¿Por qué los niños con hiperactividad toman anfetaminas?

Why do children with hyperactivity take amphetamines?

Mike Munay

I recently saw an Instagram reel of a comedian doing a monologue about doctors.

He laughed at the idea that doctors prescribe amphetamines to hyperactive children. That if a child can't sit still anymore, the medical solution is to give them a stimulant drug.

And of course, the joke was obvious: "What is this, adding fuel to the fire?"

I laughed. Because the joke was well done and the comedian had wit.

But when I stopped laughing, I realized that many people must have the exact same question.

And it's not a silly question. For decades, even within medicine, this mechanism wasn't well understood.

If amphetamines are stimulant drugs, if they increase alertness, energy, and brain activity, how is it possible that they are used to treat hyperactivity? In adults? In children?

Intuition tells us that this should worsen the problem, not improve it. That something doesn't add up. That there's a textbook medical contradiction.

Behind what seems like nonsense lies a solid, coherent explanation deeply rooted in neuroscience. This explanation involves dopamine, brain circuits, attention regulation, and the fact that hyperactivity isn't exactly what it appears to be.

So no, it's not medical madness or a bad joke. It's science.

What do we really mean by hyperactivity

When we talk about hyperactivity, we often imagine someone who moves around a lot, who can't sit still, who seems to have too much energy. But from a clinical and neurobiological point of view, that definition is deeply misleading.

Hyperactivity is not an excess of energy, but a problem of regulation. It involves regulating attention, impulses, mental focus, and behavior. It's not that the brain works too fast, but rather that it struggles to maintain control over where it allocates its resources.

That's why many people with ADHD (attention deficit hyperactivity disorder) aren't hyperactive all the time, or in every situation. They can spend hours focused on something that stimulates them, and yet be unable to sustain their attention on simple or unmotivating tasks. The problem isn't ability, it's self-regulation.

This is the predominant mechanism in many cases, but it does not explain all the variability of ADHD.

Hyperactivity results from an alteration in the brain circuits responsible for self-regulation, particularly in the prefrontal cortex. In these circuits, there is insufficient dopaminergic and noradrenergic signaling, which reduces the brain's ability to maintain attention, inhibit impulses, and prioritize relevant stimuli. As a consequence, the nervous system enters a state of functional instability: the brain constantly shifts focus and seeks external stimuli to compensate for this lack of internal activation.

Hyperactivity is not an excess of energy, but the visible result of a control system that is functioning below its optimal threshold.

The brain and the self-regulation of attention

To understand hyperactivity, we must move beyond visible behavior and look at the brain. Specifically, at the networks responsible for deciding what deserves attention and what doesn't, what drives an action and what inhibits it.

This is where the prefrontal cortex comes into play, a key region for:

  • Plan
  • Inhibit impulses
  • Maintain attention
  • Regulating behavior according to context

When these circuits are functioning properly, the brain can choose relatively easily what to do and what to ignore. When they malfunction, the brain jumps from stimulus to stimulus, not because it wants to, but because it cannot stabilize its focus.

Hyperactivity begins to be understood here: as a difficulty in maintaining executive control, not as excessive movement.

The role of dopamine (and the great misunderstanding)

At this point, a very famous and much misunderstood word appears: dopamine.

For years, dopamine has been simplified as the pleasure hormone. That idea is convenient, but false. Dopamine is not pleasure. It's a signal. A signal of relevance, of motivation, of "this matters, pay attention to it."

In the brain of someone with ADHD, certain key areas, especially those involved in control and attention circuits, show reduced dopaminergic activity. It's not that there's a lack of dopamine throughout the brain, but rather that it doesn't reach its intended destinations effectively.

Although dopamine is central, ADHD involves the interaction of multiple systems (dopamine, norepinephrine, and frontostriatal networks), which explains its enormous clinical variability.

The result is a brain that has difficulty with:

  • Maintaining attention on unstimulating tasks
  • Feeling sustained motivation
  • Regulate impulses

And here an important consequence appears: when basal dopamine is low, the brain constantly seeks stimuli to compensate.

The reward circuit and hyperactivity as a strategy

The reward circuit is not a pleasure system, but a learning and motivation system. It tells the brain what deserves effort, attention, and repetition.

When this circuit functions suboptimally, the brain enters a very specific mode: a constant search for stimulation. Movement, interruptions, changes of focus, impulsivity. Not as a moral failing, but as an unconscious strategy.

In this context, hyperactivity begins to be seen differently: not as a primary symptom, but as an adaptive response, but not adaptive in the sense of beneficial, but as an imperfect compensatory response to a deficient regulatory system.

The brain moves more, changes more, searches more… because it needs to raise its activation level to function even minimally well. Hyperactivity isn't the original problem: it's the attempt to compensate for it.

What are amphetamines really (beyond the stigma)

The word “amphetamine” carries a heavy cultural weight. It’s associated with abuse, recreational drugs, and excessive stimulation. But in pharmacology, things are less emotional and more precise.

At therapeutic doses and in medical contexts, amphetamines:

  • They increase the availability of dopamine and norepinephrine.
  • They improve signage in key care circuits
  • They do not indiscriminately accelerate the brain.

Like any drug that acts on the brain, its use requires rigorous diagnosis, adjusted doses, and medical monitoring.

They don't make someone more nervous by default. They modulate specific circuits that were functioning below their optimal level.

Calling them simply stimulants is technically correct, but clinically incomplete.

At a chemical level, amphetamine is a small, lipophilic molecule structurally similar to endogenous catecholamines, especially dopamine and norepinephrine. This similarity is not accidental: it is precisely what allows it to interact with the same neuronal systems.

Once in the body, amphetamine easily crosses the blood-brain barrier and acts primarily on dopaminergic and noradrenergic neurons. It doesn't "activate everything," but rather interferes quite specifically with how these neurons manage their neurotransmitters.

Dopaminergic neurons are those that produce and release dopamine. They are especially involved in motivation, sustained attention, and the ability to decide which stimuli deserve focus and effort.

Noradrenergic neurons, on the other hand, regulate alertness, vigilance, and the ability to respond adaptively to the environment. They do not generate hyperactivity themselves; rather, they adjust the overall "volume" of the nervous system.

The main mechanism of action of dopamine includes three key effects:

  • It enters the neuron through the dopamine (DAT) and noradrenaline (NET) transporters.
  • It displaces dopamine stored in synaptic vesicles into the cytosol
  • It partially reverses the function of the transporters, favoring the release of dopamine and noradrenaline into the synaptic space.

The result is a controlled increase of these neurotransmitters precisely in the circuits where they were functioning below their optimal level.

This distinction is important: amphetamine does not "create" new dopamine nor does it indiscriminately stimulate all areas of the brain. It redistributes and amplifies a signal that already existed, but which was insufficient to sustain attention, motivation, and executive control.

At the level of neural networks, this translates into an improved signal-to-noise ratio: less interference, fewer chaotic jumps between stimuli, and a greater capacity to maintain a stable focus. It's not a speedy brain. It's a better-synchronized brain.

Therefore, in a brain without regulatory deficits, high doses or non-medical uses can produce overstimulation. But in a brain with ADHD, where these circuits start from a hypoactive base, the effect is exactly the opposite: functional normalization.

The difference isn't in the molecule. It's in the neurobiological context in which it acts.

The key point: why a stimulant can reduce hyperactivity

This is where the mental click happens.

If hyperactivity were simply an excess of energy, a stimulant would worsen it. But it isn't. It's a consequence of a functional deficit in regulatory circuits.

When a drug like amphetamine:

  • It increases dopamine where it is lacking.
  • Improves signal in the prefrontal cortex
  • It stabilizes the reward circuit.

…the brain no longer needs to compensate.

  • The constant search for stimulation decreases
  • Impulsivity is reduced
  • Attention becomes more stable

Not because the brain is "more doped up", but because it finally has the neurochemical resources it needed to self-regulate.

Hyperactivity doesn't increase. It disappears because it's no longer needed.

This does not mean that all restlessness is ADHD or that every restless child should be medicated.

The final key idea

Stimulant treatment for ADHD is not a medical contradiction. It is the logical result of understanding that:

  • The problem is not over-activation
  • The problem is a lack of regulation
  • And dopamine plays a central role in that regulation

What from the outside seems like adding fuel to the fire, from the inside is like turning off an engine that was running erratically.

This does not imply that all restless behavior should be treated with medication, nor does it make stimulants a universal tool for improvement. It is merely a technical explanation of the specific case in which hyperactivity is treated with amphetamine.

It's not magic, paradox, or contradiction. It's neuroscience, properly understood.

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