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History (nerve compression)
See also: history of nerve decompression

The treatment of each peripheral nerve entrapment has its own history, making any single narrative incomplete.

Theories on the causes of neuropathic pain have been closely intertwined with surgical research in a feedback loop. Theories of neuropathic pain would inform surgical experimentation, and surgical experimentation would lead to observations or discoveries from which new or modified theories would be developed. By the early 20th century the concept of mononeuropathies due to nerve lesions would be discussed (often called nerve palsy, neuropathy, or neuritis), however causes were still debated. One especially poorly understood form of neuropathy was a delayed onset nerve palsy, called tardy nerve palsy. While some cases of tardy nerve palsy could be ascribed to obvious causes such a structural lesion (e.g. broken wrist) or tumors, many cases of tardy nerve palsy had no clear cause and so were deemed idiopathic (also called spontaneous compression). Various surgical observations led to the theory that the median nerve could be compressed spontaneously under the transverse ligament of the wrist, an area that would later be known as the carpal tunnel in carpal tunnel syndrome. This theory was supported by surgical observations and successfully treated case studies. The development of carpal tunnel syndrome was of particular interest for other idiopathic tardy nerve palsies. Carpal tunnel served as a model for how nerves could be squeezed by narrow anatomic compartments and soon other tunnel syndromes were conceptualized, such as cubital tunnel syndrome, and tarsal tunnel syndrome.

While the concept of a tunnel causing a slow-onset, chronic, low-grade nerve injury due to pressure was now understood, the pathophysiology of nerve compression was unclear. It would not be until the 1970s and 1980s where this would be more fully understood. While the nerves of the limbs (legs and arms), head, and subcutaneous nerves (nerves near the skin) were generally accessible with open surgery, the nerves of the pelvis were much more difficult to reach and subsequent advancements required new surgical technology. With more difficult surgical access, there were fewer surgical discoveries, and theories were slower to develop. The development of endoscopic surgery in the late 20th century greatly expanded the potential to access pelvic nerves. The sacral pelxus, sciatic nerve, and pudendal nerve where now much more surgically accessible. Surgical exploration again led to new discoveries: the existence of fibrous bands as a major cause of sciatic nerve entrapment. The findings from sciatic nerve explorations eventually gave birth to deep gluteal syndrome. The ability to surgically access and treat pelvic nerves gave birth to a new medical specialty called neuropelveology.

1916 - tardy nerve palsy described in ulnar nerve

1932 - spinal disc herniation described

1949 - compression at the thoracic outlet described

1947 - piriformis syndrome described

1950 - carpal tunnel syndrome described

1958 - cubital tunnel syndrome described

1962 - tarsal tunnel syndrome described

1962 - mechanism of trigeminal neuralgia described

1970s/1980s - studies on the pathophysiology of nerve compression

1987 - pudendal neuralgia described

1988 - hypothesis that majority of diabetic peripheral neuropathy symptoms due to multiple nerve entrapments.

2008 - Nantes criteria developed for pudendal neuralgia

2015 - deep gluteal syndrome described; neuropelveology described (a discipline dedicated just to the pelvic nerves)

History (nerve decompression)
See also: history of nerve compression

The treatment of each peripheral nerve entrapment has its own history, making any single narrative incomplete.

The symptoms of nerve injury in the early 1900s were called nerve palsy (today neuropathy is a more common term). The concept of injuries causing nerve palsy was understood at that time. For example, wrist fractures were known to be a cause of nerve palsy through compression, and this could be treated by liberating the nerve. It was freeing the nerve after post-traumatic injuries that early nerve decompressions occurred. However, non-traumatic causes of nerve palsy were less clear, in some cases having no known explanation (idiopathic). It was the development of carpal tunnel syndrome that became the foundation of nerve compression at anatomic areas of narrowing. This expanded the indications for nerve decompression both to idiopathic neuropathies as well as many parts of the body that exhibited anatomic areas of narrowing in the vicinity of a nerve.

Nerve decompressions have benefitted from advances in technology and peripheral nerve surgery. For example, use of the operating microscope (surgery that uses this microscope is now known as microsurgery) was important to the development of the Jannetta procedure for trigeminal neuralgia. Endoscopic surgery was an important advancement, as this allowed greatly expanded surgical access compared to open surgery. In particular, endoscopic surgery gave much better access to the pudendal nerve as well as the sciatic nerve, and allowed the possibility of decompressing the sacral plexus. The use of image-guided diagnostic nerve blocks provided better capabilities to identify the entrapped nerve as well as the site of entrapment, leading to more accurate diagnosis and reducing the need for surgical exploration. The use of magnetic resonance neurography (MRN) and diffusion tensor imaging (DTI) have allowed better visualization of nerves, at times identifying the site of entrapment without the need for extensive surgical exploration. Robot-assisted surgery is still in the early stages, not yet achieving widespread use for nerve decompressions, however it can provide dexterity, precision, and stability not possible by hand which is important given the delicate nature of peripheral nerve surgery.

1878: first ulnar nerve decompression. However, it did not gain much traction at the time.

1933: first published carpal tunnel surgery for post-traumatic compression

1946: first carpal tunnel surgery for idiopathic compression

1958: cubital tunnel surgery described

1962: tarsal tunnel surgery described

1967: Janetta procedure for trigeminal neuralgia

1989: endoscopic carpal tunnel surgery

1992: Magnetic resonance neurography described. First clinical study on nerve decompressions to relieve symptoms of diabetic peripheral neruopathy.

1994: Diffusion tensor imaging described

1997 endoscopic pudendal nerve decompression

2000: correlation found between brow lifts and migraine reduction. This is the precursor to modern migraine surgery.

2003: arthroscopic piriformis muscle release

2005: Magnetic resonance neurography and image-guided injections used in a clinical research study to improve nerve decompression outcomes

2010: endoscopic sciatic nerve decompression

2015: sacral plexus decompression; robotic pudendal nerve decompression

Causes (nerve compression syndrome)
Abnormal biomechanics can be associated with nerve compression. Ischiofemoral impingement (where the femur and ischium come too close together) can squeeze the sciatic nerve. Hip-spine syndrome is another example. Hip-spine syndrome is the co-existence of hip and spine pathologies, and this relationship is thought to be biomechanic (hip movement disorders changes spine biomechanics, or vice versa). Some hip pathologies cause nerve compression, such as ischiofemoral impingement. Some spine pathologies cause nerve compression, such as a herniated disc. The nature of this chain of causality is a biomechanical.

hip-spine syndrome: the co-existence of hip and spine disorders as a common observation.

Some hip range of motion abnormalities cause sciatic nerve compression (e.g. ischiofemoral impingement)

Some spine pathologies cause nerve root compression (disc herniation, Spondylolisthesis, bone spur)

Direct link is not proven though, kind of circumstantial right now.

Controversy
Surgical treatment for nerve compression has caused controversy across various medical specialties. The controversy is not for nerve decompression as a whole but rather for the use of nerve decompressions for specific syndromes (e.g. piriformis syndrome, or pudendal neuralgia, or migraines, etc.)

Critics
Critics generally believe the results of specific nerve decompression surgeries are attributable to either the placebo effect (patient expectations influencing outcomes) or natural history (patients getting better on their own). Critics sometimes reject the validity of nerve decompression surgery because the thesis of nerve compression conflicts with preexisting theories about how certain diseases work. In diabetic peripheral neuropathy (treatable in some cases with multiple nerve decompressions ) and migraines (migraine surgery is a nerve decompression ), critics dispute the interpretation of the results because the majority of studies are of retrospective case series (reports of surgeries performed in the past) rather than prospective randomized controlled trials (RCTs), and so any positive results of surgery could be influenced by methodological flaws such as lack of proper control groups. Critics may believe that given the lack of RCTs on nerve decompression surgery, and the known risk of surgical complications (however small), nerve decompression should not be recommended.

Proponents
Proponents have alleged that the success of treating previously untreatable patients validates decompression as a treatment. That RCTs in surgical research have ethical issues, as a proper control group would receive a placebo surgery and be exposed to surgical complications. That prospective RCTs should not be the only way to reason about whether a therapy is effective given the challenges in using RCTs to study surgery (a suggested alternative is to compare surgery to the best existing treatments). That potential bias in existing studies doesn't account for the large, reproducible effects of nerve decompression, so the results should not be discounted just because the studies aren't RCTs. That the improvement from surgery is clearly much larger than the studied magnitude of the placebo effect, and so cannot be explained by it. That suggesting surgery is placebo is a double standard when these same treatment-resistant patients never seem to benefit from the placebo effect of failed non-surgical treatments and even prior failed surgical treatments. Proponents have noted that nerve compressions are seen in many other nerves, and that we should expect to see some number of patients with entrapments of any given peripheral nerve. Proponents have asserted that some critics have gone beyond healthy skepticism, exaggerated proponents' claims, argued against positions the proponents did not make, levied non-constructive criticism, and misinterpreted the placebo effect in ways not supported by peer-reviewed research.

Controversy
Nerve compression syndromes and their surgical treatment has caused controversy across various medical specialties.

In some cases, critics have disputed whether specific pain syndromes (which are now considered nerve compression syndromes) are real clinical entities, especially if the diagnosis and pathophysiology are not well understood. Even when there is agreement that a syndrome exists, there are disputes over the validity of diagnostic criteria as many nerve compression syndromes are partially a diagnosis of exclusion. There has been skepticism over whether these syndromes can be said to really be nerve entrapment, as the diagnosis may be clinical which doesn't necessarily prove nerve compression.

Proponents have alleged that the success of treating previously untreatable patients with therapies designed to relieve nerve compression validates the etiology of nerve entrapment. Proponents have noted that nerve compressions are seen in many other nerves, and that we should expect to see some number of patients with entrapments of any given peripheral nerve. Proponents have asserted that some critics have gone beyond healthy skepticism, exaggerated proponents' claims, argued against positions the proponents did not make, levied non-constructive criticism, and misinterpreted the placebo effect in ways not supported by peer-reviewed research.

Difficulty finding diagnosis and treatment
historically this was an impossible problem and so nobody really tried; neurologists don't diagnose and treat nerve entrapment; requires a sophisticated understanding of neuroanatomy and diagnostic tools most don't have; patients see many specialists to fine one that can help; they often have undertreated chronic pain. Result is patients have to go through many doctors, and their pain syndromes undertreated.

Surgery (neuropathic pain)
If neuropathic pain is caused by nerve compression, this may be treatable with a nerve decompression. When nerves are subject to chronic pressure, they exhibit a pathological progression resulting in reversible and partially reversible nerve injuries that cause pain, paresthesias, and potentially muscle weakness. In a nerve decompression, a surgeon explores the entrapment site and removes tissue around the nerve to relieve pressure. In many cases the potential for nerve recovery (full or partial) after decompression is excellent, as chronic nerve compression is associated with low-grade nerve injury (Sunderland classification I-III) rather than high-grade nerve injury (Sunderland classification IV-V). Nerve decompressions are associated with a significant reduction in pain, in some cases the complete elimination of pain.

For patients with diabetic peripehral neruopathy (which affects 30% of diabetes patients ) and superimposed nerve compression, this may be treatable with multiple nerve decompressions. The theory behind this procedure is that diabetic peripheral neuropathy (DPN) predisposes peripheral nerves to compression at anatomic sites of narrowing, and that the majority of peripheral DPN symptoms may actually be attributable to nerve compression rather than DPN itself. The surgery is associated with lower pain scores, higher two-point discrimination (a measure of sensory improvement), lower rate of ulcerations, fewer falls (in the case of lower extremity decompression), and fewer amputations.

Surgery (diabetes)
Diabetic peripheral neuropathy (DPN) affects 30% of all diabetes patients. When DPN is superimposed with nerve compression, DPN may be treatable with multiple nerve decompressions. The theory is that DPN predisposes peripheral nerves to compression at anatomical sites of narrowing, and that the majority of DPN symptoms are actually attributable to nerve compression, a treatable condition, rather than DPN itself. The surgery is associated with lower pain scores, higher two-point discrimination (a measure of sensory improvement), lower rate of ulcerations, fewer falls (in the case of lower extremity decompression), and fewer amputations.

Surgery (peripheral neuropathy)
Peripheral neuropathy due to nerve compression is treatable with a nerve decompression. When a nerve is subject to localized pressure or stretching, the vascular supply is interrupted leading to a cascade of physiological changes that causes nerve injury. In a nerve decompression, a surgeon explores the entrapment site and removes tissue around the nerve to relieve pressure. Common sites of entrapment are spaces of anatomic narrowing such as osteofibrous tunnels (e.g. carpal tunnel in carpal tunnel syndrome). In many cases the potential for nerve recovery (full or partial) after decompression is excellent, as chronic nerve compression is associated with low-grade nerve injury (Sunderland classification I-III) rather than high-grade nerve injury (Sunderland classification IV-V). Nerve decompressions are associated with a significant reduction in pain, in some cases the complete elimination of pain. The outcomes tend to vary by the nerve decompressed, the severity/duration of symptoms, and surgical technique.

references:

Nerve entrapment due to nerve swelling
As nerves well in diabetic neuropathy patients, nerves become predisposed to entrapment at osseofibrous tunnels. As the cross-sectional volume of the contents increases in the tunnel, so does the pressure. Studies on nerve entrapment have shown that the microvascular system of nerves becomes compromised at 30mm Hg. Sustained increases of pressure disrupting the microvascular supply of nerves creates a cascade of physiological changes associated with nerve entrapment that results in progressive levels of nerve damage.

sources:

Surgery
Diabetic peripheral neuropathy (DPN) with superimposed nerve compression may be treatable in the limbs with multiple nerve decompressions. The theory behind this procedure is that DPN predisposes patients to nerve compression at anatomic areas of narrowing, and that a majority of symptoms of DPN are actually attributable to nerve entrapment, a treatable condition. The surgery is associated with lower pain scores, higher two-point discrimination (a measure of sensory improvement), lower rate of ulcerations, fewer falls (in the case of lower extremity decompression), and fewer amputations. Multiple nerve decompression is unusual in that it can reverse some symptoms (e.g. lower pain and increased sensation), while also providing protection against serious foot complications (e.g. ulcers and amputations).

sources:

"Decompression surgery represents a paradigm shift in treatment protocols because it both relieves pain and restores protective sensation, while providing significant protection against a cascade of serious foot complications"

"It is concluded that a positive Tinel sign is a reliable indicator of successful outcome from decompression of the tibial nerve in patients with diabetes with symptomatic neuropathy, and in patients with symptomatic idiopathic neuropathy."

"For more than 30 years, peripheral nerve decompression in patients with DPN has been explored as one of the promising treatment options, and multiple studies have shown encouraging results"

"Surgical decompression may help relieve pain in select cases"

"Based on the “double crush” hypothesis,21,22 they have proposed that diabetic neuropathy may be due, in part, to compression of the nerves at sites of anatomic narrowing and that surgical decompression of these nerves may be an effective way to alleviate the neuropathic somatosensory symptoms and prevent complications."