Neuropatia de ulnar la cot Flashcards
Care este cea mai frecventa neuropatie de entrapment la membrele superioare?
neuropatia de median la pumn prin sdr de canal carpian
Care este a doua cea mai frecventa neuropatie de entrapment la membrele superioare?
Neuropatia de ulnar la cot
Ce leziuni pot mima o neuropatie de ulnar la cot?
entrapment la nivelul pumnului
plexopatie de trunchi inferior
radiculopatie C8-T1
Anatomia nervului ulnar
Nv ulnar deriva din radacinile C8-T1;
Trunchiul inferior din plexul brahial;
Cordonul medial al plexului brahial - extensia terminala la acestui cordon devine nv ulnar; Nv senzitivi cutanati brahial medial si nv cutanati antebrahial medial si alte ramuri pt nv median deriva tot din cordonul medial;
Nv median coboara la nivelul bratului medial si nu da nici un ram;
Trece prin septul intermuscular medial la nivelul jumatatii bratului si trece prin arcada lui Struthers (fascia profunda, fb ms din capul medial al tricepsului si ligamentul brahial intern);
Apoi nv median trece medial si distal spre cot.
La cot: nv intra in santul ulnar (intre epicondilul medial si procesul olecranian) ;
Putin mai distal de sant in antebratul proximal, nv ulnar trece pe sub arcada tendinoasa a celor 2 capetele a ms FCU = aponevroza humerala-ulnara = tunelul cubital.
se desprind apoi ramurile musculare pt FCU si divizia mediala a FDP deg 4,5
Apoi nv coboara prin antebratul medial fara sa dea vreun ram pana dupa pumn.
La 5-8 cm proximal de pumn, iese ramul senzitiv cutanat dorsal ulnar - pt sensib fetei dorsale mediale a mainii si a deg 4,5.
La nivelul apofizei stiloide ulnare, ramul senzitiv cutanat palmar pt sensibil palmei mediale proximale.
Nv intra prin pumn medial prin canalul Guyon pt sensib pt deg 5 si partea mediala a deg 4 si musculatura eminentei hipotenare, interososii palmari si dorsali, lumbricali III, IV si 2 muschi ai eminentei tenare (adductor pollicis si capul profund al FPB)
Anatomia cotului
Nv ulnar devine superficial cand se apropie de santul ulnar;
de obicei nv medial trece prin santul ulnar; rar trece medial pe deasupra la epicondil;
la unii exista o banda fibrotendinoasa densa sau ms epitrohleoanconeu accesor intre epicondilul medial si olecran;
distal de santul ulnar este tunelul ulnar-loc de entrapment;
0-22 mm intre epicondilul medial si tunelul cubital;
!!! de aia stimulezi la 3 cm sub sant si deasupra santului;
In tunelul cubital, nv ulnar se continua pe sub FCU si iese printre fascia profunda ce separa FCU si FDP - la 3-7 cm distal de santul cubital; ramul pt FCU la unii e distal de tunelul cubital 93%.
Etiologia neuropatiei de ulnar la cot
compresiune mecanica cronica / intindere la nivelul santului cubital sau la n_ivelul tunelului_;
rar: la sant: ganglion, tumori, benzi fibroase, ms accesori;
majoritatea: compresiune externa sau traumatisme repetate;
fractura de cot anterioara (si cu cativa ani) sau artroza de cot => paralizie ulnara tardiva;
traumatisme minore cronice / compresiuni (sprijin pe cot)
imobilizare postoperatorie; compresiune in timpul anesteziei sau comei;
subluxatie a nv ulnar in afara santului ulnar (in timpul flexie cotului);
Distal de sant, in tunelul cubital:
compresiune a nv ulnar sub tunelul cubital ingust congenital;
flexie persistenta si repetata intinde nv ulnar si creste presiunea in tunelul cubital;
Clinica in neuropatia de ulnar la cot
e la fel pt compresiune in sant sau in tunelul cubital;
DDx cu CTS (simpt senzitive mai proeminente) - predom simpt motorii, mai ales cronice;
- deficit motor fara simpt senzitive - compresiune mecanica lent progresiva;
- Majoritatea ms intrinseci ai mainii sunt inervati de ulnar=> slabiciune in acesti ms: pierderea dexteritatii; scaderea fortei pensei;
- atrofie la nivelul eminentei hipotenare si tenare (adductor pollicis si FPB capul profund)
adductia deg mare e crutata (inervata de median si radial);
Posturi ale mainii prin slabiciunea ms din ulnar:
- postura Benediction - de binecuvantare: deg inelar si deg mic sunt inclestate, cu artic metacarpofalangiana in hiperextensie si artic interfalangiene proximale si distale flectate (date de slabiciunea lumbricali III, IV), deg si deg mare sunt tinute in usoara abductie (slabiciune interososi si adductor pollicis);
- semnul Wartenberg - deg 5 e in adductie pasiva prin slabiciune de ms al 3-lea interosos palmar; pacientul isi prinde deg mic in buzunar cand incearca sa bage mana;
- semnul Froment - cand pac incearca sa piste un obiect sau o foaie de hartie. To compensate for intrinsic ulnar hand weakness, the long flexors to the thumb and index finger (median innervated) are used, creating a flexed thumb and index finger posture.
Examination of the patient’s grip often reveals it to be abnormal. Weakness of the ulnar-innervated FDP will result in the inability to flex the joints of the ring and little fingers. This often can be demonstrated just by having the patient make a fist (Figure 19–6). Patients with ulnar neuropathy may not be able to flex the distal fourth and fifth fingers completely when making a grip; in contrast, the median- innervated second and third distal digits flex normally.
In UNE, sensory disturbance, when present, involves the volar and dorsal fifth and medial fourth digits and the medial hand (Figure 19–7). The sensory disturbance does not extend proximally much beyond the wrist crease. Sensory involvement extending into the medial forearm implies a higher lesion in the plexus or nerve roots (i.e., this is the territory of the medial antebrachial cutaneous sensory nerve, which arises directly from the medial cord of the brachial plexus). Another important skin territory to check is the dorsal medial hand. Sensory abnormalities here are important because they indicate that the dorsal ulnar cutaneous sensory nerve territory also is involved. This finding excludes an ulnar neuropathy at the wrist as the dorsal ulnar cutaneous sensory nerve arises proximal to the wrist.
Pain, when present, may localize to the elbow or radiate down to the medial forearm and wrist. Paresthesias may be reproduced by placing the elbow in a flexed position or by applying pressure to the groove behind the medial epi- condyle. The ulnar nerve may be palpably enlarged and tender. The nerve may also be palpably taut with decreased mobility, especially in patients with ulnar neuropathy at the cubital tunnel.
Diagnosticul diferential al neuropatiei de ulnar la cot
The differential diagnosis in a patient suspected of having UNE (Table 19–1) principally includes C8–T1 radiculopa- thy, lower trunk or medial cord brachial plexopathy, and ulnar neuropathy at the wrist. Very rare cases of ulnar nerve entrapment in the proximal arm and more distally in the forearm have also been reported.
A cervical radiculopathy at the C8–T1 level, although seen less frequently than radiculopathy at the C6 and C7 root levels (which are more commonly affected in cervi- cal disc disease or spondylosis), may be difficult to differ- entiate clinically from ulnar neuropathy. Neck pain and radiation into the arm, sensory disturbance extending into the forearm, and weakness involving the median and radi- ally innervated C8–T1 muscles are the major differentiat- ing features. Of course, weakness often is minimal and sensory loss often vague in radiculopathy, making the dif- ferentiation between a mild C8–T1 radiculopathy and an ulnar neuropathy demanding, if based on clinical find- ings alone.
Lower trunk/medial cord brachial plexopathies are uncommon. Entrapment of the lower trunk by a fibrous band or hypertrophied muscle results in neurogenic thoracic outlet syndrome (see Chapter 30). Lower trunk plexopa- thies may also result from infiltration by neoplasm, prior radiation, or self-limited inflammatory processes (e.g.,
neuralgic amyotrophy). Like C8–T1 radiculopathy, lower trunk plexopathies may demonstrate weakness of non- ulnar-innervated C8–T1 muscles and sensory disturbance that extends into the medial forearm.
Other than in the region of the elbow, entrapment of the ulnar nerve in the arm or forearm is rare. In the arm proper, entrapment under the arcade of Struthers has been reported. In the forearm, infrequent cases of ulnar neu- ropathy occur at the exit of the cubital tunnel. The entraping structure is the deep fascia between the FCU and FDP. Unusual cases of ulnar neuropathy in the distal forearm have also been reported due to a fibrovascular band supply- ing blood to a hypertrophied FCU muscle. Clinical differentiation of these unusual cases from typical UNE is difficult. They are usually discovered either by careful elec- trophysiologic examination, at the time of surgery, or at the time of a second surgery after a failed ulnar surgery at the elbow.
Evaluarea electrofiziologica in neuropatia de nerv ulnar la cot
Like other mononeuropathies, the goal of nerve conduction studies and electromyography (EMG) is to demonstrate abnormalities that are limited to one nerve, in this case the ulnar nerve. Although in most cases the lesion is at the elbow, entrapment at the wrist, at the medial cord or lower trunk of the brachial plexus, or at the C8–T1 nerve roots can mimic a UNE clinically. Patterns of nerve conduction and EMG abnormalities often can be used to differentiate these possibilities (Table 19–2). If the ulnar nerve lesion is demyelinating, nerve conduction studies may demonstrate conduction velocity slowing, conduction block, or both at the lesion site. Unfortunately, in many cases of UNE, the pathophysiology is that of axonal loss, and nerve conduction studies demonstrate only a non-localizable ulnar neuropa- thy. The EMG study, if abnormal, then can be used to localize the lesion only at or proximal to the takeoff to the most proximal muscle affected on EMG. Because there are no ulnar-innervated muscles above the elbow, the electro- physiologic impression often is one of an ulnar neuropathy at or proximal to the FCU muscle (the most proximal ulnar-innervated muscle).
Nerve Conduction Studies
The goal of nerve conduction studies in patients with UNE is to demonstrate, when possible, focal demyelination across the elbow (Box 19–1). Focal demyelinating lesions may manifest as slowing of conduction velocity or conduc- tion block between proximal and distal stimulation sites (Figure 19–8). As for focal slowing, one needs to consider how much slowing is abnormal. In general, conduction velocities of more proximal nerve segments are the same as, or more often faster than those of, distal segments. This is due to a combination of (1) larger nerve fiber diameter and less tapering of the nerve more proximally (the reason that conduction velocities are faster in the upper than in the lower extremity) and (2) warmer temperatures in the proximal limb compared to the distal limb. In ulnar motor nerve conduction studies, however, this relationship may not hold true unless the position of the elbow is controlled.
Differential Slowing: Flexed versus Extended Elbow Conduction Techniques
One of the more complicating factors in ulnar conduction studies is the position of the elbow and its effect on the calculated conduction velocity across the elbow. It has been well established in many studies that the position of the elbow during ulnar conduction studies strongly influences the calculated conduction velocity. Ulnar conduction studies performed in the extended (i.e., straight) elbow position often show artifactual slowing of conduction veloc-
ity across the elbow due to underestimation of the true nerve length (Figure 19–9). This is because in the extended
elbow position, the ulnar nerve is slack with some redun- dancy. In normal subjects, this results in ulnar conduction velocities being slower in the across-the-elbow segment than in the segment above or below it, if the study is per- formed with the elbow in the extended position. Autopsy studies have confirmed that the length of the ulnar nerve across the elbow is measured more accurately with the elbow flexed (i.e., bent).
In several studies of normal controls, the mean differen- tial slowing comparing the across-the-elbow conduction velocity to forearm conduction velocity in the flexed elbow position (90–135 degrees) was 0 m/s, with an upper limit of normal of 10 to 11 m/s. In contrast, in the extended elbow position, mean slowing was 10 to 11 m/s, with an upper limit of normal in the range of 25 to 30 m/s (to reemphasize, in normal controls!). This extent of factitious conduction velocity slowing across the elbow, in the extended elbow position, is poorly appreciated in some EMG laboratories. Some laboratories arbitrarily use a value of 10 m/s differential slowing across the elbow, in the extended elbow position, to localize an ulnar neuropathy to the elbow. However, appreciation of the large range of variability in normal subjects, with the elbow in an extended position, is crucial to avoid erroneously diagnosing UNE in the normal population. An arbitrary cutoff value of 10 m/s differential slowing between the forearm and across elbow segments, in the extended elbow position, will result in many false-positive diagnoses of UNE. A patient with sensory loss in the little finger from a C8 radiculopathy would not be pleased to undergo ulnar nerve surgery simply based on a conduction velocity slowing of 10 m/s across the elbow compared to the forearm segment, if tested in the extended elbow position (as this is a normal finding in the extended elbow position).
Similar considerations apply to the absolute conduction velocity across the elbow in normal controls. The lower limit of normal for absolute conduction velocity across the elbow is 38 m/s in the extended elbow position, but never drops below 49 m/s in the flexed elbow position. Some have found that the absolute conduction velocity across the elbow is a better measure than differential conduction velocity slowing for detecting abnormalities in patients with ulnar neuropathy. Although absolute conduction velocity across the elbow may be considered a sensitive indicator of ulnar neuropathy, it does not localize the lesion. In any patient with significant axonal loss and dropout of the largest conducting fibers, conduction velocity will decrease across all nerve segments. An ulnar conduction velocity across the elbow segment of 40 m/s has little localizing value if the forearm conduction velocity is also 40 m/s.
In studies comparing the relative usefulness of the flexed versus extended elbow position in demonstrating focal slowing across the elbow, in those patients who had local- izing electrophysiology, the flexed elbow position has been found to be more sensitive than the extended position. The difference in the yield between the flexed and extended positions likely is related to the greater range and variability found in normal subjects for differential and absolute con- duction velocities across the elbow when tested in the extended elbow position, leading to lower cutoff values.
Thus, the flexed elbow position is considered the preferred technique when performing ulnar nerve conduction studies across the elbow. However, the flexed elbow position is more demanding in terms of measuring the curved ana- tomic course of the ulnar nerve around the elbow. In addi- tion, the flexed position has the drawback of undercalling patients with UNE and subluxable ulnar nerves, which might lead to an overestimation of the true nerve length (see below). Nevertheless, it is far better to undercall UNE in this uncommon patient group, using the flexed technique, than to erroneously diagnose UNE in normal patients, using the extended position, with inappropriate low cutoff values.
Conduction Block
In addition to focal slowing, the other electrophysiologic marker of demyelination is conduction block (Figure 19–8). There is some controversy regarding how much the ampli- tude or area must drop between distal and proximal sites to be considered conduction block (see Chapter 3). Ulnar motor conduction studies in normal subjects have shown a maximum drop in compound muscle action potential (CMAP) amplitude of 10% comparing below and above elbow and 20 to 25% comparing wrist and above-elbow sites. Accordingly, any drop in amplitude of more than 10% between below and above the elbow, especially if associated with a very small change in stimulating electrode position (see the following section) or an abrupt drop in conduction velocity, likely represents true demyelination and is of localizing value.
The other issue that must be considered in the proper interpretation of a conduction block is to not confuse a Martin–Gruber anastomosis (MGA) with a conduction block. Almost always, an MGA is recognized on routine ulnar motor nerve conduction studies as a drop in ampli- tude and area between the wrist and below-elbow stimula- tion sites (i.e., mimicking a conduction block in the forearm). The site of the MGA is typically between 3 and 10 cm distal to the medial epicondyle, a location that is not thought to interfere with electrodiagnostic evaluation of UNE. However, there are rare reports of very proximal MGAs wherein the drop in amplitude and area occurs between the below-elbow and above-elbow stimulation sites – that is, across the elbow. Thus, in all cases of ulnar conduction block across the elbow, it is prudent also to check for an MGA (by stimulating the median nerve at the wrist and antecubital fossa, and recording the ulnar muscle) (see more below in the Nerve Conduction Pitfalls section).
Short Segment Incremental Studies (“Inching”)
In a technique similar to that used for CTS, short segment incremental studies (SSIS), also known as “inching,” can be performed effectively on the ulnar nerve across the elbow to try to localize the lesion, looking for an abrupt change in either latency or amplitude. The technique is performed as follows:
- Either the abductor digiti minimi (ADM) or first dorsal interosseous (FDI) muscle is recorded. A mark is first placed halfway between the medial epicondyle and the olecranon to mark the ulnar groove. The location of the ulnar nerve is then mapped out. This process is basically identical to that of ensuring that the stimulator is directly over the nerve, as described in Chapter 3. This is accomplished by using a sub- maximal current (10–25% supramaximal), and stimulating medial to and lateral to the suspected nerve location in successive sites across the elbow. Several locations are tested sequentially from the below-elbow to above-elbow sites. At each site, the location that gives the highest CMAP amplitude is the one that is closest to the nerve, and is marked with a marker pen. A line is then drawn across the elbow “connecting all the dots” to mark exactly where the nerve lies.
The spot between the medial epicondyle and olecranon is marked as the “zero” point along the line that was drawn across the elbow, and denotes the spot adjacent to the medial epicondyle. Next, 1 cm increments are carefully marked off, along the line that was drawn, from 4 cm below the “zero” point (medial epicondyle) to 4 or 6 cm above.
The ulnar nerve is stimulated supramaximally at each location at successive 1 cm intervals from below to above the medial epicondyle (Figure 19–10).
Any abrupt increase in latency or drop in amplitude between successive stimulation sites implies focal demyelination. In normal individuals, the latency between two successive 1 cm stimulation sites usually is 0.1 to 0.3 ms and rarely 0.4 ms (Figure 19–11). Any greater latency shift (i.e., ≥0.5 ms) suggests focal slowing and demyelination (Figure 19–12). The inching technique is very sensitive but technically demanding. Any error in measurement is magni- fied when such short distances are used. The technique has the advantage of potentially being able to directly locate the lesion either at the groove or at the cubital tunnel. This may be of more than just academic interest, because it may be of some help in deciding the best surgical technique to use (e.g., a lesion of the cubital tunnel may be best handled by a simple release rather than a transposition).
Recording the First Dorsal Interosseous
In entrapment neuropathies, it is well known that nerve fibers to certain muscles may be preferentially affected whereas others are preferentially spared. Within a nerve, bundles of nerve fibers to different muscles run in separate fascicles separated by connective tissue. External compres- sion may preferentially affect the fibers within the fascicle nearest to the compression, thereby preferentially affecting the muscle that those fibers innervate (Figure 19–13). Thus, recording from different muscles sometimes can increase the yield of demonstrating either focal slowing or conduction block. Some studies have shown that recording the first dorsal interosseous (FDI) may be a slightly more sensitive technique than recording the ADM in UNE. When recording the FDI, it is best to place the active electrode over the muscle belly and the reference over the metacarpophalangeal joint of the thumb (Figure 19–14). If the reference electrode is placed on the metacarpophalan- geal joint of the index finger, an initial positive deflection often will be seen, which complicates latency measure- ments (Figure 19–15).
Mixed and Sensory Nerve Conductions
Mixed and sensory ulnar nerve conductions across the elbow may increase the yield of identifying focal slowing in patients with UNE. Sensory conductions can be performed antidromically or orthodromically from the fifth digit using the wrist, below-elbow, and above-elbow sites for either stimulating or recording, respectively. Likewise, a mixed nerve potential can be recorded below and above the elbow, stimulating the mixed nerve at the wrist.
Although these studies may have increased sensitivity for identifying UNE, they involve significant technical difficul- ties. Both sensory and mixed nerve potentials dramatically decrease in amplitude when recorded at greater distances because of the normal phenomena of temporal dispersion and phase cancellation (Figure 19–16). For instance, a normal antidromic ulnar sensory nerve action potential (SNAP) amplitude may be 20 μV when stimulated at the wrist; however, stimulating at the below-elbow site, the amplitude may fall to 5 μV and above the elbow to 2 μV. In patients with ulnar neuropathy, these potentials are often low if axonal loss has occurred. In such cases, the potential at the below-elbow and above-elbow sites may be very low or absent. Averaging is frequently required, and identification of the onset latency of these very small potentials is often difficult. These techniques may be best suited for mild cases of UNE, in which the distal sensory and mixed nerve potentials are of relatively normal ampli- tude. It is important to emphasize that when performing these studies, one is looking for focal slowing across the elbow and not for conduction block. Because of the normal drop in amplitude of sensory and mixed nerve fibers over distance, separating conduction block from normal tempo- ral dispersion and phase cancellation may be very difficult (unless the stimulation sites are very close, such as the 1 cm increments used in inching across the carpal tunnel).
Dorsal Ulnar Cutaneous Sensory Study
Recording the dorsal ulnar cutaneous sensory nerve can be a useful technique to perform in patients with suspected ulnar neuropathy. The dorsal ulnar cutaneous sensory nerve arises 5 to 8 cm proximal to the wrist to supply sensation over the dorsal medial hand, as well as the dorsal fifth and medial fourth digits. The dorsal ulnar SNAP can be recorded by placing recording electrodes in the dorsal web space between the fifth and fourth digits and stimulating 8 to 10 cm proximally just below the ulnar styloid with the hand placed in a pronated position (Figure 19–17). Usually, the potential can be recorded using a small stimulating current (e.g., 5–15 mA). A normal antidromic response is greater than 8 μV, but, as in other uncommonly performed sensory nerve conduction studies, comparison with the contralateral asymptomatic side frequently is helpful. Any potential that is less than 50% that of the contralateral asymptomatic side likely is abnormal.*
With knowledge of the anatomy of both the routine digit 5 ulnar SNAP and the dorsal ulnar SNAP, one can predict the expected patterns of abnormalities in lesions of the ulnar nerve at the elbow and at the wrist (Figure 19–18). In patients with UNE, one would expect both SNAPs to be abnormal, provided there has been axonal loss. If the lesion is pure demyelination at the elbow, both distal sensory responses will be normal. Conversely, the presence of a normal dorsal ulnar SNAP with an abnormal digit 5 ulnar sensory response suggests that the lesion is at the wrist (the dorsal ulnar branch arises proximal to the wrist). Nevertheless, this latter pattern does not completely exclude the possibility of UNE. In some patients with defi- nite UNE and axonal loss, the dorsal ulnar cutaneous SNAP is spared. This finding is thought to be due to preferential fascicular sparing of the dorsal ulnar cutaneous sensory fibers at the elbow. Studies of the microanatomy of the fascicle that forms the dorsal ulnar cutaneous sensory branch have shown that it commonly separates from the main ulnar trunk above the elbow and effectively travels as a separate nerve next to the ulnar nerve in the forearm. Therefore, care must be taken in interpreting the findings of an abnormal digit 5 ulnar SNAP and a normal dorsal ulnar cutaneous SNAP. This pattern has limitations as a diagnostic marker and cannot be used alone to reliably localize the site of the lesion to the wrist. Electrophysio- logic measurement of the dorsal ulnar SNAP is useful, but only in those cases where it is abnormal, implying localiza- tion of the lesion proximal to the wrist. To summarize, although an abnormal dorsal ulnar cutaneous SNAP indi- cates that the lesion is proximal to the wrist, the converse is not necessarily true.
Nerve Conduction Study Pitfalls
When performing routine ulnar nerve conduction studies, one must keep in mind several important technical factors:
- When stimulating at the below-elbow site, the stimulator must be located 3 cm distal to the groove to ensure that the stimulation point is distal to the cubital tunnel.
- Care must be taken not to stimulate too distally at the below-elbow site. The mistaken impression of UNE may occur if the below-elbow stimulation site is too distal and the patient has a coexistent high Martin–Gruber anastomosis (see Chapter 7). In this situation, one could see a drop in amplitude between the below-elbow and above-elbow stimulation sites. Thus, the optimal position to stimulate the below- elbow site is 3 cm distal to the medial epicondyle, not less, not more. In addition, as the nerve runs deep under the FCU, higher current is required at the below-elbow site, and supramaximal stimulation may be difficult to achieve.
- The distance from the below-elbow site to the above-elbow site ideally should be 10 cm. If shorter distances are used, slight errors in measurement may create large differences in calculated conduction velocities. If longer distances are used, a longer length of normal nerve may dilute any conduction velocity slowing across the elbow, yielding normal or equivocal results.
- The examiner should be cautious of any apparent conduction block between the wrist and below-elbow sites (Figure 19–19). Although there are very rare ulnar lesions in the forearm (e.g., exit of the cubital tunnel, fibrovascular bands in the forearm), this finding usually indicates a Martin–Gruber anastomosis, which is a normal finding. In these situations, stimu- lating the median nerve at the wrist and antecubital fossa, while recording the ulnar muscle (ADM or FDI), is essential to demonstrate that an anastomosis is present.
- As noted above, a Martin–Gruber anastomosis is usually recognized on routine ulnar motor nerve conduction studies as a drop of amplitude and area between the wrist and below-elbow stimulation sites. However, there are rare reports of a very proximal MGA wherein the drop in amplitude and area occurs between the below-elbow and above-elbow stimula- tion sites (i.e., across the elbow), mimicking a conduction block across the elbow. The optimal site for the below-elbow stimulation site is 3 cm distal to the medial epicondyle. It should be more than 2 cm in order to be distal to the cubital tunnel, and less than 4 cm to avoid the nerve being so deep that it is difficult to stimulate. Although almost all MGAs occur in the forearm and do not interfere with electrodiagnostic determination of conduction block at the elbow, some reports have found an MGA to be as proximal as 3 cm distal to the medial epicondyle (Figure 19–20). Thus, in this very unusual situation, one could confuse an MGA (a normal finding) with an ulnar conduction block across the elbow. This under- scores that the correct site to stimulate the ulnar nerve below the elbow is 3 cm distal to the medial epicondyle. In all cases where an ulnar conduction block is found across the elbow, it is prudent to check for an MGA (by stimulating the median nerve at the wrist and antecubital fossa, and recording the ulnar muscle).
- Rarely, flexing the elbow causes the ulnar nerve to sublux out of the groove medially over the medial epicondyle. Recurrent subluxation of the ulnar nerve has been a suggested cause of repetitive ulnar trauma and UNE. Thus, in a situation where a patient does have UNE and a subluxed nerve when in the elbow flexed position, the measured distance around the groove will actually overestimate the length of the nerve, resulting in a spuriously fast conduction velocity across the elbow (see Figure 19–21). In one recent study of normal individuals with a subluxed ulnar nerve at the elbow, the average change in distance across the elbow segment was overestimated by 1.6 cm (range, 0.6 to 2.5 cm), which equated to an overestimated ulnar conduction velocity across the elbow an average of 7.9 m/s (range, 3.0 to 13.0 m/s). One can see how this could result in a false-negative study in a person with UNE, if the conduction velocity across the elbow were overestimated, and did not meet the cutoff criteria for absolute and differen- tial focal slowing across the elbow. It is important to emphasize that a subluxed ulnar nerve interferes with determination of the true conduction velocity across the elbow, but not conduction block across the elbow. These cases emphasize the value of SSIS (“inching”) in suspected UNE, as this technique maps out the exact location of the ulnar nerve, and is able to detect the precise area of slowing.
Electromyographic Approach
The strategy in the EMG examination of UNE is directed toward identifying denervation or reinnervation limited to the ulnar-innervated muscles of the hand and forearm (Box 19–2). Useful muscles to check are the FDI, FDP (to digit 4 or 5), and FCU. Of the intrinsic ulnar hand muscles, testing of the FDI is usually tolerated best by patients. Testing of the ADM often is perceived as more painful, similar to the abductor pollicis brevis (APB). Median- and radial-innervated C8 muscles are screened to rule out
evidence of a C8 radiculopathy or lower trunk brachial plexopathy. Useful muscles to check are the APB, flexor pollicis longus, and extensor indicis proprius. If a cervical radiculopathy is suggested based on clinical history, then sampling the cervical paraspinal muscles is also indicated.
Of interest, the FCU is either normal or minimally affected in many surgically proven cases of UNE. Overall, involvement of the FCU correlates with the severity of the ulnar neuropathy both clinically and electrically. The finding of FCU involvement is slightly more common in lesions at the groove than at the cubital tunnel. Although sparing of the FCU was classically thought to be due to the muscular branch to the FCU arising proximal to the groove, cadaver anatomic studies have found this not to be the case. The true etiology of FCU sparing likely is related to either dif- ferential fascicular susceptibility (i.e., different fascicles are involved or spared depending on their position within the nerve trunk in relationship to the compression site) or the “dying back” concept of nerve lesions (i.e., the most distal muscles are maximally affected and the proximal ones are relatively preserved). This EMG pattern of an abnormal FDI and FDP to digits 4 and 5, but a spared FCU, is impor- tant to recognize in patients with UNE.
Unfortunately, there is no ulnar-innervated muscle above the elbow. If all ulnar-innervated muscles, including the FCU, are abnormal and the nerve conduction studies do not identify any focal slowing or conduction block around the elbow, the best electrophysiologic diagnosis that can be reached is one of an ulnar neuropathy that can only be localized at or proximal to the takeoff to the FCU muscle. Although most such cases will in fact be cases of UNE, the electrophysiologic examination cannot exclude an unusual ulnar neuropathy in the proximal arm or a lower brachial plexopathy that selectively involves ulnar fibers. Examina- tion of the medial antebrachial cutaneous sensory nerve, which comes directly off the medial cord of the brachial plexus, may help identify a lower brachial plexus lesion.
