What can neuropsychologists learn by studying individuals with damaged brains?

Introduction One of the best ways to learn about the normal functioning of the brain is to study how it functions when it is damaged (Rosvold, Mirsky, Sarason, Bransome et al., 1956). This paradigm for research in neuroscience involves comparing the neural functioning and performance on cognitive tasks of normal controls to that of patients with brain damage (for example, Fellows and Farah, 2003). Studies of localised brain damage can have especially important implications, since the impaired functional area is likely to be associated with that location in the brain containing the lesion. Though this is just one paradigm used in mapping the functional areas of the brain, other methods involve using only healthy participants and studying the pattern of neural activation during specific tasks designed to stimulate different cognitive faculties. But by comparing the functioning of healthy individuals to patients with brain damage it has been possible to distinguish very specific areas of the brain b ased on their functional purpose. Purpose of specific areas is either based around sensation and perception, information processing, memory or executive decision-making. This essay will examine some of the most pertinent findings gleaned from studies of brain damaged patients and elaborate on the avenues for future research in this context. The review of literature will proceed in a systematic manner evaluating the function of various brain areas through examination of the effects of lesions in these areas, as well as elaborating on the limitations of the methodologies employed. There are many ways in which the brain can be damaged, but the factor that seems more important in determining the effects of brain damage rather than how the brain damage occurred is the location of the damage. Evidence for this comes from reviews such as Ommaya and Genarelli (1974) who correlated clinical and experimental observations with the location of lesions in the brain. This essay will now proceed by analysing the effects of brain damage in different functional areas and the neural correlates of these effects. Brain damage can have a diverse range of effects depending on the region that is damaged, including disturbances in emotion, attention, memory and executive decision-making (Brewer and Perret, 1971). Prominent in this field of research are studies such as that of Robinson, Kubos, Starr, Rao and Price (1984) who studied patients with stroke lesions in various locations in the brain. Their findings showed a greater incidence of depression in individuals with anterior lesions on the left cerebral hemisphere. The inverse was true of right cerebral lesions, with posterior lesions leading to more depressed mood. This suggests that the location of lesions has an effect on the form that mood change takes following a stroke. To generalise further from this, different areas of the brain are differently responsible for emotional regulation and the cerebral hemispheres are oppositely arranged with regard to the operation of emotion. This research however was purely correlational, and therefore s uggests nothing of the mechanism behind the effect, and in fact cannot imply cause and effect at all between observations. Also, only depression was taken into account, measured with standard instruments for gauging levels of the disorder. This methodology misses a potential wealth of nuanced information on the subtle temperament changes that surely accompany mood disorders following stroke, qualitative methods could perhaps have uncovered more, and future research is needed to investigate other aspects of mood effects of brain damage. Brain damage can also profoundly affect memory in various ways as well as affecting mood and demeanour (Graham and Hodges, 1997). The effects of brain damage on memory are as variable as the forms of memory itself. The empirical research into this area has elucidated not only the effects of brain damage but also the processes by which different kinds of memory are encoded, stored and retrieved and the structures primarily involved. This is possible through deduction based on the pattern of impairment in a particular patient in relation to their specific lesion (Graham and Hodges, 1997). In the case of working memory, research has shown that even patients with mild brain damage show a tendency towards enhanced activation of circuitry associated with information-processing when tested on the same working memory tests as controls (McAllister, Sparling, Flashman, Guerin, Mamourian and Saykin, 2001). This kind of research has elucidated the structures and pathways associated with working memory, but it cannot rule out the possibility that these areas of the brain are involved in multiple pathways necessary for other cognitive processes. This is perhaps only a fraction of the information which could be extracted by study of working memory circuitry and how it functions in conjunction with the rest of the brain. Although this research has highlighted areas relevant to working memory it says little about the processes involved or how the brain functions as a whole in this function. In addition to working memory, damage in different areas has been shown to affect long-term memory which will now be explored. Research into dementia and Alzheimer’s disease as well as patients with frontal lobe damage has uncovered information about the encoding and storage of long-term memory (Graham and Hodges, 1997). Graham and Hodges (1997) investigated the role of subcortical structures in the formation of new memories through the study of patients with degradation of hippocampal structures (Alzheimer’s patients) as compared to those with comparably spared hippocampal structures but atrophy in neocortical areas (patients with semantic dementia). Their findings show that patients with spared hippocampal structures had greater recall for recent memory than more distant memory, whereas patients with Alzheimer’s disease showed the opposite pattern. These observations have helped to establish the pathway via which short-term memory passes into long-term memory, and thus has important implications of our understanding of the storage of memory in the brain. This study does provide strong evidence for the proposed conclusion, although the specific mechanisms by which short-term memory is transferred and stored between regions remains mysterious. Indeed, the actual location of long-term memory storage itself remains mysterious. It seems likely then that this process is not as simple as is proposed here. Of course not all stimuli are represented the same way in memory, some are emotionally charged. This essay will now explore how research into brain damage has helped the understanding of emotional activation in the brain. Emotional memory and functioning is another area in which study of brain damage can supplement valuable information. It is well known that the amygdala plays a large role in the experience of emotion, so it follows that Cahill, Babinsky, Markowitsch and McGaugh (1995) found that memory for emotionally charged stimuli and events was impaired in patients with damage to the amygdala, whereas memory for neutral autobiographical events and experimental stimuli was within the normal range. The benefits of research on brain damaged patients can perhaps best be seen in this area because of the rarity of patients with selective lesions localised in the amygdala (Adolphs, Tranel, Damasio and Damasio, 1994). Although research into the function of the amygdala in healthy participants successfully revealed that it is involved broadly in emotion (for example, LeDoux, 2003) research into the rare cases of localised damage to the amygdala (with normal functioning elsewhere) have enabled researchers to add clarity and specificity to this statement. Adolphs et al. (1994) discovered that the amygdala functions with a social dimension as well as an emotional one. Specifically, it is essential for the recognition of emotion (especially fear) in other people, but it is not necessary to discern individual identity from faces. This shows a clear contribution to the knowledge base from studies of brain damage; the constraints were added to the general statement that the amygdala is simply involved in emotion. It would have been difficult to discern this information from examining only the activation patterns in the brain and behavioural functioning of healthy participants, as the lone influence of the amygdala could not easily be isolated from the rest of the brain without it being removed. Necessarily though, such studies lack a certain ecological validity because the observations are naturally limited to such a low number of cases due to the rarity of localised amygdala damage. Anoth er important functional area brain damage can influence is cognition and executive decision-making. By studying patients with frontal lobe damage it has been possible to determine the role it plays in cognition, problem-solving and decision-making. In procedures such as the Wisconsin card-sorting test, participants can be accurately assessed for frontal lobe damage based on how well they can sort the cards into categories and their flexibility in doing so with shifting classification criteria (Stuss, Levine, Alexander, Hong, Palumbo, Hamer and Izukawa 2000). This task can even be used to distinguish the location of the damage within the frontal lobe by varying the amount of specificity in external direction. The fact that cognitive functioning can so accurately reflect the location of damage in the brain shows again the opportunity for mapping brain functions based on data collected from patients with impaired functioning in specific areas. This kind of test has particularly good reliability since the test thoroughly assesses cognitive decision-making with the absence of activation in only one very specific area. A criticism must be that the task is probably quite dissimilar from anything the participants are likely to perform in their daily life; it is contrived to be carried out under experimental conditions, and therefore the results may not be as valid as they appear in naturalistic situations. Although the accuracy with which the test can distinguish the specific location of damage gives it criterion validity. This concludes the review of research into the influence of brain damage on functional ability and demeanour. This essay has presented research on the effects of damage in various locations within the brain on behaviour, sensation, memory and cognitive processing. The contribution to knowledge of the purpose and integration of various regions in the brain have been discussed, the general conclusion being that it would be difficult to gain the same insight into the specific role of structures and the form of neural pathways without the study of patients with localised brain damage. Other paradigms exist in neuroscience, but studying the pattern of impairment in patients with localised brain damage compared to controls provides perhaps one of the best ways to assess the function and contribution of that particular damaged area. There are of course confounding variables though such as the way the damage occurred, and individual differences in participants. References Adolphs, R., Tranel, D., Damasio, H., & Damasio, A. (1994). Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature, 372(6507), 669-672. Brewer, C., & Perrett, L. (1971). Brain Damage due to Alcohol Consumption: An Air?encephalographic, Psychometric and Electroencephalographic Study. British Journal of Addiction to Alcohol & Other Drugs, 66(3), 170-182. Cahill, L., Babinsky, R., Markowitsch, H. J., & McGaugh, J. L. (1995). The amygdala and emotional memory. Nature, 377(6547), 295-296. Fellows, L. K., & Farah, M. J. (2003). Ventromedial frontal cortex mediates affective shifting in humans: evidence from a reversal learning paradigm. Brain,126(8), 1830-1837. Graham, K. S., & Hodges, J. R. (1997). Differentiating the roles of the hippocampus complex and the neocortex in long-term memory storage: Evidence from the study of semantic dementia and Alzheimer’s disease. Neuropsychology, 11(1), 77. LeDoux, J. (2003). The emotional brain, fear, and the amygdala. Cellular and molecular neurobiology, 23(4-5), 727-738. McAllister, T. W., Sparling, M. B., Flashman, L. A., Guerin, S. J., Mamourian, A. C., & Saykin, A. J. (2001). Differential working memory load effects after mild traumatic brain injury. Neuroimage, 14(5), 1004-1012. Ommaya, A. K., & Gennarelli, T. A. (1974). Cerebral concussion and traumatic unconsciousness correlation of experimental and clinical observations on blunt head injuries. Brain, 97(4), 633-654. Robinson, R. G., Kubos, K. L., Starr, L. B., Rao, K., & Price, T. R. (1984). Mood disorders in stroke patients: importance of location of lesion. Brain, 107(1), 81-93. Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome Jr, E. D., & Beck, L. H. (1956). A continuous performance test of brain damage. Journal of consulting psychology, 20(5), 343. Stuss, D. T., Levine, B., Alexander, M. P., Hong, J., Palumbo, C., Hamer, L.., †¦ & Izukawa, D. (2000). Wisconsin Card Sorting Test performance in patients with focal frontal and posterior brain damage: effects of lesion location and test structure on separable cognitive processes. Neuropsychologia, 38(4), 388-402.