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Hippocampal Lesions

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Hippocampal Lesions

            Buried deep in the medial temporal lobe is the hippocampus which resembles a zucchini or a horseshoe and is characteristic of millions and millions of cells (neurons) organized into a network that is unlike any other part of the nervous system. Structurally it is a bulb like shape and protrudes into the lateral ventricles. Its formation is a group of areas in the brain that consist of the dentate gyrus, subiculum, hippocampus, presubiculum, parasubiculum and the entorhinal cortex. Since it is located in the medial temporal lobe, it thus forms a part of the telecephalon as well as belonging to the limbic system.

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Basically, hippocampal functions are defined with respect to inhibition, memory and space and olfaction in certain instances though there is no direct evident that functionally connects the hippocampus to olfaction. It is therefore only prudent that a discourse on the hippocampal lesions follow the direction of the discourse on hippocampal functions.

            This basic layout of neurons in the hippocampus is similar for all mammals (Andersen et al 3).

Functionally, as part of the limbic system the hippopotamus been implicated in short term memory. Both neuroscientists and psychologists agree that the hippocampus is not only responsible for the generation of new memory about personal experiences, especially autobiographical or rather episodic memory. The presence of hippocampal lesions have been incriminated in the production of short term memory deficits. In contrast to the magnitude of animal experiments that have yielded extensive evidence on the linkage between hippocampal damage to spatial memory deficits, human studies have only confirmed that hippocampal bilateral damage causes amnesia and this effect is related to the hippocampal function in memory. In humans the media; temporal lobe is responsible for declarative memory.

            Any substantial bilateral damage to the hippocampal region and the medial temporal lobes invariably results to amnesia which is characterized by a significant decrease in the memory component of the intelligence quotient (MIQ). This drop is 20 points in relation to the full scale IQ (Anderson et al 733). When this is coupled to the paucity of data on the functions of the hippocampal region in relation to memory, conclusive affirmations can not be made contrarily to the adjacent cortical regions. This aside, some general points can be made on this relationship. Ubiquitous deficit in memory usually accompanies hippocampal lesions. For instance, an anterograde deficiency in episodic memory. Another effect that accompanies the development of hippocampal lesion is the deficit in the spared procedural and working memory. The degree of retrograde amnesia varies across patients and can be over a patients’ lifetime or just over a short periods of time after the development of lesion. However, this observation is limited with regard to lesions in the for nix (Anderson et al 734).

Some studies attest to the considerable sparing of the semantic memory and also in familiarity-based recognition in instances where the damage is localized in the focal hippocampus. These findings are more in consistence with results from monkey studies since relative sparing of recognition memory in such animals is more dependent on the nearby cortical regions. In humans it is right to reiterate that the hippocampus especially the right hemisphere is functionally critical in spatial navigation.

            The nature of learning that is always dependent on the medial temporal lobe is usually accompanied by what is learned (Gazzaniga & Bizzi 692). In a study carried out to determine the relationship between awareness and the medial temporal lobe, the researchers enlisted a perpetual learning task in which healthy volunteers were subjected to the search of a 90° rotated, colored T among colored right angles. These participants were asked to indicate the exact direction that the base of the colored T was pointing. After some practice these participants were able to correctly indicate the direction faster in comparison to new displays. Memory impaired patients were also included in the study and their performance was comparatively dismal. However, the results also indicated that in contrast to the expectation both groups were unable to recognize specifically which displays were repeated in the displays. Thus, performance of all the participants was not accompanied by awareness. A subsequent study enlisted patients with hippocampal damage with an aim of determining which part of the brain was responsible for the dismal performance. In this case the participants responded much faster to the repeated displays as opposed to new displays just as the first participants. Contrastingly, patients with large medial temporal lobe lesions could not be able to detect the repeated displays(Gazzaniga & Bizzi 693). This implied that the performance of the task was dependent on the integrity of the hippocampus due to deficits in short term memory.

            With regard to recognition memory: the ability to judge a recently observed item is an example of declarative memory, and therefore any bilateral damage that is restricted to the hippocampal region impairs the performance of standard tasks that are dependent on the recognition memory. In cases where there are any additional damage to the adjacent medial temporal cortex, performance is additionally impaired(Gazzaniga & Bizzi 693). For patients with perinatal hippocampal damage, recognition memory is unusually good due to the presence of a preserved ability to judge bases on familiarity. This assertion may be limited to instances of developmental amnesia usually occasioned by the functional reorganization during the developmental process as well as the acquisition of alternative learning strategies. Studies of neuroimaging data show that retrieval of information from memory (remembering) is associated with additional activation in comparison to retrieval associated with knowing.

            In humans, monkeys and rats, recognition memory is largely dependent on the integrity of the hippocampus region (Levy et al 794). Among human beings the effect on recognition memory due to an impairment of hippocampal region has also been demonstrated by non verbal and verbal materials and nonsense sounds. Generally in all these experimentations, the effect of hippocampal lesions present as short term memory deficits, given the relatedness of hippocampal function among vertebrates it can be conclusively surmised that these deficits are applicable to all vertebrates.

            Many studies have concentrated on the effect of hippocampal lesions on recognition memory. These demonstrations have been achieved through a variety of tasks. Additionally, hippocampal lesions affect olfactory recognition memory as well. Levy et al evaluated the capacity of memory impaired patients to recognize a list of odors. After a retention delay of about one hour, the olfactory recognition memory of these patients thought to have hippocampal lesions was considerably impaired even though olfactory sensitivity remained intact. Olfactory recognition memory just like all the other recognition memory sensory modalities is directly dependent on the integrity of the hippocampal region. In many situation such observations could as well been explained by abnormal olfactory sensitivity but even in such situations abnormal olfactory insensitivity cannot account for the impairment in olfactory recognition memory (495).

            Thus, apart from the highly studied effect on hippocampal lesions on recognition memory, this study provides additional evidence that hippocampal lesions present a multimodal human memory impairment. In essence, olfaction was one of the earliest ideas of the function of the hippocampus. This suggestion was mainly due to its location in the brain and its proximity to the olfactory cortex. This specific association between other recognition memory modalities and olfactory recognition memory points to the existence of an indirect linkage between the hippocampus and the functional component of olfaction.

            These studies constitute just a small fraction of data that attempt to precisely define the roles of the medial temporal lobe in learning and memory. A prominent theory posits that the hippocampal formation (comprising the dentate gyrus, hippocampus, subiculum, presubiculum, parasubiculum, and entorhinal cortex) is critical in the processing of relational information (Eichenbaum 43). In rodents, the role of the hippocampus on spatial relational learning and memory has been studied extensively. For instance, the formation and utilization of allocentric representations of space (Nadel & Hardt 475). Other studies have focused on the distortion of learning and memory and its association with the integrity of the hippocampal formation.

            The hippocampus is functionally important in the storage and processing of spatial information. Cells referred to as space cells in the hippocampus have firing fields in which the cells fire when movement proceeds to a particular location, regardless of the direction in which the animal is traveling towards. Studies in rats have yielded information on the context dependent space cells that are capable of altering their firing retrospectively or progressively. In humans the specificity of the firing with respect to location has been studied by the aid of a virtual reality town (Maguire et al 4399). In effect, the hippocampal region is the animal’s cognitive map that provides a neural representation of the environmental layout. An intact hippocampal region is a necessity for tasks requiring spatial memory. Without the benefit of a fully functional hippocampus, animals may not be able to retrieve memory necessary for detecting the direction of movement or any familiarity with a location.

            Evidence from brain imaging of humans tested against a computer simulated virtual navigation task show that when navigating, the hippocampi is extremely active not only in navigating according to memory retrieval of the layout of the location but also finding short cuts as well as new routes(Maguire et al 4401). Hippocampal lesions exhibit a marked distortion or impairment of an individual to perform simple tasks that require retrievals of spatial memory.

            In a study carried out by Lavenex et al (2006) to discriminate between allocentric and egocentric spatial representations with respect to spatial learning and memory, the researchers enlisted six monkeys that had received bilateral hippocampal ibotenic acid lesions and analyzed them against a control sample of six adult monkeys that had been taken through a sham surgery. These monkeys were released and left to forage for food located in distinct locations. To limit reliance on egocentric strategy, multiple goals and pseudo-randomly chosen entrance points were included in the study. In the first test local cues were used to direct the monkeys to the food locations, the second test eliminated the local cues to make the monkeys use an allocentric strategy to discriminate these food locations. Based on observations when a local cue was used all monkeys (both the control sample and the hippocampal-lesioned sample) located the food locations. In the second case where the local cues were eliminated, the hippocampal-lesioned monkeys were completely unable to locate the food locations (473–476). Thus, the study attested to the fact that hippocampal lesions are responsible for a defect in the development and use of allocentric spatial representations.

             Analyzing on the basis of the local cue condition, the researchers demonstrated that hippocampal lesioned monkeys were completely able to discriminate the potential baited locations that were marked with local cues. This analysis was presented graphically as;

Figure; Hippocampal-lesioned (A) and control (B) monkeys’ strategy in the local cue condition. Pot IN, Potentially-baited locations at the corners of the inner hexagon (locations 13, 15, 17); Pot OUT, potentially-baited locations at the corners of the outer hexagon (locations 4, 8, 12); Equ IN, never-baited locations at the corners of the inner hexagon (locations 14, 16, 18); Equ OUT, never-baited locations at the corners of the outer hexagon (locations 2, 6, 10); Other, never-baited locations on the sides of the outer hexagon (locations 1, 3, 5, 7, 9, 11). The number of choices in each category (n) is normalized according to the probability of making that choice (n of 3 for Pot IN, Pot OUT, Equ IN, and Equ OUT; n of 6 for Other)[Adapted from Lavenex et al 4550]

            In relation to the spatial relational condition, an analysis of individual trials demonstrated that there exist significant group differences with regard to the spatial relational condition. For their first choice monkeys with hippocampal lesions preferred locations on the inner array and were unable to successfully discriminate between the cups that were potentially baited and those that were never baited but positioned in the inner array.  Even though these monkeys, exhibited significant preference for the inner locations in the array they were nonetheless unable to discriminate between the cups.

            To surmise, unlike the normal monkeys who had only undergone a sham surgery, the hippocampal lesioned were unable to discriminate the potentially baited cups in the absence of markings of local cues. All in all, the hippocampal lesioned monkeys had lost the ability to exhibit preference for the potentially baited cups because of the absence of spatial relational learning in the context of the spatial relational condition. These results were represented graphically as follows;

Figure; Hippocampal-lesioned (A) and control (B) monkeys’ strategy in the spatial relational condition.

            Since hippocampus functions in spatial cognition and anxiety, hippocampal lesions predispose species to impairments in spatial cognitions but anxiety is not uniformly diminished for all species. In a study done using hippocampal lesioned mice, it was demonstrated that tasks such as the formation of nests, hoarding and burrowing are done poorer and less frequently when compared with the control population. In response top anxiety tests, lesioned mice were comparatively less anxious. Additionally, lesions also reduce locomotion and grooming. The reduction in anxiety can be explained by the reduced baseline in the hyponeophagia in response to anxious stimuli. These results cannot be extrapolated across species, since the tests only employed species related behaviors (Deacon & Rawlins 243).

             Different effects of hippocampal and septal lesions prescribe different behaviors. Rewarded responses are elevated as septal lesions increase, but this elevation is not shown when hippocampal lesions increase. Intraspecies aggression is elevated by an increase in septal lesions but a decrease in hippocampal lesions. Therefore, septal lesions play a more profound role in emotionality as compared to hippocampal lesions (Zuckerman 158).

            Redundancy compression can occur with the enlistment of contextual cues as well as experimentally controlled conditioning of stimuli. For instance, if a phasic cue labeled A is repeatedly presented in a context X without reinforcement(XA pre-exposure) then its representation will be undergo compression with the tonic cues with which it appears since neither the tonic tunes nor A  are predictive of any reinforcement. The effect increases the generalization between the tonic tunes and A. Subsequently, in the next phase the presence of A predicts reinforcement (XA+, X training). Thus the represent of A will need to be differentiated from the contextual cue representation. This slows down learning comparative to the control condition. This is what is referred to as latent inhibition and is observable in normal intact animals. This effect can be eliminated by the a aspiration lesions of the hippocampus (Zornetzer et al 82).

            When more selective hippocampal lesion techniques are used in studying the relationship between inhibition and hippocampal lesions, it can be demonstrated that not only does hippocampal lesions impair latent inhibition but that they may as well spare, or even facilitate latent inhibition. Buhusi & Schmanjuk (1997) employed a neural network model to explain the contradictions that exist in experimental data on the effects of hippocampal lesions on latent inhibition. In the context of the neural network model, these contradictory patterns are a result of the interactions between cognitive mechanisms like cognitive mapping and the attentional feedback mechanisms which tracks the sum of all the novelty in the environment. By using computer simulations under controlled experimental conditions, the model succeeds in counter intuitively predicting a facilitation of latent inhibition (LI) after hippocampal lesions (314).

            With regard to this experimental set up, the main determinants of the interaction are the pre-exposure time and the experimental procedure. Both selective and non selective lesions cause the impairment of latent inhibition under experimental conditions that are favorable to latent inhibition in non hippocampal lesioned animals. Alternatively, the same lesions preserve latent inhibition with experimental parameters that are favorable to latent inhibition in normal animals (315).

Works Cited

Andersen, P., Morris, R., Amaral, D., O’Keefe, J. (2007). The hippocampus book. Oxford           University Press US.

Buhusi, C.V. Schmajuk, N.A. (1997). Hippocampal lesions may impair, spare, or facilitate latent             inhibition: a neural network explanation. Neural Networks. Volume: 1: 312-317

Deacon, Robert, MJ & Rawlins, J NP (2005) Hippocampal lesions, species-typical behaviours    and anxiety in mice. Behav Brain Res, 156(2):241-9.

Eichenbaum H (2000) A cortical-hippocampal system for declarative memory. Nat Rev Neurosci            1:41–50.

Gazzaniga, S. Micheal & Bizzi, E. (2004). The Cognitive Neurosciences: Third Edition. MIT       Press.

Lavetex, B. Pamela., Amaral, G. David & Lavetex P. (2006). Hippocampal Lesion Prevents       Spatial Relational Learning in Adult Macaque Monkeys. The Journal of Neuroscience,     April 26, 2006, 26(17):4546-4558

Levy, A. Daniel., Hopkins, O. Ramona., Squire, R. Larry. (2004). Impaired odor recognition      memory in patients with hippocampal lesions.  Learn. Mem. 2004. 11: 794-796

Maguire, EA; Gadian DG, Johnsrude IS, Good CD, Ashburner J, Frackowiak RS, Frith CD      (2000). Navigation-related structural change in the hippocampi of taxi drivers. PNAS 97:             4398–4403.

Nadel L, Hardt O (2004) The spatial brain. Neuropsychology. 18:473–476.

Zornetzer, F. Steven., Davis, L. Joel., Lau. C., McKenna, M. Thomas. (1995). An Introduction to           Neural and Electronic Networks. Morgan Kaufmann Press.,

 

Cite this Hippocampal Lesions

Hippocampal Lesions. (2016, Oct 06). Retrieved from https://graduateway.com/hippocampal-lesions/

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