Memory: How the brain constructs dreams
Deep inside the temporal lobe of the brain, the hippocampus has a central role in our ability to remember, imagine and dream.
- Department of Psychology and Program in Neuroscience, Furman University, United States
Our most vivid dreams are a remarkable replication of reality, combining disparate objects, actions and perceptions into a richly detailed hallucinatory experience. How does our brain accomplish this? It has long been suspected that the hippocampus contributes to dreaming, in part due to its close association with memory: according to one estimate, about half of all dreams contain at least one element originating from a specific experience while the subject was awake (Fosse et al., 2003). Although these dreams are rarely a faithful replication of any one memory, fragments of various recent experiences intermingle with other memories (usually related remote and semantic memories) to create a novel dream. Given all this, one might guess that dreams are created by those regions of the brain responsible for memory. However, studies dating back to the 1960s have suggested that patients with a damaged hippocampus still dream (Torda, 1969a; Torda, 1969b; Solms, 2014) and, somewhat amazingly, such patients can have dreams involving recent experiences of which they have no conscious memory (Stickgold et al., 2000)!
But are the dreams of patients with damage to hippocampus truly ‘normal’? Or alternatively, might such damage, while not preventing dreams, alter the form in which they are expressed? Indeed, there is reason to think that the hippocampus supports crucial aspects of dream construction beyond the simple insertion of memories. Recent work in the cognitive neurosciences has established that the hippocampus, in addition to being involved in the formation of memories, is also part of a brain system that is involved in using memory to construct novel imagined scenarios and simulate possible future events (Hassabis et al., 2007; Hassabis and Maguire, 2009; Schacter and Addis, 2007). As a result, patients without a hippocampus find it difficult to imagine scenes that are coherent, possibly because the hippocampus is responsible for combining different elements of memory into a spatially coherent whole.
Now, in eLife, Eleanor Maguire of University College London (UCL) and colleagues – including Goffredina Spanò as first author – report that the dreams of four amnesia patients lacking a hippocampal memory system do not have the richness of detail found in most dreams (Spanò et al., 2020). Besides reporting substantially fewer dreams than the patients in a control group, the four patients with amnesia also reported dreams that were markedly less detailed: their dreams contained fewer details of spatial location (e.g., descriptions like ‘behind the bar’ or ‘to my left I can see’) and fewer sensory details. These observations support the emerging view that dreams are generated by networks in the brain similar to the networks that are involved in recalling memories and constructing imagined scenarios during wakefulness (Fox et al., 2013; Graveline and Wamsley, 2015). Like memory and imagination, a vivid dream requires the construction of detailed, memory-based imagined scenes – and this process appears to rely on the hippocampus.
These observations partially echo the reports of Clara Torda from more than a half century ago, who characterized the dreams of amnesia patients as ‘shorter’, ‘simpler’, ‘repetitious’ and ‘stereotyped’ (Torda, 1969a). But Torda’s papers were written before the invention of noninvasive methods for imaging the brain, so it is not completely clear which structures may have been damaged in her patients. In contrast, the patients in the work of Spanò et al. all have well-characterized lesion sites with damage restricted solely to the hippocampus. This allows us to confidently attribute their impoverished dreams to the loss of the hippocampus itself, rather than to other regions of nearby temporal lobe which might also have a role in dreaming.
As with many studies of rare neurological patients, the latest work must be interpreted with caution due to the small sample size. For example, patient dreams were not significantly shorter than control dreams, leading to an apparently selective deficit in specific types of details reported (such as spatial details and sensory details), rather than a general deficit in the length of the dream. On average, however, the control dreams contained more than twice the number of informative words as the patient dreams, and the lack of a statistical difference between the two groups may be a mere artifact of the low sample size.
Nonetheless, these observations and a handful of similar studies are helping us to understand how the hippocampus contributes to the dreaming process. The work of Spanò et al. – who are based at UCL, the Royal Free Hospital in London, University Hospital Bonn and the universities of Arizona and Oxford – suggests hippocampal damage disrupts dreaming in ways that mirror how it also disrupts imagination. This suggests that, rather than being an entirely distinct phenomenon, dreaming is a part of a continuum of spontaneous, constructive thought and imagery continuously generated across the sleep and waking states.
References
-
Dreaming and episodic memory: a functional dissociation?Journal of Cognitive Neuroscience 15:1–9.https://doi.org/10.1162/089892903321107774
-
Dreaming as mind wandering: evidence from functional neuroimaging and first-person content reportsFrontiers in Human Neuroscience 7:412.https://doi.org/10.3389/fnhum.2013.00412
-
Dreaming and waking cognitionTranslational Issues in Psychological Science 1:97–105.https://doi.org/10.1037/tps0000018
-
The construction system of the brainPhilosophical Transactions of the Royal Society B: Biological Sciences 364:1263–1271.https://doi.org/10.1098/rstb.2008.0296
-
The cognitive neuroscience of constructive memory: remembering the past and imagining the futurePhilosophical Transactions of the Royal Society B: Biological Sciences 362:773–786.https://doi.org/10.1098/rstb.2007.2087
-
Dreams of subjects with bilateral hippocampal lesionsActa Psychiatrica Scandinavica 45:277–288.https://doi.org/10.1111/j.1600-0447.1969.tb07128.x
Article and author information
Author details
Publication history
Copyright
© 2020, Wamsley
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 49,838
- views
-
- 813
- downloads
-
- 3
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Memory: How the brain constructs dreams
eLife 9:e58874.
https://doi.org/10.7554/eLife.58874
Further reading
-
- Neuroscience
Systems consolidation theories propose two mechanisms that enable the behavioral integration of related memories: coordinated reactivation between hippocampus and cortex, and the emergence of cortical traces that reflect overlap across memories. However, there is limited empirical evidence that links these mechanisms to the emergence of behavioral integration over time. In two experiments, participants implicitly encoded sequences of objects with overlapping structure. Assessment of behavioral integration showed that response times during a recognition task reflected behavioral priming between objects that never occurred together in time but belonged to overlapping sequences. This priming was consolidation-dependent and only emerged for sequences learned 24 hr prior to the test. Critically, behavioral integration was related to changes in neural pattern similarity in the medial prefrontal cortex and increases in post-learning rest connectivity between the posterior hippocampus and lateral occipital cortex. These findings suggest that memories with a shared predictive structure become behaviorally integrated through a consolidation-related restructuring of the learned sequences, providing insight into the relationship between different consolidation mechanisms that support behavioral integration.
-
- Neuroscience
Astrocytes derive from different lineages and play a critical role in neuropathic pain after spinal cord injury (SCI). Whether selectively eliminating these main origins of astrocytes in lumbar enlargement could attenuate SCI-induced neuropathic pain remains unclear. Through transgenic mice injected with an adeno-associated virus vector and diphtheria toxin, astrocytes in lumbar enlargement were lineage traced, targeted, and selectively eliminated. Pain-related behaviors were measured with an electronic von Frey apparatus and a cold/hot plate after SCI. RNA sequencing, bioinformatics analysis, molecular experiment, and immunohistochemistry were used to explore the potential mechanisms after astrocyte elimination. Lineage tracing revealed that the resident astrocytes but not ependymal cells were the main origins of astrocytes-induced neuropathic pain. SCI-induced mice to obtain significant pain symptoms and astrocyte activation in lumbar enlargement. Selective resident astrocyte elimination in lumbar enlargement could attenuate neuropathic pain and activate microglia. Interestingly, the type I interferons (IFNs) signal was significantly activated after astrocytes elimination, and the most activated Gene Ontology terms and pathways were associated with the type I IFNs signal which was mainly activated in microglia and further verified in vitro and in vivo. Furthermore, different concentrations of interferon and Stimulator of interferon genes (STING) agonist could activate the type I IFNs signal in microglia. These results elucidate that selectively eliminating resident astrocytes attenuated neuropathic pain associated with type I IFNs signal activation in microglia. Targeting type I IFNs signals is proven to be an effective strategy for neuropathic pain treatment after SCI.
