What does damage to the hippocampus do

For all participants, awakenings occurred after sleep onset, throughout the night. We aimed to assess dreams from both NREM and REM sleep, and we therefore staggered awakenings at intervals that allowed for entry into these stages, or approximately between 30—90 min intervals.

For example, a participant may have been woken at 30 min, returned to sleep and was woken again at 90 min. A maximum of 10 awakenings were scheduled per night. Every participant had a different sleep onset and duration, and so the awakenings were not scheduled at precisely the same clock time across participants. However, as shown in Supplementary file 2 , the sleep quality of the patients and the controls was well-matched, and this included total sleep time, bedtime and midpoint of the night.

Once a decision to awaken a participant was made, after a 3 min period without stage shift of either NREM or REM sleep, the other sleep researcher played a non-stressful Hz neutral tone via a two-way, Bluetooth intercom system equipped with a camera for continuous visual monitoring. After the tone was played, if the participant did not wake up, his name was spoken. This two-step awakening procedure was repeated up to five times, if required Dumel et al.

After awakening, participants were instructed by intercom to tell the experimenter everything that was going through their mind before they were woken up. What they said was recorded and subsequently transcribed.

Participants were occasionally probed e. Probing followed a structured protocol. This involved first asking participants to freely describe what was in their minds immediately after awakening. Can you give us any more specifics about the conversations or anything else that you recall? Crucially, this probing never involved leading the participant, as can be observed in the examples provided in Figure 2. This approach is very similar to that of well-established tasks that assess autobiographical memory recall Levine et al.

Transcriptions of dream reports were analysed by a researcher who was blind to participant group membership. We assessed across-experimenter agreement with inter-class correlation coefficients, with a two-way random effects model looking for absolute agreement, which indicated excellent agreement between the experimenters' scoring range: 0.

A dream was defined as any report that included at least one person, one place or one event Foulkes and Rechtschaffen, Dream frequency was calculated as the total number of dreams divided by the total number of awakenings.

Word count included words that provided information about the dream i. Dream complexity was experimenter scored on a 6-point scale using an adaptation of the Orlinsky score Oudiette et al. This ranged from a participant remembering a specific topic, but in isolation, for example a fragmentary action, scene, object, word, or idea unrelated to anything else, to a participant remembering an extremely long and detailed dream sequence of five or more stages.

Vividness referred to the clarity and detail of a dream, and was experimenter scored using the 6-point scale of De Gennaro et al. The emotional valence of a dream was scored using a 5-point Likert scale ranging from very negative to very positive, with three indicating a neutral tone. For self-references, one point was awarded per dream report if a participant reported he was the agent of an action, thought or feeling e.

We used two other scoring methods that are often employed for examining complex mental events in order to probe the dream reports further. The internal details score is the sum of these subcomponents. The external details score is the sum of these subcomponents. A second method we employed, the Scene Construction Test Hassabis et al. The content score is the sum of these subcomponents.

Equipment was then removed by a researcher the following morning upon awakening. All statistical analyses were performed with SPSS Given that the data did not meet the assumptions of normality and homogeneity necessary for parametric statistics, between-group analyses were performed using non-parametric Mann-Whitney U tests. In all analyses, the significance level was set at 0.

The dream data for every participant for every measure are provided in the file Table 2-Source data 1. In the interests of transparency, eLife publishes the most substantive revision requests and the accompanying author responses. This is a timely and elegant study exploring dreaming in patients with bilateral hippocampal damage due to LGI1-antibody-complex LE.

Studies like this have a strong potential to inform us about the neural basis of dreaming, which remains largely unknown. Thank you for submitting your article "Dreaming with hippocampal damage" for consideration by eLife.

Your article has been reviewed by three peer reviewers, one of whom is a member of our Board of Reviewing Editors, and the evaluation has been overseen by Laura Colgin as the Senior Editor.

The following individual involved in review of your submission has agreed to reveal their identity: Jess Payne Reviewer 3. The reviewers have discussed the reviews with one another and the Reviewing Editor has drafted this decision to help you prepare a revised submission.

In recognition of the fact that revisions may take longer than the two months we typically allow, until the research enterprise restarts in full, we will give authors as much time as they need to submit revised manuscripts. This is a timely and interesting study from the Maguire lab exploring the role of the hippocampus in dreaming. Four patients with bilateral hippocampal damage, due to LGI1-antibody-complex LE were tested at home using a tightly controlled forced awakening protocol informed by PSG.

These patients are extremely rare, presenting with selective memory disturbances due to circumscribed hippocampal insult, which adds to the novelty of the study. The authors used an elegant experimental design including a habituation protocol and the use of PSG to guide awakenings in participants.

Interestingly, the current study findings are in line with older papers by Torda from the s emphasising dream abnormalities in amnesia, as opposed to more recent investigations which characterise dreaming as largely intact in such patients Solms, Stickgold.

While the reviewers were all enthusiastic about this study, a number of methodological concerns were nevertheless raised. It is argued that these studies are flawed for several reasons, including because damage actually extended beyond the hippocampus and patients had broader cognitive impairments.

This may be the case, but the clear presence of dreaming in these patients e. Torda, studies; Stickgold et al. The current study is therefore not the first to test whether dreaming requires the hippocampus and such statements should be tempered accordingly.

It is stated that participants were awoken after a solid 3min period of REM or NREM sleep, but how, specifically, was the timing and number of awakenings determined? How often were they awoken, and at what time of night? Were awakenings stopped when some maximum number was reached? Was the clock time of awakenings equivalent between patients and controls? Further details would be helpful to address these comments. Subtle differences in how questions are posed have a large effect on the quantity and quality of dream reports.

Thus, it is ideal to use pre-recorded verbal prompts for all participants, avoiding systematic bias in the way that dream reports are elicited from patients vs from controls.

In this regard, it could be a problem that participants "were occasionally prompted e. While the number of prompts did not differ significantly between control and patient groups, the study is underpowered to detect all but the largest differences here. Numerically, control participants were prompted for more information more often than the patients. There also could have been subtle differences in the quality of interaction between researchers and participants that affected reporting.

There exists no validated measure of dreaming other than participants' subjective report, and there is no evidence that participants can meaningfully distinguish between having had a dream that they cannot recall and having not had a dream at all. It is therefore of questionable validity to presume that "blank dreams" indicate that dreaming occurred and was forgotten, whereas "no dream" reports indicate lack of dreaming.

While a large sample is not feasible with this rare and difficult-to-test population, strong conclusions based on non-significant differences between groups should be avoided. For example, it is unclear whether patients are not just describing their dream experiences using fewer words than controls. Importantly, some of the methods used to score richness of detail for example that used in Hassabis et al.

The figures currently present the group means, but individual data points should be included to enable the reader to see the spread of scores across patient and Control groups. A case series would enable the authors to further compare and contrast the case who had no dream reports and to potentially understand the heterogeneity across these patients. It may be that aggregating the dreaming performance across these patients masks important individual differences, as for some measures Controls appear to outperform patients by almost double e.

It was suggested that the authors should be a bit more cautious in their language given that most HC output is believed to be blocked during REM sleep which is where most imagery rich dreaming occurs. In fact, given that REM sleep dreaming may be mostly cortical temporarily devoid of HC input , these results become even more interesting, because the REM sleep dreams obtained here were still degraded compared to controls.

In Clive Wearing, a British conductor, composer and musician, suffered a viral encephalitis , which caused major damage to the left and right hippocampus. Although his intellectual skills are intact, he has serious problems with his memory and he cannot create new declarative memories consciously accessible factual knowledge.

He cannot enter into a conversation because he constantly forgets the previous sentence of the conversation. He cannot go outside because he does not know where he is, where he comes from and where he is going. Every day he wakes up as if awakened from a coma, unaware of where he is. This fact was discovered in the s by the famous case of Henry Molaison. Henry, who suffered from severe epilepsy, underwent surgery to eliminate his seizures.

Because of the loss of his hippocampus, Henry would suffer from severe anterograde amnesia for the rest of his life. This meant that his ability to form new memories was impaired. He could remember facts and experiences from before his surgery, but nothing afterward. Most patients after a traumatic brain injury do not have near as extreme of symptoms as Henry did. They can still create some new memories, but they will have a much harder time doing so. For example, they might need to ask the same question multiple times because they cannot remember the answer.

While the hippocampus mainly controls declarative memory, damage to it can also cause symptoms of depression. In individuals with depression and post-traumatic stress disorder, brain scans reveal that their hippocampal volume is actually reduced. Not only that, but their hippocampus appears to be smaller during periods of depression than during periods of remission. To explain this fact, some psychologists developed a theory of depression known as the neurogenic hypothesis.

This hypothesis suggests that an impaired ability to produce new brain cells contributes to depression. Interestingly, the hippocampus actually plays a role in the production of new brain cells. Therefore, the fact that hippocampus activity decreases during depression supports this idea. Next, we will discuss exactly how the hippocampus plays a role in neuron production, and how that helps with recovery for individuals with hippocampus brain injuries.

One of the most fascinating things about the hippocampus is the role it plays in neurogenesis , which refers to the creation of new brain cells. That is because it is one of the only areas in the adult brain that produces progenitor cells. These cells can transform into different types of brain cells and migrate into brain regions that need replenishing. Thus, the hippocampus can heal brain damage by replacing damaged nerve cells. Because the hippocampus is so intimately involved in neurogenesis, activating that process may help reverse some of the damage.

You can help your hippocampus do this by boosting the production of brain-derived neurotrophic factor BDNF in your brain. BDNF acts as fuel to activate neurogenesis. Exercise, particularly aerobic exercise, is one of the best ways to boost BDNF levels and improve hippocampal function.

For example, a now-famous study compared the brains of two groups of mice. One group had access to a running wheel, and one did not.

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