The Effects of Hippocampal Damage - Dissertation Example

?The effects of hippocampal damage Introduction The hippocampus is a major constituent of human brains and other vertebrates. It plays a vital role in information consolidation from the short term memory to the long term memory and the spatial navigation. Just like other mammals, humans have two hippocampi one on each side of the brain. In primates, hippocampus is a part of the cerebral cortex and is located underneath the cortical surface in the medical temporal lobe. The hippocampus is among the first brain regions to suffer damage in the event of Alzheimer’s disease. It is also vulnerable to disorientation and memory loss in the early symptoms. The hippocampal damage can result from encephalitis, hypoxia (oxygen starvation), or medical temporal lobe epilepsy. People suffering from bilateral and extensive hippocampal damage sometimes experience anterograde amnesia (inability to retain or form new memories) (Kirkpatrick, 2007). This paper seeks to discuss the extent to which the effects of hoppocampal damage could be explained in terms of an impairment of associative learning with reference to spatial learning and recognition memory. The hippocampal damage implicates the permanent loss of memory in people with medical temporal lobe resections. In the past studies, it was noted that bilateral hippocampus ablations in the impaired performance on the task of the associative learning and on the task of the object discrimination retention. The studies assessed the long term impacts of hippocampal resections and to extend the analysis of the impacts of hippocampal resection to recognition memory (Mondragon, Bonardi & Hall, 2003). The opinion of the experts has remained divided on the concern of whether the system of hippocampus functions in spatial information processing exclusively. For example, in understanding spatial relations, or in navigation, or whether it performs a broad function in the brain, the expert opinion has remained divided. The past studies on rats and monkeys tended to concur with the explanation of the extent to which the effects of hippocampal damage are explained in terms of an impairment of associative learning. The hippocampal damage impairs the functions of episodic memory, declarative knowledge, understanding relations among objects, and word learning (Jennings, 2007). One influential theory hypothesizes a wide role for the system of hippocampus in associative learning, with the focus on associations learned recently and rapidly. A long with the past theoretical and clinical studies, the influential theory indicates that the hippocampal system is important for associative learning whether or not there is a component of the association depending on spatial information. The system of hippocampus plays a pivotal role in associative learning with no regard to the relevance of spatial information to any particular aspect of the association. Fornix transected monkeys were impaired in efforts of learning response associations and new stimulus even when the stimuli were very familiar. The problem in this case is associating stimulus with a response, in contrary to the deficit in distinguishing the stimuli from the others (Graham, Hall & Mitchell, 2005). On the other hand, the fornix transaction do not impair performance where a familiar stimuli instructs a response in relation to the already learned association indicating that the problem is learning new association instead of retrieval or retention of previously learned association. Together, these assertions indicate that fornix transection results into a long lasting associative learning impairment outside the spatial domain, in a way consistent with the theories of the system of hippocampal function that emphasizes the general role in the rapid acquisition of associative knowledge (Aggleton, Hunt & Rawlins, 2002). There has been numerous and continuous debate on the extent to which the effects of hoppocampal damage impair of associative learning with regards to spatial learning and recognition memory. Past researches have detailed the effect of hippocampal damage of associative learning. This has been done with reference to whether the function of rodent hippocampus in memory is constrained to the spatial domain (Bonardi & Jennings, 2009). This controversy has been recently highlighted with social transmission of food preference studies, an association task that do not have spatial requirement. Several other studies and reports have detailed that hippocampal damage impairs memory in this aspect; however, there are concerns on the degree of the hippocampal damage that is essential to lead to impairment. In addition, studies on hippocampus system have found no particular impact of lesions of hippocampus on memory. However, hippocampal lesions lead to impairment on spatial delayed alternation though not on the social transmission of food preference memory. The damage of the hippocampal system results into severe and equivalent memory impairment for the food preference acquired socially. It is hence important to note that subiculum and hippocampus play together a crucial function in the formation of this form of relational and non-spatial memory (Aggleton, Hunt & Rawlins, 2002). The neuroimaging and lesion evidence shows that the hippocampus is an essential node in the neural network that supports the retrieval of the autobiography memory, and hence the focal hippocampal damage may result into a functional impact and consequence to the general network structure. The hippocampal damage has a significant effect on the connectivity ad engagement of the autobiographic memory network. The result encompass retreaving specific autobiographic memory activity in residual tissue of the hippocampus and across the autobiographic memory network as well as the temporal poles, medial prefrontal cortex, lateral parietal cortex, and retrosplenial cortex (Tam & Bonardi, 2012). The hippocampal damage also results into a reduced strength of connections that involve the hippocampus system. On the contrary, the effect of the hippocampal damage leads to the strengthened connections in the extra-hippocampal nodes like the medial prefrontal cortex and the left retrosplenial cortex. This reflects possibly a compensatory mechanism. It has been noted in the past studies that the left hippocampus and the effect of hippocampal damage is an essential node in autobiographic network, and plays a dominant role in starting other network node engagement. The hippocampal damage has significant effect on the connectivity and the functional organization of the neural network that support the retrieval of the autobiographic network (Bonardi & Jennings, 2009). The findings of the major studies on the effects of hippocampal damage on the impairment of associative learning with reference to spatial learning and recognition memory reveal that the effects of hippocampal damage are complicated, varied and complex. The effects are characterized by both the changes in connectivity and reduction of activation. There is clear evidence on the vital role of the hippocampus in the autobiographic memory network. Most probably as with other network hubs, when hippocampus is damaged, there is an appearance of a surge of effects on numerous levels (Kirkpatrick, 2007). The episodic quality of autobiographic memory network is diminished behaviorally, and at the neural level, the activity is minimized. This decrease of the activity is not only in the hippocampal damage, but the whole autobiographic memory network is down regulated. Effective analysis of connectivity shows that the successful autobiographic memory network retrieval is supported by a modified network that bypasses the hippocampal node damage, and insicates an increased dependency on the other constituents of the autobiographic memory network. In this regard, the effects of hippocampal damage on the impairment of associative learning can be witnessed with reference to spatial learning and recognition memory in the autobiographic memory network (Jennings, 2007). Historically, the effect of hippocampal damage has been associated with the impairment of associative learning. This has specifically been associated with recognition memory and spatial learning. The broadly held hypothesis concerning this is that the hippocampus is entailed in olfaction (Bonardi, 2007). The whole idea has been in the past cast into doubt by numerous anatomical studies that failed to access direct projections in the hippocampus system from the olfactory bulb. The later studies of the same confirmed that olfactory bulb project into the ventral part of the entorhinal lateral cortex. This has led to the continuity in the interest in the olfactory responses of the hippocampus, specifically the role of the hippocampus system in odors memory. However, a small number of specialists believe today that olfaction is the primary function of the hippocampus system. On the impairment of associative learning with respect to the recognition memory and spatial learning, there are three major ideas of the functions of hippocampus that has dominated the hippocampal literature in studies: memory, inhibition, and space (Dunn, 2005). The theory of inhibition behavior asserts that animals experiencing hippocampal damage particularly tend to be hyperactive. In addition, the behavioral inhibition theiry states that these species with hippocampal damage normally experience difficulty learning that inhibit responses that have been taught previously, particularly when the responses needs a passive avoidance test, remaining quiet. On the hippocampus memory, the hippocampal damage results into the inability to form episodic memories and inability to remember any specific event that took place before the damage (Bonardi, Hall & Ong, 2005). Patients with hippocampal damage tend to remember events that took place several years before the hippocampal damage. It is conventionally agreed due to the past studies that hippocampus system play essential role in memory. The concise role of memory played by hippocampus system after the hippocampal damage remains broadly debated. Finally, the hippocampal function is also associated with spatial theory. The spatial theory explains as with the memory theory, that spatial coding plays a pivotal function in hippocamapal role, although the specifics remain widely debated (Graham, Hall & Mitchell, 2005). Hippocampal damage produces a complicated range of cognitive deficits, for instance in spatial learning, but association formation is often said to be in one piece, implying that associative learning does not in any circumstance underlie the affected skills in the event of damage to hippocampus. In addition, numerous studies indicate that some sorts of associative learning may be impaired after damage occurs to hippocampus. This implies that impairment to an associative learning could go between the impacts if for example hippocampal damage on spatial learning. The effects of hippocampal damage on the impairment of associative learning can be perceived with reference to spatial learning and recognition memory as indicated in this paper. There are numerous aspects of associative learning that are practically impaired by damage on hippocampus (Blair, Bonardi & Hall, 2004). In many such aspects and instances, learning is impaired and we can use the associative theory to look into this deficit. In a research by Dr Helen Cassaday, it was found out that schizophrenia is characterized by high impulsivity that is much evident in inhibitory learning as a deficit. In addition, deficit in performance on tasks that employ cues of setting tasks also characterizes schizophrenia. Alzheimer’s disease has a broad range of cognitive impairments and much of this is not characterized in associative terms precisely. These findings give explanations of the effect of hippocampal damage on associative learning with regards to spatial learning and cognitive memory (Mondragon, Bonardi & Hall, 2003). The extents to which the effects of hippocampal damage affect associative learning differ between children and adults. When the degree of effects of hippocampal damage on associative learning in children is compared to that in adults, there is relatively little known concerning autobiographical memory and the capability of imagining future and fictitious scenes in children, in spite of the significance of these roles in independent living and development (Bonardi & Ong, 2003). There is much less mastered concerning the effect of early damage on hippocampus on the memory and imagination abilities of children. Recent studies on the effects of hippocampal damage suggest that healthy children are able to recall autobiographical events that include specific episodic details and spatiotemporal information (Bonardi, 2001). In contrary, children with a neonatal hypoxia or ischaemia experience had impaired recall, with very specific episodic details being lost. In spite of this substantial loss in memory and deficit, the children are still able to have fictitious scenarios constructed. This is very contrasting in the case of adults with damage on the hippocampus and has typical autobiographic memory impairment and deficits in future and fictitious scenario constructions. This speculates that children are relatively intact some functionality and/ or semantic memory in their residual hippocampi might underpin their ability to construct a scenario (Bonardi & Ward-Robinson, 2001). In an attempt to explain the effect of hippocampal damage on associative learning in relation to spatial learning and cognitive memory, it is vital to note that the hippocampus work in concert with various cortical brain regions in a healthy human brain. The function of hippocampus is linked to the brain network with the precuneus beings its central hub. This brings about the remote effects of the unilateral damage to hippocampus on the functional connectivity between the distant regions of the brain that are associated with the human brain default network. This underline the effects of pathology circumscribed on the brain regions connected functionally (Byrne, 2008). The hippocampus is grouped with structures near its location (under medial temporal lobe) such as the dentate gyrus: hippocampal formation. Hippocampus plays a vital role in the formation of fact memories and new autobiographic memories. It sometimes functions as a gateway memory through which any particular new memory have to pass prior to entering its permanent storage located in the brain. Therefore any damage in the hippocampus significantly affects associative learning in relation to spatial learning and cognitive memory. This is because hippocampal damage leads to anterogade amnesia: the entire loss of individual ability to create new memories, even though the old memories may remain intact (Philippe, 2007). That is to say, people who sustain substantial injury in the hippocampus are prone to have intact memory of events that took place during childhood and several years before the injury, but this is not the case with the memory of anything that took place after the memory as total loss of cognitive memory may be inevitable. Evidence also shows that some forms of memory like the memory for new habits and skills can be created even without hippocampus. Current research and studies also seek to determine the exact forms of learning and memory that can uphold damage in the hippocampus, as well as how these forms of learning and memory can be utilized in guiding rehabilitation (Sharp, 2002). The effect of hippocampal damage on associative learning has been noted variedly among children and adults as explained in the earlier paragraphs. The hippocampus is particular sensitive to reductions in the level of oxygen in the body. Among both children and adults, it has been noted from the past studies that periods of hypoxia (oxygen deprivation) not particularly fatal may lead to hippocampal damage. This could specifically occur during respiratory failure, heart attack, carbon monoxide poisoning, near drowning, and sleep apnea among other conditions. Hippocampus is also not a unique focus in medical epilepsy and may be damaged by chronic seizures. Hippocampal damage may also be as a result of diseases like herpes encephalitis. In addition, hiipocampus is the first area in the brain that indicates damage in Alzheimer’s disease. Therefore any damage in the hippocampus results into a subsequent effect in the associative learning (Howard, 2002). Conclusion In summary, hippocampus is a major constituent of human brains. Hippocampus plays a vital role in consolidation of information from the short term memory to the long term memory and the spatial navigation. Humans have two hippocampi just like any other animal with one on each side of the brain (Henri, Duvernoy & Cattin, 2005). Hippocampus is a part of the cerebral cortex and is located underneath the cortical surface in the medical temporal lobe in primates. The hippocampus is among the first brain regions to indicate damage in the event of Alzheimer’s disease. As explained in earlier paragraphs, hippocampus is vulnerable to disorientation and memory loss in the early symptoms. Some of the major causes of hippocampal damage include encephalitis, hypoxia (oxygen starvation), or medical temporal lobe epilepsy. Those who suffer from bilateral and extensive hippocampal damage sometimes experience anterograde amnesia (Per Andersen et al., 2007). This paper has discussed the extent to which the effects of hoppocampal damage could be explained in terms of an impairment of associative learning with reference to spatial learning and recognition memory. Bibliography Aggleton JP, Hunt PR, Rawlins JN.2002. The effects of hippocampal lesions upon spatial and non?spatial tests of working memory. Behav Brain Res, 19: 133–46. Blair, C.A.J., Bonardi, C., & Hall, G.  2004.   Differential effects of 8-OH-DPAT on two forms of appetitive Pavlovian conditioning in the rat.   Behavioral Neuroscience, 118, 1439-1443.  Bonardi, C. 2001.   Dorsal hippocampal lesions impair appetitive classical conditioning to localized cues.  European Journal of Neuroscience, 13, 1435-1443.  Bonardi, C. 2007. Occasion setting is specific to the CS-US association. Learning and Motivation, 38, 208-228. Bonardi, C., & Jennings, D. 2009.  Learning about associations: Evidence for a hierarchical account of occasion setting.  Journal of Experimental Psychology: Animal Behavior Processes, 35, 440-445. Bonardi, C., & Ong, S.Y. 2003.  Learned irrelevance: a contemporary overview.  Quarterly Journal of Experimental Psychology, 56B, 80-89. Bonardi, C., & Ward-Robinson, J. 2001.  Occasion setters: Specificity to the US and the CS-US association.  Learning and Motivation, 32, 349-366.  Bonardi., C., Hall., G., & Ong, S. Y. 2005. Analysis of the learned irrelevance effect in appetitive Pavlovian conditioning.  Quarterly Journal of Experimental Psychology, 58B, 141-162. Byrne, J. 2008. Learning and Memory: A comprehensive reference. London: Elsevier Dunn, M. 2005.  Attenuation of D-amphetamine-induced disruption of conditional discrimination performance by alpha-flupenthixol.  Psychopharmacology, 177, 296-306. Graham, S., & Hall, G, & Mitchell, C. 2005.  Acquired distinctiveness and equivalence in human discrimination learning: Evidence for an attentional process.  Psychonomic Bulletin & Review, 12, 89-92.  Henri M. Duvernoy, F. Cattin 2005. The Human Hippocampus: Functional Anatomy, Vascularization, and Serial Sections with MRI. London: Springer. Howard Eichenbaum 2002. The Cognitive Neuroscience of Memory. New York: Oxford University Press Jennings, D. 2007. Occasion setting of timing behaviour. Journal of Experimental Psychology:  Animal Behavior Processes, 23, 339-348. Kirkpatrick, K, 2007.  Stimulus duration effects in overshadowing. Journal of Experimental Psychology: Animal Behavior Processes, 33, 464-475. Mondragon, E., Bonardi, C., & Hall, G.  2003. Negative priming and occasion setting  in an appetitive Pavlovian procedure.  Learning and Behavior, 31, 281-291. Per Andersen et al., 2007 The Hippocampus Book. Oxford: Oxford University Press. Philippe Taupin 2007. The Hippocampus: Neurotransmission and Plasticity in the Nervous System. London: Nova Publishers. Sharp, P. 2002. The Neural Basis of Navigation: Evidence from Single Cell Recording. Boson: Springer. Tam, S.K.E., & Bonardi, C.  2012. Dorsal hippocampal involvement in appetitive trace conditioning and interval timing Behavioural Neuroscience 126, 258-269. Read More