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Disease/ Disorder

Definition

Ulnar mononeuropathy at the wrist (UMW) refers to an injury of the distal portion of the ulnar nerve resulting in motor and/or sensory deficits in its distribution. It is also known as Guyon’s canal syndrome or ulnar tunnel syndrome.1 Common causes include external compression caused by repetitive hand usage and compression from ganglia or other mass lesions. The clinical presentation is determined by the location of the injury with respect to the branches of the distal ulnar nerve.

Etiology

Disagreement exists in the literature with regards to the most common cause(s) of UMW.1,2 Injury to the distal ulnar nerve may occur due to compression, trauma, or vascular insufficiency. External compression from repetitive use and ganglia in the region of the wrist are variably cited as the most common causes.3 Additional causes4 include lipomas, rheumatoid arthritis (causing synovial cysts or synovial proliferation), tumors, and anomalous anatomical structures (including aberrant hand muscles).

Epidemiology including risk factors and primary prevention

Epidemiology of UMW is not well-known or studied at this time. Ulnar neuropathies are the second most common upper limb entrapment neuropathy, after the median nerve, and the wrist is the second most common entrapment point of the ulnar nerve, after the elbow.5 Risk factors include occupations, activities, and hobbies that put increased pressure at the base of the palm or wrist.3,6 Cycling has been identified as an activity that is associated with UMW.7 Diabetes has also recently been proposed as a risk factor for ulnar nerve entrapment.8 Primary prevention includes avoiding prolonged pressure at the base of the palm or wrist and the use of padded gloves and/or padded handlebars with cycling. It is also important to ensure adequate fit of any casts, braces, or splints that encompass the wrist to prevent compression of the ulnar nerve.

Patho-anatomy/physiology

Guyon’s canal is a tunnel at the wrist between the hook of the hamate and the pisiform bone. The floor of the tunnel is formed by the transverse carpal ligament and the pisohamate ligament. The roof is formed by volar carpal ligament and palmaris brevis muscle.

In the forearm, the ulnar nerve gives off the palmar cutaneous branch (supplying sensation to the proximal/ulnar portion of the palm) and, more distally, the dorsal ulnar cutaneous (DUC) nerve that supplies sensation to the dorsal/ulnar aspect of the hand. Neither the palmar cutaneous branch nor the DUC nerve traverse Guyon’s canal, and sensation in the distribution of these nerves is spared in UMW.

The ulnar nerve then enters Guyon’s canal where it divides into the deep and superficial branches. The superficial branch supplies sensation to the volar aspects of the fifth and medial half of the fourth digits in addition to the distal/ulnar palmar surface. The superficial branch also innervates the palmaris brevis muscle. The deep branch provides a branch to the hypothenar muscles before supplying the interosseous muscles and 3rd and 4th lumbricals. Symptoms of UMW are dependent on the location of the lesion and which nerve branches it affects.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Depending on the source, UMW can be divided into 3, 4, or 5 types.  Here, four types will be discussed, as described in Stewart’s Focal Peripheral Neuropathies.1 It should be noted that only Type 1 involves a lesion that is actually in Guyon’s canal.

  1. Type 1 involves compression of both the deep and superficial branches of the ulnar nerve.  Compression occurs at the entrance of Guyon’s canal (main trunk of the ulnar nerve) or within Guyon’s canal (both deep and superficial branches).  Both sensation and strength are affected, though the distributions of the palmar cutaneous branch and DUC are spared.
  2. Type 2 involves compression only of the deep branch of the ulnar nerve, affecting both the hypothenar branch and the terminal branch to the interossei and lumbricals.  Sensory function is spared.  Compression occurs distal to Guyon’s canal and proximal to the hypothenar branch.
  3. Type 3 involves compression of the deep branch distal to the hypothenar branch. The hypothenar muscles are spared, while the interossei and 3rd and 4th lumbricals are affected.  Sensory function is spared as the superficial branch is not involved.
  4. Type 4 involves compression of only the superficial branch.  Motor function is spared (with the exception of the palmaris brevis muscle). Compression occurs distal to Guyon’s canal. Type 4 is least common type and is rare.

Compression occurs in the following order of frequency: Type 3 (most common), Type 1, Type 2, Type 4 (least common).

Specific secondary or associated conditions and complications

Complications of untreated UMW may include loss of hand function related to weakness and numbness, and an ulnar claw deformity secondary to weakness of the two lumbricals on the thenar side and unopposed action of the medial half of the flexor digitorum profundus.

Essentials of Assessment

History

History should focus on the distribution of symptoms – especially numbness and weakness, potential risk factors, prior trauma, and exacerbating and alleviating factors. Clinicians should also clarify if there is clinical history suggestive of an ulnar lesion at the elbow (which is a much more common site of ulnar neuropathy), such as elbow pain or external compression of the elbow. The history should also be used to explore for the possibility of other diagnoses in the differential including neck pain radiating into the arm suggestive of a C8 or T1 radiculopathy, or history suggestive of a brachial plexus injury. In patients with purely motor syndromes, the differential diagnoses would include amyotrophic lateral sclerosis, monomelic amyotrophy, and multifocal motor neuropathy with conduction block, thus the possibility of systemic symptoms and/or symptoms outside the distribution of the ulnar nerve should be explored.

Physical examination

Inspection should be performed first, looking for atrophy of the hand intrinsic and abductor digiti mini muscles, an ulnar claw hand, or other deformities. Any atrophy of muscles outside the distribution of the ulnar nerve should raise suspicion for alternative/additional diagnoses. Close inspection for fasciculations in ulnar-innervated muscles, as well as other muscles, should be performed.

Manual muscle testing of all major muscle groups should be performed, particularly on hand intrinsic musculature. Ulnar-innervated muscles of the hand may be affected, but ulnar-innervated forearm muscles would be spared – this can help differentiate an ulnar nerve lesion at the wrist from one more proximal.

A thorough sensory examination should be performed.  Sensory disturbance of the volar fifth and medial fourth digits may be seen if the superficial sensory branch is affected. Careful attention should be paid to the sensory distributions of the DUC nerve and the palmar cutaneous branch of the ulnar nerve.  These branches should both be spared in an ulnar nerve lesion at the wrist but can both be affected in a lesion of the ulnar nerve at the elbow. It should be noted that, in Type 2 and Type 3 lesions, sensation should not be affected. Sensory deficits in the upper limb above the wrist/hand should raise suspicion of a nerve lesion more proximal (ie plexus, nerve root).

Froment’s sign and Wartenberg’s sign may help identify an ulnar nerve lesion, but these are not specific to ulnar neuropathy at the wrist. Froment’s sign is a sign from weakness of pinch strength between digits one and two and is due to weakness of the thumb adductor pollicis muscle, which is innervated by the deep branch of the ulnar nerve. Froment’s sign thus appears as thumb interphalangeal joint flexion when a patient attempts to grasp a thin object (ie piece of paper) between the thumb and index finger, as the weakened adductor pollicis is overtaken by the median nerve-innervated flexor pollicis longus during this pinching maneuver. Wartenberg’s sign is performed by placing the patient’s hand on a flat surface, with palm down and fingers extended and passively abducted. The patient is then asked to actively adduct the fingers. Inability to fully adduct the fifth digit is a positive Wartenberg sign, indicating weakness in the ulnar nerve-innervated intrinsic hand muscles, along with unopposed action of the extensor digiti minimi, innervated by the posterior interosseous nerve, from the deep branch of the radial nerve. Palmaris brevis sign may be seen in severe lesions of the deep branch of the ulnar nerve. This sign is positive when the fifth digit is abducted and a prominent contraction of the palmaris brevis may be seen, as a result of atrophy of the intrinsic hand muscles with sparing of the palmaris brevis muscle.

Functional assessment

The patient’s function must be assessed to determine if the neuropathy is causing impairment of self-care and activities of daily living, including hobbies and recreational pursuits.

Laboratory studies

Laboratory studies are not necessary for the diagnosis of UMW; however, they may help clarify medical status and any underlying etiologies. If rheumatoid arthritis is a concern, the clinician could consider checking rheumatoid factor, anti-cyclic citrullinated peptide antibodies, erythrocyte sedimentation rate, and C-reactive protein. Hemoglobin A1c, fasting blood glucose, and vitamin B12 levels can help identify confounding or coexisting neuropathies. In addition, certain medications for treating symptoms of pain and paresthesias may warrant investigation of renal or hepatic function.

Imaging

Plain radiographs are of limited utility in the evaluation of UMW unless a history of trauma is present or underlying pathology such as rheumatoid arthritis is considered. Computed tomography (CT) can also identify fractures, especially hamate fractures. Magnetic Resonance Imaging (MRI), MR Neurogram, and ultrasound may be useful in detecting enlargement of the ulnar nerve that can result from chronic compression. Also, these modalities can identify anomalous anatomic structures (such as an aberrant abductor digiti minimi muscle) or other space occupying lesions that may cause compression of the ulnar nerve (such as lipomas or ganglion cysts). Ultrasound may also reveal abnormalities in echogenicity that can occur with nerve compression. In addition, Doppler ultrasound can be used to evaluate for ulnar artery thrombosis.

Supplemental assessment tools

The electrodiagnostic evaluation is a key component of the evaluation of UMW.1 EMG and NCS can help localize the lesion, determine the severity and chronicity, and exclude other potential diagnoses in the differential.

  1. Sensory nerve conductions studies should be performed in the distribution of the ulnar nerve and surrounding nerves. It is important to keep in mind that in Type 2 and Type 3 lesions, no sensory abnormalities are expected. In Type 1 and Type 4 lesions, abnormalities in the ulnar sensory nerve conduction to the small finger may include slowing (indicating demyelination in the sensory fibers of the ulnar nerve) or decreased amplitude (indicating axon loss).  The DUC sensory nerve conduction study may be useful in differentiating an UMW from a lesion of the ulnar nerve at the elbow.  In a lesion at the wrist, the DUC should be normal.  In a lesion at the elbow, decreased amplitude may be observed in the DUC.  Decreased amplitude in the DUC and Medial Antebrachial Cutaneous nerve, along with the ulnar sensory nerve conduction study to the small finger, may occur in a lesion of the brachial plexus that may mimic the symptoms of ulnar neuropathy.
  2. Motor nerve conduction studies should be performed when stimulating the ulnar nerve and recording over the first dorsal interosseous (FDI) and abductor digiti minimi (ADM) muscles.  In Type 3 lesions, distal motor latency and amplitude should be normal while recording at the ADM, while recording at the FDI would be expected to show abnormalities.  Particularly when recording at the FDI, comparison to the contralateral (unaffected) limb may be useful to identify abnormalities. In Type 1 and Type 2 lesions, abnormalities may be seen in the distal motor latencies and amplitudes when recording at both the ADM and FDI. In Type 4 lesions, no abnormalities are expected in motor nerve conduction studies. Stimulation of the ulnar nerve in the palm may help identify conduction block caused by demyelination in the ulnar nerve in the wrist region. Careful attention should be paid to the conduction velocity in the ulnar nerve in the across-elbow segment to exclude the possibility of an ulnar nerve lesion at the elbow.  Median motor nerve conduction studies are also an important part of the examination. Simultaneous abnormalities in both median and ulnar motor nerve conduction studies should raise suspicion for a systemic neuropathy, motor neuron disease, brachial plexopathy, or cervical radiculopathy.
  3. Short segment incremental studies of the ulnar nerve in the wrist region may be useful to identify a point of focal slowing in the ulnar nerve.
  4. Needle electrode examination should be performed in hand intrinsic muscles supplied by the ulnar nerve (including the FDI and ADM) as well as the median nerve (including the abductor pollicis brevis and/or opponens pollicis).  Proximal ulnar-innervated muscles, such as the flexor digitorum profundus to digits 4 and 5 and flexor carpi ulnaris, should be sampled to exclude a proximal ulnar mononeuropathy, although normal findings in these muscles do not rule out an ulnar nerve lesion at the elbow. Denervation in the FDI with sparing of the ADM should raise suspicion for a Type 3 lesion, while a Type 1 or Type 2 lesion would be expected to affect both muscles.  Denervation in the abductor pollicis brevis, opponens pollicis, flexor carpi ulnaris, or flexor digitorum profundus should not occur in UMW and should result in consideration of alternative diagnoses.  Motor neuron disease would be expected to result in widespread or diffuse denervation as well as prominent fasciculations.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Treatment is based, first, on obtaining a correct diagnosis, and second, on identifying the underlying cause. Treatment should be aimed at alleviating the underlying cause and treating any associated symptoms. According to the European HANDGUIDE study,9,10 recommended treatment options include activity modification, splinting, and surgery. Mild symptoms may be treated conservatively with activity modification, occupational therapy, or splinting. More severe symptoms, especially those functionally limiting the patient, such as progressive weakness, severe numbness, and deformity, should be referred for surgical evaluation.

At different disease stages

New onset/acute:

Most experts have recommended activity modification with a combination of patient instructions and splinting in the setting of acute/subacute and mild symptoms. The patient should be advised to minimize pressure to the wrist and base of the palm, which can be done with a neutral wrist splint or by simply avoiding pressure and mechanical overload to the area. Occupational therapy may be beneficial to help maintain muscle strength and assist with occupational accommodations. Cyclists with UMW should be encouraged to use padded gloves, padded handlebars, and/or modify their grip. Medications, such as nonsteroidal anti-inflammatories, tricyclics, opioids, and anticonvulsants, are also frequently used to help minimize symptoms, although experts have agreed that they have not proven useful in treatment. Similarly, corticosteroids are occasionally injected into the area of entrapment to help reduce pain and inflammation despite lack of evidence demonstrating benefit to this intervention. Surgical intervention to relieve pressure on the nerve can be an option for severe cases.

Chronic/progressive:

If weakness and symptoms progress, then surgical intervention should be considered. Ulnar tunnel release has produced particularly successful outcomes in ulnar tunnel syndrome resulting from trauma or aberrant muscles.

Coordination of care

Care of a patient with UMW may involve a primary care provider, physiatrist, radiologist, electrodiagnostician, occupational therapist, and surgeon. Coordinating care with clear treatment goals is important for appropriate treatment of this issue.

Patient & family education

Patients should be educated on signs and symptoms of UMW, the basic anatomy, and pathophysiology. Especially when patients are being treated conservatively, it is important to educate the patient on signs that the lesion is progressing, such as worsening numbness, weakness, hand muscle atrophy, or hand deformity.  Education regarding activity modifications is important to attempt to avoid progression of nerve injury.

Cutting Edge/ Emerging and Unique Concepts and Practice

Ultrasound imaging of Guyon’s canal is a new imaging technique under investigation.11 As physiatrists become more comfortable with utilizing ultrasound in their clinical practice, it can be used as a readily available, safe, relatively inexpensive method to evaluate for signs of nerve compression and/or space-occupying lesions in Guyon’s canal. Sonographically-guided injections may be an option for improved accuracy.

Gaps in the Evidence-Based Knowledge

There is some controversy on the types of UMW, with various authors suggesting as few as 3 and as many as 5 types.1,2 These types are described based on their clinical and electrodiagnostic characteristics and refer to the location of entrapment within Guyon’s canal. When evaluating a patient, it is important to describe the clinical findings and perform the electrodiagnostic evaluation in sufficient detail to identify the entrapment point in the canal. Due to a lack of large-scale trials, comprehensive guidelines regarding diagnosis and management of UMW have not been well established. The use of MRI and ultrasound is still relatively new. The role and order of different diagnostic tests have yet to be clarified in the context of disease severity and duration. There is also limited data on the success of conservative measures to treat UMW.

References

  1. Stewart, J., Focal Peripheral Neuropathies. 2010 West Vancouver, Canada: JBJ Publishing.
  2. Donofrio, P., Textbook of Peripheral Neuropathy. 2012, New York, NY: Demos Medical.
  3. Murata, K., J.T. Shih, and T.M. Tsai, Causes of ulnar tunnel syndrome: a retrospective study of 31 subjects. J Hand Surg Am, 2003. 28(4): p. 647-51.
  4. Harvie, P., N. Patel, and S.J. Ostlere, Ulnar nerve compression at Guyon’s canal by an anomalous abductor digiti minimi muscle: the role of ultrasound in clinical diagnosis. Hand Surg, 2003. 8(2): p. 271-5.
  5. Stewart, J.D., The variable clinical manifestations of ulnar neuropathies at the elbow. J Neurol Neurosurg Psychiatry, 1987. 50(3): p. 252-8.
  6. Ginanneschi, F., et al., Ulnar nerve compression neuropathy at Guyon’s canal caused by crutch walking: case report with ultrasonographic nerve imaging. Arch Phys Med Rehabil, 2009. 90(3): p. 522-4.
  7. Akuthota, V., et al., The effect of long-distance bicycling on ulnar and median nerves: an electrophysiologic evaluation of cyclist palsy. Am J Sports Med, 2005. 33(8): p. 1224-30.
  8. Rydberg, M., et al., Diabetic hand: prevalence and incidence of diabetic hand problems using data from 1.1 million inhabitants in southern Sweden. BMJ Open Diabetes Res Care, 2022. 10(1).
  9. Hoogvliet, P., et al., How to treat Guyon’s canal syndrome? Results from the European HANDGUIDE study: a multidisciplinary treatment guideline. Br J Sports Med, 2013. 47(17): p. 1063-70.
  10. Chen, S.H., et al., Prospective outcome analysis of ulnar tunnel syndrome: Comparing traumatic versus non-traumatic etiologies. Asian J Surg, 2022.
  11. Aleksenko D, V.M., Guyon Canal Syndrome, in StatPearls [Internet]. 2022, StatPearls Publishing: Treasure Island, FL.

Original Version of the Topic

Bradeigh S. Godfrey, DO. Ulnar nerve mononeuropathy at the wrist. 9/20/2013

Previous Revision(s) of the Topic

Kevin Fitzpatrick, MD. Ulnar nerve mononeuropathy at the wrist. 2/13/2018

Author Disclosures

Thomas Chai, MD
Nothing to Disclose

Eliana Ege, MD
Nothing to Disclose