Keywords
Lacerto Fibrosus Syndrome - median nerve entrapment - hand surgery - WALANT
Introduction
Carpal tunnel syndrome (CTS) corresponds to the clinical manifestation of compression of the median nerve under the flexor carpi retinaculum and is recognized as the most frequent site of nerve compression in the upper extremities.[1]
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[4] Compression of the median nerve around the elbow is a lesser-known and often underdiagnosed entity. Its existence is controversial because it is difficult to confirm by common methods as it is a pathology that occurs due to dynamic compression, and its incidence in the general population is still unknown.[1]
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[7] It is necessary to highlight that both nerve compressions can occur simultaneously in the context of double compression or Double Crush Syndrome.[8]
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[12] On the other hand, the lack of complete resolution of symptoms after surgical treatment of the carpal tunnel could be the result of undiagnosed proximal compression.[1]
Compressive neuropathy of the median nerve that occurs in the proximal portion of the forearm can be the product of compression at various points, such as the proximal arch of the flexor digitorum superficialis (FDS) muscle, between the two heads of the pronator teres (PT) muscle, which is known as “pronator syndrome” and under lacertus fibrosus (LF) described as Lacertus Fibrosus Syndrome.[1]
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LF syndrome has been described in recent studies as the most common cause of proximal median nerve entrapment.[1]
[5] It corresponds to a dynamic compression so the usefulness of the electrodiagnostic and imaging study is limited.[14] Clinical evaluation is essential for the correct diagnosis and it is necessary to carry out a targeted search for clinical signs that suggest the presence of this neuropathy.[1]
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Conservative treatment is the first approach. In the event of its failure and persistence of symptoms, surgical release of the LF may be indicated. It is a relatively simple surgery, which can be performed under local anesthesia with the patient awake, which also has the advantage of allowing immediate clinical evaluation of the recovery of strength of some finger and wrist flexor muscles intraoperatively.[16]
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[20] This technique has been shown to have favorable results in the literature.[7]
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The purpose of the following work is to describe in detail the anatomy, clinical, and physical examination, emphasizing the techniques for a correct diagnosis, as well as the LF release surgery with local anesthesia technique without ischemia cuff and without sedation, WALANT (wide -awake local anesthesia no tourniquet). We believe that it is essential to recognize this pathology to avoid errors in diagnosis and, above all, underdiagnosis.
Anatomy
The median nerve originates from the union of a nerve contribution from the lateral bundle with a nerve contribution from the medial bundle of the brachial plexus, with contributions from the roots of C5 to T1.[12] It descends through the anteromedial region of the arm and elbow, on the medial edge in the antecubital fossa where it runs immediately under the LF, together with the brachial artery ([Fig. 1]). In its distal path it descends between both heads of the PT muscle and then deep to the proximal arch of the FDS muscle where it continues its path in the central region of the forearm towards the wrist, passing then under the transverse carpal ligament in the carpal tunnel. In its mid-proximal course in the forearm, the branches that make up the anterior interosseous nerve (AIN) emerge and the distal mid-segment of the palmar cutaneous nerve emerges.
Fig. 1 Anatomy of the anterior region of the elbow. LF = Lacertus Fibrosus; NM = Median Nerve.
The LF corresponds to an aponeurotic extension of the proximal portion of the bicipital tendon towards the medial edge of the antebrachial aponeurosis in the proximal-medial region of the forearm, involving the flexopronator muscles.[21] Its functions are to protect the underlying neurovascular structures, contribute to proprioception, and act as a stabilizing structure for the biceps tendon.[21] It is usually rectangular in shape, whose dimensions are usually between 4.5 to 6.2 cm long by 0.5 to 2.5 cm wide.[21]
In the cadaveric study of Dubois et al.[22] they emphasize the role of the LF as a compression structure, reporting that in 42% of the cases, the median nerve was in direct contact with the LF versus only 1 case (2.7% of the specimens) where the compression occurred at the level of the two heads of the PT.[22]
Pathophysiology of Dynamic Compression
Pathophysiology of Dynamic Compression
Compression of the median nerve in the proximal region of the forearm is an eminently dynamic compression and is defined as “Sunderland Zero”,[1]
[23] this means that the compression does not produce an anatomical alteration in the structure of the nerve, but rather causes a functional alteration, due to changes in axonal transport.
In the fascicular anatomy of the median nerve at the elbow, the most superficial fascicles are located in the anteromedial portion of the median nerve, they correspond to the fascicles of the anterior interosseous branch that innervates the flexor pollicis longus (FPL) and flexor profundus of the second finger (FPD2) and the branch for the flexor carpi radialis (FCR), which explains the clinical presentation of paresis of these muscles in particular.[24]
Surgical release of the LF could decrease pressure on the median nerve by up to 81%.[25] This, added to the predominantly dynamic nature of the compression, without the presence of axonal damage, makes it reasonable to expect a complete recovery of clinical symptoms after surgical release.[7]
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Clinical History and Physical Examination
Clinical History and Physical Examination
The symptoms of patients with LF syndrome are often mistakenly interpreted as CTS or may go unnoticed. It is very important to highlight that both pathologies can coexist and the symptoms may correspond to a “Double Crush” of the median nerve where proximal compression predisposes to distal compression or vice versa.[1]
[8] Hagert et al.[12] describe the presence of this double compression pattern in 25.1% of patients operated on for LF syndrome over 10 years and describe that 12.7% of all patients had previous surgery for CTS.
Within clinical history, it is essential to define the location and time at which the symptoms appear. Unlike carpal tunnel, the patient's clinical symptoms include intermittent, daytime pain that worsens with pronating activities and is in the anterior and medial region of the proximal portion of the forearm and extends across the anterior surface of the forearm. Pain is present in up to 35–40% of cases.[12]
Patients usually complain of fatigue, clumsiness, or lack of strength, especially in certain hand movements. They usually describe difficulty in performing fine clamp tasks between the thumb and index finger and may report paresthesia around the proximal thenar eminence, due to involvement of the palmar sensory branch of the median nerve.[12] In the absence of concomitant CTS, we should not find paresthesias of the rest of the innervation territory of the median nerve.[16]
It is crucial to perform a thorough physical examination with a targeted search for areas of hypoesthesia, tenderness on palpation, evaluation of the strength of the affected muscles, and identification of clinical signs associated with nerve compressions.
Tenderness on digital palpation should be specifically assessed in the anterior and medial portion of the proximal forearm, where the FDS is anatomically located, approximately 1 cm below the elbow crease. It is also common to find a positive "Tinel's sign" at this site.[14]
In the proximal compression of the median nerve, it will be necessary to evaluate directly and comparatively with the contralateral extremity, evaluating the strength of the FCR muscle, through wrist flexion against resistance, the FPL, and FPD2. The presence of decreased strength and asymmetry with respect to the contralateral side, when the contralateral is a healthy side, supports the diagnosis.[1]
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A dynamic way to evaluate the strength of the FPL and FPD2 muscles is through the physical test of the “OK” sign in which the patient is asked to perform a terminal pinch between the thumb and index finger while extending the rest of the fingers. The rest of the long fingers. The patient is asked to resist the force that the examiner exerts to separate the fingers in a pincer[26] ([Fig. 2]). Pinch strength can also be objectified using objective tools such as pinch dynamometers.[10]
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Fig. 2 “OK” Sign.
Martinel et al.[15] recently described the clinical sign “Lacertus Antagonist Test” in which, through manual mobilization or the use of “Kinetic Taping” a medial displacement of the pronator is performed, which reduces the tension exerted by the LF on the proximal median nerve, relieving compression, resulting in strength recovery when performing the “OK” test, emulating a LF release.[14]
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The “Scratch Collapse Test” is a diagnostic test used to discriminate the location of compression of the different nervous structures in both the upper and lower extremities.[28]
[29] It consists of evaluating the external rotation strength of both upper extremities simultaneously and against resistance and repeating the maneuver after performing a superficial stimulus on the suspected site of nerve compression ([Fig. 3]). It has been described for LF syndrome, CTS and compression of the ulnar nerve at the elbow, among others.[1]
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[29] In the literature, its usefulness is still considered controversial with results of sensitivity and specificity that do not agree between different studies.[28]
[29] Even so, we believe that despite being an operator-dependent test and requiring a learning curve, in trained hands it is an important tool in the diagnosis of this pathology.
Fig. 3 Scratch Collapse Test.
For all these reasons, LF syndrome is a diagnostic challenge for the clinician, given that its diagnosis is based on clinical tests. This is why Hagert describes the diagnostic triad ([Fig. 4]) that includes: the presence of motor deficit of the FCR, FPL, and FDP2 which can be objectified by the loss of terminal thumb-index clamp strength (as a sign most evident and frequently found clinical condition), the presence of pain on superficial compression or positive “Tinel” sign at the level of the LF and the presence of positive “Scratch Collapse Test”.[1]
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Fig. 4 Hagert's Triad. Diagnostic triad described by Hagert for the diagnosis of Lacertus Fibrosus Syndrome (LF), which includes motor weakness, pain in the LF, and a positive Scratch Collapse Test.
Complementary Studies
As previously mentioned, LF syndrome is clinically diagnosed, and complementary studies are of lesser relevance. It is important to emphasize that a thorough search for concomitant pathologies, such as CTS, and the exclusion of other associated conditions are essential for an accurate diagnosis.
Imaging studies with ultrasound and magnetic resonance imaging have limitations, as no consistent imaging signs confirm the diagnosis of LF syndrome. However, these methods are recommended for differential diagnosis and to investigate other potential causes of compression.
Although the specificity and sensitivity of electromyographic studies for diagnosing LF syndrome have not been thoroughly studied, the dynamic pathophysiology of nerve compression suggests that their sensitivity may be limited. The absence of electrodiagnostic findings may lead to the false conclusion of excluding LF syndrome as a diagnosis, potentially resulting in diagnostic errors.[14]
Treatment
There is an agreement in the literature that the initial management of this pathology should be conservative treatment.[1]
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[14] Patients are recommended to modify their lifestyle by reducing activities that involve repeated flexion and pronation, especially against resistance. At the same time, for symptomatic relief, anti-inflammatory medications and the use of physical therapy can be indicated, where management with “Kinetic Taping” takes place, which has been seen to improve the symptoms.[14]
Ultrasound-guided injection with corticosteroids is a minimally invasive alternative that has shown good results in other nerve entrapments. Its results in the management of LF syndrome are still unknown.[14]
Ultrasound-guided injection with corticosteroids is a minimally invasive alternative that has shown good results in other nerve entrapments. Its results in the management of LF syndrome are still unknown.[1]
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[19] It is a minimally invasive procedure that has demonstrated good clinical and functional results.[10]
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Hagert describes the use of the tripod method ([Fig. 5]) to locate the LF prior to surgery. The injection of the mixture of epinephrine with lidocaine, buffered with bicarbonate, is performed as described by Lalonde,[18]
[19] which is injected slowly and deliberately to avoid pain associated with the injection. The surgical technique consists of making a transverse incision approximately 2 cm long, followed by careful blunt dissection until the superficial fascia of the PT and LF muscles are located ([Fig. 6]). This is completely excised, completely releasing the compression of the median nerve under the LF. Since the patient is fully awake and can collaborate during surgery, it is recommended that strength evaluation tests be performed again and confirm immediate recovery.[10]
[12] Postoperative recovery and rehabilitation depend on the patient's level of activity, but rest from heavy activity is usually suggested, stimulating active mobilization of the elbow, hand, and fingers from the first day. Usually, the patient's subjective sensation of improvement is instantaneous, and the functional results are maintained over time.[14]
Fig. 5 Tripod technique for locating the LF.
Fig. 6 Minimally invasive surgical technique for LF release. *Image from Int Orthop. 2023;47(11):2781-2786 with permission from Azócar et al.
Percutaneous release guided under ultrasound[30] has been described with good results, although studies with a higher level of evidence are necessary to be able to make a clinical recommendation; however, it is recognized as a plausible technique.
Discussion
“The eye only sees what the mind is prepared to understand."
Robertson Davies
LF syndrome remains a controversial diagnosis among international hand surgery societies. Some surgeons question its existence, and the debate has even been likened to a matter of belief.
Recent reports suggest that LF syndrome is far more prevalent than previously recognized and often goes unnoticed if not actively sought. It should always be considered as a potential diagnosis in patients with only partial improvement following CTS release, which has a failure rate ranging from 10–20%.[1] This could be due to an initial misdiagnosis or the presence of concurrent compressions, known as "Double Crush Syndrome."[11]
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Patients with LF syndrome exhibit signs and symptoms indicative of more extensive involvement in the proximal forearm, often reporting strength deficits. These deficits must not be underestimated and require targeted evaluation through specific motor tests. The diagnosis is clinical, as commonly used complementary studies often yield normal results.
Understanding functional anatomy is essential to grasp the concept of dynamic nerve compression and to appreciate the rapid recovery of strength following surgical release.
Expanding scientific knowledge on this condition is crucial to improving care for patients who may otherwise be underdiagnosed and undertreated.
