REVIEW ARTICLE
Differential Diagnosis of Finger Drop Aravinthan Varatharaj, BM, BCh, MA(Oxon), MRCP,* Ashwin Pinto, BM, BCh, FRCP, DPhil,* and Mike Manning, MB, ChB, FRCSw
Abstract: Finger drop is a useful clinical sign which is easy to elicit. This article presents a logical approach for assessing patients with finger drop and outlines the important causes, and how to differentiate them. Patients with finger drop may present either to orthopedic surgeons or to neurologists, and both specialists should be aware of important diagnoses in their complementary fields. Key Words: finger drop, posterior interosseous nerve, peripheral neuropathy
(The Neurologist 2015;19:128–131)
FINGER DROP A good clinical sign is quick and easy to elicit, objective in interpretation, and has a relatively short list of potential causes. “Finger drop” is such a sign. It is elicited by asking the patient to hold both arms out, with the wrists and fingers held straight, and palms facing the floor. The sign is considered positive when there is inability to maintain extension of one or more fingers at the metacarpophalangeal joints (MCPJs), despite good extension at the wrist (Fig. 1). Concomitant flexion at the wrist joint (wrist drop) is a distinct clinical sign, usually associated with radial nerve palsy; although there is some overlap in causes, this article deals only with the differential diagnosis of finger drop.
THE ANATOMY OF FINGER DROP Finger extension at the MCPJs is controlled by the extensor digitorum communis (EDC), which arises from the lateral epicondyle of the humerus and passes down the posterior compartment of the forearm. The muscle provides separate tendons to all 4 fingers, although with the exception of that passing to the index finger the tendons are joined by fibrous bands and cannot act independently. The extensor digiti minimi and the extensor indicis provide additional tendons to the little and index fingers, respectively. All 3 muscles are supplied by the posterior interosseous branch of the radial nerve, which contains only motor fibers to these and other muscles of the extensor compartment (the few sensory fibers in the nerve supply the interosseous membrane and are not clinically relevant). Do not test the long extensors by asking the patient to open their hand from a fist, as even if the EDC is compromised the interossei and lumbricals will extend the interphalangeal joints and open the hand. The best way to identify weakness in the EDC is to look for finger drop as described above, and to test the ability to maintain finger extension against resistance. From the *Wessex Neurological Centre, Southampton; and wDepartment of Orthopaedics, Whiston Hospital, Prescot, UK. The authors declare no conflict of interest. Reprints: Aravinthan Varatharaj, BM, BCh, MA(Oxon), MRCP, Wessex Neurological Centre, Tremona Road, Southampton, SO16 6YD, UK. E-mail: [email protected]. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 1074-7931/15/1905-0128 DOI: 10.1097/NRL.0000000000000021
128 | www.theneurologist.org
As an aside, when testing finger abduction and adduction in the presence of finger drop one should take care to ensure that the fingers are passively held extended in the plane of the metacarpals. If not, the flexed position compromises the lever and reduces the force applied by the interossei, creating the illusion of weakness in these muscles.
“NEUROLOGICAL” CAUSES OF FINGER DROP Multifocal Motor Neuropathy With Conduction Block (MMN-CB) A chronic pure motor neuropathy of likely immune etiology, MMN-CB typically presents as asymmetrical distal weakness affecting primarily the upper limbs. The disease is more common in men than women and typically presents in the middle age. There is often differential involvement of fibers of the posterior interosseous nerve, resulting in drop of Z1 fingers; typically the third or fourth fingers are affected.1 The ability of MMN-CB to selectively attack a subset of fibers within a motor nerve is a characteristic feature of the disease. Finger drop may be the only feature of the illness. Early on in the disease there may be profound weakness without wasting (as there is no denervation), and marked fasciculation is less common than in motor neuron disease. Nerve conduction studies may show discrete areas of conduction block outside areas considered typical for nerve entrapment, although conduction block is not detected in all clinical cases. A subset of patients produce anti-GM1 ganglioside antibody, although the diagnostic value of testing is limited.2 A standard course of intravenous immunoglobulin (IVIg) typically results in a swift improvement, although regular infusions are necessary to maintain response. Corticosteroids are ineffective and may worsen symptoms.
Motor Neuron Disease The early stages of amyotrophic lateral sclerosis are often monomelic, with involvement of only 1 limb. Denervation of the long extensors may lead to finger drop with a paucity of signs outside the affected limb. However, electromyography (EMG) often shows subclinical denervation in other muscles, and one would expect clinical progression over time. Wasting and fasciculations may be more prominent early on than in MMN-CB, and nerve conduction studies are helpful to exclude the presence of conduction block. The coexistence of upper motor neuron signs would strongly suggest a diagnosis of amyotrophic lateral sclerosis.
Posterior Interosseous Nerve Palsy The posterior interosseous nerve arises from the radial nerve at the level of the lateral epicondyle, passes through the supinator in the arcade of Frohse, and descends down the forearm along the interosseous membrane. Palsy is commonly due to compression by fibrous bands in the arcade of Frohse, which may be related to repetitive pronation-supination movements (eg, screwdriver use). Compression can also occur The Neurologist
Volume 19, Number 5, May 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
The Neurologist
Volume 19, Number 5, May 2015
Differential Diagnosis of Finger Drop
Syringomyelia An expanding syrinx disrupts the anterior horn cells and, as the disease typically begins in the cervicothoracic cord, motor neuron pools supplying the finger extensors (C7, C8) may be affected, resulting in a finger drop. The small muscles of the hand are typically involved, and wasting and fasciculation may be apparent. There is usually loss of pain and temperature sensation because of the interruption of spinothalamic fibers which decussate soon after entering the cord. Neuropathic injuries on the hands are common, reflecting the cutaneous anesthesia. Magnetic resonance imaging is the investigation of choice. Treatment is largely supportive; although in cases associated with a Chiari malformation decompression of the foramen magnum may be attempted. FIGURE 1. An example of finger drop.
due to a mass in the forearm, commonly a lipoma.3 The nerve may be damaged in trauma to the upper limb, typically as a complication of the Monteggia fracture-dislocation or because of penetrating injury.4 The nerve is also vulnerable during elbow surgery, for example, when making a lateral incision for open reduction and internal fixation of a fractured proximal radius.5 Posterior interosseous nerve palsy may be suspected based on a characteristic pattern of muscle weakness (Table 1) and an absence of sensory signs. Sparing of extensor carpi radialis longus allows the wrist to extend in radial deviation but not in ulnar deviation, though is a difficult feature to elicit. Incomplete lesions may affect extension of 1 or 2 fingers only. In the case of compression by fibrous bands, there is often tenderness over the arcade of Frohse and the pain is exacerbated by resisted supination. Neurophysiology and imaging of the forearm may be helpful to confirm the diagnosis and the cause. Treatment depends on the underlying cause. In idiopathic posterior interosseous nerve palsy, surgical exploration and release of the arcade of Frohse should be considered.
Myasthenia Gravis The finger extensors may be preferentially affected in distal forms of myasthenia gravis, although finger abduction and wrist extension are often involved as well. One review written in 1948 noted that “paresis of y the extensor of one finger may be the only recognizable involvement for a long period of time.”6 Variable weakness with fatiguability is suggestive. Bilateral involvement is more typical, and more proximal muscles may also be involved. Distal weakness may be the presenting feature of myasthenia gravis, or more commonly may develop later in the course of generalized disease. Muscle wasting is unusual. Antibodies to the acetylcholine receptor are typically present, and electrodiagnostic confirmation is achieved with demonstration of a decremental response to repetitive nerve stimulation, or jitter (and block) on single-fiber EMG. TABLE 1. Muscles Supplied by the Posterior Interosseous Nerve Extensor digitorum communis (finger extension at MCPJs) Extensor digiti indicis and minimi (index and little finger extension at MCPJs) Extensor carpi ulnaris (extension and ulnar deviation at wrist) Extensor pollicis brevis (extension of thumb at MCPJ) Extensor pollicis longus (extension of thumb at IPJ) Supinator (supination of forearm) IPJ indicates interphalangeal joint; MCPJ, metacarpophalangeal joint.
Copyright
r
Distal Myopathies Welander myopathy occurs due to a mutation in the TIA1 protein and is mainly found in Sweden and Finland, although Sumner et al7 described cases in England. Onset is around the fourth or fifth decade and weakness begins in the hands, most commonly in the finger and wrist extensors. Over time the intrinsic hand muscles are involved, and there is slow progression to the feet with weakness of the toe and ankle extensors. Serum creatine kinase tends to be normal or only mildly raised. EMG is myopathic, and muscle biopsy shows rimmed vacuoles and sarcoplasmic inclusions similar to those found in inclusion body myositis. Genetic testing is confirmatory. Other distal myopathies may also present with finger drop, such as the myofibrillar myopathy caused by mutations in ZASP (Z-band alternatively spliced PDZ motif-containing protein).8
Cortical Hand Finger drop can also be due to a central pathology, originally described by Lhermitte as “pseudoperipheral palsy.”9 The “cortical hand” results from a lesion, usually an infarct, in the hand area of the motor strip in the contralateral precentral gyrus. Given the dense somatotopic representation of the hand, this area forms a readily identifiable “knob” on the precentral gyrus. Anatomic studies suggest that the radial fingers are represented laterally in the hand area while the ulnar fingers are placed medially,10 and a clinical series correlating infarct location with finger weakness was supportive of this theory.11 The pattern of weakness is variable, but finger extension is often involved, hence the finger drop. If more proximal arm weakness is also present, with ipsilateral leg weakness or other hemispheric signs such as hemisensory loss, then the diagnosis may be more clear; but in the case of isolated distal hand weakness, a central cause is easy to forget. Spasticity and brisk reflexes will not be present acutely. If the lesion involves only the precentral gyrus, then sensory features will be absent. A clue to point against a peripheral etiology maybe the involvement of muscles supplied by multiple peripheral nerves, for example, extensor digitorum (radial), abductor pollicis brevis (median), and the interossei (ulnar). A sudden onset of symptoms in a patient with appropriate risk factors would suggest a vascular cause. The investigation of choice is diffusion-weighted magnetic resonance imaging, looking for a lesion in the relevant cortical area (Fig. 2) (Table 2).
“ORTHOPEDIC” CAUSES OF FINGER DROP Ruptured Extensor Tendon This is usually associated with rheumatoid arthritis. Extensor tendon disruption occurs because of friction against
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.theneurologist.org |
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
129
The Neurologist
Varatharaj et al
Volume 19, Number 5, May 2015
FIGURE 2. Magnetic resonance images in axial section showing an acute infarction in the hand knob of the right precentral gyrus, with a lesion (see arrow) bright on diffusion-weighted imaging (A), and dark on the apparent diffusion coeffficient map (B).
abnormal bony surfaces, microvascular inflammation, or through erosion by inflamed synovium. The tendon of extensor digiti minimi typically goes first, followed by the tendon of EDC going to the little finger, the tendon of EDC going to the ring finger, and then the extensor pollicis longus. On examination, one should note the finger drop and any coexisting TABLE 2. Summary of “Neurological” Causes of Finger Drop
Conditions MMN-CB
Motor neuron disease (amyotrophic lateral sclerosis form) Posterior interosseous nerve palsy Myasthenia gravis
Syringomyelia
Distal myopathies Cortical hand
Motor Features Weakness without prominent wasting or fasciculation; differential finger drop Weakness with prominent wasting and fasciculation; spasticity; brisk reflexes; extensor plantars Weakness of muscles innervated by posterior interosseous nerve only Fatigable weakness; bilateral involvement; associated proximal weakness Weakness typically beginning in hand and ascending; wasting of small muscles Slowly progressive weakness; family history Involvement of muscles supplied by multiple peripheral nerves; sudden onset (if vascular)
Sensory Features None
Extensor Tendon Subluxation None
None
As each long extensor tendon passes over the dorsal aspect of the MCPJ, it is made to sit over the midline of the joint by a sling of fibrous tissue known as the sagittal band. In this way the tendons are held away from the center of rotation of the MCPJ and thus exert a greater force on the phalanges. When the sagittal bands are weak or broken, the extensor tendons are liable to sublux ulnarly into the valleys between
None
Loss of pain and temperature sensation in characteristic distribution None If present may be in cortical pattern (eg, agraphaesthesia, astereognosis)
MMN-CB indicates multifocal motor neuropathy with conduction block.
130 | www.theneurologist.org
features of rheumatoid arthritis, and then instruct the patient to hold their elbow flexed (preferably resting on the arm of a chair), with the forearm vertical, wrist extended, and fingers curled naturally. In this position, one may best demonstrate the so-called “tenodesis effect”; whereby as the examiner passively flexes the wrist, the fingers automatically extend due to tension on the long extensors (Fig. 3). This natural effect is preserved in neurological causes of finger drop and in posterior interosseous nerve palsy, but lost in tendon rupture. If identified early the best treatment is surgical repair through side-toside transfer of adjacent tendons.
FIGURE 3. Normal appearance of the tenodesis effect; the fingers extend as the wrist is flexed. Note the natural cascade of the fingers, whereby resting flexion increases from the radial to the ulnar side.
Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
The Neurologist
Volume 19, Number 5, May 2015
Differential Diagnosis of Finger Drop
TABLE 3. Summary of “Orthopedic” Causes of Finger Drop
Conditions
Differentiating Features
Posterior interosseous nerve palsy Ruptured extensor tendon Extensor tendon subluxation Trigger finger
Depending on cause; history of trauma, surgery, or repetitive strain, palpable lipoma Associated with rheumatoid arthritis; typically affects little finger firs; loss of tenodesis effect Unable to actively extend, but can be passively extended and held in place Characteristic story of locking; palpable nodule over metacarpal head
MCPJs, and in doing so the mechanical advantage of extensor digitorum is compromised. This may occur after a laceration about the dorsal surface of the MCPJs, through a twisting force on the fingers, or secondary to rheumatoid synovitis of the MCPJs. On examination, one notes finger drop and finds an inability to actively extend the flexed finger. However, the examiner may passively extend the finger, and in doing so the extensor tendon is brought to lie back in the correct position. The patient may then hold the extended finger in place. In an acute sagittal band injury, a primary surgical repair may be possible. In chronic extensor tendon subluxation, repair is complicated and one may attempt to centralize the wayward tendon through a combination of releasing the sagittal band on the ulnar side and both reefing (tightening) the sagittal band radially and anchoring it to the radial collateral ligament of the MCPJ.
Trigger Finger Also known as stenosing tenovaginitis, this is a condition in which the sheath containing the finger flexor tendons become stenosed near the base of the digit. The flexor tendon proximal to the constriction becomes swollen and may be palpable as a tender nodule over the metacarpal head. The patient has difficultly flexing and extending the affected finger and experiences locking and clicking as the swollen tendon is forced through the narrowed sheath. The finger may lock in any position and the patient typically resorts to using the other hand to click the finger back into the range of movement. With the finger locked in flexion, this condition may mimic finger drop. The etiology of trigger finger is unclear but the condition is certainly more common in diabetics. Treatment includes splintage, physiotherapy, steroid injection into the tendon sheath, or surgical release of the first part of the tendon sheath (Table 3).
CONCLUSIONS Finger drop is a useful clinical sign which is easy to elicit and has a relatively short list of causes. Careful clinical examination can help to narrow down the differential. As a rule, if the tenodesis effect is lost then the problem is with the tendons rather than the nerves. In a patient with appropriate vascular risk factors, the acute onset of finger drop without
Copyright
r
trauma should prompt the search for a cortical infarct. The distinction made here between “neurological” and “orthopedic” causes is of course arbitrary and clearly patients may present to either specialist. As well as providing a system with which to approach the patient with finger drop, hopefully this article also illustrates the value of a more perfect union between neurology and orthopedics. ACKNOWLEDGMENT The authors thank Medical Photography at Whiston Hospital for their help with preparing the images. REFERENCES 1. Slee M, Selvan A, Donaghy M. Multifocal motor neuropathy: the diagnostic spectrum and response to treatment. Neurology. 2007;69:1680–1687. 2. Nobile-Orazio E, Cappellari A, Priori A. Multifocal motor neuropathy: current concepts and controversies. Muscle Nerve. 2005;31:663–680. 3. Werner P, Furtner M, Lo¨scher WN, et al. A case of posterior interosseous nerve palsy: good recovery despite diagnostic delay. J Neurol Neurosurg Psychiatry. 2007;78:1408–1409. 4. Sunderamoorthy D, Chaudhury M. An uncommon peripheral nerve injury after penetrating injury of the forearm: the importance of clinical examination. Emerg Med J. 2003;20:565–566. 5. McRae R, Esser M. Practical Fracture Treatment. 5th ed. Edinburgh: Churchill Livingstone; 2008. 6. Harvey AM. Some preliminary observations on the clinical course of myasthenia gravis before and after thymectomy. Bull N Y Acad Med. 1948;24:505–522. 7. Sumner D, Crawford M, Harriman DGF. Distal muscular dystrophy in an English family. Brain. 1971;94:51–60. 8. Selcen D, Engel AG. Mutations in ZASP define a novel form of muscular dystrophy in humans. Ann Neurol. 2005;57:269–276. 9. Lhermitte J. De valeur semiologique des troubles de la sensibilite a disposition radiculaire dans les lesions de l’encephale [Semiological value of radicular sensory disturbance caused by a cerebral lesion]. Sem Med. 1909;24:277–293. 10. Penfield W, Boldrey E. Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain. 1937;60:389–443. 11. Kim JS. Predominant involvement of a particular group of fingers due to small, cortical infarction. Neurology. 2001;56:1677–1682.
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.theneurologist.org |
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
131
Differential Diagnosis of Finger Drop Aravinthan Varatharaj, BM, BCh, MA(Oxon), MRCP,* Ashwin Pinto, BM, BCh, FRCP, DPhil,* and Mike Manning, MB, ChB, FRCSw
Abstract: Finger drop is a useful clinical sign which is easy to elicit. This article presents a logical approach for assessing patients with finger drop and outlines the important causes, and how to differentiate them. Patients with finger drop may present either to orthopedic surgeons or to neurologists, and both specialists should be aware of important diagnoses in their complementary fields. Key Words: finger drop, posterior interosseous nerve, peripheral neuropathy
(The Neurologist 2015;19:128–131)
FINGER DROP A good clinical sign is quick and easy to elicit, objective in interpretation, and has a relatively short list of potential causes. “Finger drop” is such a sign. It is elicited by asking the patient to hold both arms out, with the wrists and fingers held straight, and palms facing the floor. The sign is considered positive when there is inability to maintain extension of one or more fingers at the metacarpophalangeal joints (MCPJs), despite good extension at the wrist (Fig. 1). Concomitant flexion at the wrist joint (wrist drop) is a distinct clinical sign, usually associated with radial nerve palsy; although there is some overlap in causes, this article deals only with the differential diagnosis of finger drop.
THE ANATOMY OF FINGER DROP Finger extension at the MCPJs is controlled by the extensor digitorum communis (EDC), which arises from the lateral epicondyle of the humerus and passes down the posterior compartment of the forearm. The muscle provides separate tendons to all 4 fingers, although with the exception of that passing to the index finger the tendons are joined by fibrous bands and cannot act independently. The extensor digiti minimi and the extensor indicis provide additional tendons to the little and index fingers, respectively. All 3 muscles are supplied by the posterior interosseous branch of the radial nerve, which contains only motor fibers to these and other muscles of the extensor compartment (the few sensory fibers in the nerve supply the interosseous membrane and are not clinically relevant). Do not test the long extensors by asking the patient to open their hand from a fist, as even if the EDC is compromised the interossei and lumbricals will extend the interphalangeal joints and open the hand. The best way to identify weakness in the EDC is to look for finger drop as described above, and to test the ability to maintain finger extension against resistance. From the *Wessex Neurological Centre, Southampton; and wDepartment of Orthopaedics, Whiston Hospital, Prescot, UK. The authors declare no conflict of interest. Reprints: Aravinthan Varatharaj, BM, BCh, MA(Oxon), MRCP, Wessex Neurological Centre, Tremona Road, Southampton, SO16 6YD, UK. E-mail: [email protected]. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 1074-7931/15/1905-0128 DOI: 10.1097/NRL.0000000000000021
128 | www.theneurologist.org
As an aside, when testing finger abduction and adduction in the presence of finger drop one should take care to ensure that the fingers are passively held extended in the plane of the metacarpals. If not, the flexed position compromises the lever and reduces the force applied by the interossei, creating the illusion of weakness in these muscles.
“NEUROLOGICAL” CAUSES OF FINGER DROP Multifocal Motor Neuropathy With Conduction Block (MMN-CB) A chronic pure motor neuropathy of likely immune etiology, MMN-CB typically presents as asymmetrical distal weakness affecting primarily the upper limbs. The disease is more common in men than women and typically presents in the middle age. There is often differential involvement of fibers of the posterior interosseous nerve, resulting in drop of Z1 fingers; typically the third or fourth fingers are affected.1 The ability of MMN-CB to selectively attack a subset of fibers within a motor nerve is a characteristic feature of the disease. Finger drop may be the only feature of the illness. Early on in the disease there may be profound weakness without wasting (as there is no denervation), and marked fasciculation is less common than in motor neuron disease. Nerve conduction studies may show discrete areas of conduction block outside areas considered typical for nerve entrapment, although conduction block is not detected in all clinical cases. A subset of patients produce anti-GM1 ganglioside antibody, although the diagnostic value of testing is limited.2 A standard course of intravenous immunoglobulin (IVIg) typically results in a swift improvement, although regular infusions are necessary to maintain response. Corticosteroids are ineffective and may worsen symptoms.
Motor Neuron Disease The early stages of amyotrophic lateral sclerosis are often monomelic, with involvement of only 1 limb. Denervation of the long extensors may lead to finger drop with a paucity of signs outside the affected limb. However, electromyography (EMG) often shows subclinical denervation in other muscles, and one would expect clinical progression over time. Wasting and fasciculations may be more prominent early on than in MMN-CB, and nerve conduction studies are helpful to exclude the presence of conduction block. The coexistence of upper motor neuron signs would strongly suggest a diagnosis of amyotrophic lateral sclerosis.
Posterior Interosseous Nerve Palsy The posterior interosseous nerve arises from the radial nerve at the level of the lateral epicondyle, passes through the supinator in the arcade of Frohse, and descends down the forearm along the interosseous membrane. Palsy is commonly due to compression by fibrous bands in the arcade of Frohse, which may be related to repetitive pronation-supination movements (eg, screwdriver use). Compression can also occur The Neurologist
Volume 19, Number 5, May 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
The Neurologist
Volume 19, Number 5, May 2015
Differential Diagnosis of Finger Drop
Syringomyelia An expanding syrinx disrupts the anterior horn cells and, as the disease typically begins in the cervicothoracic cord, motor neuron pools supplying the finger extensors (C7, C8) may be affected, resulting in a finger drop. The small muscles of the hand are typically involved, and wasting and fasciculation may be apparent. There is usually loss of pain and temperature sensation because of the interruption of spinothalamic fibers which decussate soon after entering the cord. Neuropathic injuries on the hands are common, reflecting the cutaneous anesthesia. Magnetic resonance imaging is the investigation of choice. Treatment is largely supportive; although in cases associated with a Chiari malformation decompression of the foramen magnum may be attempted. FIGURE 1. An example of finger drop.
due to a mass in the forearm, commonly a lipoma.3 The nerve may be damaged in trauma to the upper limb, typically as a complication of the Monteggia fracture-dislocation or because of penetrating injury.4 The nerve is also vulnerable during elbow surgery, for example, when making a lateral incision for open reduction and internal fixation of a fractured proximal radius.5 Posterior interosseous nerve palsy may be suspected based on a characteristic pattern of muscle weakness (Table 1) and an absence of sensory signs. Sparing of extensor carpi radialis longus allows the wrist to extend in radial deviation but not in ulnar deviation, though is a difficult feature to elicit. Incomplete lesions may affect extension of 1 or 2 fingers only. In the case of compression by fibrous bands, there is often tenderness over the arcade of Frohse and the pain is exacerbated by resisted supination. Neurophysiology and imaging of the forearm may be helpful to confirm the diagnosis and the cause. Treatment depends on the underlying cause. In idiopathic posterior interosseous nerve palsy, surgical exploration and release of the arcade of Frohse should be considered.
Myasthenia Gravis The finger extensors may be preferentially affected in distal forms of myasthenia gravis, although finger abduction and wrist extension are often involved as well. One review written in 1948 noted that “paresis of y the extensor of one finger may be the only recognizable involvement for a long period of time.”6 Variable weakness with fatiguability is suggestive. Bilateral involvement is more typical, and more proximal muscles may also be involved. Distal weakness may be the presenting feature of myasthenia gravis, or more commonly may develop later in the course of generalized disease. Muscle wasting is unusual. Antibodies to the acetylcholine receptor are typically present, and electrodiagnostic confirmation is achieved with demonstration of a decremental response to repetitive nerve stimulation, or jitter (and block) on single-fiber EMG. TABLE 1. Muscles Supplied by the Posterior Interosseous Nerve Extensor digitorum communis (finger extension at MCPJs) Extensor digiti indicis and minimi (index and little finger extension at MCPJs) Extensor carpi ulnaris (extension and ulnar deviation at wrist) Extensor pollicis brevis (extension of thumb at MCPJ) Extensor pollicis longus (extension of thumb at IPJ) Supinator (supination of forearm) IPJ indicates interphalangeal joint; MCPJ, metacarpophalangeal joint.
Copyright
r
Distal Myopathies Welander myopathy occurs due to a mutation in the TIA1 protein and is mainly found in Sweden and Finland, although Sumner et al7 described cases in England. Onset is around the fourth or fifth decade and weakness begins in the hands, most commonly in the finger and wrist extensors. Over time the intrinsic hand muscles are involved, and there is slow progression to the feet with weakness of the toe and ankle extensors. Serum creatine kinase tends to be normal or only mildly raised. EMG is myopathic, and muscle biopsy shows rimmed vacuoles and sarcoplasmic inclusions similar to those found in inclusion body myositis. Genetic testing is confirmatory. Other distal myopathies may also present with finger drop, such as the myofibrillar myopathy caused by mutations in ZASP (Z-band alternatively spliced PDZ motif-containing protein).8
Cortical Hand Finger drop can also be due to a central pathology, originally described by Lhermitte as “pseudoperipheral palsy.”9 The “cortical hand” results from a lesion, usually an infarct, in the hand area of the motor strip in the contralateral precentral gyrus. Given the dense somatotopic representation of the hand, this area forms a readily identifiable “knob” on the precentral gyrus. Anatomic studies suggest that the radial fingers are represented laterally in the hand area while the ulnar fingers are placed medially,10 and a clinical series correlating infarct location with finger weakness was supportive of this theory.11 The pattern of weakness is variable, but finger extension is often involved, hence the finger drop. If more proximal arm weakness is also present, with ipsilateral leg weakness or other hemispheric signs such as hemisensory loss, then the diagnosis may be more clear; but in the case of isolated distal hand weakness, a central cause is easy to forget. Spasticity and brisk reflexes will not be present acutely. If the lesion involves only the precentral gyrus, then sensory features will be absent. A clue to point against a peripheral etiology maybe the involvement of muscles supplied by multiple peripheral nerves, for example, extensor digitorum (radial), abductor pollicis brevis (median), and the interossei (ulnar). A sudden onset of symptoms in a patient with appropriate risk factors would suggest a vascular cause. The investigation of choice is diffusion-weighted magnetic resonance imaging, looking for a lesion in the relevant cortical area (Fig. 2) (Table 2).
“ORTHOPEDIC” CAUSES OF FINGER DROP Ruptured Extensor Tendon This is usually associated with rheumatoid arthritis. Extensor tendon disruption occurs because of friction against
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.theneurologist.org |
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
129
The Neurologist
Varatharaj et al
Volume 19, Number 5, May 2015
FIGURE 2. Magnetic resonance images in axial section showing an acute infarction in the hand knob of the right precentral gyrus, with a lesion (see arrow) bright on diffusion-weighted imaging (A), and dark on the apparent diffusion coeffficient map (B).
abnormal bony surfaces, microvascular inflammation, or through erosion by inflamed synovium. The tendon of extensor digiti minimi typically goes first, followed by the tendon of EDC going to the little finger, the tendon of EDC going to the ring finger, and then the extensor pollicis longus. On examination, one should note the finger drop and any coexisting TABLE 2. Summary of “Neurological” Causes of Finger Drop
Conditions MMN-CB
Motor neuron disease (amyotrophic lateral sclerosis form) Posterior interosseous nerve palsy Myasthenia gravis
Syringomyelia
Distal myopathies Cortical hand
Motor Features Weakness without prominent wasting or fasciculation; differential finger drop Weakness with prominent wasting and fasciculation; spasticity; brisk reflexes; extensor plantars Weakness of muscles innervated by posterior interosseous nerve only Fatigable weakness; bilateral involvement; associated proximal weakness Weakness typically beginning in hand and ascending; wasting of small muscles Slowly progressive weakness; family history Involvement of muscles supplied by multiple peripheral nerves; sudden onset (if vascular)
Sensory Features None
Extensor Tendon Subluxation None
None
As each long extensor tendon passes over the dorsal aspect of the MCPJ, it is made to sit over the midline of the joint by a sling of fibrous tissue known as the sagittal band. In this way the tendons are held away from the center of rotation of the MCPJ and thus exert a greater force on the phalanges. When the sagittal bands are weak or broken, the extensor tendons are liable to sublux ulnarly into the valleys between
None
Loss of pain and temperature sensation in characteristic distribution None If present may be in cortical pattern (eg, agraphaesthesia, astereognosis)
MMN-CB indicates multifocal motor neuropathy with conduction block.
130 | www.theneurologist.org
features of rheumatoid arthritis, and then instruct the patient to hold their elbow flexed (preferably resting on the arm of a chair), with the forearm vertical, wrist extended, and fingers curled naturally. In this position, one may best demonstrate the so-called “tenodesis effect”; whereby as the examiner passively flexes the wrist, the fingers automatically extend due to tension on the long extensors (Fig. 3). This natural effect is preserved in neurological causes of finger drop and in posterior interosseous nerve palsy, but lost in tendon rupture. If identified early the best treatment is surgical repair through side-toside transfer of adjacent tendons.
FIGURE 3. Normal appearance of the tenodesis effect; the fingers extend as the wrist is flexed. Note the natural cascade of the fingers, whereby resting flexion increases from the radial to the ulnar side.
Copyright
r
2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
The Neurologist
Volume 19, Number 5, May 2015
Differential Diagnosis of Finger Drop
TABLE 3. Summary of “Orthopedic” Causes of Finger Drop
Conditions
Differentiating Features
Posterior interosseous nerve palsy Ruptured extensor tendon Extensor tendon subluxation Trigger finger
Depending on cause; history of trauma, surgery, or repetitive strain, palpable lipoma Associated with rheumatoid arthritis; typically affects little finger firs; loss of tenodesis effect Unable to actively extend, but can be passively extended and held in place Characteristic story of locking; palpable nodule over metacarpal head
MCPJs, and in doing so the mechanical advantage of extensor digitorum is compromised. This may occur after a laceration about the dorsal surface of the MCPJs, through a twisting force on the fingers, or secondary to rheumatoid synovitis of the MCPJs. On examination, one notes finger drop and finds an inability to actively extend the flexed finger. However, the examiner may passively extend the finger, and in doing so the extensor tendon is brought to lie back in the correct position. The patient may then hold the extended finger in place. In an acute sagittal band injury, a primary surgical repair may be possible. In chronic extensor tendon subluxation, repair is complicated and one may attempt to centralize the wayward tendon through a combination of releasing the sagittal band on the ulnar side and both reefing (tightening) the sagittal band radially and anchoring it to the radial collateral ligament of the MCPJ.
Trigger Finger Also known as stenosing tenovaginitis, this is a condition in which the sheath containing the finger flexor tendons become stenosed near the base of the digit. The flexor tendon proximal to the constriction becomes swollen and may be palpable as a tender nodule over the metacarpal head. The patient has difficultly flexing and extending the affected finger and experiences locking and clicking as the swollen tendon is forced through the narrowed sheath. The finger may lock in any position and the patient typically resorts to using the other hand to click the finger back into the range of movement. With the finger locked in flexion, this condition may mimic finger drop. The etiology of trigger finger is unclear but the condition is certainly more common in diabetics. Treatment includes splintage, physiotherapy, steroid injection into the tendon sheath, or surgical release of the first part of the tendon sheath (Table 3).
CONCLUSIONS Finger drop is a useful clinical sign which is easy to elicit and has a relatively short list of causes. Careful clinical examination can help to narrow down the differential. As a rule, if the tenodesis effect is lost then the problem is with the tendons rather than the nerves. In a patient with appropriate vascular risk factors, the acute onset of finger drop without
Copyright
r
trauma should prompt the search for a cortical infarct. The distinction made here between “neurological” and “orthopedic” causes is of course arbitrary and clearly patients may present to either specialist. As well as providing a system with which to approach the patient with finger drop, hopefully this article also illustrates the value of a more perfect union between neurology and orthopedics. ACKNOWLEDGMENT The authors thank Medical Photography at Whiston Hospital for their help with preparing the images. REFERENCES 1. Slee M, Selvan A, Donaghy M. Multifocal motor neuropathy: the diagnostic spectrum and response to treatment. Neurology. 2007;69:1680–1687. 2. Nobile-Orazio E, Cappellari A, Priori A. Multifocal motor neuropathy: current concepts and controversies. Muscle Nerve. 2005;31:663–680. 3. Werner P, Furtner M, Lo¨scher WN, et al. A case of posterior interosseous nerve palsy: good recovery despite diagnostic delay. J Neurol Neurosurg Psychiatry. 2007;78:1408–1409. 4. Sunderamoorthy D, Chaudhury M. An uncommon peripheral nerve injury after penetrating injury of the forearm: the importance of clinical examination. Emerg Med J. 2003;20:565–566. 5. McRae R, Esser M. Practical Fracture Treatment. 5th ed. Edinburgh: Churchill Livingstone; 2008. 6. Harvey AM. Some preliminary observations on the clinical course of myasthenia gravis before and after thymectomy. Bull N Y Acad Med. 1948;24:505–522. 7. Sumner D, Crawford M, Harriman DGF. Distal muscular dystrophy in an English family. Brain. 1971;94:51–60. 8. Selcen D, Engel AG. Mutations in ZASP define a novel form of muscular dystrophy in humans. Ann Neurol. 2005;57:269–276. 9. Lhermitte J. De valeur semiologique des troubles de la sensibilite a disposition radiculaire dans les lesions de l’encephale [Semiological value of radicular sensory disturbance caused by a cerebral lesion]. Sem Med. 1909;24:277–293. 10. Penfield W, Boldrey E. Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain. 1937;60:389–443. 11. Kim JS. Predominant involvement of a particular group of fingers due to small, cortical infarction. Neurology. 2001;56:1677–1682.
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.theneurologist.org |
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
131
