[2] Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness.

The origin of the term is due to the association of the condition with a night spent in alcoholic stupor with the arm draped over a chair or bench.

Mechanical compression of the radial nerve in the spiral groove can also occur as a result of the continuous use of crutches or prolonged kneeling in a "shooting" position.

[14] The so-called "cyclist palsy" is caused by prolonged grip pressures on handlebars, and has been postulated to be an entrapment neuropathy of the ulnar nerve in the Guyon canal of the wrist.

[15] Occupational exposure to forceful handgrip work and vibration, such as construction workers, increased the risk for surgical treatment of radial nerve entrapment.

[16] Posture induced common peroneal nerve (CPN) palsy is usually produced during the prolonged squatting or habitual leg crossing while seated, especially in Asian culture and is manifested by the onset of foot drop.

Alternatively, there may be expansion of the tissues around a nerve in a space where there is little room for this to occur, as is often the case in carpal tunnel syndrome.

This may be due to weight gain or peripheral oedema (especially in pregnancy), or to a specific condition such as acromegaly, hypothyroidism or scleroderma and psoriasis.

There are anatomical regions in which segments of peripheral nerves are vulnerable or predisposed to become trapped and suffer from chronic compression.

[27] In sciatic nerve decompression study, compromising structures were piriformis muscle, fibrovascular bundles, and adhesion with scar tissues.

[28] In another endoscopic neurolysis study, the presence of fibrovascular bands and bursal tissue was the most common cause, followed by musculotendinous structures.

Previously, physicians thought repetitive wrist and hand motions were the only cause of carpal tunnel syndrome, especially in frequent computer users.

[30] Gene variants associated with musculoskeletal growth and extracellular matrix architecture have been implicated in carpal tunnel syndrome.

[5] Specifically, increased pressure on a nerve compresses the neural microvasculature and alters the blood flow dynamics.

[32] Experimental studies suggest a dose response curve such that the greater the duration and amount of pressure, the more significant is neural dysfunction.

[33] Prolonged ischaemia and mechanical compromise may induce downstream effects such as inflammation, demyelination, scarring, and eventually axon degeneration.

Neuroinflammation sensitizes injured and uninjured axons and nociceptors in target tissue, contributing to neuropathic pain initiation and maintenance.

[34] The initial changes are a break-down in the blood nerve barrier, followed by sub-perineurial edema and fibrosis; localized, then diffuse, demyelination occurs, and finally Wallerian degeneration.

[36] As successful blocks require accurate targeting of the nerve, this is done under image guidance such as fluoroscopy, ultrasound,[37] CT,[37] or MRI.

[38] Ultrasound is popular choice because of its soft-tissue contrast, portability, lack of radiation, and low cost, but is not good at depicting deeper structures like the deep pelvic nerves.

[32] There is substantial evidence to support an association between certain work activities and carpal tunnel syndrome that involve repetitive motion.

[54] Certain recreational activities such as bicycling are associated with pudendal neuralgia due to increased pressure on Alcock's canal.

[61][62][63] The effectiveness of botox injections is predicated on muscular entrapment such that atrophying a muscle reduces pressure on a nerve.

The decision to proceed with surgical interventions is a matter of when the severity of subjective symptoms outweighs the potential risks and complications.

It is a common clinical experience, that even chronic entrapments with longstanding muscle weakness and sensory disturbances sometimes show a very rapid reversibility of some or all of the symptoms after surgical decompression of the nerve.

Neuromodulation is symptomatic treatment and does not attempt to address the root cause of compression, but rather to alter the signals sent along the nerves to the brain.

It can be a suitable choice when the source of compression has been removed, but the positive sensory symptoms such as pain aren't fully resolved.

[75] A challenge with these new treatment is that peripheral nerves are highly mobile, and it is difficult to fix a wire (called an electrical lead) or tube to something that's constantly moving, and it may migrate after implantation.

[77] The prevalence is measured by sending screen questionnaires to a large random sample of a population, and giving the positive cases a full clinical and electrophysiological investigation.

[110] Some proponents have noted that failing to mention these syndromes as a real diagnosis is a disservice to the many patients who could benefit from its correct treatment every year.