Paresthesia is the medical term for the sensation of “pins and needles,” or a prickling, burning, or crawling feeling on the skin. While this common sensation often occurs when a limb falls asleep, experiencing it while sick suggests a temporary neurological symptom linked to the body’s fight against infection. The illness itself triggers systemic changes that disrupt normal nerve function.
How Inflammation Affects Nerve Endings
When the body detects an invader, the immune system releases a cascade of chemical signals into the bloodstream. These immune molecules, known as proinflammatory cytokines (including interleukin-6 and tumor necrosis factor-alpha), travel throughout the body. They act not just on immune cells but also on the peripheral nervous system.
The cytokines instruct other cells to produce inflammatory mediators, notably prostaglandins, which cause general sickness symptoms such as fever and body aches. Prostaglandins and cytokines directly sensitize the peripheral nerve endings located beneath the skin. This process lowers the activation threshold of these nerves.
This heightened sensitivity, or hyperalgesia, means that nerves fire signals to the brain in response to otherwise harmless stimuli, such as light touch or a change in air temperature. The brain interprets these exaggerated signals as tingling, burning, or increased pain. Once the infection clears and the immune response subsides, the concentration of these inflammatory chemicals drops, allowing the nerves to return to normal sensitivity.
Systemic Conditions Exacerbated by Illness
Beyond direct chemical irritation, the systemic effects of illness contribute to paresthesia. Fever, vomiting, or diarrhea often cause dehydration and electrolyte imbalance. Severe fluid loss reduces blood volume, which temporarily limits blood flow and oxygen delivery to peripheral nerve cells, causing them to malfunction and send erratic signals.
Electrolytes such as sodium, potassium, and calcium are necessary for the proper transmission of electrical impulses along nerve pathways. When an illness causes a drop or spike in these mineral levels, the nerve signal transmission becomes unstable. This instability can manifest as temporary numbness or tingling.
Another factor is hyperventilation, which occurs during high anxiety, severe pain, or respiratory distress accompanying an illness. Rapid, deep breathing causes a temporary drop in the blood’s carbon dioxide levels, leading to respiratory alkalosis. This change in blood chemistry can cause blood vessels to constrict and decrease the amount of free ionized calcium circulating in the plasma.
The sudden reduction in available calcium increases the excitability of nerve tissue. This metabolic change commonly causes tingling sensations, particularly in the hands, feet, and around the mouth. This specific type of paresthesia resolves soon after normal breathing patterns are restored.
When Tingling Is a Warning Sign
While transient tingling during illness is common, certain characteristics of paresthesia warrant immediate medical attention. Tingling or weakness that is strictly unilateral, meaning it only affects one side of the body, should be taken seriously. This symptom, especially alongside sudden, severe weakness in a limb, difficulty speaking, or facial drooping, may indicate a stroke.
Paresthesia that persists long after the acute illness has resolved is a red flag for potential nerve damage or an underlying neurological condition. Tingling that becomes chronic, constant, or symmetrical in a “glove-and-stocking” distribution in the hands and feet may suggest peripheral neuropathy. This condition involves damage to the peripheral nerves and requires medical evaluation.
A blistering rash appearing in a single stripe or band on one side of the body, preceded by intense tingling or burning, is characteristic of Shingles (herpes zoster). This condition is caused by the reactivation of the varicella-zoster virus, which lies dormant in nerve roots. Prompt antiviral treatment for Shingles is important to minimize the risk of developing long-term nerve pain known as postherpetic neuralgia.