Knee pain is commonly understood as a mechanical problem involving joint structures like cartilage, ligaments, or tendons. However, a significant subset of knee discomfort originates from the nervous system, a condition known as neuropathic pain. This type of pain occurs when a nerve is damaged, irritated, or compressed, causing it to send abnormal pain signals to the brain. Nerve damage can cause pain in or around the knee, requiring specialized diagnostic and therapeutic approaches.
Nerves That Transmit Knee Pain Signals
The knee joint and surrounding skin receive sensation from peripheral nerves branching off larger nerves originating in the lumbar spine. These sensory branches are collectively known as the genicular nerves, which transmit pain signals from the joint capsule. Damage to these nerve endings can result in chronic pain that mimics or coexists with joint issues.
The major nerves contributing to knee sensation are the femoral, sciatic, and obturator nerves, which give off branches near the knee. The saphenous nerve, a large sensory branch of the femoral nerve, travels down the inner thigh and is a frequent source of neuropathic knee pain, particularly its infrapatellar branch. The common peroneal nerve, a division of the sciatic nerve, is vulnerable to injury as it wraps around the head of the fibula. Irritation or injury along the course of these nerves registers as pain localized to the knee area.
Causes of Nerve Damage Leading to Knee Pain
Nerve damage leading to knee pain arises from direct physical trauma, systemic diseases, or surgical interventions. Iatrogenic injury, meaning damage caused by medical treatment, is a recognized cause, particularly following total knee arthroplasty (TKA). The surgical incision during TKA frequently severs the infrapatellar branch of the saphenous nerve, leading to numbness or chronic pain at the surgical site. This severed nerve end can sometimes form a painful, localized growth known as a neuroma, which continues to fire pain signals.
Entrapment or compression is another common source of nerve-related knee pain. The common peroneal nerve is susceptible to entrapment as it runs superficially around the fibular head, often compressed by tight casts, prolonged squatting, or habitual leg crossing. The saphenous nerve can also become compressed as it passes through the adductor canal in the inner thigh, resulting in medial knee and thigh pain.
Systemic conditions represent a third major cause, with diabetes mellitus being the most prevalent example leading to diabetic neuropathy. High blood sugar levels impair nerve function, causing a peripheral neuropathy that often begins in the feet and progresses into the lower leg and knee area. This neuropathy typically manifests as bilateral symptoms, including spontaneous pain, tingling, and burning sensations in the lower extremities.
Identifying Nerve-Related Knee Pain
Differentiating neuropathic pain from typical mechanical joint pain is crucial for accurate diagnosis. Mechanical pain is often described as a dull ache, stiffness, or grinding sensation that worsens with movement and improves with rest. Nerve-related discomfort is typically characterized by distinct sensory qualities, often described as burning, shooting, stabbing, or electrical shock-like pain. Patients may also experience allodynia (pain caused by light touch) or hyperalgesia (an exaggerated response to a mildly painful stimulus).
The diagnostic process relies on a detailed physical examination and specialized testing. Clinicians test sensation and reflexes and look for a Tinel’s sign, a tingling sensation elicited by tapping over the irritated nerve. To objectively assess nerve function, electrodiagnostic testing is employed, including Nerve Conduction Studies (NCS) and Electromyography (EMG). NCS measures the speed and strength of electrical signals, while EMG evaluates the electrical activity of the muscles the nerve supplies, helping to pinpoint the damage location.
Targeted Treatments for Neuropathic Knee Pain
Treating nerve-related knee pain requires strategies that target the nervous system, rather than joint inflammation or structural damage. Pharmacological interventions rely on medications originally developed for other conditions that calm overactive nerves. First-line treatments include anti-seizure medications, such as gabapentin and pregabalin, and certain antidepressants like tricyclic antidepressants or serotonin-norepinephrine reuptake inhibitors. These agents modulate the chemical signals that transmit pain impulses, reducing the spontaneous firing of damaged nerves.
Interventional procedures offer targeted relief, especially for localized pain unresponsive to medication. A genicular nerve block, involving an injection of a local anesthetic near the sensory nerves, can be used both diagnostically and therapeutically. If a diagnostic block temporarily alleviates the pain, radiofrequency ablation (RFA) may be considered. RFA uses heat energy to temporarily interrupt the ability of these small sensory nerves to transmit pain signals to the brain.
Physical therapy also plays a role through techniques designed to restore normal nerve movement and reduce sensitivity. Nerve gliding, or nerve flossing, involves specific movement patterns that gently mobilize the affected nerve, such as the femoral or sciatic nerve. This gentle movement helps the nerve slide freely within surrounding tissues, reducing adhesions and desensitizing the nerve to movement and pressure.