The Science of How We Get Motivated

What Moves You?

Smiling woman working out with friends in crossfit gym
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The words motion, motivation, and emotion all contain the same word root. When we think about motivation, we may ask about emotion with the words "what moves you?" All of this hints at a neurological fact- many of the regions that are associated with drive and motivation physically connect our emotions with action.

The Anterior Cingulate Cortex

A previously vivacious and engaged political organizer suffered a hemorrhagic stroke from an aneurysm in her anterior communicating artery.*

After the stroke, she was awake and alert, but barely responsive to anything around her. Her family's voices and even physical discomfort seemed to mean nothing to her. She wouldn't eat unless food was placed in her mouth, and she wouldn't speak except in single syllables. The doctors diagnosed her with akinetic mutism, an extremely severe lack of motivation.

A CT scan suggested that the blood from the aneurysm had pushed into her anterior cingulate cortex (ACC), a region at the very back of what is considered the frontal lobes, in the middle of the brain about as far back as her temples. The anterior cingulate cortex is part of the limbic system, the network of brain structures that demonstrate and elicit emotion.

The bottom part of the ACC is connected with the amygdalae, critical regions for emotion, as well as the prefrontal cortex, which is involved with emotional regulation. It is also connected with the hypothalamus and the brainstem, through which the ACC influences our heart rate, blood pressure, and other autonomic aspects of emotion.

The top part of the ACC is connected to the frontal lobes, which help us guide attention and make plans. The ACC also directly connects to premotor cortex, which stimulates the first parts of coordinated movement. In combination, the top and bottom parts of the ACC make it ideally situated to integrate emotional information and channel it towards action.

Disorders of the Anterior Cingulate Cortex

Unfortunately, the ACC can be damaged by medical disorders such as tumors, hemorrhage, strokes and more. When this happens, an important connection between emotion and action is severed, and we lose our emotional drive. This results in apathy, also called abulia, in which people don't feel a need to respond to practically anything in their environment, including things that would normally have been very important to them, like family, friends, or sometimes even physical pain. The most severe form is akinetic mutism, in which a person is so demotivated they do not even move or speak.

The Dopaminergic Reward Pathway

In addition to lack of motivation, there are also occasions when we are motivated inappropriately. Addiction is one of the best examples in which we are motivated to behave in ways that we know are contrary to our interests.

James Olds and Peter Milner from McGill University demonstrated that stimulation of the mesolimbic reward center at the bottom and front of the brain acted as a reward in rats.

Electrodes were placed in the brains of rats so that the animal could stimulate itself by pressing a lever. Animals would use this lever sometimes over a thousand times in an hour. The same circuits were later demonstrated in monkeys by other researchers.

The ventral tegmental area, also known as the mesolimbic reward center projects to many different structures involved with emotion and drive, including the anterior cingulate cortex and the amygdala. It also projects to the prefrontal cortex, which allows us to judge and weigh the potential for reward associated with an event of object in our environment.

One of the most important structures in the ventral tegmental area is the nucleus accumbens. The nucleus accumbens consists of two regions: the core and the shell. Lesions of the core abolish some behavioral responses to conditioned stimuli, and so appears to be related to movement associated with emotional significance. The core appears to amplify conditioned behavior-for example if amphetamine is infused into the core, the animal is more likely to work towards a goal that has been associated with reward in the past. The shell seems more related to new objects and events.

Disorders of the Dopaminergic Reward Pathway

Neurochemically, the reward pathway depends on the neurotransmitter dopamine. Drug addiction has been tightly associated with increased dopamine transmission in this system. Similarly, some drugs intended to increase levels of dopamine in the brain, such as drugs intended to treat symptoms of Parkinson's disease, can also impact this system, leading to addictive behaviors such as pathological gambling.

If someone who abuses cocaine or amphetamine stops using the drug, they can suffer from a depletion in dopamine in the mesolimbic reward system, which leads to feelings of apathy and depression during withdrawal. This effect can actually also be helpful to some doctors treating agitated or violent patients-giving medications such as Haldol diminishes levels of dopamine, leading to reduction in the patient's drive and thereby calming them down. Serotonin stimulants can have a similar though less dramatic effect, and may avoid some of the side effects of antipsychotics.


Regions of the brain are highly interconnected, which can make it difficult to determine exactly why someone has a symptom like apathy. While I've discussed two major areas associated with drive, other regions like the anterior insula can also be involved.

Disorders of motivation are not necessarily permanent. The brain is very adaptable, and other systems can partially compensate for damage to a particular region. The woman who suffered a hemorrhage into her anterior cingulate cortex did improve with time as the body reabsorbed the blood, though she continued to suffer symptoms of decreased motivation reminiscent of depression.

It's important to recognize that while we are our brains, this also means we are adaptable and are able to overcome damage that would otherwise limit our desire to act.

*Personal details have been changed to protect confidentiality.


Barris R, Schuman H (1953): Bilateral anterior cingulate gyrus lesions; syndrome of the anterior cingulate gyri. Neurology. 3:44-52.

Nielsen J, Jacobs L (1951): Bilateral lesions of the anterior cingulate gyri; report of case. Bulletin of the Los Angeles Neurological Society. 16:231-234.

Sollberger, M., Rankin, K. P., & Miller, B. L. (2010). Social cognition. Continuum Lifelong Learning Neurol, 16(4), 69-85.

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