Imaging in the diagnosis of ulnar nerve pathologies—a neoteric approach

Following the carpal tunnel syndrome, compressive neuropathy of the ulnar nerve at the cubital tunnel is the most common cause of compressive neuropathy [1, 2]. Conventionally, neuropathies have been diagnosed by clinical examination, Tinel’s sign and electrodiagnostic (nerve conduction velocity and electromyography) findings which provide information about the nerve involved and the possible site of injury but do not provide any accurate anatomical information. Introduction of high-frequency ultrasound probes have made direct visualisation of peripheral nerves possible, thus providing anatomical details about the nerve. Ultrasonographic findings of peripheral nerves were first reviewed by Fornage in 1988 [3]. Since then, technological advances like increased frequency and variable sizes of footprints of linear transducers have escalated the use of ultrasound in peripheral nerve pathologies. Exact site, extent and type of involvement, local cause of neuropathy, continuity of nerve and architectural distortion can be identified for accurate diagnosis and planning the management. Ultrasound is quick, cost effective, has no contraindications and provides detailed imaging of the entire length of the nerve. MR imaging adds to soft tissue details, change in muscles supplied by the affected nerve and helps in characterising the nerve lesion. In-spite of these advantages, imaging remains underutilised in cases of peripheral neuropathy. The aim of this pictorial essay is to demonstrate the use of imaging in diagnosing the ulnar nerve neuropathies due to various aetiologies. Various previous publications have mentioned methods to identify the nerve in specific anatomical locations and various peripheral nerve pathologies, centred around the Guyon’s canal and Cubital tunnel [3‐7]. With this review, we provide a neoteric review which combines ultrasound and MR imaging of commonly encountered causes of ulnar neuropathies.

The nerve arises from the medial cord of the brachial plexus carrying fibres from the C8-T1 nerve roots. It lies posteromedial to the brachial artery in the anterior compartment of the upper arm and descends down to enter the posterior compartment by piercing the medial intermuscular septum (Fig. 1). This is a potential site of compression of the nerve under the ‘Arcade of Struther’ [8] which is described as a fibrous canal on the medial aspect of the middle- and lower-third of the arm, consisting of the medial head of the triceps brachii muscle and its aponeurotic expansion, which extends into the intermuscular septum and internal brachial ligament and covers part of the ulnar nerve. Thereafter, the ulnar nerve runs behind the medial epicondyle with the superior ulnar collateral vessels under the ‘Cubital tunnel’ [9‐11]. The roof of the cubital tunnel is formed by the Osborne’s ligament or the Cubital retinaculum which is a ligament spanning from the medial epicondyle to the olecranon process, continuous with the fascia connecting the humeral and ulnar heads of the flexor carpi ulnaris (FCU). Alternatively, the roof may be formed by the anconeus epitrochearlis muscle [12]. The floor is formed by the medial collateral ligament (MCL) and elbow joint capsule, while the medial epicondyle and olecranon form the walls on either side [13]. Flexion of the elbow decreases the height, area and sagittal curvature of the tunnel, with maximum nerve compression occurring at 135° of flexion according to a study by James et al. [14]. At this level, the ulnar nerve gives off an articular branch to the elbow joint.

Thereafter, the ulnar nerve descends into the forearm, passing between the two heads of the flexor carpi ulnaris muscle (FCU) [15]. The nerve provides motor supply to the FCU and medial half of the flexor digitorum profundus. It continues distally along the ulna, lying deep to the FCU. About 5 cm distal to the medial epicondyle, the ulnar nerve pierces the flexor-pronator aponeurosis which is the fibrous common origin of the flexor and pronator muscles. Another aponeurosis extends between the flexor digitorum superficialis of the ring finger and the humeral head of the flexor carpi ulnaris, known as the ligament of Spinner, which attaches to the medial epicondyle and can cause kinking of the nerve following an anterior transposition. Near the wrist, the ulnar nerve moves lateral to the FCU, courses medial to the ulnar artery to enter the palm through the Guyon’s canal. The volar carpal ligament forms the roof of the canal while the transverse carpal ligament and the hypothenar muscles form the floor. The medial and lateral walls are formed by pisiform, pisohamate ligament, abductor digiti minimi muscle belly on the ulnar side and the hook of hamate on the radial side [16]. Near the wrist, the motor innervation of the ulnar nerve includes the thenar muscles: the adductor policis, deep head of flexor pollicis brevis (FPB); dorsal and palmar interossei and 3rd and 4th lumbricals, hypothenar muscles: abductor digiti minimi, opponens digiti minimi and flexor digiti minimi. The ulnar nerve gives dorsal and palmar cutaneous branches and a few superficial terminal branches to provide sensation to the ulnar fourth and entire fifth finger and the medial aspect of the forearm.

The normal peripheral nerve has a honeycomb appearance which is readily identified on imaging. The central spots are the nerve fascicles which are formed by bundles of nerve fibres surrounded by the perineurium. Each nerve fibre is also surrounded by an endoneurium which is not visible on imaging with the currently available resolution. The fascicles are in turn embedded and surrounded by epineurium which forms the sheath of the peripheral nerve [17]. Normal maximum cross-sectional area of the ulnar nerve at the level of cubital tunnel in a study by Wiesler et al. proved to be 0.065 cm² [18].

Ulnar neuropathy can result in sensory symptoms only or can cause progressively worsening motor deficit. It usually starts as altered sensation in the ulnar nerve sensory distribution, including the ulnar fourth and entire fifth finger which may progress to involve the motor fibres leading to muscular weakening and muscular atrophy over time [12, 22]. Elbow flexion can result in exaggerated symptoms as the cubital tunnel height and area decrease on flexion with resultant nerve compression [14]. Elbow flexion during sleep can result in night symptoms severe enough to cause awakening. The fibres of the intrinsic muscles of hand are located more peripherally in the nerve while the FCU and FDP fibres are more centrally placed. Chronic severe injury progressively leads to weakening of the FCU and FDP resulting in the typical ‘Ulnar claw hand’ [12]. When the ulnar nerve is divided at the wrist, only the opponens pollicis, superficial head of the flexor pollicis brevis and lateral 2 lumbricals are functioning, all of which are supplied by the median nerve.

Ulnar neuropathy can occur due to entrapment of the nerve at anatomical sites, chronic irritation of the nerve due to local causes or transection of the nerve following penetrating injuries.

The most common site of ulnar nerve entrapment is at the elbow, within the cubital tunnel or the epicondylar groove [23] while the second most common site is at the wrist, commonly in the Guyon’s canal [24‐27].

Another common cause of ulnar neuropathy is the ‘tardy ulnar nerve palsy’ as described by Panas et al. [28‐30] in which chronic nerve irritation occurs due to prior trauma or osteoarthritis.

Common sites of nerve compression include a site in the upper arm where the ulnar nerve pierces the intermuscular septum, beneath the arcade of Struther, alongside the medial epicondyle particularly in patients with cubitus valgus deformity, in the ulnar groove, within the cubital tunnel and between the two heads of FCU. More distally, it can get compressed where it exits the FCU and perforates a fascial layer between the flexor digitorum superficialis and the flexor digitorum profundus [31, 32].

Guyon’s canal is the commonest site of direct nerve trauma following penetrating injuries as the nerve is superficial in this region [27]. Three zones have been identified in relation to the ulnar nerve pathology near the Guyon’s canal—zone 1: encompassing the area proximal to the bifurcation of the ulnar nerve; zone 2: encompassing the motor branch of the nerve after it has bifurcated; and zone 3: encompassing the superficial or sensory branch of the bifurcated nerve.

Other aetiologies include compression during general anaesthesia, blunt trauma, deformities, transient occlusion of brachial artery, cigarette smoking, entrapment within scar tissue, local hematomas, subdermal contraceptive implants and following venepuncture [33‐37]. Thermal and burn injuries are another cause of ulnar nerve palsy which may also include other nerves in the region of the burn. Tumour and tumour like lesions involving the ulnar nerve include peripheral nerve sheath tumours (PNSTs), fibrolipomatous hypertrophy, intraneural lipomas, intraneural ganglion, true neuromas and pseudo neuromas.

Clinical examination and electrodiagnostic studies (nerve conduction velocity (NCV) and electromyography (EMG)) are the conventional diagnostic tools in neuropathies as they provide essential information about the type of dysfunction and help in clinical monitoring. Tinel’s sign helps in assessing the possible site of injury and to assess response to treatment. Nerve injuries have been classified by Seddon in 1943 and expanded by Sunderland in 1951. Mackinnon and Dellon in 1992 added grade VI injury to Sunderland grading scheme which was defined as a mixed type of injury which denotes various types of injuries across the cross section of the nerve [38‐40]. Table 1 illustrates this classification along with imaging findings in different types of nerve injuries. Imaging helps by providing unmatched anatomical details about the nerve involved. Plain radiographs show fracture sites, soft tissue swellings and orthopaedic implants. It may also demonstrate a fat stripe of lipoma or a bony lesion in proximity to the course of the nerve. High-resolution ultrasound and MRI help in direct visualisation of the nerve with anatomical delineation of the pathological segment. Hypo-echogenicity of the nerve on ultrasound and hyperintensity on MRI are markers of neuropathy. Normal nerves do not show any intra-neural vascularity. Appreciation of intra-neural vascularity is a marker of neural compression or inflammation and co-relates with severity of affection of nerve [41]. These imaging modalities also provide essential information about the surrounding soft tissue and the muscles innervated by the injured nerve.

One of the principal causes of ulnar neuropathy in the Indian subcontinent is infection by lepra bacilli. Nerve involvement in leprosy may vary from involvement of an intradermal nerve in the cutaneous patch to a major lesion in the peripheral or the cranial nerve trunk [47]. Nerve damage in leprosy may present itself as silent neuropathy without overt signs and symptoms or as clinically manifest disease which may present as weakness, atrophy or contracture.

Imaging features may range from a hypoechoic nerve with loss of fascicular architecture to frank abscess formation and intra neural hypervascularity. Figure 13 shows cases of ulnar nerve involvement in different stages of leprosy.

The ulnae nerve has a superficial course near the wrist where it passes under the Guyon’s canal. It can be commonly injured in penetrating injuries to the wrist. Figure 14 shows a case with discontinuity in ulnar nerve following a penetrating injury to forearm. Another case with glass cut injury shows a neuroma in continuity in the ulnar nerve in Fig. 15 along with soft tissue oedema.

Peripheral nerve sheath tumours (PNSTs) include neurofibroma and schwannoma which may be benign or malignant. Deep-seated neurofibromas may have neurological symptoms while superficial neurofibromas are usually small painless masses. Plain radiography is usually normal in PNST while high-resolution ultrasound shows a hypoechoic fusiform mass in continuity with the parent nerve. MRI is the imaging modality used to differentiate between PNST and traumatic neuromas. PNST are characterised by T1 iso-hypointense, T2 hyperintense fusiform mass in continuity with the nerve which may show low signal intensity in the centre on T2-weighted images corresponding to the higher fibro-collagen content in the centre which co-relates with the organised histological architecture. Another sign is the split fat sign best seen on T1-weighted images wherein the hyperintense fat around the fusiform mass suggests intermuscular location of the lesion. Fascicular pattern may be detected within the mass which also supports its neurogenic origin [48]. It has been suggested that post contrast scans show enhancement in PNST while there is no enhancement in traumatic neuromas which form due to regeneration and scarring of the nerve [48]. However, a study by Ahlawat et al. suggests that absence of target sign and history of trauma are the most reliable signs of a traumatic neuroma. Their study showed enhancement in 88% of traumatic neuromas, which might be attributed to a broken blood-nerve barrier [50]. Figure 16 shows a PNST in continuity with the ulnar nerve in the arm in a patient with soft tissue swelling and no neural symptoms. Neurofibroma in ulnar nerve is seen in Fig. 17 in a patient with neurofibromatosis.

Conservative treatment of ulnar neuropathy focuses on pain relief, inflammation reduction, and rehabilitation. Patients are advised to avoid aggravating activities, use night splints and use NSAIDs and steroids to decrease inflammation [12, 15]. Surgery is indicated when conservative management fails or for decompression and in cases of primary repair of the nerve.

Diffusion tensor imaging and tractography are now being used for peripheral nerve pathologies. Jengojen et al. [51] used diffusion tensor imaging and tractography to assess acute changes in radial and median nerve following compression and demonstrated changes in radial nerve metrics. Razek et al. [52] carried out a prospective study in 39 patients with mild to moderate carpal tunnel syndrome and found positive correlation between findings of diffusion tensor imaging, electrodiagnostic tests and clinical assessment.

Neuropathic segments tend to have a lower fractional anisotropy value as compared to the normal segment [53].

Use of high-resolution ultrasound in imaging of peripheral neuropathy is a relatively new use of this age-old modality. Ultrasound is a rapid, cost effective, widely available modality with no contraindications. It allows quick assessment of the nerve throughout its length and provides unmatched data about anatomical details of the affected nerve. Technical issues like inability to image through bone, orthopaedic implants, poor resolution of deeper nerves with higher frequency transducers, suboptimal scan in patients with higher fatty tissue due to increase in depth and similar echogenicity limit its use to a certain extent. Operator dependence and need for in-depth knowledge of the anatomical details is another limiting factor.

Ulnar nerve is the second most common nerve involved in compressive neuropathies of the upper limb. Patients presenting with symptoms of ulnar nerve palsy have been conventionally diagnosed using clinical and electrodiagnostic findings. Use of high-resolution ultrasound and MRI will usher in a new era of multimodality approach in the diagnosis and treatment of nerve pathologies. It allows direct visualisation of the nerve with precise anatomical details and points towards the aetio-pathogenesis of the palsy, facilitating better clinical decision making and patient management. This pictorial essay describes the hallmark of imaging findings in a wide spectrum of ulnar nerve pathologies as diagnosed using imaging modalities.