Perineural Injection Therapy

Perineural Injection Therapy (PIT) targets the neurogenic component of chronic pain by directly treating sensitized peripheral nerves. Peripheral nerves can become chronically sensitized and inflamed, and when they do, they actively sustain and amplify pain long after the original tissue injury has healed. This pain remains often without any visible findings on X-ray or MRI.

When peripheral nerves are injured, compressed or entrapped, or persistently stressed, they trigger neurogenic inflammation. These inflamed and sensitized nerve fibers begin releasing signals, neuropeptides such as Calcitonin Gene-Related Peptide (CGRP) and Substance P, into the surrounding tissue. These chemicals cause local inflammation, sensitize nearby pain receptors, and drive a self-sustaining cycle: the nerve releases inflammatory signals, those signals worsen the nerve's environment, and the nerve responds by releasing more.

Conventional pain management (anti-inflammatory medications, corticosteroids, acetaminophen) are often inadequate at addressing this form of pain, and most orthopedic treatments rarely address this issue since these changes can't be seen on imaging modalities like X-rays and MRI's. Patients who present with fibromyalgia-like widespread pain, allodynia, diffuse tenderness, or pain that doesn't map neatly to a structural diagnosis often have substantial peripheral nerve sensitization as a primary driver.

PIT interrupts this chronic cycle of neurogenic inflammation and nerve entrapment by delivering a low-concentration dextrose solution (5% dextrose) subcutaneously along the course of sensitized nerve pathways. Not only is there a biological effect on the nerves treated, but a physical decompression of the nerve is often part of the treatment as well, sometimes referred to as a nerve hydrodissection. A perineural injection treatment can sometimes have an immediate effect on pain, and involves essentially no downtime post-treatment either.

When peripheral nerves become entrapped or compressed, they release inflammatory compounds and create a self-sustaining cycle of pain and sensitization. By delivering dextrose directly to the nerve environment and mechanically decompressing it, PIT restores normal metabolic function and interrupts the cycle.

Perineural injection therapy targets the root cause of nerve pain that rarely responds to other treatments. When nerves travel from deep origins to superficial destinations, they pass through layers of muscle, fascia, and connective tissue. Sometimes, they pass through small fibro-osseous tunnels between bone and a thin layer of dense connective tissue. During repetitive motions, chronically sustained abnormal or atypical postures, or periods of local injury and inflammation, these nerves can become entrapped and compressed, causing a local nerve injury called neuropraxia.

When injured, these nerves release inflammatory neuropeptides CGRP and Substance P, causing local inflammation, sensitizing nearby pain receptors, and depriving the nerve of adequate nutrition — the nerve essentially becomes starved. Evidence suggests that peripheral nerve fibers deprived of adequate glucose become hyperexcitable and pro-inflammatory.

By delivering dextrose directly to the subcutaneous nerve environment and simultaneously mechanically decompressing the nerve, normal metabolic function is restored and the cycle of chronic inflammation is interrupted. The TRPV1 (transient receptor potential vanilloid 1) receptor is a key driver of neurogenic inflammation and pain amplification. Research suggests dextrose may competitively block this receptor, reducing the sensitized nerve's inflammatory output and its capacity to sustain the pain cycle.