Definition
About 6% of the population reports nerve pain. Nerve pain or expert neuralgia is pain that manifests itself in and is caused by the innervated area of one or more nerves. This distinguishes neuralgia from other types of pain such as back pain.
These can also be caused by muscle cramps, for example. Nerve pain, however, is the direct result of damage to a tissue belonging to the nervous system. This leads to an activation of the pain-recognizing and conductive nerve endings, which can belong to sensory peripheral nerves, but also to the spinal cord and brain.
Cause
Damage to a nerve or a structure belonging to the nervous system can have various causes. Mechanical effects in the form of cuts or pressure, such as a herniated disc, and toxic chemical burns or radiation can damage nerves through external influences. Among the so-called neurotoxins are heavy metals such as lead, cyclic hydrocarbons, alcohol, but also some drugs.
Other causes are inflammatory processes, as in shingles (herpes zoster), or metabolic processes, such as the metabolic disorder diabetes mellitus. Inflammatory processes are usually caused by infections. Varicella (chickenpox pathogens), borrelia and others also attack the peripheral nerves or the nerve cells themselves when infected.
Inflammation can also be caused by autoimmunological processes, i.e. diseases in which the body’s own immune system attacks cells and structures of the body. These diseases, which can also cause nerve pain, include multiple sclerosis and Guillain-Barre syndrome. Disturbances in the metabolism of nerve cells or myelin sheaths can be triggered not only by diabetes mellitus but also by diseases of the intestine and the resulting poorer absorption (malabsorption) of vitamins such as thiamine.
Diseases of the liver or kidneys can also be the cause of metabolic disorders. In addition, the exact nature of the nerve pain is influenced by the pattern of the damage. If the myelin sheath of a nerve is damaged, it becomes “demyelinated” and the nerve loses its protective insulating layer.
Without this layer, electrical signals from sensitive nerves that react to touch can jump to pain-conducting fibers. This pattern can be caused by causative diseases such as multiple sclerosis and viral infectious diseases such as shingles (herpes zoster). Metabolic diseases such as diabetes mellitus can also be responsible for this form of damage.
If not only the protective myelin sheath but the entire nerve fiber is damaged, the flow of information can be completely blocked, a process known as deafferentiation. The blockage causes a lack of information in the central nervous system, so that inhibitory effects controlled by the central nervous system are no longer activated due to the absence of ascending stimuli. These so-called deafferentiation pains occur, for example, after amputations or in paraplegia.
This topic might also be of interest to you: Pinched nerveThe severing of large nerves occurs mainly after amputations, which can lead to deafferentation and/or phantom pain. As already mentioned, deafferentiation pain is caused by the loss of inhibitory A-? fibers, which are sensitive to pressure and touch.
These fibers normally inhibit the transmission of pain impulses in the spinal cord via interneurons. If this inhibition fails, an excessive activity of the no longer inhibited neurons can occur, resulting in pain. The exact cause of phantom pain is not yet sufficiently understood.
It is known that every part of the body is represented at a specific location on the cortex of the brain. One explanation is that when a limb is severed in the cortex, these representations are reorganized. The perceived pain can then arise from a conflict situation between the new and old pattern of the respective representation.
If the expected response of the missing limb to a signal of the representation in the cortex is absent, the signal intensity of the representation is amplified as a compensation mechanism, which can be perceived as pain by the patient.In addition to the nerve pain occurring in the peripheral nervous system, there is also the central pain. Central nerve pain is caused in the CNS, i.e. directly in the brain or spinal cord, by damage to the neurons located there. There is a division into thalamic pain, which is caused by damage to the nerve cells in the thalamus, and pseudothalamic pain, which is caused by damage in other regions of the CNS.
Even more specifically, the tractus spinothalamicus in the spinal cord and the nucleus ventralis posterolateralis of the thalamus can be named as frequent damage sites. These lesions (damage) are often based on causative diseases. In diseases such as multiple sclerosis or syringomyelia, degenerative processes occur, which can lead to the failure of inhibitory structures in the CNS as well as to irritation of the sensitive pathway for pain and temperature. If peripheral nerve pain lasts longer, a kind of learning process can lead to an adaptation of the nerve cells in the CNS. Thus, nerve pain can become centrally chronic even though the actual peripheral cause has long since healed, for example in post-zosteric neuralgia.
