Principal understandings of memory
Lesion studies have fuelled developments in numerous areas of cognitive research, foremostly memory processes and their corresponding neural architecture. The pioneering case was H.M., where excision of the medial temporal lobe induced selective impairment in new long-term memory acquisition (Corkin, 2002). This led to formulation of the most recognized taxonomy of memory to date, the dissociation between declarative and non-declarative memory (Squire, 2004). Challenging conventional paradigms of memory as a one-dimensional unit, significant efforts were launched to formulate novel theories of memory formation, specifically categorizing and substantiating existence of coalescing subsystems.
Amnesic individuals provided compelling support for this cognitive modularity. Contrary to collective deficits in long-term memory, amnesiacs were selectively impaired on conscious recollection tasks (cued recall), whilst preserving abilities to complete tests independent of deliberate recall (word completion) through priming (Warrington & Weiskrantz, 1970). Researchers were consequently able to dissociate implicit from explicit memory and assign discrete neural structures governing these. The latter process recruits medial temporal lobe structures, foremostly the hippocampus and amygdala, whilst implicit memory draws from sub-cortical structures, the neocortex and basal ganglia (Petri & Mishkin, 1994).
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Permanent lesion studies have therefore built the groundwork in isolating structures necessary for specific processes, but offer fairly static representations of memory. Its chronological nature, in which even conceptually discrete phases are rarely unitary and often mediated by dissociated regions, renders permanent lesions ineffective at disentangling sequential processes and establishing causal relations.
Comprehensive understanding of this multi-faceted domain necessitates not only determination of cerebral location, but examination of temporal relations, lateralization, functionality and cortical reorganization within separate systems. Reversible methods' ability to selectively activate and inactivate regions permits identification of individual neural structures' contributions at different cognitive processing stages (Floel & Cohen, 2007). Similarly, exposing regions that mediate separate but temporally overlying functions deepens understanding of the interactions underpinning memory formation.
This gains relevance regarding encoding and retrieval mechanisms in long-term episodic memory, referring to transfer of information into and out of short-term and long-term storage. According to the Hemispheric-Encoding-Retrieval-Asymmetry (HERA) model (Tulving et al., 1994), lateralization of prefrontal cortex (PFC) activation leads to left PFC recruitment during encoding, whilst the right mediates information retrieval. Lesion studies were previously restricted in isolating relative prefrontal contributions to the dissociated processing stages.
Challenges to the model suggested asymmetry of prefrontal activity was modulated by type of processed stimuli (verbal vs. non-verbal), where lateralization was thought not to hold valid for non-verbal materials (Wagner et al., 1998b). Offering a technique to directly test the model's predictions, multiple rTMS studies now provide conclusive evidence that episodic memory processing in both stimuli types pertains to the model, exhibiting consistent prefrontal activation asymmetry (Floel et al., 2004; Epstein et al., 2002; Habib et al., 2003).
In conclusion, localized lesions have established long-term memory not as a solitary component but characterized by various subsystems sustained by dissociable neural structures. Non-invasive techniques corroborate and extend these neural models by offering a means of investigating temporal organization and relevance of specific structures to distinct stages of memory processes.
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Corkin, S. (2002). What's new with the amnesic patient H.M.? Nature Reviews Neuroscience, 3 (2), 153-160.
Epstein, C.M., Sekino, M., Yamaguchi, K., Kamiya, S., Ueno, S. (2002). Asymmetries of prefrontal cortex in human episodic memory: effects of transcranial magnetic stimulation on learning abstract patterns. Neuroscience Letters, 320 (1-2). 5-8.
Floel, A., & Cohen, L. G. (2007). Contribution of non-invasive cortical stimulation to the study of memory functions. Brain Research Reviews, 53, 250-259.
Floel, A., Poeppel, D., Buffalo, E. A., Braun, A., Wu, C. W., Seo, H. J., Stefan, K., Knecht, S., & Cohen, L. G. (2004). Prefrontal cortex asymmetry for memory encoding of words and abstract shapes. Cerebral Cortex, 14, 404-409.
Habib, R., Nyberg, L., & Tulving, E. (2003). Hemispheric asymmetries of memory: The HERA model revisited. Trends in Cognitive Science, 7(6), 241-245.
Petri, H. L. & Mishkin, M. (1994). Behaviorism, cognitivism and the neuropsychology of
memory. American Scientist, 82, 30-37.
Squire, L.R. (2004). Memory systems of the brain: a brief history and current perspective. Neurobiology of Learning and Memory, 82 (3), 171-177.
Tulving, E., Kapur, S., Craik, F.I., Moscovitch, M., Houle, S. (1994). Hemispheric encoding/retrieval asymmetry in episodic memory: positron emission tomography findings. Proceedings of the National Academy of Sciences of the United States of America, 91 (6), 2016-2020.
Wagner, A. D., Poldrack, R. A., Eldridge, L. L., Desmond, J. E., Glover, G. H., & Gabrieli, J. D. (1998b). Material-specific lateralization of prefrontal activation during episodic encoding and retrieval. NeuroReport, 9 (16), 3711-3717.
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Describe the main methods by which an experimenter can introduce lesions to brain areas, together with advantages and disadvantages for each.
Developments in variety and sophistication of permanent and reversible deactivation techniques have yielded powerful research tools. The most established method is mechanical ablation by surgical excision and fibre bundle transaction or electrocauterization, burning inserted electrodes' surrounding tissue (Chow, 1967). Aspiration removes peripheral cortical structures using suction pipettes. The techniques' crudeness damage fibers of passage and constrain normal blood supply, influencing adjacent neural systems' activity.
Chemical ablation avoids undercutting cerebral tissue, enabling selective deactivations on subsets of neurons and metabolic systems of interest. Injecting excitotoxic pharmacological agents (kainic or ibotenic acid) overstimulates glutamate receptors, inducing cell death by Ca+ excess (Storey et al., 1992). Immunolocalization (Nilsson et al., 1992) utilizes antibodies that identify specific surface antigens to direct toxins and genetic interventions employ specified gene expression for targeted toxin production (O'Kane & Moffat, 1992). Lengthy cell degeneration rates restrict usefulness and poor neurotoxin spread confinement produces lesion variability.
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Histological assessment is necessary to verify intended permanent lesion extent/location, where MRI-directed stereotaxic methods permit evaluation in vivo, facilitating reproducibility (Saunders et al., 1990). However, recovery of function via cerebral reorganization means remaining tissues' activity is measured, instead of removed regions' normal functioning. Beyond ethical concerns, many cognitive processes remain inaccessible in animals and are simplistic representations, limiting generalizations.
Cryogenic techniques (thermo-electric plates, cryoloop systems, cryotips) induce reversible dysfunction by cooling tissue (Campeau & Davis, 1990). Repeated deactivation is possible, where neural degeneration occurs only in excessive consecutive cooling. High precision and control is exertable over deactivation onset, continuance and recovery, with lesion magnitudes easily reproducible. Inactivations are restricted to smaller surface regions and necessitate complicated technical requirements. Thick cooling probe insulations increase overlying tissue damage risk.
Chemical inactivation via Na+ channel blockers (tetrodoxin, temporary anaesthetics) transiently obstructs signal generation (Martin & Ghez, 1999). Neurotransmitter agonist and antagonists (i.e. GABA-A agonist muscimol) temporarily block synaptic transmission. Delivery through minute cannulae limits fibers of passage damage and highly receptor-selective deactivation agents disengage focal regions in surface and deeper structures. Lesions are enlarged only by multiple penetrations, complicating replication. Excessive repetition incurs irreversible damage and inconsistent deactivation/recovery times confound data collection.
Transcranial magnetic stimulation is a non-invasive, reversible technique delivering single/repetitive pulse sequences of magnetic stimulation to cortical areas, disturbing cognitive processes with great temporal resolution. Repeated application and measurement facilitates causal inferences between activations and behaviour and temporal investigations, highlighting when structures are recruited during processes (Pascual-Leone et al., 1999). Utilization of healthy subjects reduce interferences from secondary brain damage/pathological neural correlates.
Application is restricted to peripheral structures and poorly localized, effects projecting to adjacent /interconnected regions. Stimulation may evoke muscular spasms, aches and seizures, confounding behavioural measurements. Intended and actual stimulated regions may not correspond, due to internal structural inconsistencies between subjects.
Reversible techniques require less subjects, each being their own control, enhancing findings' reliability. Impermanent dysfunction means plasticity and recruitment of secondary neural structures no longer confound measurements. Increased temporal regulation over lesion induction and multiple site deactivations allow investigation of inner double dissociations, subcomponents and interactions of cognitive processes (Lomber, 1999).
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Campeau, S., & Davis, M. (1990). Reversible neural inactivation by cooling in anesthetized and freely behaving rats. Journal of Neuroscience Methods, 32, 25-35.
Chow, K.L. (1967). Effects of ablation. In: Quarton, G.C., Melnechuk, T., Schmitt, F.O. (Eds.), The Neurosciences (pp. 705-713). New York: Rockefeller University Press.
Nilsson, O.G., Leanza, G., Rosenblad, C., Lappi, D.A., Wiley, R.G., Bjorklund, A. (1992). Spatial Learning Impairments in Rats with Selective Immunolesion of the Forebrain Cholinergic System. NeuroReport, 3, 1005-1008.
Lomber, S.G. (1999). The advantages and limitations of permanent or reversible deactivation techniques in the assessment of neural function. Journal of Neuroscience Methods, 86, 109-117.
Martin J.H., Ghez, C. (1999). Pharmacological inactivation in the analysis of the central control of movement. Journal of Neuroscience Methods, 86 (2), 145-149.
(O'Kane, C.J. & Moffat, K.G. (1992). Selective Cell Ablation and Genetic Surgery. Current Opinion in Genetics & Development, 2 (4), 602-607.
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Saunders, R.C., Aigner, T.G., Frank, J.A. (1990). Magnetic resonance imaging of the rhesus monkey brain: use for stereotactic neurosurgery. Experimental Brain Research, 81, 443-446.
Storey, E., Hymen, B.T., Jenkins, B., Brouillet, E., Miller, J.M., Rosen, B.R., Beal, M.F. (1992). I-Methyl-4-Phenylpyridinium Produces Excitotoxic Lesions in Rat Striatum as a Result of Impairment of Oxidative Metabolism. Journal of Neurochemistry, 58 (5), 1975-1978.
What are the relative strengths and weaknesses of single-case vs. group human lesion methods?
The fundamental goal of lesion methods is delineating the neural correlates underlying cognition. The relative effectiveness of two key experimental methods adopted in realizing this objective, the single case and group study, will be reviewed.
When a rare cognitive impairment challenges well established theories of cognition, single cases provide valuable data illustrating novel theoretical arguments. These often alter courses of future research, e.g. individual focal retrograde amnesia reports led to redefining traditional models of anterograde and retrograde amnesia (Kapur, 1993).
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Comprehensive examination and description of one individual's information processing abilities permits deeper understanding of the exact nature of impairment. This level of detail is often distorted when combining data, where normalization onto standard space can misrepresent anatomical locations (Caramazza, 1986). Furthermore, assumption of universality is violated in brain damaged individuals, where behavioural inconsistencies cannot be ignored as 'noise' (Robertson et al., 1993) and averaged scores do not necessarily echo performance of single individuals (Miceli et al., 1989).
However, cortical re-organization means individuals also undergo neural change and variability, where averaging data from single patients tested repeatedly over time faces similar challenges (Zurif et al., 1989). Natural lesions are also rarely focal, encompassing numerous regions which restricts inferences about exact anatomical bases relevant to observed deficits.
Single-case studies are often selected as extreme representatives, potentially reflecting exaggerated idiosyncratic features about individuals and are therefore not reliably demonstrative of general populations (Robertson et al., 1993). Whilst between-subjects discrepancies are resolved, it forfeits generalizablity and runs risks of relying on chance findings. By establishing objective behavioural and anatomical inclusion parameters, the group approach may facilitate pure replication, study evolvements and disproving of outcomes (Zurif et al., 1991), indispensible factors when seeking to verify and substantiate experimental theories.
Selection criteria are however inadequately specified and unable to entirely exclude heterogeneity, where neural damage manifestation varies considerably, as do associated cognitive impairments. Due to the idiosyncratic nature of lesions, patients may display homogeneity regarding inclusion criteria, but fail to display this in experimental task performance (Gazzaniga et al., 1998). Specifically, reliance on syndromes for group categorization, i.e. Gerstmann's Syndrome, renders conclusions from averaging undependable (Badecker & Caramazza, 1985). Impairments occurring conjointly in syndromes may have a common functional deficit or result from adjacent, albeit dissociated neural structures. This distinction is blurred through averaging, increasing the risk of over-interpreting and confounding functional and anatomical associations.
Cognitive neuroscience has recently encouraged utilizing cognitive deficits to define not only neural locations, but functionality of information processing. Single-case studies are restricted in modelling neural processes in terms of underlying neuroanatomy, where correlational designs require large samples to test hypotheses and establish cause- effect associations amongst two variables (Robertson et al., 1993). This necessitates the two approaches complementing each other, capitalizing on respective strengths, where descriptive single-case studies are influential in providing comprehensive accounts of specific and exceptional cases. These offer useful approximations for devising novel hypothesis, where subsequent testing of cognitive models and validation/refutation of claims by group studies provides valuable insights into cognitive modularity and dynamic brain-behaviour associations.
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