memories for particular events of one’s life
what are semantic memories
explicit memories for general facts or information
what is another term for episodic memories
autobiographical
Describe the case of Tulving’s patient KC
completely normal semantic memory, but complete inability to perform mental time travel to the past or future, and inability to remember any episodic memories
describe the Vargha-Khadem study on medial temporal lobe amnesia
followed the maturation of 3 people with the damage from early life - they processed through all of the typical stages in school and what not with not improvement in their episodic memory
is it easy to diagnose episodic memory deficits?
no, sometimes patients are good at filling in, but one can ask very specific and pointed questions that can only be answered by reference to a particular experience
what is global cerebral ischemia, and what does it often cause
complete loss of blood to their entire brains,
- often medial temporal lobe amnesia
where was the damage to R.Bs brain mostly found (the bungled operation)
- what did this suggest in reference to medial temporal lobe amnesia
- why isn’t this conclusive evidence?
the pyramidal cell layer of the CA1 subfield of the hippocampus
- maybe dmg to the hippo is alone sufficient to induce mt amnesia
- but in the case of global cerebral ischemia, we can’t tell if theres other damage thats just harder to spot
what is the strongest evidence that selective hippo dmg can cause medial temporal lobe amnesia? define and explain
- transient global amnesia
sudden onset of severe anterograde amnesia and moderate retrograde amnesia for explicit memories
amnesia tends to only last for 4-6 hours - we have found damage to the same CA1 subfield of the hippo as in the case of RB
what is Korsakoff's syndrome explain those it effects (1) explain phsyiological cause (1) explain symptoms (5) explain neurological pathology and their loci (3/4 depending)
- memory disorder common in people who have consumed a lot of booze
- largely attributed to the brain damage associated with the thiamine deficiency that accompanies heavy alcohol consumption
- sensory and motor problems, extreme confusion, personality changes, risk of death from liver, gastrointestinal or heart disorders
- lesions to the medial diencephalon (medial thalamus and hypothalamus)
- diffuse damage to other brain structures (neocortex, hippocampus and cerebellum)
what are the similarities between the symptoms of Korsakoff’s syndrome and MT amnesia?
early stages of Korsakoff’s - anterograde, explicit, episodic amnesia is the most prominent
- there do appear to be problems with implicit memory, depending on the test, but less severe than explicit
what are the main differences between Korsakoff’s and MT amnesia in terms of symptomology
Progression…
1. middle stages - retrograde amnesia into childhood
why does the insidious onset of Korsakoff’s make it difficult to study the resulting retrograde amnesia?
never clear whether amnesia for recent events is because of retrograde or anterograde blockage
what has been a problem with identify which part of Korsakoff’s brain deterioration is the cause of amnesia?
how diffuse the pathology is
what was the first hypothesis pertaining to the neural basis of korsakoff amnesia
what disproved this?
damage to mammillary bodies of the hypothalamus was responsible
- cases of Korsakoff’s where there was no pathology to these bodies
what do we now believe to be the neural basis of Korsakoff’s amnesia? is it probably this site alone?
damage to the mediodorsal nuclei of the thalamus
Nah, probably fairly diffuse
what is Medial encephalic amnsesia
amnesia like that found in Korsakoff syndrome, where there is damage to medial diencephalon
Describe the case of medial encephalic amnesia in NA
what brain structures were damaged? (3)
stabbed through his cribriform plate into his brain
- unable to recall any events that occurred 2 years before his accident
- when retested 3 years later, his retrograde amnesia had decreased in duration, covering only those events than had happened 2 weeks before
- slight imrpvmt of day to day recall, recalling random memories of no significance
MRI found extensive medial diencephalic damage, including damage to the mediodorsal nuclei and mammillary bodies
where have efforts to study the neural basis of Alzheimer’s amnesia focussed? why?
predementia patients with alzheimers, who have much more general memory deficits than those with any of the other disorders we’ve spoken about
- major anterograde and retrograde deficits in explicit memory
- deficits in short term memory
- some deficits in implicit memory
- ie; verbal and perceptual material is deficient
- sensorimotor learning is fiiiine
what is the leading theory of why patients with alzheimers have amnesia?
greatly diminished levels of acetylcholine
which brain structure is degenerated in Alzheimer’s patients leading to the decrease in ACH
the basal forebrain, a midline area just about the hypothalamus, the brains main source of the neurotransmitter.
what is a piece of evidence that suggests that the basal forebrain and ACH is causal in Alzheimer’s amnesia?
strokes in the basal forebrain also cause amnesia
do we believe that aCH deficiencies are the sole cause of Alzheimer’s amnesia?
no, there is a lot of diffuse brain deterioration
this includes areas like the medial temporal lobes and prefrontal cortex which are super relevant for memory
what do we call amnesia following a non penetrating blow to the head
Posttraumatic amnesia
can we get comas after head trauma
yes, they usually last for only a little while but can last for weeks in severe cases
what do people who suffer from non-penetrating head trauma experience when they wake up from a coma?
confusion
when do we test people who have had head trauma
what does this testing usually reveal
after the period of confusion if at all.
- reveals permanent retrograde amnesia for the events leading up to the blow and anterograde during the confused period
why are the memory deficits associated with closed head injuries so strange?
because the person might seem perfectly lucid during their confused state and them remember none of that shit
describe the durational hierarchy that is common in closed head injuries
confusion and anterograde period is longer than the coma, which is longer than the period of retrograde
what do more severe head injuries tend to produce?
longer comas, periods of confusion and amnesia
what are islands of memory
surviving memories for isolated events that occurred during periods for which other memories have been wiped out
what does the gradient of retrograde amnesia after concussion provide support for? why?
memory consolidation, the fact that older memories are preserved suggests they have been strengthened (consolidated)
explain Hebb’s theory of memory consolidation
short term memories are stored by reverberating or circulating neural activity in closed circuits, which can be disrupted by trauma leading to memory loss. Once they induce structural changes in the involved synapses (consolidation) they become more stable.
what have proven to be a good method of studying memory consolidation in a controlled environment
electroconvulsive shock treatments which attempts to stop consolidation by disrupting the neural activity, hopefully only erasing short term memory and leaving the longer, structurally stored memories intact.
what do ECS experiments allow us to estimate in theory?
The length of the period of retrograde amnesia produced would provide an estimate for the amount of time it takes to induce consolidation
what doe ECS studies show about Hebb’s theory?
consolidation probably takes a lot longer than he anticipated
Describe the Squire, Slater and Chase study on ECS induced retrograde amnesia
Five ECS treatments disrupted memory of information pertaining to TV shows that had been played within the last three years, but not earlier
what its he current view of memory consolidation
continues for a very long time, if not indefinitely
- lasting memories become more and more resistant throughout ones life
- each time we activate a memory, it is updated, linked with other ones, which increase its resistance to disruption
what is the standard consolidation theory? whaat is another name for it?
the theory that memories are stored in the hippo until they can be transferred into more stable cortical storage
aka dual trace theory
is the standard consolidation theory still widely accepted? why or why not?
no, temporally graded amnesia is in a lot of types of amnesia, so its unlikely that the hippo plays any special role
what is the more modern version of the dual trace theory
when conscious experience occurs, it is rapidly and sparsely encoded in a throughout the hippo and other structures
what was Nadel and Moscovitch’s position on the reason for the increase in memory resistance over time?
each time a similar experience occurs or an original memory is recalled, a new engram (brain change that stores a memory) is established and linked to the original, making the memory easier to recall and the original harder to disturb
what is an engram
a brain change that stores a memory
define reconsolidation
each time a memory is retrieved from long term storage, it is temporarily held in labile (unstable) short term memory, where it is once again susceptible to trauma
