When we experience a stubbed finger, a hot stove, or the sting of a cut, that is our peripheral nervous system — the vast network of nerves that carries signals between the body and the brain, doing the heavy lifting behind the scenes. But not all nerves are the same. Some deliver fast, sharp signals; others carry slow, lingering sensations. To understand chronic pain—and how therapies like Scrambler Therapy work—we first need to know the different nerve fibers and what they do.

HOW NERVES TRANSMIT SIGNALS

Nerve fibers transmit electrical impulses, called action potentials, from sensory receptors in the skin and organs to the spinal cord and brain. These fibers are categorized by:

• Diameter (larger = faster)

• Myelination (a fatty sheath that speeds transmission)

• Conduction velocity

• Function

The key players:

A-BETA FIBERS: THE GENTLE GIANTS

• Large diameter

• Heavily myelinated

• Very fast (35–90 m/s)

• Function: Light touch, vibration, proprioception

Role: “Good news” nerves; tell your brain when your hand is on something soft or you’re upright. Under normal conditions, they don’t carry pain signals.

A-DELTA FIBERS: THE FIRST ALARM RESPONDERS

• Small diameter

• Lightly myelinated

• Moderate speed (5–35 m/s)

• Function: Sharp, acute pain and temperature (cold)

Role: Alert you quickly to immediate, localized threats (pinprick, sharp objects).

C FIBERS: THE SMOLDERING EMBERS

• Very small diameter

• Unmyelinated

• Slow (0.5–2 m/s);

• Function: Dull, aching, burning pain; warmth;

Role: Carry chronic or slow-onset pain—the deep, throbbing ache after an injury or ongoing neuropathy. Signals arrive late and linger.

WHY THIS MATTERS FOR PAIN?

Chronic pain often involves overactivation or dysfunction of C and A-delta fibers. Understanding their behavior helps us identify how pain becomes chronic—and how we might reverse it.

Key clinical takeaways:

• Neuropathic pain often involves sensitized or damaged C-fibers.;

• Referred pain can involve abnormal cross-talk between different types of fibers.;

• Touch and vibration therapies often target A-beta fibers to modulate pain.;

BEYOND SENSATION: NERVE FIBER PLASTICITY

These fibers don’t just transmit signals—they change over time. With chronic pain:

• C-fibers may become hyperresponsive.;

• A-beta fibers (normally non-painful) may start carrying pain signals through “crossed wiring” at the spinal cord level.;

WHEN PAIN PERSISTS — THE SCIENCE OF CENTRAL SENSITIZATION

Imagine burning your hand on a hot stove. The pain is immediate, sharp, and intense, but with time it heals. But what if, long after the burn has healed, simply touching your skin still caused pain—or worse, the pain spread beyond the original site and intensified over time?

This is what is called central sensitization — a phenomenon where the central nervous system (brain and spinal cord) becomes abnormally sensitive to pain signals. It’s a key player in many chronic pain conditions, and understanding how it works helps us target it with treatments like Scrambler Therapy.

MORE ON CENTRAL SENSITIZATION?

Central sensitization is a state in which the central nervous system (CNS)—particularly the spinal cord and brain—becomes hypersensitive to sensory input.

It occurs when:

• Normal sensory input is perceived as painful (allodynia);

• Painful input is perceived as more intense than it should be (hyperalgesia);

In short, the “volume” on pain is turned up permanently—even in the absence of an injury.

THE BIOLOGY BEHIND IT

Let’s explore how this amplification occurs:

1. Wind-Up in the Spinal Cord

Repeated stimulation of C-fibers leads to persistent activation of dorsal horn neurons in the spinal cord. Over time, this causes:

• Increased release of neurotransmitters like glutamate and substance P

• Increased excitability of spinal neurons;

• Lower thresholds for pain signal transmission;

This is known as “wind-up”—a progressive, activity-dependent increase in pain sensitivity.

2. NMDA Receptor Activation

NMDA (N-methyl-D-aspartate) receptors in the spinal cord are critical for learning and memory—but in chronic pain, they become hijacked.

• Prolonged activation of NMDA receptors makes spinal neurons more responsive to input.;

• Even gentle stimuli (like touch) can trigger strong pain responses.;

This contributes to neuronal plasticity that favors pain persistence.

3. Loss of Inhibition

Normally, inhibitory neurons and neurotransmitters like GABA and glycine help “gate” pain signals at the spinal level. But in central sensitization:

• These inhibitory pathways are diminished or dysfunctional

• The CNS loses its natural “brakes,” allowing pain to run unchecked;

4. Glial Cell Activation and Neuroinflammation

Glia (microglia and astrocytes) release pro-inflammatory cytokines, prostanoids, and chemokines. It creates a feedback loop that sustains and amplifies pain signals.

CLINICAL MANIFESTATIONS

Patients with central sensitization often describe:

• Widespread pain

• Fatigue and poor sleep

• Sensitivity to touch, light, sound, or temperature

• Brain fog or cognitive issues

This is a feature of many chronic pain syndromes, including:

• Fibromyalgia

• Complex regional pain syndrome (CRPS)

• Chronic low back pain

• Post-surgical pain syndromes

• Migraine

• Irritable bowel syndrome

THE BRAIN’S ROLE

It’s not just the spinal cord—the brain gets involved too. A functional MRI shows increased activity in pain-processing areas (insula, anterior cingulate cortex, prefrontal cortex). The brain anticipates pain, reinforcing it through attention, emotion, and memory loops. The entire pain matrix can become hyper-reactive—a concept known as central amplification.

WHY IS THIS SO IMPORTANT?

If pain is driven by central changes, addressing only the peripheral cause (e.g., a bulging disc) may not relieve the pain. Many medications, especially opioids, may not help and can even worsen sensitivity. We need approaches that target the nervous system itself—and neuromodulation, including Scrambler Therapy, is one such approach.