Memory+and+technology

=Learning outcome=
 * Discuss the use of technology in investigating cognitive processes (for example, MRI (magnetic resonance imaging) scans in memory research, fMRI scans in decision‑making research). **
 * ** PET scans and Alzheimers **
 * ** MRI scans and memory research **
 * ** fMRI and what it tells us about how experience affects neural networks ** (for this one, see the Maguire handout)

**Refer back to the Biological level of analysis**
You will need to review information for a quick summary of the technology and how it can be used. Brain scanning technology

=Examples=

PET scans and Alzheimers

 * To what extent can knowledge from PET scans be applied in the context of Alzheimer's disease? **
 * Crane & Hadad - page 86
 * http://www.radiology-info.org/nuclear-medicine-positron-emission-tomography/pet-scan-alzheimers-disease.html

=MRI scans and memory research=
 * How has the MRI changed our knowledge of amnesia? **

The case of HM
//**(N.b.** H.M. died December 2008 in a nursing home at the age of 82 from respiratory pneumonia - see "[|H.M. - an unforgettable amnesiac]"//)

//**Journal of Neuroscience**//
 * Study by Corkin et. al. (1997)**

**Volume 17, Number 10, Issue of May 15, 1997 pp. 3964-3979**
http://www.jneurosci.org/cgi/content/full/17/10/3964

HM underwent 2 scanning sessions of MRI, after an ECT in 1992 determined it was safe to do so (he has 3 clips placed on the dura mater from an earlier procedure and there was concern these would move or heat up) Session 1 - May '92 Session 2 - August '93

__**Aim**__ Previously, hypotheses related to the localization of function as connected to his amnesia were simply based on the information provided by the surgical report by Dr Scoville (who performed the original surgery to alleviate H.M's epilepsy) //This uncertainty has prompted speculation (Horel, 1978) that lesions in structures other than the hippocampal formation may explain the memory impairment. Moreover, recent studies in animal models of human amnesia have raised questions about which temporal lobe structures included within the ablation in H. M. contribute to normal memory function (Mishkin and Murray, 1994). For example, the perirhinal cortex has been shown to be an important component of the medial temporal lobe memory system in the monkey (Zola-Morgan et al., 1989c, 1993; Meunier et al., 1993; Suzuki et al., 1993), but it is currently unclear to what extent this region is damaged in H. M.//
 * - to identify the precise extent of the temporal lobe lesion (bilateral resection) and to document any other possible brain abnormalities**

__**Findings**__ The lesion was bilaterally symmetrical and included:
 * MRI studies indicated that:**
 * the medial temporal polar cortex,
 * most of the amygdaloid complex,
 * most or all of the entorhinal cortex, and
 * approximately half of the rostrocaudal extent of the intraventricular portion of the hippocampal formation (dentate gyrus, hippocampus, and subicular complex).

The temporal lobe resection was **less** than originally described in Scoville's report - 5cm, not 8cm of the rostrocaudal (front to back) removal

For example:
 * Certain adjacent cortical structures appeared to show signs of impact**
 * //The caudal 2 cm, approximately, of the hippocampus body (normal length, ~4 cm) was intact, although atrophic.//
 * //the cerebellum demonstrated marked atrophy,//


 * Limitations**
 * //Whether this preserved tissue is functional and capable of mediating any cognitive processes awaits the results of ongoing functional **imaging ** studies.//
 * //The severity of the memory impairment in H. M., compared with that in other amnesic patients with selective hippocampal lesions, **may** be related to the inclusion of portions of his entorhinal, perirhinal, and parahippocampal cortices in the medial temporal lobe removal.//

Allow one to dismiss the "temporal stem" hypothesis of medial temporal lobe amnesia (Horel, 1978). But:
 * Strengths**
 * Horel speculated that the human amnesic syndrome was not attributable to damage of the hippocampal formation, but rather to damage of the white matter, the temporal stem, located immediately dorsal to the hippocampal formation.
 * In HM's case the temporal stem was not directly damaged bilaterally
 * nor were most of the neocortical regions that contribute fibers to the temporal stem

Caudal half of the hippocampus, and the fornix and mammillary nuclei remained - therefore argues that these are insufficient to sustain normal memory function
 * //This finding would argue against Gaffan's view that these connections, rather than hippocampal cortical connections, are primarily responsible for the role of the hippocampal formation in memory (Gaffan, 1992c).//

**Conclusions** //This MRI study has confirmed that the lesions responsible for the amnesic syndrome in H. M. are confined to the medial temporal lobe. Given the severity and permanence of the anterograde amnesia in H. M., it is clear that the remaining 2 cm of posterior, intraventricular hippocampal formation, approximately, (of a total rostrocaudal extent of ~4 cm) is not sufficient to support normal memory functions.// //**These findings reinforce the view that lesions of the hippocampal formation and adjacent cortical structures can produce global and enduring amnesia and can exacerbate amnesia beyond that seen after more selective hippocampal lesions.**//

=Further information=

http://tech.mit.edu/V129/N58/hmbrain.html
 * H.M. brain dissection**

If you are interested, live streaming of the dissection may be found [|here]