Nerve compression syndrome | |
---|---|
Other names | Entrapment neuropathy |
Radial nerve compression is an example of nerve compression syndrome | |
Specialty | Neurology, neurosurgery, orthopedic surgery, plastic surgery, Gynaecology |
Symptoms | pain, tingling, dull ache, numbness, shooting pain, muscle weakness |
Diagnostic method | clinical exam, diagnostic blocks, imaging, and electrophysiology testing |
Nerve compression syndrome, or compression neuropathy, or nerve entrapment syndrome, is a medical condition caused by chronic, direct pressure on a peripheral nerve. [1] It is known colloquially as a trapped nerve, though this may also refer to nerve root compression (by a herniated disc, for example). Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. The diagnosis is largely clinical and can be confirmed with diagnostic nerve blocks. Occasionally imaging and electrophysiology studies aid in the diagnosis. Timely diagnosis is important as untreated chronic nerve compression may cause permanent damage. A surgical nerve decompression can relieve pressure on the nerve but cannot always reverse the physiological changes that occurred before treatment. Nerve injury by a single episode of physical trauma is in one sense an acute compression neuropathy but is not usually included under this heading, as chronic compression takes a unique pathophysiological course.
nerve | location | usually referred to as |
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supraorbital nerve | supraorbital notch [2] | migraine / frontal headache |
nerve | location | usually referred to as |
---|---|---|
Median | carpal tunnel | carpal tunnel syndrome |
Median (anterior interosseous) | proximal forearm | anterior interosseous syndrome |
Median | pronator teres | pronator teres syndrome |
Median | ligament of Struthers | Ligament of Struthers syndrome |
Ulnar | cubital tunnel | Cubital tunnel syndrome |
Ulnar | Guyon's canal | Guyon's canal syndrome |
Radial | axilla | Radial nerve compression |
Radial | spiral groove | Radial nerve compression |
Radial (Posterior interosseous) | proximal forearm | posterior interosseous nerve entrapment |
Radial (Superficial radial) | distal forearm | Wartenberg's Syndrome |
Suprascapular | Suprascapular canal | suprascapular nerve entrapment |
nerve | location | usually referred to as |
---|---|---|
Common peroneal | fibular neck | peroneal nerve compression |
Tibial | tarsal tunnel | tarsal tunnel syndrome |
Saphenous | Roof of Adductor canal | Saphenous nerve entrapment syndrome |
Lateral cutaneous nerve of thigh | inguinal ligament | meralgia paraesthetica |
Sciatic | piriformis | piriformis syndrome |
Sciatic | gluteal space | deep gluteal syndrome [3] |
Iliohypogastric | lower abdomen | iliohypogastric nerve entrapment |
Obturator | obturator canal | obturator nerve entrapment |
Pudendal | Alcock's canal | pudendal nerve entrapment |
Pudendal | sacrospinous ligament | pudendal nerve entrapment |
anterior intercoastal nerves | lateral rectus abdominis muscle | anterior cutaneous nerve entrapment syndrome (ACNES) |
posterior femoral cutaneous | gluteal space | posterior femoral cutaneous nerve entrapment |
middle cluneal | posterior sacroiliac ligament | middle cluneal nerve entrapment (MCN-E) |
sacral plexus (s1-s4) | pelvis | sacral plexus entrapment or lumbosacral plexus entrapment |
superior cluneal | posterior iliac crest | super cluneal nerve entrapment (SCN-E) |
Symptoms vary depending on whether the affected nerve contains motor and/or sensory fibers. Sensory nerve entrapment presents with paresthesias. These paresthesias may be painful, such as shooting pain, burning, or a dull ache. They may also be pain-free, such as numbness or tingling. Motor nerve entrapment may present with muscle weakness or paralysis for voluntary movements of the innervated muscles. Entrapment of certain pelvic nerves can cause incontinence and/or sexual dysfunction. [4] Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness. Muscle weakness is usually noticed later, and is often associated with muscle atrophy.[ citation needed ]
The distribution of symptoms is highly specific to the nerve entrapped and the way the nerve courses and branches beyond the entrapment point. For a given entrapment neuropathy, symptoms will only present in the areas innervated by that nerve and distal to the entrapment point. The symptom distribution is highly dependent on a patient's neuroanatomy, which may mean that two patients can present differently despite having the same nerve entrapped.[ citation needed ]
The timing/duration of symptoms may be continuous, intermittent, and/or positional. This is dependent on the underlying cause of entrapment and the specific nerves involved. For example, pain while sitting is associated with inferior cluneal nerve entrapment, pudendal nerve entrapment, and anococcyeal nerve entrapment. [5] [6] [7]
Certain occupations, postures, and activities can put prolonged pressure on a nerve. The term "Saturday night palsy" is used for a radial nerve injury caused by prolonged compression of the nerve at the spiral groove. 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. [8] 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. [9] Occupational exposure to forceful handgrip work and vibration, such as construction workers, increased the risk for surgical treatment of radial nerve entrapment. [10] 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. [11] One sport-related cause of lateral femoral cutaneous nerve entrapment is seen in scuba divers where the weight belt worn around the waist directly compresses the nerve. [12] Prolonged periods of cycling can be associated with pudendal nerve entrapment, as there is often direct compression on the pudendal nerve between the nose of the bicycle seat and pubic bone. [13] Tight fitting goggles can put pressure on the supraorbital nerve, also known as "swimmer's headache". [14] Tight fitting handcuffs can compress the superficial branch of the radial nerve, known by several names such as Cheiralgia paresthetica, Wartenberg's syndrome, and handcuff neuropathy. [15] The use of a thick wallet in the rear pocket can compress the sciatic nerve when sitting. [16]
Nerve compression can be secondary to other medical conditions. Entrapment neuropathies are remarkably common in diabetes. [17] A well defined lesion such as a tumor, hypertrophic muscle, cyst, hernia, hematoma, etc. can increase pressure on surrounding soft tissue, including nerves. 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 is increasing research that some forms of nerve entrapment, such as those in the hip/pelvis, can be secondary to abnormalities of the hip/spine leading to abnormal biomechanics. [18] With abnormal biomechanics, even normal postures and activities can put pressure on nerves.[ citation needed ]
Entrapment can be caused by injuries. Surgical injuries can cause entrapment by the development of scar tissue around the nerve as well as the decreased ability of the nerve to glide, increasing strain during movements. Radial nerve entrapment is seen after fracture manipulation when the nerve is unknowingly entrapped between bone and an installed plate, compressed by a bone fragment or if excessive nailing of the bone occurs. [19] Accidents are also associated with nerve entrapment as swelling puts pressure on the nerve and the development of scar tissue nearby may provide a hard surface for the nerve to be squeezed against, such as pudendal neuralgia in cyclists where repetitive trauma creates fibrotic entrapment of the pudendal nerve. [20]
Surgical and anatomic research has shed some light on the proximate causes of entrapment. There are anatomical regions in which segments of peripheral nerves are vulnerable or predisposed to become trapped and suffer from chronic compression. Neural compression occurs especially in osteofibrous tunnels but may also occur at points of passage of the peripheral nerve through the muscles or near a band of fibrous tissue. [21] In sciatic nerve decompression study, compromising structures were piriformis muscle, fibrovascular bundles, and adhesion with scar tissues. [22] In another endoscopic neurolysis study, the presence of fibrovascular bands and bursal tissue was the most common cause, followed by musculotendinous structures. [23]
Genetics may play a role in creating the necessary conditions for entrapment to occur. Previously, physicians thought repetitive wrist and hand motions were the only cause of carpal tunnel syndrome, especially in frequent computer users. But now doctors understand that the syndrome is probably a congenital predisposition in that some individuals have bigger carpal tunnels as compared to others. [24] Gene variants associated with musculoskeletal growth and extracellular matrix architecture have been implicated in carpal tunnel syndrome. [25] A rarer genetic cause is HNPP.
Acute and chronic compression of a nerve in a given area can lead to a cascade of physiological changes resulting in impaired function and then anatomical changes in the later stages. [26] Specifically, increased pressure on a nerve compresses the neural microvasculature and alters the blood flow dynamics. [27] 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. Focal demyelination is a hallmark of entrapment neuropathies, which are often characterized by nerve conduction slowing or block. [28] 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. [29]
Animal models demonstrate that extraneural pressures as low as 20 to 30 mm Hg disrupt intraneural venous circulation. These pressures are often reached in patients with entrapment neuropathies. In several animal models, low magnitude, chronic nerve compression causes a biological response of: endoneurial edema, demyelination, inflammation, distal axon degeneration, extensive fibrosis, new axon growth, remyelination, and thickening of the perineurium and endothelium. Axonal degeneration was correlated with degree of endoneurial edema. [30]
In a few case reports (surgical resection of nerve, autopsy with known disease) the nerve at the site of injury was compared to a site proximal or distal to the injury. In each case, the site of injury demonstrated thickening of the walls of the microvessels in the endoneurium and perineurium along with epineurial and perineurial edema, thickening and fibrosis. Myelin thinning was also noted along with evidence of fiber degeneration and regeneration. [30] Experimental studies suggest a dose response curve such that the greater the duration and amount of pressure, the more significant is neural dysfunction. [29]
Clinical diagnosis can often identify compression neuropathy on signs and symptoms alone. While there are variations in how nerves course and branch, the anatomical territory of major nerves do not change from patient to patient. Some forms of nerve entrapment can have characteristic symptoms, such as sitting and pudendal pain. Pudendal neuralgia, for example, is diagnosed by the Nantes criteria with four out of five criteria being clinical. [31]
Diagnostic nerve blocks are very effective for identifying sensory entrapment points. Their strength is that they can directly measure whether a given nerve is contributing pain, or not. They are precise and reproducible. [32] As successful blocks require accurate targeting of the nerve, this is done under image guidance such as fluoroscopy, ultrasound, [33] CT, [34] or MRI. [35] 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. For deeper structures, CT and MRI are more appropriate, although the equipment is more expensive [36] [37] [38] . [34] [35]
The challenge with diagnostic blocks is that there often not good information to indicate exactly where the entrapment point may be. For example, symptoms may be poorly localized [39] , and the symptoms may be imprecise [40] . Consequently, multiple blocks may need to be performed on different nerves to find the correct one. A successful diagnostic block will lead to immediate and significant resolution of symptoms up to complete pain relief [40] [41] . The duration of the block will last several hours depending on the anesthetic used. [42]
MR and ultrasound can be used for peripheral nerve imaging. [43] Ultrasound is common for superficial nerves of the upper extremity such as carpal tunnel syndrome. [44] MR imaging is not always reliable in that often the clinical assessment and imaging do not match for peripheral neuropathies. [45] That is, there are false positives and false negatives which bring into question how reliable these scans are for diagnosis and surgical planning. There are known limitations of MR for the identification of nerve entrapment:
Despite these limitations, MR imaging studies can rule out certain causes of entrapment such as a mass lesion. Increasingly used are specialized forms of MRI such as MR neurography [46] (MRN) and MR tractography (MRT). Of the two MRT is more effective as it has a high correlation with intraoperative findings. [47]
The main electrophysiological studies are the nerve conduction study (NCS) and electromyography (EMG). The benefit of nerve conduction studies has not been proven beyond distal entrapment neuropathies (carpal tunnel syndrome and cubital tunnel syndrome). [48] An EMG is limited to just providing information on motor nerves, and provides limited information on the location, extent, and etiology of nerve injury. Electrophysiology is not very useful in pelvic sensory neuropathies or for interrogation of the deep pelvic nerves. [46]
The major limitation of extra-operative electrophysiology studies is that they do not have direct access to the nerve. In contrast, intra-operative electrophysiology studies can be done with direct access to the nerve, and this is a useful tool for nerve decompression surgery. During surgery the studies can be used to identify which nerves innervate given myotomes, identify which blood vessels are essential for a nerve, and to compare nerve conduction before and after decompression.[ citation needed ]
When an underlying medical condition is causing the neuropathy, treatment should first be directed at this condition. Several systemic conditions have been implicated in the development of nerve compression syndromes, including diabetes, thyroid disease, heavy alcohol use, generalized edema, and systemic inflammatory disease. [27] There is substantial evidence to support an association between certain work activities and carpal tunnel syndrome that involve repetitive motion. [49] Certain recreational activities such as bicycling are associated with pudendal neuralgia due to increased pressure on Alcock's canal. [50]
Non-surgical treatments includes rest and activity modification, physical therapy, ergonomic modifications, pain management, and steroid blocks. About 50% of the time, symptoms will improve only conservative measures. [51] [52] Opioids can provide short-term pain relief in highly selected patients. [53] Steroid blocks can have a short-term benefit but have not shown to have long-term therapeutic benefit. [54] [55]
In select cases botox injections may also be an effective option, such as piriformis syndrome or migraines. [56] [57] [58] 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. With muscle wasting or electromyographic evidence of denervation, timely surgical decompression is clearly indicated. [27]
Nerve decompressions aim to surgically access and explore some segment of nerve, removing any tissue that may be causing compression. In this way a nerve decompression can directly address the underlying cause of entrapment. A nerve decompression can either be done by open surgery or laparoscopic surgery. In some cases, like carpal tunnel syndrome, either approach is viable. [59] For deeper nerves, a laparoscopic approach is the only choice. New laparoscopic techniques allow surgeons to get access to previously unreachable pelvic structures such as the sacral plexus. [20] Nerve decompressions and resections are the only treatments with a known cure rate. 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. [26]
A large number of nerve decompression surgeries achieve 25+% cure rate, and 75+% success rate. [60] [61] [62] [63] It is not known why separate surgeries would have similar outcomes.
Nerve resections aim to eliminate the dermatome entirely along with any positive sensory symptoms such as pain. While nerve decompression may be used on any nerve, nerve resection should only be used on purely sensory nerves when the loss of sensation is acceptable. The superior cluneal nerves, middle cluneal nerves, posterior femoral cutaneous nerve, lateral femoral cutaneous nerve are all sensory and resection may simply be a more "complete" option, as nerve decompressions can't explore every part of the nerve and may miss some entrapment points. Outcomes for nerve resection is similar to nerve decompression. [64] [65] One disadvantage of nerve resections is that traumatic injury to the nerve is unavoidable, and a neuroma may form at the point of resection. There are surgical approaches to prevent neuroma formation [66] such as targeted muscle reinnervation [67] which have shown very good results, however the risk of neuroma formation is not completely eliminated.
Other surgical treatments include general neuromodulation treatments. 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. If neuromodulation is used without removing the source of compression, tissue injury might progress leading to worse outcomes when the source of compression is eventually removed. Better known neuromodulation treatments include the spinal cord stimulator and the intrathecal catheter. The disadvantage of these treatments is that they are not targeted for peripheral nerves (implantation is typically in the spinal cord), can only address sensory symptoms, can expose unrelated nerves to injury during implantation if placed in the spine, and have a high failure rate due to device migration. The spinal cord stimulator in particular has a very high complication rate, as high as 40%. [68] Advancements have been made to move these devices closer to peripheral nerves such as peripheral nerve stimulation [69] and the peripheral nerve catheter. [70] 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. For example, lead migration is a common long-term complication of both spinal cord stimulators and peripheral nerve stimulators. [68] [71]
The prevalence of nerve entrapment is not known, however a rough bound can be determined by data on lower and upper estimates. A lower bound is the prevalence of the most common entrapment neuropathy, carpal tunnel syndrome (CTS). [72] 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. Studies in Sweden, Egypt, and the US have found the same general prevalence for CTS, of between 3.3% - 3.8%. [73] [74] [75] An upper bound is the prevalence of chronic pain with neuropathic characteristics. Not all neuropathic pain is nerve entrapment, but all nerve entrapment will cause neuropathic symptoms. The most reliable studies have an estimated prevalence of between 6.9% - 10%. [76]
The concept of nerve entrapment has gained acceptance in large part due to surgical research. [77] The successful experimental treatment of previously intractable conditions necessitated an explanation for how these treatments worked. As pain and nerves are poorly understood, nerve decompression outcomes are some of the clearest evidence that neuropathic pain can be causally linked to nerve compression. Consequently our understanding of nerve entrapment is closely linked to advances in surgical research.
1764: Domenico Cotugno describes sciatica as a disease of nervous origin. [78]
1881: Lasegue's sign is described for the diagnosis of sciatica. [79]
1934: Theory that a spinal disc pressing on the spinal cord can cause sciatica is introduced. [80]
1947: Piriformis syndrome is described as a cause of sciatica. [81]
1950: Carpal tunnel syndrome is described as being due to medial nerve compression. [82]
1987: Pudendal nerve compression is described in cyclists. [83]
1990: Study using a nerve decompression to treat Meralgia Paresthetica [84]
1992: Study positing nerve decompressions can treat diabetic polyneuropathy. [85] Magnetic resonance neurography is invented. [86]
1996: Study on microvascular decompression for trigeminal neuralgia [87]
2008: Nantes criteria introduced for clinical diagnosis of pudendal neuralgia. [88]
2011: Study on endoscopic techniques to decompress the sciatic nerve [61]
2014: Study on endoscopic technique to decompress the pudendal nerve [89]
Circa 2015: Diffusion tensor imaging matures as a way to image peripheral nerves. There are literature reviews, and it is considered reliable and reproducible. [90] [91]
2015: Early study on endoscopic lumbosacral plexus decompression outcomes. [60] Deep gluteal syndrome is introduced to describe sciatic nerve entrapment in the gluteal space. [32] [40] Neuropelveology is introduced to apply concepts from nerve entrapment to chronic pelvic pain. [92]
Carpal tunnel syndrome (CTS) is the collection of symptoms and signs associated with nerve compression of the median nerve at the carpal tunnel. Most CTS is related to idiopathic compression of the median nerve as it travels through the wrist at the carpal tunnel. Idiopathic means that there is no other disease process contributing to pressure on the nerve. As with most structural issues, it occurs in both hands, and the strongest risk factor is genetics.
The pudendal nerve is the main nerve of the perineum. It is a mixed nerve and also conveys sympathetic autonomic fibers. It carries sensation from the external genitalia of both sexes and the skin around the anus and perineum, as well as the motor supply to various pelvic muscles, including the male or female external urethral sphincter and the external anal sphincter.
Sciatica is pain going down the leg from the lower back. This pain may go down the back, outside, or front of the leg. Onset is often sudden following activities like heavy lifting, though gradual onset may also occur. The pain is often described as shooting. Typically, symptoms are only on one side of the body. Certain causes, however, may result in pain on both sides. Lower back pain is sometimes present. Weakness or numbness may occur in various parts of the affected leg and foot.
Pudendal nerve entrapment (PNE), also known as Alcock canal syndrome, is an uncommon source of chronic pain in which the pudendal nerve is entrapped or compressed in Alcock's canal. There are several different types of PNE based on the site of entrapment anatomically. Pain is positional and is worsened by sitting. Other symptoms include genital numbness, fecal incontinence and urinary incontinence.
Peripheral neuropathy, often shortened to neuropathy, refers to damage or disease affecting the nerves. Damage to nerves may impair sensation, movement, gland function, and/or organ function depending on which nerves are affected. Neuropathies affecting motor, sensory, or autonomic nerves result in different symptoms. More than one type of nerve may be affected simultaneously. Peripheral neuropathy may be acute or chronic, and may be reversible or permanent.
Piriformis syndrome is a condition which is believed to result from nerve compression at the sciatic nerve by the piriformis muscle. It is a specific case of deep gluteal syndrome. The largest and most bulky nerve in the human body is the sciatic nerve. Starting at its origin it is 2 cm wide and 0.5 cm thick. The sciatic nerve forms the roots of L4-S3 segments of the lumbosacral plexus. The nerve will pass inferiorly to the piriformis muscle, in the direction of the lower limb where it divides into common tibial and fibular nerves. Symptoms may include pain and numbness in the buttocks and down the leg. Often symptoms are worsened with sitting or running.
Tarsal tunnel syndrome (TTS) is a nerve entrapment syndrome causing a painful foot condition in which the tibial nerve is compressed as it travels through the tarsal tunnel. This tunnel is found along the inner leg behind the medial malleolus. The posterior tibial artery, tibial nerve, and tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus muscles travel in a bundle through the tarsal tunnel. Inside the tunnel, the nerve splits into three segments. One nerve (calcaneal) continues to the heel, the other two continue on to the bottom of the foot. The tarsal tunnel is delineated by bone on the inside and the flexor retinaculum on the outside.
A neurectomy, or nerve resection is a neurosurgical procedure in which a peripheral nerve is cut or removed to alleviate neuropathic pain or permanently disable some function of a nerve. The nerve is not intended to grow back. For chronic pain it may be an alternative to a failed nerve decompression when the target nerve has no motor function and numbness is acceptable. Neurectomies have also been used to permanently block autonomic function, and special sensory function not related to pain.
The superior cluneal nerves are pure sensory nerves that innervate the skin of the upper part of the buttocks. They are the terminal ends of the L1-L3 spinal nerve dorsal rami lateral branches. They are one of three different types of cluneal nerves. They travel inferiorly through multiple layers of muscles, then traverse osteofibrous tunnels between the thoracolumbar fascia and iliac crest.
Ulnar tunnel syndrome, also known as Guyon's canal syndrome or Handlebar palsy, is ulnar neuropathy at the wrist where it passes through the Guyon canal. The most common presentation is a palsy of the deep motor branch of the ulnar nerve causing weakness of the interosseous muscles. Many are associated with a ganglion cyst pressing on the ulnar nerve, but most are idiopathic. Long distance bicycle rides are associated with transient alterations in ulnar nerve function. Sensory loss in the ring and small fingers is usually due to ulnar nerve entrapment at the cubital tunnel near the elbow, which is known as cubital tunnel syndrome, although it can uncommonly be due to compression at the wrist.
Idiopathic Ulnar neuropathy at the elbow is a condition where pressure on the ulnar nerve as it passes through the cubital tunnel causes nerve dysfunction (neuropathy). The symptoms of neuropathy are paresthesia (tingling) and numbness primarily affecting the little finger and ring finger of the hand. Ulnar neuropathy can progress to weakness and atrophy of the muscles in the hand. Symptoms can be alleviated by attempts to keep the elbow from flexing while sleeping, such as sticking one's arm in the pillow case, so the pillow restricts flexion.
Magnetic resonance neurography (MRN) is the direct imaging of nerves in the body by optimizing selectivity for unique MRI water properties of nerves. It is a modification of magnetic resonance imaging. This technique yields a detailed image of a nerve from the resonance signal that arises from in the nerve itself rather than from surrounding tissues or from fat in the nerve lining. Because of the intraneural source of the image signal, the image provides a medically useful set of information about the internal state of the nerve such as the presence of irritation, nerve swelling (edema), compression, pinch or injury. Standard magnetic resonance images can show the outline of some nerves in portions of their courses but do not show the intrinsic signal from nerve water. Magnetic resonance neurography is used to evaluate major nerve compressions such as those affecting the sciatic nerve (e.g. piriformis syndrome), the brachial plexus nerves (e.g. thoracic outlet syndrome), the pudendal nerve, or virtually any named nerve in the body. A related technique for imaging neural tracts in the brain and spinal cord is called magnetic resonance tractography or diffusion tensor imaging.
In medicine, Carnett's sign is a finding on clinical examination in which (acute) abdominal pain remains unchanged or increases when the muscles of the abdominal wall are tensed. For this part of the abdominal examination, the patient can be asked to lift the head and shoulders from the examination table to tense the abdominal muscles. An alternative is to ask the patient to raise both legs with straight knees.
Anterior interosseous syndrome is a medical condition in which damage to the anterior interosseous nerve (AIN), a distal motor and sensory branch of the median nerve, classically with severe weakness of the pincer movement of the thumb and index finger, and can cause transient pain in the wrist.
Pronator teres syndrome is a compression neuropathy of the median nerve at the elbow. It is rare compared to compression at the wrist or isolated injury of the anterior interosseous branch of the median nerve.
Carpal tunnel surgery, also called carpal tunnel release (CTR) and carpal tunnel decompression surgery, is a nerve decompression in which the transverse carpal ligament is divided. It is a surgical treatment for carpal tunnel syndrome (CTS) and recommended when there is constant (not just intermittent) numbness, muscle weakness, or atrophy, and when night-splinting no longer controls intermittent symptoms of pain in the carpal tunnel. In general, milder cases can be controlled for months to years, but severe cases are unrelenting symptomatically and are likely to result in surgical treatment. Approximately 500,000 surgical procedures are performed each year, and the economic impact of this condition is estimated to exceed $2 billion annually.
Nerve glide, also known as nerve flossing or nerve stretching, is an exercise that stretches nerves. It facilitates the smooth and regular movement of peripheral nerves in the body. It allows the nerve to glide freely along with the movement of the joint and relax the nerve from compression. Nerve gliding cannot proceed with injuries or inflammations as the nerve is trapped by the tissue surrounding the nerve near the joint. Thus, nerve gliding exercise is widely used in rehabilitation programs and during the post-surgical period.
A nerve decompression is a neurosurgical procedure to relieve chronic, direct pressure on a nerve to treat nerve entrapment, a pain syndrome characterized by severe chronic pain and muscle weakness. In this way a nerve decompression targets the underlying pathophysiology of the syndrome and is considered a first-line surgical treatment option for peripheral nerve pain. Despite treating the underlying cause of the disease, the symptoms may not be fully reversible as delays in diagnosis can allow permanent damage to occur to the nerve and surrounding microvasculature. Traditionally only nerves accessible with open surgery have been good candidates, however innovations in laparoscopy and nerve-sparing techniques made nearly all nerves in the body good candidates, as surgical access is no longer a barrier.
Deep gluteal syndrome describes the non-discogenic extrapelvic entrapment of the sciatic nerve in the deep gluteal space. It is an extension of non-discogenic sciatic nerve entrapment beyond the traditional model of piriformis syndrome. Symptoms are pain or dysthesias the buttocks, hip, and posterior thigh with or without radiating leg pain. Patients often report pain when sitting. The two most common causes are piriformis syndrome and fibrovascular bands, but many other causes exist. Diagnosis is usually done through physical examination, magnetic resonance imaging, magnetic resonance neurography, and diagnostic nerve blocks. Surgical treatment is an endoscopic sciatic nerve decompression.
Nerve entrapment involves a cascade of physiological changes caused by compression and tension. Some of these changes are irreversible. The magnitude and duration of the forces determines the extent of injury. In the acute form, mechanical injury and metabolic blocks impede nerve function. In the chronic form, there is a sequence of changes starting with a breakdown of the blood-nerve-barrier, followed by edema with connective tissue changes, followed by diffuse demyelination, and finally followed by axonmetesis. The injury will often be a mixed lesion where mild/moderate compression is a combination of a metabolic block and neuropraxia, while severe compression combines elements of neuropraxia and axonmetesis.
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