Skin sensitivity to touch is defined by the feeling of pain or discomfort caused by a normally harmless stimulus, such as a light touch or the pressure of clothing. This heightened reaction involves a complex interplay between peripheral nerves and the central nervous system. The sensation of touch is interpreted differently due to changes in the biological machinery responsible for processing signals. Understanding this hyper-responsiveness requires examining how the normal sensory pathway becomes altered.
How the Body Registers Normal Touch
The sensation of normal, non-painful touch begins with specialized nerve endings in the skin called low-threshold mechanoreceptors (LTMRs). These sensory cells respond only to gentle mechanical stimuli like pressure, vibration, or stretch, not to harmful input. Different types of LTMRs exist, such as Meissner’s corpuscles, which detect light touch, and Pacinian corpuscles, which sense deeper pressure.
When these receptors are stimulated, they generate an electrical signal that travels rapidly along large, myelinated peripheral nerve fibers toward the spinal cord. The signal enters the central nervous system, is relayed through a series of neurons, and crosses over to the opposite side of the body. It then ascends to the thalamus and is finally projected to the somatosensory cortex for conscious perception.
Localized Causes of Over-Reactivity
One mechanism contributing to heightened skin sensitivity is peripheral sensitization, involving changes at the site of the nerve endings in the skin. This local over-reactivity is typically triggered by tissue damage, inflammation, or infection, such as a severe sunburn, an outbreak of eczema, or a local nerve injury. When tissue is damaged, non-neuronal cells like immune cells release potent signaling chemicals, including inflammatory mediators like prostaglandins and cytokines.
These chemicals bind to receptors on the peripheral nerve fibers, causing a change that significantly lowers the nerve’s activation threshold. Nerves that once needed a strong stimulus to fire are now hyper-excitable, firing with even a gentle input. This chemical environment allows a light brush that was previously ignored to trigger a strong, potentially painful, signal to the spinal cord.
Central Nervous System Signal Amplification
If peripheral sensitization continues, it can lead to central sensitization, a more complex phenomenon involving neuroplastic changes in the spinal cord and brain. In this state, the central nervous system becomes persistently hyper-responsive to all incoming sensory information. This involves increased excitability and enhanced synaptic transmission of neurons in the dorsal horn of the spinal cord, essentially amplifying all signals.
One manifestation of this change is “wind-up,” where repeated, low-level stimulation causes a progressive buildup in the response of spinal cord neurons, leading to an amplified signal. These central changes can cause a non-painful stimulus, like air movement or the weight of a sheet, to be interpreted as pain, a condition known as allodynia. Central sensitization can also result in hyperalgesia, which is an exaggerated pain response to a truly painful stimulus. The process is maintained by excitatory neurotransmitters, such as glutamate and Substance P, which enhance communication between nerve cells.
Real-World Examples of Tactile Hypersensitivity
Tactile hypersensitivity is a defining feature of several chronic pain conditions, driven by varying degrees of peripheral and central changes. Fibromyalgia, for example, is dominated by central sensitization, where the brain and spinal cord misinterpret normal sensory input as pain. Patients often experience widespread pain and allodynia, reflecting the nervous system’s generalized hypersensitivity.
A condition like Post-Herpetic Neuralgia, which is chronic pain following a shingles infection, begins with significant peripheral nerve damage. This initial damage leads to a cascade that often results in prominent allodynia due to the subsequent development of central sensitization in the spinal cord. Similarly, painful diabetic neuropathy, caused by nerve damage from high blood sugar, starts peripherally. However, long-term changes in the central nervous system often contribute to the persistent, burning, and hypersensitive pain. These examples demonstrate how a damaged or overstimulated nervous system can transform the simple sensation of touch into a painful experience.