Different patterns of neurogenic quadrilateral space syndrome: a case series of undefined posterior shoulder pain

Cahill and Palmer first described the entrapment syndrome of the axillary nerve (AN) and the posterior humeral circumflex artery (PHCA) within the quadrilateral space (QS) in 1983 [1].
The QS is bounded by the upper border of teres major inferiorly, the lower border of teres minor superiorly, the long head of triceps medially, and the surgical neck of the humerus laterally [1]. Within the QS, the axillary nerve divides into three distinct fascicular groups that innervate different fibers of the deltoid and teres minor. Several anatomic variants have been described [2–5].
Notably, in approximately 14% of individuals, the long head of triceps brachii is partially or entirely innervated by a branch of the axillary nerve [6, 7].
It predominantly affects young male athletes (20-40 years old) who perform shoulder abduction and external rotation (AER) movements, such as swimmers and tennis, volleyball, and baseball players [8]. Athletes are at higher risk for dynamic stress on the axillary nerve compared with the general population; the presumed prevalence in a cohort of beach volleyball athletes was estimated to be 2.2% [9, 10]. Fibrous bands or other space-occupying lesions can be responsible for the symptoms [10].
Quadrilateral space syndrome (QSS) can present with neurological signs and symptoms such as posterior shoulder pain, nondermatomal paresthesias, tenderness over the quadrilateral space, and isolated deltoid atrophy [11]. The epidemiology of QSS is not fully understood; a small number of cases have been described so far, and the heterogeneity of clinical presentation makes the diagnosis challenging even for senior clinicians, as posterior shoulder pain is frequently vague and difficult to interpret. It is worth noting that all the patients described in our case series were competitive athletes in overhead sports. This consideration helped us in making the diagnosis and choosing the appropriate treatment. Moreover, when QSS affects the posterior humeral circumflex artery, known as “Pitcher syndrome,” symptoms may include thrombosis, aneurysms, embolisms, and digital or hand ischemia [8, 10] the undefined shoulder pain may be aggravated by AER movements [8].
Some cases of painless QSS have also been described in beach volleyball athletes that presented anterior deltoid atrophy and weakness in forward flexion. It is frequently associated with atrophy of the teres minor, though cases with normal or hypertrophic teres minor are also observed [11].
A complete clinical assessment of all common causes of posterior shoulder pain is crucial for making a diagnosis. We suggest including the evaluation of posterior labral injury, posterior instability, and suprascapular nerve entrapment. The Mayo Clinic classifies QSS into neurogenic and vascular types [10].
Neurogenic QSS includes silent del- toid atrophy, persistent shoulder pain, non dermatomal paresthesias, tenderness over the quadrilateral space, movement limitations unrelieved by common painkillers, and fasciculation of the posterior deltoid or long head of the triceps brachii. Vascular quadrilateral space syndrome encompasses thrombosis and embolisms, characterized by pallor, coolness, and cyanosis of the hand and digits. Tenderness over the quadrilateral space suggests QSS, confirmed by ultrasound-guided injection of 5 mL of 1% plain lidocaine into the quadrilateral space. If the anesthetic spreads between the infraspinatus and the teres minor, the test might not be specific, as the anesthetic could involve both the suprascapular nerve and the axillary nerve [12].
To avoid misleading examinations, the procedure should be performed by an expert ultra – sound technician. Electromyography (EMG) is not always indicative of QSS because the condition is sometimes caused by a dynamic compression within the quadrilateral space muscular belly, thus the examination should be performed during AER movements. When EMG is performed at rest, it can exclude suprascapular nerve entrapment or significant axillary nerve involvement [13].
MRI is useful for evaluating cystic ganglion or space occupying lesions, and examining the muscle belly may show the first signs of denervation or nerve damage, such as muscle edema or atrophy of the teres minor and deltoid muscle. Two weeks after denervation, it is possible to observe diffused belly edema on STIR images, which sometimes are the first signs of nerve distress [14].