Muscle anomalies are difficult to differentiate from soft tissue tumors [
7], particularly if the abnormality appears unilaterally, causing asymmetry [
9]. The existence of accessory muscles may confuse surgeons intraoperatively and cause neurovascular compression during active movement. The course and direction of the ABs may occasionally create tunnel formations, in which the MN and the BA may be entrapped [
12,
15]. The MN during its course, in the upper limb, may pass through several musculoaponeurotic structures, that are constituted by relatively thick layers of connective tissue and have been reported as the main potential sites of neurovascular entrapment, thus explaining the pathophysiology of neuropathy [
22]. Mehta et al. [
12] described an intramuscular tunnel created by the B, that entrapped brachial vessels and the MN, in the distal arm third. The topography of the above-referred neurovascular structures within the B would possibly render them extremely vulnerable to trauma in case of a fracture of the distal humeral shaft. Since B is a key flexor of the arm, its contraction could compress these neurovascular structures, and its prolonged contraction could lead to paresthesia and numbness. The probability of MN compression proximal to its entrance into the forearm should be taken into consideration. Moreover, remnants of CB variants, such as the CB longus (its accessory tendon), may cross anterior to the MN and BA [
6], thus causing neurovascular compression. Gessini et al. [
7] reported that the hypertrophic CB longus may be an etiological factor for potential entrapment of the MN, and/or vascular disturbances, due to BA compression.
In the present series, three different muscle variants of the arm are described. Two muscular ABs originating from the CB and BB short head and joining the TB medial head (first case), musculofascial ABs between BB short head and the upper arm fascia (third case), and two musculofascial tunnels (second and fourth case), arising from the CB superficial and deep heads, and joining the upper arm fascia, and the TB medial head. Musculofascial tunnel formations may entrap the deeply situated nerves (MCN and MN), as well as the BA. The muscle or musculofascial tunnels’ variant could lead to diagnostic and therapeutic challenges regarding high MN neuropathy [
5]. The meticulous clinical examination may exclude possible areas of entrapment, while morphological details of the nerves supplying the arm muscles are greatly facilitated by magnetic resonance imaging (MRI), which may be utilized in challenging cases [
10,
18]. MN entrapment and irritation may lead to high neuropathy [
5] including loss of muscle strength, involving all muscles innervated by the nerve, including elbow flexion and forearm supination, as well as sensitivity disruptions, mainly at the forearm’s radial side. Vascular symptoms may also present with homeostasis disturbances of the hand [
7], while brachial vessels’ compression may lead to claudication and in more severe cases to edema and/or ischemia. Entrapment of the MN at the anterior arm compartment would lead to motor, as well as sensory deficits. Particularly, it would affect the strength of the superficial volar forearm muscles, including pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis, and the deep flexors, including flexor digitorum profundus, flexor pollicis longus, and pronator quadratus. Furthermore, the hand muscles, such as the first and second lumbricals, the opponens pollicis, the abductor pollicis brevis, and the flexor pollicis brevis may also be affected. Sensory changes could include the palmar cutaneous branch, as well as the radial 3–1/2 digits. These symptoms could differentiate MN entrapment, at the anterior arm compartment, from carpal tunnel syndrome, anterior interosseous nerve compressive neuropathy, and/or pronator syndrome. In carpal tunnel syndrome, the flexor forearm muscles would show no impairment, at anterior interosseous nerve neuropathy, there would be no sensory deficits, while in pronator syndrome, there would be pain at the proximal volar forearm, sensory changes over the palmar cutaneous branch, and positive Tinel's over the proximal volar forearm. Furthermore, the knowledge of abnormal CB insertion is significant because it can be used as a transitional flap to replace soft tissue deficits in infraclavicular and axillary areas during post-mastectomy reconstruction [
8]. The CB flap’s high feasibility may also be exploited for facial reanimation [
20], or the own muscle may serve as a guide for anaesthesiologists to locate the MCN [
14]. Additionally, keeping in mind that the BB accessory tendon is crucial while performing tendon reconstruction and repair and treating a fracture followed by unusual displacement of the bone fragment [
4]. In general, the possibility of a variant should be kept in mind by radiologists when assessing MRI scans, as these features can be misinterpreted [
21] and by clinicians when diagnosing or treating patients with weakness or pain in the anterior arm compartment.