Why It Feels Like Your Pain Is “All in Your Head”: Understanding Central Sensitization

If you’ve lived with chronic pain long enough, have had enough failed treatments, seen enough unremarkable imaging results, and have experienced enough chamges to your pain, you've probably asked yourself this very question. "Is this all in my head?"

That question doesn’t arise because you’re weak, suggestible, or imagining symptoms. It arises because chronic pain follows a different set of biological rules than acute pain, and those rules are rarely explained.

There is, however, a very real physiological reason chronic pain can feel this way. It’s called central sensitization—sometimes referred to as pain centralization—and it represents a shift in how the nervous system processes danger.

How Normal Pain Processing Works

To understand central sensitization, we first have to understand normal pain processing.

Under typical circumstances, pain begins in the periphery. Specialized sensory receptors called nociceptors detect potentially damaging stimuli. Pressure, temperature, and chemical irritation stimulate them which causes the nerves to fire from the source all the way to your spinal cord and up to your brain. It is here that the nerve impulse is interpreted as pain.

Here’s an important detail that’s rarely discussed: nerves do not fire in gradients. A nerve either fires or it doesn’t. When it fires, it fires at full intensity. Pain is not determined by how hard the nerve fires—it’s determined by how much of that signal is allowed through the spinal cord to the brain.

That filtering process happens largely in the spinal cord.

Descending Inhibition: The Nervous System’s Volume Control

Inside the spinal cord are networks of inhibitory interneurons. These neurons act as gatekeepers, regulating how much incoming sensory information is permitted to reach the brain. As pain signals ascend your spinal cord, these inhibitory interneurons descend to halt some of those signals. Not all of them, but a calculated amount.

This process is known as descending inhibition.

Your brain continuously evaluates context and threat: Is this dangerous? Is this familiar? Is this life-threatening or inconsequential?

That evaluation determines how much inhibition is applied.

This is why bumping your elbow and stubbing your toe feel dramatically different, even though the nerve fibers involved fire with the same electrical intensity. Your brain perceives one as trivial and the other as potentially destabilizing. The “volume” is turned up or down accordingly.

Pain, in other words, is a judgment, not a direct measurement of tissue damage.

When the System Starts Getting It Wrong

In chronic pain, the problem is not that the nervous system is broken. It’s that it has learned the wrong lesson.

Central sensitization is the process by which your central nervous system (brain and spinal cord) gradually take over pain generation, independent of ongoing tissue damage. Instead of responding to real-time danger signals from the body, the central nervous system begins predicting pain based on memory, expectation, and perceived threat.

At this point, pain no longer requires a nociceptor to be activated. The spinal cord itself becomes the source of the signal.

This is why chronic pain can feel like it’s coming from “nowhere.” It’s also why people often describe it as confusing, unpredictable, or disconnected from activity or injury.

It is no wonder your pain feels like it is "all in your head!"

Pain as Learned Protection

A helpful way to understand central sensitization is to compare it to muscle memory.

You don’t consciously think about how to walk, type, or drive. Those patterns live in the spinal cord and brainstem, allowing the brain to conserve energy. Chronic pain uses the same learning pathways.

If a particular movement, posture, or situation once caused pain—especially severe or repeated pain—the nervous system stores that association. The next time you approach that movement, pain may appear before any tissue stress occurs.

This is not imagination. It is anticipatory protection.

The nervous system’s job is not accuracy. It’s survival. And survival favors false alarms over missed threats.

Why Chronic Pain Feels So Real—and So Personal

One of the most distressing aspects of central sensitization is how intimate it feels. Pain appears without warning. It fluctuates with stress, sleep, illness, or emotional load. It doesn’t obey structural logic.

That leads many people to assume the pain must be psychological.

But in reality, real physiological changes are occuring in your brain and spinal cord on a physical and biochemical level. Central sensitization is ----------

The Physical Changes Inside a Sensitized Nervous System

There are three prominent, physical changes that occur with central sensitization.

1. With persistent pain signaling, gene expression begins to shift. The body produces more pain receptors and fewer opioid receptors, making the system more sensitive and less capable of self-modulation.

2. In your brain, the sensory homunculus changes shape. Your sensory homunculus is a

brain map of your body proportional to the concentration of sensory receptors in your body. Areas associated with chronic pain become disproportionately large, drawing more attention and neural resources. Pain quite literally occupies more “space” in the brain.

3. Meanwhile, structures such as the dorsal root ganglia, where peripheral nerves join the spinal cord, become hyperexcitable. Signals that would once have been filtered out now pass through easily.

The brakes weaken. The accelerator sticks.

The Biochemical Side Most People Never Suspect

Central sensitization is also driven by changes in neurotransmitter balance.

Descending inhibition depends heavily on serotonin, norepinephrine, and dopamine. When these neurotransmitters are low—as they often are in chronic stress, poor sleep, inflammation, or long-term pain—the inhibitory system loses strength.

At the same time, excitatory neurotransmitters like glutamate increase, further amplifying incoming signals.

This creates a system that is chemically biased toward pain, regardless of structural findings. Importantly, these biochemical changes are not mood disorders masquerading as pain. They are shared regulatory pathways that influence both emotional tone and pain sensitivity.

Emotional Drivers Without Psychological Blame

Emotional factors play a role in central sensitization, but not in the way patients are often led to believe.

Experiences such as adverse childhood events (ACEs), trauma, chronic anxiety, catastrophizing thoughts, or prolonged stress alter autonomic tone, cortisol rhythms, immune signaling, and neurotransmitter availability. The nervous system interprets these states as ongoing threat.

Pain increases not because someone is “too emotional,” but because the body is biochemically primed for defense.

This is why addressing emotional regulation through appropriate mind-body therapies is not dismissive—it’s neurologically relevant.

Why Imaging No Longer Explains the Pain

Central sensitization is not detectable on even the most advanced imaging. It can only be diagnosed through a thorough history and physical exam. But the problem doesn't stop here.

Once pain is centrally generated, the relationship between tissue damage and pain intensity breaks down. Studies across all chronic pain conditions show that there is no correlation between pain intensity and tissue damage. You can have significant degeneration with little pain, or severe pain with minimal findings. This phenomenon is surely the greatest reason why people start to question themselves and wonder if their pain truly is "all in their head."

So… Is the Pain in Your Head?

No!

But it is being generated closer to the brain than you were ever told to look.

Your pain is not imagined. It is not exaggerated. It is not a character flaw. It is the result of a nervous system that has learned—through experience, chemistry, and adaptation—to stay on guard.

Central sensitization explains why conventional treatments often fail, why medications lose effectiveness, and why isolated structural fixes don’t resolve a system-level problem.

Chronic pain is very real and certainly not all in your head.

Written By:

Dr. Jason Winkelmann

Chronic Pain Specialist and Educator

Frequently Asked Questions

If my pain is coming from my nervous system, does that mean it’s psychological?

No. Central sensitization involves real, measurable changes in the brain and spinal cord, including altered gene expression, neurotransmitter balance, and nerve excitability. While emotional states can influence these systems, the pain itself is generated through physiological and biochemical processes—not imagination or psychological weakness.

Why does my pain feel unpredictable or disconnected from injury or activity?

In central sensitization, the nervous system shifts from reacting to real-time tissue damage to predicting danger based on past experiences. This means pain can appear without a clear trigger, fluctuate with stress or sleep, and persist long after tissues have healed. The pain feels inconsistent because it is being driven by learned neural patterns rather than current injury.

Why don’t imaging tests explain my chronic pain?

Once pain becomes centrally generated, the relationship between tissue damage and pain intensity breaks down. Imaging can identify structural changes, but it cannot detect altered pain processing in the spinal cord or brain. This is why many people experience severe pain despite “normal” scans—or minimal pain despite significant degeneration.

Can a sensitized nervous system be retrained?

Yes. While central sensitization develops through learning and adaptation, those same neural pathways are capable of change. Effective treatment focuses on restoring inhibitory control, improving biochemical balance, reducing perceived threat, and gradually retraining the nervous system’s response to stimuli rather than simply blocking pain signals.