If you grew up with siblings, it is likely that you have heard the phrase, ”Imitation is the sincerest form of flattery.” However, it wasn’t until a groundbreaking finding in the 1990s that the neural correlate to imitation was discovered in a class of neurons called mirror neurons. These neurons were discovered in the macaque monkey but have since been identified and visualized through neuroimaging techniques in humans. Mirror neurons are responsive both when performing a goal-directed action and when seeing another perform the same action. In other words, the same neurons that fire when you throw a baseball also fire when you watch someone throw a baseball!
We know that brain activity generates rhythms, which can be measured through techniques such as EEG (electroencephalography). One of these rhythms, mu rhythm, is a 10 Hz oscillatory pattern generated across activity of the motor cortex. Mu rhythm is generated when a person is at rest, aka not performing a physical activity. However, when an individual performs an action, mu rhythm is suppressed or desynchronized. Sometimes, mu rhythm is even suppressed when a person simply imagines performing an action! This close connection to the activity of mirror neurons has led some to believe that the mirror neuron system could influence the synchronization of mu rhythm.
Since their discovery, mirror neurons have taken the neuroscience world by storm. In less than twenty years, over 1,500 papers have been published studying the phenomenon that is mirror neurons. Why all the popularity? These so-called “imitation neurons” were discovered through their activity when a subject observes an action, but researchers quickly theorized that mirror neurons could play a much larger role in the brain. The existence of these neurons opens the door for studying much more complex types of behavior, cognition, and phenotype including empathy, attention, and even Autism Spectrum Disorder (ASD).
ASD is a phenotypically complex disease, with hallmark characteristics including deficits in language acquisition and social communication. These aspects of ASD have been studied extensively due in part to the theorized role of the mirror neuron network in empathy and social cues. In fact, many of the brain regions associated with empathy and comprehending others’ emotions (anterior cingulated cortex and insula) are functionally connected to brain regions housing a mirror neuron system! However, researchers realized that mirror neuron deregulation was far from the only explanation for behaviors associated with ASD. Alongside the social interaction symptoms of ASD are non-social related symptoms, including repetitive behaviors and restricted interests, neither of which connect to the potential role of the mirror neuron system.
A recent study investigates the link between the mirror neuron system and ASD through a task comparing the reaction times to imitate a simple movement (finger lifting or dot movements) between ASD participants and healthy controls. This task taps into the mirror neuron system, which, if deregulated in ASD participants, should manifest with an increased reaction time in this imitation task.
Interestingly, ASD participant movements did not differ in reaction time from healthy controls in this task, which the authors interpret as evidence arguing against a globally deregulated mirror neuron system in ASD participants. Instead, the researchers found that the deficit in ASD participants was dependent upon the presentation mode during the task. When the task involved seeing a visual stimulus before hearing a tone indicating they should perform an action, ASD individuals had a difficult time discriminating the two (visual vs. tone). It was not until the researchers made the task significantly more challenging that ASD participants displayed a deficit in reaction time. This specificity in the ASD individual deficit challenges the “broken mirror theory,” or the idea of generalized mirror neuron deregulation in ASD participants.
So if these ASD symptoms do not arise from general deregulation of the mirror neuron system, what could be causing it? One possible mechanism is the “underconnectivity theory of autism” model. Using fMRI (functional magnetic resonance imaging), a neuroimaging technique that allows researchers to measure brain activity in a variety of tasks, we can begin to understand what brain regions co-activate or synchronize during a behavioral task. The “underconnectivity theory” postulates that individuals with ASD have lower synchronization between temporal lobes. Think of this like a game of telephone: information has to quickly and accurately migrate from one side of your brain to the other. If there is difficulty in communicating, the message will not be clearly received. In the “underconnectivity theory,” this manifests as lower synchronization. Evidence for a deficit in neural synchronization has arisen from a number of fMRI studies analyzing different tasks including language, executive function, social processing, and working memory.
Both the mirror neuron system and ASD symptoms are complex, multi-layered phenomena that are far from fully understood. While it is generally accepted that ASD does not involve a general dysfunction of the mirror neuron system, where and how mirror neuron deregulation contributes to ASD symptoms remains a widely debated topic. The discovery of these neurons has given us a neurobiological basis for sensations that marvel many of us – empathy, imitation, and social awareness. The next time that someone tells you, “Imitation is the sincerest form of flattery,” maybe it will be a little less annoying and a little more interesting!
Iacoboni, M., Dapretto, M. (2006). The mirror neuron system and the consequences of its dysfunction, Nature Reviews, 7 942 – 951.
Schunke, O., Schottle, D., Vettorazzi, E., Brandt, V., Kahl, U., Baumer, T., Ganos, C., David, N., Peiker, I., Engel, A., Brass, M., Munchau, A. (2016). Mirror me: Imitative responses in adults with autism. Autism, 20(2) 134 – 144.
Just, M., Keller, T., Malave, V., Kana, R., Varma, S. (2012). Autism as a neural systems disorder: A theory of frontal-posterior underconnectivity, Neurosci Biobehav Rev, 36(4) 1292 – 1313.