The concept of neuropathic pain is based on a hypothesis that was first proposed in the 18th century. At that time, the Italian physician and physicist Cotugno (1736-1822), who was still following the Hippocratic humoral medicine, suspected that nerves, like the spinal cord and brain, were surrounded by a fluid. At the same time, the Italian physician and anatomist Luigi Galvani discovered by chance that the dissected thigh muscles of a frog could contract by static electricity. Also by accident, he discovered that immersing an arm in an electrically charged liquid caused a burning, shooting sensation. Galvani and later Volt were convinced that a liquid with its laws could not only store electricity but also spontaneously generate it when stimulated. Thus radiating, burning, shooting, electrical pain was explained as a reaction to a spontaneously generated electrical impulse which continued in the course of the nerve through the surrounding fluid.
In 1828, the English physician Thomas Brown (Brown 1828), who worked at the Royal Infirmary in Glasgow, introduced the term "spinal irritation" based on this hypothesis. An entrapment or irritation of a nerve or nerve root was now regarded as the cause of this electrical impulse. He was thus the first doctor to find the cause of sciatica and back pain in a connection between the spinal column and the spinal nerves radiating from it.
In a 1934 publication by the neurosurgeon Mixter and the orthopaedic surgeon Barr, the damaged intervertebral disc (caused by bone tumours, which were still common at the time) was shown to be a regular cause of back pain, even without neurological symptoms. Radiating pain (sciatica) was now defined as nerve pain with irritation of the nerve roots due to a damaged intervertebral disc. However, it remained difficult to make solid diagnoses of radiating pain and to develop effective treatment plans. The lack of clear (neurological) criteria for surgery caused not only the number of operations to explode, but also the number of people whose operations did not produce the desired result. Around 1970, surgeons (including Waddel) were accused of leaving "more tragic human wrecks than any other operation in history".
Reason for other renowned but critical physicians such as Mayer (1849), von Leyden (1832-1910) and the neurologist Heinrich Romberg (1795-1873) to study the phenomenon of spinal irritation intensively. They came to the conclusion that it was unacceptable from a medical-scientific point of view to consider spinal irritation as a real disease.
The German physiologist Hering (Hering 1884) built on the concept of nerve pain and, based on measurements of the electrical currents of nerve fibres after stimulation, postulated the hypothesis that abnormal conditions could arise at damaged nerve sites, causing not only new impulses but also electrical charges to jump from one fibre to another. He called these impulses abnormal impulse transfers or ephapses. Friedrich Strian (Strian 1996) extended this hypothetical model, similar to the scientifically founded model for synapses, to include crosstalk: the transmission of discharges becomes possible because ephapses can form at the damaged sites where the myelin sheath has been lost. This would allow a transition from sympathetic to sensory fibres or from low-density sensory fibres to high-density nociceptive fibres. However, scientific proof of this hypothesis has never been provided.
In the 1950s, the Swiss neurologist Alois Brügger discovered that not all radiating pain symptoms could be attributed to peripheral nerve stimulation and introduced the term pseudoradicular syndrome. The disappointing results of spinal surgery at that time also led to the suspicion that the view that nerve pain was the result of compression of the nerve roots could not be correct.
Due to the extraordinary technical development of radiological imaging techniques that clearly demonstrate stenosis, disc herniation or disc pathology as the cause of nerve pain and have meanwhile gained a firm (first) place within spinal diagnostics, the image of neuropathic pain in the form of (cervical or lumbar) radicular syndrome has come to the fore again and can enjoy wide acceptance. The (surgical) treatments based on this diagnosis are increasing enormously every year, while the results are disappointing. Obviously, despite the tremendous development of radiological imaging, it is still not possible to make an irrefutable diagnosis of back and radiation pain and to develop effective treatment strategies for it. The theoretical framework of neuropathic pain caused by irritation of the nerves exiting the spine is clearly inadequate for a correct diagnosis.
The International Association for the Study of Pain (IASP 2014), which is primarily concerned with neuropathic or nerve pain, defines it as a hypothetical lesion or dysfunction of the central or peripheral nervous system that results in impairment of the nociceptive nervous system.
A definitive diagnosis can only be made if the pain is due to a detectable lesion or dysfunction of the somatosensory system that is relevant to pain perception. For this purpose, technical devices are used that can "accurately" measure the conduction velocity and thus the function of the nerves via electrodes on the skin. The diagnostic value of these measurements is limited because the conduction velocity of selective fibres cannot be measured.
Similarly, the IASP counts phantom limb pain, pain after brain haemorrhage and in multiple sclerosis, pain due to spinal cord injury, metabolic diseases such as diabetes mellitus, viral diseases such as shingles, alcohol abuse and chemotherapy as neuropathic pain.
Sandkühler (2001) describes chronic pain as a pathological change in central neurological signal processing that influences pain perception (wind-up phenomenon - Long Term Potentization - LTP - Long Term Depression - LTD - classical central sensitisation (pain memory) - neuro-immune - interaction - influencing synaptic stimulus transmission).
More and more researchers are finding an explanation for chronic pain syndromes in neuroinflammatory processes. The lowering of the stimulus threshold leads to an earlier and faster perception of pain signals (peripheral and central sensitisation processes). So a person with chronic pain is actually suffering from a blocked protective mechanism in the brain.
Meacham et al. (2017) attempt to explain chronic neuropathic pain by the presumed existence of an independent pain-producing system in the nervous system. In contrast to nociceptive pain, no electrical impulses are generated during pain stimuli. Thus, no action potential is generated by the stimulation of a sensory organ.
In 2017, the IASP introduced the concept of "nociplastic pain" - pain that results from altered nociception despite the absence of clear evidence of actual or impending tissue damage leading to activation of peripheral nociceptors, or evidence of disease or lesion of the somatosensory system causing the pain", as a third explanatory mechanism for pain alongside the nociceptive and neuropathic concepts. Central and peripheral sensitisation is thought to be an important mechanism. The three pain mechanisms can co-exist, making diagnosis very difficult.