OBJECTIVE. The purpose of this article is to review advanced MRI techniques and describe the MRI findings of pure sensory mononeuropathy with relevant clinical and anatomic correlation.
CONCLUSION. Peripheral sensory mononeuropathy can be challenging to evaluate with MRI because of the small caliber of pure sensory nerves and the lack of changes in secondary muscular denervation. Advances in MRI afford the necessary signal-intensity contrast and resolution for adequate evaluation of many of these small peripheral nerves.
MRI is increasingly being used for noninvasive diagnostic evaluation of suspected peripheral nerve abnormalities [1, 2]. High-resolution MRI can depict pathologic macrostructural changes in the nerve, such as loss of continuity and deviation from the expected course, and microstructural changes, such as increased size and abnormal signal intensity, which may reflect altered myelination and axonal loss. With improved signal-to-noise ratio (SNR), spatial resolution, and contrast resolution, MRI can be used to assess for a variety of pathologic entities, including compression and entrapment neuropathy, traumatic injury, neoplasms, and inflammatory processes, including demyelinating conditions [3, 4]. Most important, peripheral nerve MRI results have been found to influence clinical management and patient care [1, 5, 6], and the technique may also be used to directly guide nerve blocks .
Peripheral nerves with pure sensory function pose an imaging challenge because of their small caliber (sometimes < 1 mm ) and lack of associated muscle denervation, which can be seen with motor nerve abnormalities [3, 5, 9]. Examples of pure sensory nerves referred for evaluation to our MRI department, from most to least common, are the lateral femoral cutaneous nerve (LFCN), the sural nerve at the ankle, the saphenous nerve at the knee, digital nerves within the hand and foot, the superficial branch of the radial nerve (SBRN) within the distal forearm, the lateral and medial antebrachial cutaneous nerves (LABCN and MABCN) at the elbow, and rarely the palmar cutaneous branch of the median nerve (PCBMN) at the wrist (Table 1). Focal sensory mononeuropathy can have traumatic, iatrogenic, idiopathic, and compressive causes . We present an overview of high-resolution MRI findings of sensory peripheral nerve disease with clinical and electrophysiologic correlation.
TABLE 1: Examples of Pure Sensory Nerves Associated With Routine Requests for MRI Evaluation
Superficial branch of radial nerve
Dorsal aspect of radial side of the hand and digits
Cheiralgia paresthetica; Wartenberg or handcuff syndrome
Palmar cutaneous branch of the medial nerve
Proximal palm and thenar eminence
Lateral antebrachial cutaneous nerve
Radial side of the forearm
Medial antebrachial cutaneous nerve
Medial forearm, olecranon, and deep fascia of the medial epicondyle and cubital tunnel
Lateral femoral cutaneous nerve
Anterolateral and lateral thigh
Medial aspect of the thigh, leg, and foot up to the first metatarsophalangeal joint; knee
General MRI techniques for peripheral nerve imaging have been previously described in the literature and are often referred to as MR neurography . At our institution, peripheral nerve imaging is most commonly performed at 3 T for the inherent increased SNR and the greater capacity for parallel imaging to reduce time. The latter is particularly important when thin slices are used to ensure that focal abnormalities are not missed (maximum 3 mm and sometimes as thin as 0.6 mm) and when > 5 cm coverage is required in the z-direction, which can make sequences lengthy. Parallel imaging is optimized with surface coils with a larger number of channels; we typically use a 16-channel flex coil for the extremities and 32-channel coil for the pelvic and upper thigh region. These coils afford high SNR and conform to different anatomic configurations. Patients with orthopedic hardware are typically imaged with a 1.5-T system and metal artifact reduction techniques when the nerve in question is close to the orthopedic hardware, because of the inherent increased paramagnetic susceptibility effect at 3 T.
Our general peripheral nerve extremity protocol (Table 2) with a 3 T system (MR750, GE Healthcare) includes two-plane (axial, either coronal or sagittal) intermediate-weighted 2D fast spin-echo (FSE) images and an axial T2-weighted Dixon (in phase, out of phase) fat suppression sequence . Anecdotally, we have found Dixon imaging to provide more homogeneous fat suppression and increased SNR than a STIR sequence does. For evaluation of the LFCN, we use a 2-point Dixon fat-water separation sequence (Cube-Flex, GE Healthcare)  with a black-blood flow-saturation preparation pulse with venous suppression capabilities to improve nerve visualization. This vascular suppression technique may have potential for use in the extremities but does not currently provide adequate flow suppression for differentiation between very small sensory nerves and their accompanying vessels. It is also limited by spatial resolution. Alternatively, a protocol using T1- and T2-weighted imaging (including T2 spectral adiabatic inversion recovery [SPAIR, Siemens Healthcare]) has been described in the literature .
TABLE 2: Suggested 3-T MRI Parameters for Evaluation of Peripheral Nerves in the Extremities
Note—Receive-only 16-channel flex coil on GE Healthcare MR750 system. IDEAL = iterative decomposition with echo asymmetry and least squares estimation (3-point Dixon).
Slice thickness and acquisition time vary depending on length (z-coverage) required.
On MR images, a normal peripheral nerve is isointense to slightly hyperintense compared with skeletal muscle on intermediate-weighted and T2-weighted FSE images and should follow its expected anatomic course without deviation or disruption. Sensory nerves should also maintain uniform size along their paths. The expected honeycomb fascicular architecture of a normal peripheral nerve in cross-section is sometimes difficult to visualize in the case of pure sensory nerves given their small caliber. In contrast, an abnormal nerve may exhibit focal, short-segment, or diffuse enlargement, signal hyperintensity, and loss of the normal fascicular architecture. Perineural fat planes may be effaced owing to extrinsic pathologic changes . Overall, as Chhabra et al.  have noted, abnormal findings in peripheral nerves at MRI have been found to correlate with the traditional classification grading schemes of nerve injury defined by Seddon et al.  and Sunderland . For example, mild nerve enlargement and abnormal T2 hyperintensity correspond to neurapraxia (mildest type of injury affecting only the myelin sheath), whereas effacement or disruption of nerve fascicles suggests axonotmesis (axonal rupture with intact supporting connective tissue scaffold). Neurotmesis (total nerve severance) can be seen on MR images as discontinuity of the nerve .
Sensory nerves can be evaluated electro-diagnostically by use of nerve conduction studies [16–18]. Nerve conduction studies involve peripheral nerve stimulation with cutaneous electrodes and recording of the response with metal or self-adhesive active and reference recording electrodes. Ring electrodes are available for recording the response of digital nerves. The response from a stimulated sensory nerve is termed the sensory nerve action potential (SNAP) and indicates the sum of single nerve fiber action potentials . There are 3000–6000 nerve fibers within a sensory nerve, and the diameter of nerve fibers that contribute to the SNAP ranges from 8 to 12 μm . Normal SNAP amplitudes can range from 10 to over 100 μV, and therefore, comparison with the contralateral side is essential. An abnormal SNAP is suggestive of pathologic change at or distal to the dorsal root ganglion [16, 19].
Because nerve conduction studies rely on surface measurements, their accuracy in representing the underlying anatomic and pathologic features may be limited, particularly in cases of small nerves, variant anatomy, and obesity [18, 20–25]. Technical factors, such as limb temperature, and operator skill may also influence the accuracy of electrodiagnostic results .
Superficial Branch of the Radial Nerve (Cheiralgia Paresthetica)
Anatomy and Function
The SBRN provides cutaneous innervation to the dorsal aspect of the thumb, index finger, radial side of the middle finger, and the dorsal aspect of the radial side of the hand . Near the elbow joint, the radial nerve bifurcates into the SBRN and the deep branch of the radial nerve, which is termed the posterior interosseous nerve distal to the point at which it exits the radial tunnel. Within the proximal to mid forearm, the SBRN courses deep to the brachioradialis. Within the distal forearm, the SBRN emerges along the dorsal ulnar margin of the brachioradialis, between the brachioradialis and extensor carpi radialis longus tendons and immediately radial to the distal radius . At this location, the nerve is most susceptible to compression [26–28] (Fig. 1A). The SBRN then pierces the overlying fascia and enters the subcutaneous fat, where it divides into lateral, middle, and medial branches at the level of the wrist. A branch from the ulnar nerve communicates with the SBRN medial branch, possibly contributing to variability in clinical symptoms of cheiralgia paresthetica .
Cheiralgia (Greek for “hand pain”) paresthetica is mononeuropathy of the SBRN  (Fig. 1). Originally described by Wartenberg  in 1932, cheiralgia paresthetica, or Wartenberg syndrome, most commonly presents with paresthesia along the dorsal radial aspect of the hand [10, 26]. Focal hyperesthesia or hyperalgesia along the dorsal ulnar aspect of the thumb has also been described .
Anatomic entrapment is an important inciting factor of cheiralgia paresthetica and can be secondary to compression of the SBRN between the brachioradialis and extensor carpi radialis longus tendons in the distal forearm . Other potential entrapment sites include between two slips of a brachioradialis tendon [30, 31] and along a variant intramuscular course of the nerve through the extensor carpi radialis brevis . Cheiralgia paresthetica has been reported to result from compression injury due to overtightened watch straps or handcuffs  and, thus, is sometimes referred to as handcuff syndrome. Handcuff-related neuropathies can also affect sensory branches of the median and ulnar nerves  (Fig. 2). Iatrogenic causes of cheiralgia paresthetica include impingement from orthopedic hardware and stretch injury during closed reduction of a forearm fracture [27, 32]. Cephalic vein cannulation and adjacent tendon sheath injection are also reported culprits [32, 33]. Neuropathy of the SBRN may occur more frequently in patients with diabetes mellitus [10, 26] and has also been associated with de Quervain tenosynovitis .
Palmar Cutaneous Branch of the Median Nerve
Anatomy and Function
The PCBMN innervates the skin over the proximal palm and thenar eminence (Fig. 2D). The PCBMN originates from the median nerve  and courses within a tunnel in the distal arm between the superficial and deep antebrachial fascial layers before piercing the antebrachial fascia to become subcutaneous  (Fig. 3). The PCBMN provides small branches to the scaphoid and occasionally the lunate bones before entering the wrist. Within the hand, the PCBMN branches into a variable number of divisions .
Injury to the PCBMN leads to sensory loss or hyperesthesia of the palm . Iatrogenic injury can occur during surgery along the ventral aspect of the distal forearm and wrist, most commonly during treatment of carpal tunnel syndrome. Other surgical procedures that carry risk of PCBMN injury include volar synovectomy, resection of volar ganglia, and tendon transfer procedures . The PCBMN can be compressed by hypertrophic soft or scar tissue, anomalous ten-dons or muscles, and soft-tissue masses. PCBMN neuropathy secondary to repetitive trauma from competitive volleyball has also been reported .
Lateral Antebrachial Cutaneous Nerve
Anatomy and Function
The LABCN arises directly from the musculocutaneous nerve (C5 and C6 nerve roots) and courses in the arm deep to the biceps brachii muscle. The nerve then pierces the brachial fascia and emerges subcutaneously at the lateral margin of the biceps 2–5 cm proximal to the antecubital fossa [34–36] (Fig. 4). Distal to the elbow crease, the LABCN bifurcates into posterior and anterior cutaneous divisions that innervate the radial aspect of the forearm .
LABCN neuropathy is uncommon and typically presents with elbow pain, paresthesia, or both along the volar lateral forearm [34, 34]. The clinical presentation may occasionally mimic cheiralgia paresthetica because of variation in sensory innervation between the two nerves . Forced pronation and extension during a physical examination may reproduce symptoms of LABCN neuropathy . Ultrasound-guided injection of local anesthetic around the LABCN along the lateral biceps margin can be used to help confirm the diagnosis .
The LABCN is the most commonly involved sensory nerve in Parsonage-Turner syndrome . Injury to the musculocutaneous nerve or the upper trunk of the brachial plexus also usually precipitates LABCN neuropathy.
Entrapment of the LABCN where it emerges along the lateral biceps margin or where it pierces the brachial fascia is called Bassett lesion . Entrapment distal to the elbow flexion crease is rare . Possible causes of LABCN entrapment include distal biceps tendon tear and associated acute compression by the bicipital aponeurosis; biceps tendon repair; cephalic vein phlebotomy; prolonged anesthesia with unfavorable arm positioning; fractures of the distal humerus, proximal radius, or olecranon process; and chronic impingement secondary to repetitive movement .
Medial Antebrachial Cutaneous Nerve
Anatomy and Function
The MABCN provides sensation to the medial forearm, olecranon region, and deep fascia of the medial epicondyle and cubital tunnel [20, 34]. The MABCN arises from the brachial plexus medial cord with contributing fibers from the C8, T1, and T2 nerve roots [20, 34, 39]. Within the axilla, the MABCN courses medial to the axillary artery and has a ramus that provides cutaneous sensation over the biceps brachii muscle in the upper arm. The MABCN then courses along the ulnar aspect of the arm and ulnar margin of the brachial artery before piercing the brachial fascia at the basilic hiatus (Fig. 4C). The subcutaneous MABCN courses alongside the basilic vein and divides into anterior and posterior rami, which continue to descend along the forearm. Cadaveric studies have shown variability within the course and divisions of the MABCN [39, 40].
MABCN neuropathy typically causes anteromedial elbow and medial forearm pain, numbness, and dysesthesias . MABCN injury during cubital tunnel release, however, may only affect the posterior branch of the MABCN and result in posterior elbow and proximal forearm pain . Other iatrogenic causes of MABCN neuropathy include injury during anesthetic or steroid injection for medial epicondylitis, venipuncture, removal or insertion of implantable hormonal contraceptives in the arm, ulnar collateral ligament reconstruction, elbow arthroscopy, and fracture fixation . MABCN injury has also been reported as secondary to compression by a lipoma, repetitive minor trauma (e.g., tennis), and radiation therapy [20, 34].
Meralgia (derived from the Greek words for “thigh” and “pain”) paresthetica is sensory mononeuropathy of LFCN, which provides sensory innervation to the anterolateral and lateral thigh [10, 21]. The LFCN originates from the L2 and L3 nerve roots and emerges within the pelvis along the lateral border of the psoas muscle. It courses within the right iliac fossa fat and then runs obliquely along the surface of the iliacus muscle toward the anterosuperior iliac spine. The LFCN then pierces the iliac fascia to exit the pelvis in a fibrous tunnel, typically inferior to the inguinal ligament and superior to the sartorius muscle (Fig. 5A). Within the thigh, the LFCN bifurcates into anterior and posterior branches [21, 22, 41]. Cadaveric studies, however, have shown multiple variations of typical LFCN anatomy  in its position relative to the anterosuperior iliac spine and sartorius muscle where it pierces the iliac fossa to enter the thigh .
Meralgia paresthetica can range from mild symptoms to more severe, function-limiting pain (Fig. 5). Meralgia paresthetica is typically unilateral, has a peak incidence in the 4th–6th decades of life, and has a slight predilection among men [10, 21]. The incidence of meralgia paresthetica is 4.3 cases per 10,000 patient-years, although a higher incidence is observed in the diabetic population . Also known as Bernhardt-Roth syndrome, meralgia paresthetica presents with paresthesia and sometimes pain of the anterolateral and lateral thigh [10, 21]. Many patients may also experience tenderness over the inguinal ligament .
The LFCN is subject to mechanical compression anywhere along its course, although entrapment is most common where it pierces the iliac fascia. Obesity, tight clothing, direct trauma, and pregnancy are predisposing factors for compression. Other causes of meralgia paresthetica include muscle spasm, scoliosis, iliacus hematoma, compression by the sartorius muscle when the leg is turned out (e.g., in a dancer's stance), proximal sartorius enthesopathy, pelvic infection or neoplasm, and postsurgical scarring. Iatrogenic LFCN injury may occur at the time of hip and spine surgery, iliac bone marrow harvesting, appendectomy, and obstetric-gynecologic procedures [10, 21, 22, 41].
Saphenous Nerve (Gonyalgia Paresthetica)
Anatomy and Function
The saphenous nerve is the largest cutaneous branch of the femoral nerve and innervates the medial aspect of the thigh, leg, and foot up to the first metatarsophalangeal joint [42–44]. The saphenous nerve originates from the femoral nerve distal to the inguinal ligament and courses through the adductor canal (Hunter canal), where it lies anterior and medial to the superficial femoral artery and vein. At the point beyond which it exits the canal, the nerve bifurcates into sartorial and infrapatellar branches. The sartorial branch courses between the sartorius and gracilis muscles within the medial aspect of the leg. The infrapatellar branch curves anteroinferiorly below the patella and ramifies into terminal sensory branches [42, 43, 45] (Fig. 6D).
Saphenous neuritis presents clinically with medial-side thigh, knee, or calf pain that can radiate to the medial aspect of the foot (Fig. 6). Regional loss of sensation may occur, particularly in cases of nerve laceration [42, 45].
Compressive and traumatic injury to the saphenous nerve can occur at any level along its course. The most common entrapment site is where the nerve exits the adductor canal . Compression of the sartorial branch of the saphenous nerve is most frequent between the sartorius and gracilis muscles where the nerve becomes sub-cutaneous . Pes anserine bursitis can also cause saphenous neuropathy, as in prolonged kneeling or overuse of the knees by surfers to grip a surfboard [42, 45]. Soft-tissue tumors and ganglion cysts from the knee may exert direct mass effect on the saphenous nerve . Iatrogenic injury can result from varicose vein stripping, saphenous vein grafting, femoropopliteal bypass, knee surgery and arthroscopy, ankle arthroscopy, and superficial femoral artery thromboendarterectomy [42–44].
The term gonyalgia paresthetica specifically refers to mononeuropathy of the infrapatellar branch of the saphenous nerve . This branch provides sensory innervation inferior to the patella and the anteroinferior knee joint capsule . Medial knee incisions can potentially injure the infrapatellar branch of the saphenous nerve and cause a neuroma  (Fig. 7). Surgical procedures that carry risk of injury specifically to this branch include total knee arthroplasty, patellar and hamstring tendon harvesting, arthroscopy, and tibial nailing [42, 45, 46].
Anatomy and Function
The sural nerve supplies sensory innervation to the lateral ankle and foot . The nerve proper typically originates from the union of the medial sural nerve (a branch of the tibial nerve) and the lateral sural cutaneous nerve (a branch of the common peroneal nerve) [43, 44]. In some individuals, the sural nerve may arise directly from either the tibial nerve or the common peroneal nerve . The sural nerve courses between the medial and lateral heads of the gastrocnemius muscle before piercing the deep fascia in the upper calf to become subcutaneous. Distally, it courses along the posterolateral lower leg in close relation to the lesser saphenous vein and lateral to the Achilles tendon [43, 44] (Fig. 8A). At the fifth metatarsal base, the sural nerve bifurcates into medial and lateral branches .
Sural neuropathy may present with lateral ankle and foot paresthesia or pain. Symptoms are aggravated by foot inversion and plantar flexion. In some cases, sural nerve injury can manifest as chronic calf pain intensified by physical activity , and symptoms tend to be worse at night .
The most common cause of sural neuropathy is trauma  (Figs. 8 and 9). Acute traumatic injury to the sural nerve can occur, for example, in cases of fracture of the fifth metatarsal base or in the lower ankle and forefoot region [43, 45]. Sural neuropathy may develop as a result of Achilles or peroneal tendinosis or gastrocnemius injury. Iatrogenic injury to the sural nerve can occur during sural nerve biopsy, lesser saphenous vein stripping, and posterolateral ankle surgery involving the Achilles or peroneal tendon . Peripheral nerve sheath tumors of the sural nerve have also been reported .
Digital Nerves (Digitalgia Paresthetica)
Anatomy and Function
Sensory neuropathy involving the fingers or toes due to primary digital nerve abnormality is known as digitalgia paresthetica . In the hand, proper digital nerves innervate the radial and ulnar sides of the thumb and fingers  (Fig. 2D). In the foot, common digital nerves arise from the medial and lateral plantar nerves and innervate the web spaces before branching into medial and lateral digital branches that innervate the toes .
Originally described by Wartenberg in 1954 , digitalgia paresthetica can be caused by pressure on or trauma to a sensory digital nerve or, in some cases, be secondary to rheumatic disorders . In the fingers, digitalgia paresthetica has been reported as secondary to carrying heavy plastic grocery bags  and to backpacking . Perineural fibrosis of the ulnar digital nerve of the thumb is known as bowler thumb and can occur in bowlers and baseball players and in postoperative patients . Painful neuromas within the finger can also occur after laceration or surgical amputation  (Fig. 10).
Digitalgia paresthetica has been reported to occur in military recruits during the early phases of marching training . Common digital nerves of the foot are prone to perineural fibrosis in the plantar intermetatarsal region from repetitive trauma. This pathologic change is referred to as Morton neuroma and is easily detectable with MRI. Neuroma of the medial proper plantar digital nerve of the great toe is known as a Joplin neuroma .
For some patients, peripheral sensory mononeuropathy may be self-resolving or easily treated by removal of an extrinsic compressing factor [9, 10, 21, 22]. Conservative management options include activity modification, splinting and protective padding, nonsteroidal antiinflammatory medications, oral and topical analgesics, and systemic medications [34, 42, 54]. Physical therapy may be helpful in some cases , although perineural anesthetic or steroid injections may be necessary if symptoms persist [27, 32]. Kinesio taping and acupuncture have also been described in the treatment of meralgia paresthetica .
When conservative therapy fails, surgical intervention is aimed at the underlying cause. In cases of entrapment requiring decompression, nerve release or, less commonly, nerve resection can be performed . Neurectomy carries the consequence of permanent sensory loss and may not entirely alleviate symptoms, especially when associated with chronic regional pain syndrome . In cases of a transected nerve, surgical treatment options include microsurgical epineural nerve coaptation (favored by most) and neuroma excision with cauterization or ligation and proximal transposition of the proximal end of the transected nerve into bone or muscle [34, 45].
Pure sensory nerves can be injured in a variety of ways, and the injuries can lead to regional paresthesia or sensory loss that can range from mild to debilitating. Although pure sensory nerves are small in diameter, high-resolution MRI can depict many peripheral sensory nerves. A lack of secondary muscular denervation changes, however, renders MRI interpretation of peripheral sensory mononeuropathies challenging. Knowledge of the anatomic course of the nerve and appropriate selection of sequences, imaging planes, and sequence parameters can facilitate MRI acquisition and evaluation.
The Hospital for Special Surgery has an institutional research agreement with GE Healthcare.
Based on a presentation at the ARRS 2016 Annual Meeting, Los Angeles, CA.
This is a web exclusive article.
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