Do you remember the last time you were laughing and simply could not stop? Perhaps it was a situation when you should not have been laughing at all.
This happened to one of us while accompanying a friend to a family court in the middle of an unpleasant divorce case. It led to a rapid dash to the bathroom while desperately trying (and failing) to regain control – not quite the kind of emotional support this friend was looking for!
Another classic example is the cricket commentators Brian Johnston and Jonathan Agnew who laughed so much as they described the day’s play in 1991 that they could not talk at all. But how and why does this happen?
In fact, although we typically associate laughter with amusement, most of it occurs for other, social reasons. For example, you are 30 times more likely to laugh if you are with someone else than if you are on your own. And you’ll laugh more if you know your companion and like them.
Most laughter occurs during conversations, when people may laugh through contagion – catching the laughter from someone else. Studies show that when we see or hear someone laughing, this can trigger laughter in us almost automatically, promoting social bonding.
We often laugh to demonstrate agreement and understanding, and to cement friendship – for example, over shared recollections. We also laugh to reduce stress.
These common conversational laughs happen roughly six times per ten minutes of conversation, on average. They’re short, lower in pitch, and tend to start and stop quickly.
These types of laughter, which we refer to as voluntary, are different from the helpless laughter that incapacitates us, and which we cannot prevent from happening. Helpless or involuntary laughs are longer and higher pitched, involving strange squeaks and whistles.
In our latest research, we have investigated whether these two different kinds of laughter might have their roots in entirely different brain systems.
Things get difficult
When attempting to understand the brain networks that underlie the production of laughter, things can get difficult quickly.
For a start, people move a lot when they laugh. This can cause problems for brain imaging techniques such as fMRI (functional magnetic resonance imaging). It can also be extremely difficult to get people to laugh naturally under laboratory conditions.
Another issue is that different regions of the brain all appear connected to laughter. One of us (Fausto) collaborates with the epilepsy surgery unit at Niguarda Hospital in Milan, where patients with drug-resistant epilepsy undergo electrical brain stimulation for clinical purposes. Electrical stimulation is highly precise and not affected by movement.
Normally, if you stimulate the motor system, the patient will move. If you stimulate the visual system, they may experience hallucinations. And if you stimulate the auditory system, they will hear sounds. But there are five or six areas of the brain where stimulation triggers loud laughter in the patient. So, why is this?
We recently reviewed all brain stimulation studies of people laughing, and how they felt when they laughed. These studies provide evidence that the areas of the brain where stimulation evokes laughter form two different laughter networks.
In one, encompassing the anterior cingulate cortex, the temporal pole and some subcortical regions, stimulation led to laughter accompanied by pleasant sensations and happy feelings – this is the more helpless, high-pitched laughter. When there was stimulation to the other network, which is in the brain’s motor and premotor regions, laughter led to speech impairments and was not associated with any emotional state.
Evolutionary differences
The areas constituting the first, more joyous laughter network mapped on to a network for vocalising that humans share with all other mammals. This is potentially also responsible for other spontaneous emotional vocalisations such as crying out.
Activation of this network during spontaneous laughter triggers a neurochemical cascade that taps into, among other things, the opioid system. This helps to explain the sense of pleasure and reward that comes from this joyous, uncontrollable laughter. The serotonin system that regulates our sensitivity to pain is also affected, which may explain why this laughter can temporarily dull physical pain.
From an evolutionary perspective, this network is older. It originates in the spontaneous emotional responses and rough-and-tumble play systems of animals, and is therefore largely unchanged between humans and other animals.
The other, voluntary laughs mapped on to a brain network linked to voluntary movements in humans, such as speaking aloud. These have a primary role in strategic communication and social negotiation, so may explain the particular use of laughter in conversation as a sort of spoken punctuation.
This neural system is found mainly in humans, and is associated with complex vocal acts such as speaking, singing and beatboxing.
A 2022 study looking at the shapes our vocal tracts make when we laugh in this conversational way found they resemble the shapes we make when we speak. In contrast, the shapes of our vocal tract when we laugh helplessly look very unlike speech, and their motor control is simpler, consistent with their ancient origins.
This research shows that voluntary laughter requires more complex and refined motor control than spontaneous laughter, occupying a middle ground between spontaneous laughter and spoken language – not only functionally but anatomically as well.
If a person has a stroke that damages this voluntary network, they can develop severe problems with speech while still being able to laugh, cry and swear. We would argue that this is because the older network remains intact.
The science of laughter may seem like a rather frivolous subject – and neuroscientists have certainly devoted more effort to studying negative emotions such as fear, anxiety, anger and disgust.
However, research on human laughter is turning out to be something of a Rosetta Stone for understanding a surprising range of phenomena – including the origins of the social brain in mammals, the mechanisms of bonding and empathy, pain modulation, language in conversation, and emotional contagion.
The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.