The ability to foresee and shape future events using episodic memory as a source of information that facilitates action planning has been termed “mental time travel” (MTT). Suddendorf & Corballis (S&C) convincingly argue in favour of an adaptive value of such a cognitive capacity compared to fixed or instinctual ways of predicting future scenarios, as in hibernators. It is argued that MTT emerged at some point during human evolution to predict future actions of conspecifics. In other words, MTT probably evolved because selection favoured individuals who had the capacity to flexibly use MTT over others who were less able to create mental models of future events, including social interactions. S&C reason that MTT could be specific to humans, because there is little evidence for MTT in nonhuman animals. However, the authors also emphasise that testing MTT in nonhuman animals is a difficult if not impossible enterprise, partly due to the absence of verbal reports of episodic memory contents in animals.
In light of the central claim of the target article that MTT is human-specific, it is surprising that the authors fail to make use of insights from psychopathology. The possibility that evolutionary psychology and psychopathology can mutually inform each other has been outlined by one of the leading ethologists of the 20th century, Konrad Lorenz – notably in a footnote of his formerly acclaimed, but nowadays largely disregarded, book Behind the Mirror, first published in German in 1973. (Lorenz developed many of his ideas much earlier, during his time as a prisoner of war in the former Soviet Union, recently rediscovered and published as The Russian Manuscript: Lorenz 1992.) Basically, Lorenz, who was a psychiatrist himself, pointed out that analysing failures of any given behaviour might contribute more to the understanding of its physiology than studying the intact physiology itself. Although not explicitly stated, cognitive and emotional correlates of behaviour could be examined in the same way (Lorenz Reference Lorenz1973/1977).
We therefore propose that any attempt to dissect the cognitive architecture of MTT would greatly benefit from a careful consideration of certain psychopathological conditions, where one or more aspect of MTT is arguably affected by malfunctioning.
S&C define the “ingredients” of human MTT using a theatre production as a metaphor. Accordingly, imagination, self-awareness, recursion, metarepresentation, appreciation of the time dimension (including temporal distance, order, and location within time patterns), executive functioning, and prospective memory are considered key components of MTT, with episodic memory lying at the very core. Hence, mental disorders, which are characterised by the dysfunction of one or more of the key components of MTT, may not only help elucidate the neuropsychology, but also the underlying neural networks involved in MTT.
The most devastating disorders with putative deficits in MTT are probably the various forms of dementia. S&C briefly mention amnesia and damage to the frontal lobes as potential causes of disrupted MTT, without going into detail, however, about what exactly the deficits could be at both the neurotransmitter level and brain pathology. In Alzheimer's disease (AD), for example, the loss of episodic and prospective memory is profound, even in preclinical stages (Jones et al. Reference Jones, Livner and Backman2006), and this functional deterioration is associated with a progressive cholinergic deficit commencing in the nucleus basalis of Meynert. It is well known that the entorhinal cortex and the hippocampus suffer a severe loss of function through the accumulation of neuritic plaques and tangles. In contrast, it is only quite recently that researchers have discovered that the so-called spindle cells – an evolutionarily novel cell type unique to apes and humans, located in the anterior cingulate cortex where the integration of cognition, emotion, and motor control takes place – degenerate early in the course of AD (Nimchinsky et al. Reference Nimchinsky, Vogt, Morrison and Hof1995).
Similarly, in full-blown Korsakoff's syndrome – which may develop in conditions associated with a severe deficiency of vitamin B1 (in Western societies, most often chronic alcoholism) – episodic memory deficits may lead to a complete loss of personal history. Even more pronounced than in AD, patients with Korsakoff's syndrome “make up” their personal history, referred to as producing confabulations. These patients are unaware of the incorrectness of their “memories.” A striking feature of this disorder is that patients with Korsakoff's syndrome may invent a totally different story when asked the same question only minutes later. Thus, although the patients' imagination is apparently left intact, they are confined to the present, and this might be one reason for the conspicuousness of Korsakoff's syndrome compared to other forms of dementia (Sacks Reference Sacks1985). The anatomical lesion of Korsakoff's syndrome is primarily located in the corpora mamillaria.
Comparing deficits in episodic memory in AD patients to those in different types of frontotemporal lobe degeneration (FTDL) may help address the issue of the relevance of each specific component of MTT. AD patients typically show a temporally graded memory loss with more remote memories being better preserved than more recent ones, whereas patients with semantic dementia (SD) involving the anterior temporal pole show the reversed gradient. However, patients with a frontal variant of FTD (fv-FTD) do not show any temporal gradient of episodic memory deficits (Piolino et al. Reference Piolino, Desgranges, Belliard, Matuszewski, Lalevee, de la Sayette and Eustache2003). Here, the altered memory retrieval as well as executive dysfunction seem to contribute to deficits in episodic memory, which is in support of the components relevant for MTT.
The behavioural consequences of both AD and Korsakoff's syndrome are that, depending on the severity of the disorder, patients are unable to lead independent lives – partly, because their toolboxes that allow the flexible use of a vocabulary to construct future events and to refer to autobiographical memories in a meaningful personal way are irreversibly destroyed.
Interestingly, another evolutionary cost may result from the hyper-functioning of MTT. Patients with obsessive-compulsive disorder (OCD) suffer from intrusive thoughts to which they often over-ascribe meaning in order to prevent future (negative) events, perhaps as a consequence of the tendency to excessively reflect upon their cognitive processes (Janeck et al. Reference Janeck, Calamari, Riemann and Heffelfinger2003). This often precludes effective future action planning in that patients with OCD are caught in repetitive behaviours to avoid erroneously anticipated threat or danger. Notably, those brain regions involved in future action planning, as well as episodic and prospective memory retrieval, including the ACC, the prefrontal cortex, and the dorsolateral prefrontal cortex, have been found overactive in patients with OCD; and this could arguably be interpreted as an MTT overshoot (Brüne Reference Brüne2006). Here, serotonin and dopamine are probably the key players in the pathology of OCD.
These examples of failures of MTT in mental disorders certainly do not represent an exhaustive list. Schizophrenia, for instance, can be seen as another prime example, where virtually any one of the ingredients of MTT may be disrupted, including metarepresentation or “theory of mind” (Brüne & Brüne-Cohrs Reference Brüne and Brüne-Cohrs2006) and time consciousness (Vogeley & Kupke Reference Vogeley and Kupke2007).
In any event, the purpose of this commentary is to pinpoint the need for more interdisciplinary approaches to the understanding of the evolved psychology of our species, to which the study of psychopathology – particularly of human-specific domains – can contribute a lot more than is currently conceived.