I – INTRODUCTION
The subject of time and, more specifically, keeping it, has become an increasingly large area for neuroscientific research. Knowing how cells follow chronological patterns is crucial to understanding the fundamentals of brain activity and recent interest in research, such as the nobel prize winning breakthroughs in circadian rhythms of 2017 (Huang, 2018), clearly demonstrates this. However, the title is of particular interest as it pertains less to this recent focus on cells’ individual biological clocks, but rather to that of human time perception: the feeling of time passing. For clarity, the phrase ‘sense of time’ is to be defined here as a ‘conscious and subjective experience of rate’, as in how long an event feels to be taking place in comparison to the objective measure of time and in what way might disparities between these occur. Whilst this, and associated phenomena, have been well documented throughout history, there has been much less focus and research funding given to this area. Understanding key mechanisms and brain regions involved in our sense of time would not only glean something rudimentary about human experience but, could also help scientists glimpse common degenerative diseases in a new light. Bradykinesia, referring to a slowness in movement, is a common symptom of parkinsonism, a syndrome found in not only Parkinson’s but Lewy Body Dementia and a host of other common, incurable diseases of the brain (Heldman et al., 2011). Though they may seem unconnected, bradykinesia (along with many other symptoms) and sense of time appear to be inextricably linked; understanding how could be key to future treatment.
From Oliver Sacks’ early experience with catatonic patients in New York, to the recent influential experiments on temporal illusions by David Eagleman’s team, even to the effects of certain narcotics, the record of distortion in human time perception is vast. This essay aims to lay out what neuroscientists know about time perception, what they assume, and where promising research could lead us.
II – OLIVER SACKS
The disparity between one’s feeling of time passing and objective time can be hard to comprehend and the degree to which this can occur, even more so. To understand the personal element of this
Neurologist Oliver Sacks began work at the Beth Abraham Hospital in New York, helping patients who had suffered from the 1920s pandemic of encephalitis lethargica, more commonly known as ‘sleepy sickness’ (Hoffman and Vilensky, 2017). Although his patients had survived the original infection, they were left with an advanced form of parkinsonism, being slow to move and often living in a completely catatonic state for decades. In his final published work, a collection of essays entitled ‘The River of Consciousness’, Sacks recounts some remarkable cases of time distortion in these people. Describing acute sufferers as ‘frozen’, he notes a particular instance where a patient, Miron, sat outside his office completely still in a bizarre tableaux. Upon asking what Miron was doing, the man explained, simply, he was trying to wipe his nose. After trialing a new drug, L-DOPA, which returned sufferers to a normal speed of movement, Sacks noticed in severe cases the drug would push patients to the opposite extreme. Hester, normally frozen, would move much faster than normal rates, being able to play catch with such speed as to shock the doctors. Her speech was accelerated to the limits of human mechanics; asking to her count aloud would result in numbers slurring together as her jaw fought to keep up with her mind. When looking at a Necker cube, an optical illusion where the perspective of the drawing changes every few seconds to a normal person (Kornmeier and Bach, 2005), Hester saw the perspectives swap multiple times a second. These intriguing case studies relate to ‘sense of time’ as neither person felt their movements to be abnormal, instead, when Miron took several minutes to wipe his nose he felt he was moving at a normal speed but the environment was rushing around him. Similarly, Hester did not believe how fast she was moving until watching film footage of herself. These examples show that not only is there a stark difference between one’s experience of time and the objective measure but, further, that one’s experience of time can be manipulated.
In encephalitis lethargica patients, their experience of time was manipulated by a drug, L-DOPA. This drug is an amino acid made naturally in humans and acts as a precursor to the neurotransmitter dopamine (Ncbi.nlm.nih.gov, 2018), with the aim of treatment to increase dopamine levels in sufferers. When dopamine levels drop by 80%, parkinson’s sufferers begin to develop bradykinesia and speech problems but, where these levels plummet in parkinson’s, they are practically untraceable in people with sleepy sickness. Dopamine, whilst not a mechanism in of itself, could be one of the keys to understanding time perception at a chemical degree in the brain.
III – DOPAMINE
Dopamine is a neurotransmitter in the brain and acts as a precursor to the hormone, epinephrine (commonly adrenaline). It is involved in the extrapyramidal system of the brain, a part of the motor cortex responsible for controlling involuntary movements (Ncbi.nlm.nih.gov, 2018). Its role in motion has been clarified with a recent study in 2015 by Panagrahi et al where, by using a mouse model, they showed that animals with progressive depletion of dopamine (PDD) neurons experienced a similarly progressive decrease in movement and ‘vigor’. Re-establishing these dopamine connections in their brains brought with them a return of movement, confirming the importance of dopamine in control of motion.
As well as motion, dopamine (DA) neurons are also involved in the reward system of the brain. DA neurons in the midbrain, an area involved in both movement and reward processing (Queensland Brain Institute, 2018), become activated depending on how expected a reward stimulus is. An insightful study demonstrated that DA neuronal responses were smaller when the reward is more expected (Fiorillo, Newsome and Schultz, 2008). This discovery is important because it suggests that DA neurons not only predict stimuli but, do so in a linear way, that is to indicate dopamine neurons receive temporal information. This was one of the first clues to suggest that dopaminergic interactions in the brain could be involved in judgment of time intervals, however it wasn’t until 2016 that the link between DA neurons and a more complex ‘sense of time’ was made. Knowing DA neurons are activated based on expected times, a group measured and then influenced DA neurons in mice as the animals judged durations of various timed intervals. They found that when they suppressed these neurons, estimation of time sped up, consequently activation of the same neurons resulted in slower estimations. Therefore showing that DA activity directly affects and controls judgment of time.
IV – TEMPORAL ILLUSIONS
Whilst it’s clear that one’s sense of time can be manipulated by specific diseases or drugs, to the normal person how much does perception of time actually change and how easily can it be influenced?