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Magnetic resonance neurography and ultrasonogram findings in upper limb peripheral neuropathies
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.250701
Keywords: MR neurography, neuropathy, ultrasonogram
Peripheral neuropathy is defined as any disease or damage to the peripheral nerves. Though the diagnosis is predominantly clinical (which includes history, clinical examination, and electrodiagnostic tests),[1] the role of imaging studies is increasing for various reasons. Imaging provides the spatial resolution of the nerve and helps to determine the primary pathology. It gives the exact site of pathology with a high-resolution depiction of nerves. It establishes the continuity of the nerve and prognosticates the management by determining the event to be acute or chronic. The primary modalities available for nerve imaging are a high-frequency ultrasound and magnetic resonance imaging (MRI). With the advent of highly focused ultrasound, high tesla MRI scanners and dedicated coils, the specificity and sensitivity of these modalities for establishing the diagnosis of peripheral neuropathies have increased manifold. In the current article, we will limit ourselves to the discussion of peripheral neuropathies involving the upper limb.
Ultrasonogram For imaging of nerves, high-frequency ultrasound is required (usually above 12–14 Hz). Evaluation with ultrasound gives a flexible field of view and the pathological site can be readily compared to the normal site. The entire extent of the nerve can be assessed in one go in a short duration of time and multifocal pathologies can also be picked. Ultrasonogram (USG) is cheap and far more convenient to the patient. It also allows for real-time dynamic imaging. However, it depends on the operator's skill. In addition, its sensitivity markedly decreases in conditions of dense scarring and calcification or when the nerve is very deep-seated. Magnetic resonance imaging MRI has a very high inherent soft tissue contrast; thus, it detects subtle signal abnormalities on T2-weighted (T2W) sequence. Hence, MRI is more specific and sensitive than ultrasound in detecting peripheral neuropathies.[2] The interobserver and intraobserver variation is significantly low with MRI and provides more objective assessment, unlike USG. Additionally, secondary muscle denervation changes are better depicted on MR examinations (which has a role in deciding the management).[3] Muscle atrophy with fatty replacement signifies chronic denervation and either conservative management or tendon transfer would be the treatment of choice. On the other hand, in acute denervation, the patient is managed aggressively to revert the changes. However, MRI is an expensive investigation and requires a longer duration than a USG. Moreover, only a limited region can be evaluated at a time. Thus, the chances of missing a multifocal or bilateral pathology are higher.
Ultrasonogram A high-frequency linear transducer (12–14 Hz) should be used for evaluation of peripheral nerves. The entire course of the nerve should be screened to detect a multifocal pathology and comparison should be done with the other limb. Magnetic resonance imaging Higher strength scanners (3T) should be preferred along with dedicated surface coil for better signal-to-noise ratio (SNR). The MR neurography (MRN) protocol should include T1 weighted spin echo (T1 W SE) and T2 weighted fat-saturated (T2 W FS) sequences in the axial plane and isovoxel 3-dimensional T2 weighted fat-saturated (3D T2FS) sequence, which can be utilized for making reformats in a coronal and sagittal plane. Axial plane is best for delineating the normal course of the nerve and to detect any subtle pathology, whereas reformats aid in the pre-surgical mapping of the nerve for the surgeon. Newer sequences like diffusion-weighted imaging with background suppression (DWIBS) and diffusion tensor imaging (DTI) are being increasingly used these days, essentially for response assessment.[2] Appearance of normal nerve Using a high-frequency ultrasound, the nerve appears as a smooth round-to-ovoid, iso-to a mildly hyperechoic structure having a fascicular pattern in a cross-sectional view. It usually accompanies a vessel along, which can be easily distinguished by putting the color flow. It can be distinguished from a muscle or tendon by tracing the nerve in its proximal or distal course. In sagittal orientation, the nerve appears as a bundle of longitudinal fibers packed in a sheath [Figure 1].
T1W sequence is best to evaluate the morphology of the nerve on MRI. It is isointense to muscles, round-to-ovoid smooth structure having intrafascicular fat and surrounded by a thin rim of perineural fat. The peripheral nerves are typically seen in the interfacial plane between the muscles accompanying a vessel [Figure 2]. On fluid sensitive fat-suppressed T2W sequence, the nerve is isointense to mildly hyperintense to the surrounding muscles. Various curved reformats can be made to depict the entire extent of the nerve by acquiring isovoxel 3D sequences.
Radiological features suggesting abnormality in a nerve Abnormal signal intensity/echogenicity of the nerve The nerve is abnormal when it becomes hypoechoic on USG or abnormally T2 hyperintense on MRI as the nerve fascicles tend to gain fluid signal [Figure 3]a. Various theories have been proposed for such an appearance-like vascular congestion, blockade of axoplasmic flow leading to abnormal proximal accumulation of endoneurial fluid, and distal Wallerian degeneration changes.[4] When the disease is severe, the nerve becomes hypointense on T2 at the site of pathology and hyperintense both proximal and distal to it. This is known as the triple B sign (bright, black, and bright).[2]
Abnormal morphology of the nerve The normal fascicular pattern of the nerve can be visualized on MRN. The nerve loses its fascicular pattern when it becomes pathological. The surrounding perineural fat can also become scarred or effaced or inflamed in neuropathy. Change in the caliber of the nerve The nerve usually becomes enlarged to form a neuroma at the site of pathology, as the fibers tend to regenerate by growing in all directions. The nerve can also show atrophy distal to the site of pathology. Loss of continuity of the nerve This usually occurs in traumatic neuropathy when the nerve gets transected either partially or completely, thereby leading to a gap between the transected ends. Associated surrounding inflammation This is usually encountered in traumatic neuropathy wherein there is adjacent T2 hyperintensity with loss of normal architecture of soft tissue around the nerve. Denervation Group of muscles supplied by a nerve show changes of denervation when their supplying nerve is pathological. When the injury is acute, there is edema in muscles seen as T2 hyperintensity [Figure 3]b. When it is subacute, it shows both changes of edema and beginning of fatty infiltration. When the injury had occurred in the remote past, there is atrophy of muscles with fatty infiltration. Low fractional anisotropy Recent studies have established the role of DTI in peripheral neuropathy. Any normal nerve would have a high fractional anisotropy (FA) value as they show increased free water diffusion in one direction. Any disruption or injury to the nerve would restrict this directional preference of diffusion leading to a reduction in FA values. Normalization of FA value post-treatment indicates recovery. Thus, DTI plays a pivotal role in response assessment.[5] Apparent diffusion coefficient values Apparent diffusion coefficient (ADC) values help to differentiate malignant and benign nerve sheath tumors. Benign tumors depict ADC values in the range of 1.1–2 × 10-3 mm2/s whereas malignant tumors depict values ranging from 0.7–1.1 × 10-3 mm2/s. In addition, a serial increase of ADC values post-treatment indicates recovery, thereby helping in response assessment.[5]
Median nerve The median nerve is one of the major peripheral nerves of the brachial plexus formed by the median root of the medial cord and lateral root of the lateral cord, containing fibers from all the roots (C5-T1). It descends in the arm in close relation to the brachial artery, lateral to it in the upper arm then crosses in the mid-arm to run medial to the artery in the lower arm, lying superficial to the brachial muscle. It courses between the two heads of pronator teres to enter the anterior compartment of the forearm via the cubital fossa. In the upper forearm, the median nerve gives its major muscular branch, anterior interosseous nerve. Thereafter, it runs between flexor digitorum profundus and flexor digitorum superficialis to finally enter the carpal tunnel under the flexor retinaculum. Before entering the carpal tunnel, it gives off a superficial palmar branch. In the palm, it divides into multiple muscular and digital branches [Figure 4].
Ulnar nerve The ulnar nerve is another major peripheral nerve of the upper limb arising from the medial cord of the brachial plexus having fibers from C8, T1. It courses on the medial side of the arm in the anterior compartment. At the junction of upper two-third and lower one-third of the arm, it pierces the medial intermuscular septum to enter the posterior compartment. It crosses posterior to the medial epicondyle (cubital tunnel) to enter the forearm. In the proximal forearm, it again enters the anterior compartment by coursing between the two head of flexor carpi ulnaris. Thereafter, it runs medially superficial to flexor carpi ulnaris. It enters the palm superficial to the carpal tunnel in the Guyon canal. It terminates by dividing into superficial and deep branches in the palm [Figure 5].[1],[6]
Radial nerve The radial nerve is the third major peripheral nerve of the brachial plexus arising from the posterior cord from fibers C5-T1. It exits the axilla by coursing dorsal to the brachial artery runs between lateral and medial bellies of the triceps muscle. Thereafter, it runs deep, at the surface of the humerus in the spiral (radial) groove, to come to the posterolateral aspect of the arm. At the junction of upper two-third and lower one-third of the arm, the nerve pierces the intermuscular septum to enter the anterior compartment of the arm. It enters the cubital fossa laterally to reach the forearm by piercing the supinator muscle (subsequently called the posterior interosseous nerve). Before piercing the intermuscular septum, the radial nerve gives off the superficial radial nerve which courses superficially with the radial nerve to supply the dorsum of palm. Posterior interosseous nerve enters the posterior compartment to supply its muscles [Figure 6].
Classification of neuropathy The median, radial, and ulnar nerves may be affected by various peripheral neuropathies, each of which may be categorized according to its cause, as:
Traumatic neuropathy Peripheral nerve is a collection of axonal fibers surrounded by myelin sheath, which help in the transfer of information from the brain and spinal cord to the rest of the body. These nerves are fragile and can be easily damaged by trauma. The various modes of trauma include sharp cut injury, blunt trauma as in laceration or contusion, iatrogenic or electrical injury, etc. The myelin sheath surrounding the axon is called endoneurium and is composed of Schwann cells and loose connective tissue. Multiple such axons combine to form fascicles, which are surrounded by another connective tissue covering called the perineurium. Multiple such fascicles are further surrounded by loose connective tissue called the epineurium.[7] Depending on the severity of injury, nerve injuries are classified by Seddon as neuropraxia (when there is damage to myelin with maintained axonal length), axonotmesis (damage to axonal fibers with maintained myelin or connective tissue sheath), and neurotmesis (when there is disruption of axonal fibers with damage to myelin or connective tissue sheath).[8] Neuropraxia is the milder form of injury which recovers by itself, hence conservative management is recommended for this form of injury. Axonotmesis is a relatively severe form of injury, in which the axon undergoes Wallerian degeneration. A good recovery with time is expected with conservative management in such cases. On the other hand, neurotmesis is the most severe form of injury, which requires surgical management and has a dismal prognosis as it involves complete discontinuity of axons and the myelin sheath. Any nerve injury can lead to neuroma formation, which is a bunch of disorganized neural tissue along with fibrosis. This neuroma is called 'neuroma in continuity' when the continuity of the nerve is maintained [Figure 7]. It can be of spindle shape (if it occurs centrally and is having an intact perineurium) or may be a lateral neuroma (if it is present eccentrically after partial discontinuity of the perineurium occurs). When the neuroma occurs in a completely transacted nerve, it forms an end neuroma [Figure 8]. MRI can aid in differentiating between axonotmesis and neurotmesis on the basis of nerve and muscle signal intensity characteristics at different time intervals after the nerve injury.[9]
A major role of imaging (USG and MRI) in traumatic neuropathies is to correctly determine the exact site of involvement. Imaging studies also help in establishing the continuity of the nerve. If the nerve is discontinuous, it is possible to determine if there is neuroma formation. The type of neuroma can also be ascertained. The gap between the two ends of a completely transacted nerve can be determined. It is also helpful in surgical planning — whether primary nerve repair will be possible or nerve reconstruction with grafting will be required. Nerve injuries, if managed early, can prevent a permanent disability. Entrapment neuropathies Peripheral nerves are prone to get compressed at the following sites: (a) When they course through the fibro-osseous or fibromuscular tunnel, (b) while piercing through the muscle, (c) when some anatomic variation is seen, (d) when the retinacula or the fibrous tissue thickens either due to overuse or because of age-related degeneration, (e) due to adjoining mass lesion (ganglion, synovial cyst, and tumors), or fractures or dislocation.[10],[11] Various clinical entities are described according to the site of compression of the nerve. The main role of imaging in entrapment neuropathies is to determine the exact site of compression as neurophysiological studies only give an approximate idea of the location of compression. It is also possible to find the cause of entrapment to determine the feasibility of surgical intervention, e.g., if any mass lesion or a thickened retinacula causes compression of the nerve.
Median nerve Median nerve can get entrapped at the supracondylar region of distal humerus (named the supracondylar process syndrome) due to the presence of an osseous spur arising from the anteromedial surface of distal end of the humerus.[12] This is a very rare site of entrapment with an incidence rate of 0.5%. A fibrous band, called the ligament of Struthers, may be seen joining this osseous spur (supracondylar process) and the medial epicondyle, thereby forming a fibro-osseous tunnel in which the nerve gets entrapped.[13] Pronator syndrome Distally, the nerve can get entrapped between the two heads of pronator teres;[14],[15] or beneath the biceps aponeurosis which is called lacertus fibrosis; or, by the thickened proximal edge of flexor digitorum superficialis when it enters the forearm, which is called as the pronator syndrome. Patients typically complain of forearm pain which worsens with pronation/supination.[14] Rarely, the median nerve may get entrapped under the sublime bridge (tendinous arch between the radial and humeral heads of the flexor digitorum superficialis).[16] Carpal tunnel syndrome Carpal tunnel forms the most common entrapment neuropathy of the upper limb, having a prevalence of 3%. The compression of the median nerve when it enters the palm beneath the flexor retinaculum in the carpal tunnel is called carpal tunnel syndrome. This occurs whenever the pressure within the carpal tunnel increases. This may be due to systemic disorders like diabetes and hypothyroidism, or due to the presence of a mass either within the nerve or in the surrounding vicinity like a ganglion, cyst, lipoma, heterotopic calcification, fibrolipomatous hamartoma, etc.[17],[18],[19],[20],[21],[22] Patients present with classical clinical complaints of pain and paresthesia involving the radial three and a half fingers with associated thenar muscle atrophy. Diagnosis is usually clinical and imaging is required to evaluate the cause. Various parameters to diagnose this entrapment neuropathy include the flattening ratio (ratio of longitudinal to short axis diameter of median nerve at the level of hook of hamate) being greater than 3, bowing index (ratio of perpendicular distance of mid of flexor retinaculum from the line joining tubercle of trapezium and hook of hamate to the distance between tubercle of trapezium and hook of hamate) being greater than 0.14, and an abnormal T2 hyperintensity of the median nerve both proximal and distal to site of compression [Figure 9]. In addition, there is denervation of thenar muscles supplied by the median nerve.[2]
Ulnar nerve Cubital tunnel This is the second most common upper limb compressive neuropathy, where the ulnar nerve is pathologically compressed beneath the cubital retinaculum, also called Osborne ligament (fibrous band connecting the medial epicondyle to olecranon process).[11],[23],[24],[25] Multiple studies have been done to evaluate MR findings in ulnar nerve compression at the elbow which demonstrate increased caliber and altered signal intensity in symptomatic patients.[26],[27],[28],[29] However, the nerve may normally show mild T2 hyperintensity at this level. Role of MR is predominantly to look for secondary causes in symptomatic patients.[30] The ulnar nerve can also get compressed under the arcuate ligament when it crosses the two heads of flexor carpi ulnaris muscle.[31] Guyon canal Guyon canal syndrome is a result of compression of the ulnar nerve in the piso-hamate tunnel. This canal is present at the level of the wrist and is formed by pisiform and flexor carpi ulnaris medially. The hook of hamate, extrinsic flexor tendons, and transverse carpal ligament form the lateral wall while the roof is formed by the palmar carpal ligament (with palmaris brevis, if present), and the floor by flexor retinaculum, flexor digitorum profundus, transverse carpal ligament, piso-hamate, piso-metacarpal ligaments, and opponens digiti minimi. Causes of compression of the nerve at this level could be due to the presence of lesions like a cyst, lipoma, ganglion, accessory muscles [Figure 10], and vascular lesions.[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42]
Radial nerve The radial nerve can get entrapped proximally in the axilla and arm, or distally after its division in the forearm. The most common cause of entrapment in the arm is due to fracture of the humerus at the junction of the mid and distal third of the humerus. Radial tunnel syndrome The nerve gets entrapped at the elbow. Various causes of this condition are a fibrous band attached to the radiocapitellar joint, the tendinous origin of extensor carpi radialis brevis, or due to the radial recurrent vessel.[43] Supinator syndrome It refers to the entrapment of radial nerve at the level of the proximal forearm when it courses through the arcade of Frohse, piercing the supinator muscle, and is the commonest site of entrapment. Other potential sites of compression are at the anterior capsule of the radiocapitellar joint, small recurrent vessels that cross the posterior interosseous nerve (leash of Henry), the fibrous edge of the extensor carpi radialis brevis, and the distal margin of the supinator muscle, where the posterior interosseous nerve exits the supinator tunnel.[44],[45] It is usually the posterior interosseous nerve of the radial nerve which gets compressed in supinator syndrome [Figure 11]. Since posterior interosseous nerve is a pure motor nerve, hence patient presents with wrist drop and finger drop without any sensory loss.[1],[46]
Various viral and bacterial infectious agents may cause neuropathy in which the clinical symptoms mimic those of a focal nerve disturbance. Amongst the bacterial infections, leprosy, tuberculosis, and diphtheria can involve the peripheral nerves. Amongst the viral infections, the most common infectious agents include human immunodeficiency virus, varicella-zoster virus, herpes simplex virus, poliomyelitis virus, and cytomegalovirus.[1] In such cases, long segment nerve thickening with abscess formation may be seen. In addition, the presence of nodes at the local site also point towards an infective etiology [Figure 12].
Inflammatory demyelinating polyradiculoneuropathies are immune-mediated neuropathies characterized by multiple foci of demyelination and axonal degeneration of peripheral nerves. The entity chronic inflammatory demyelinating polyneuropathy (CIDP) has not been evaluated much in the past by imaging.[47],[48],[49] On MRI, this condition would predominantly involve the proximal nerves and may have thickening or altered signal of roots or cords of the brachial plexus. There can be involvement of a solitary nerve or multiple nerves at a time at multiple sites. Inflammatory neuropathy can also arise due to constant irritation of the nerve by an implant/foreign material [Figure 13]. In such cases, long segment thickening with signal alteration of the nerve is seen which gets relieved after the removal of the foreign material. Another case of long segment thickening of the median and ulnar nerve due to electric shock is shown in [Figure 14]. Few authors advocate the administration of contrast in all cases of inflammatory neuropathies. Inflammation would lead to a disruption of the blood-nerve barrier and hence would show a thin rim enhancement on postgadolinium images.[50],[51]
Mass lesions Mass lesions of peripheral nerves can be divided into lesions that arise either from the nerve or its sheath cells, or as lesions that originate from the surrounding soft tissues, i.e., intraneural or extraneural lesions. Benign neurogenic tumors include schwannomas, neurofibromas, fibrolipomatous hamartomas, lipofibromas, encapsulated neuromas, or macrodystrophia lipomatosa. Macrodystrophia lipomatosa is one of the intraneural pathologies, which is best diagnosed by MRI, which depicts a marked enlargement of the nerve with the presence of increased intraneural fat. Malignant peripheral neurogenic lesions include malignant schwannomas, malignant triton tumors, malignant neurilemomas, neurilemosarcomas, neurofibrosarcomas, neurogenic sarcomas, and neurosarcomas.[52] Mass lesions that may originate from surrounding soft tissues include ganglia and other cysts, enlarged lymph nodes, lipomas, hemangiomas, and other benign or malignant soft-tissue tumors, as well as metastases from malignancies such as melanoma or breast cancer. The nerve tumors appear as a well defined focal swelling of the nerve with complete loss of its fascicular pattern [Figure 15]. These have altered echogenicity or MR signal intensity and can have areas of necrosis or hemorrhage. No perineural fibrosis is visualized (as in traumatic neuroma).
Fibrolipomatous hamartoma is one specific condition wherein the MR findings are diagnostic without a need for biopsy. The nerve is grossly enlarged with increased intraneural fat. This condition is most commonly seen in the median nerve.[17]
Neuropathy is a broad term referring to the clinical presentation of sensory abnormalities (pain, paresthesia, and numbness) or motor weakness in the expected distribution of a particular nerve. With the advent of high-resolution ultrasound and higher field strength magnets having better surface array coils and superior software, these imaging modalities are emerging as the complementary tool of choice for assessment of peripheral neuropathies. In traumatic nerve injuries, the exact lesion localization is the central diagnostic step in the presurgical workup. MRN showed very high sensitivity in detection of the nerve involved with the additional advantage of delineating the exact site of involvement, secondary muscle changes, and in establishing continuity of the nerve which has a bearing on the management and on the prognosis of the nerve injury. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15]
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