Acute brachial neuritis was described as early as 1897 [
1], and it was further elaborated in the early 20th century in a study of 46 soldiers with shoulder pain [
2,
3]. Parsonage and Turner systematically reported varying disease patterns in their series of 136 patients and described this entity as neuralgic amyotrophy and shoulder girdle syndrome [
3,
4]. The cause of this disease remains controversial, but various hypotheses have been proposed, including post–viral immunological insult to the brachial plexus, immunization, pregnancy, surgery, radiation, heroin abuse or treatment with interferon [
5,
6]. A hereditary form of this disease, known as
hereditary neuralgic amyotrophy, also has been described, which is linked to chromosome 17q24 [
5]. In our patients, no predisposing factor could be found and no causal association could be inferred. An incidence of 1.64/100,000 person-years has been reported [
7‐
10], with most cases occurring in the third to seventh decades of life [
8]. A clear male predisposition has been reported, with a male-to-female ratio reported to range from 2:1 to 11.5:1 [
8]. Both of the patients in our present report were men, one in his early fourth decade and the other in his third decade of life, respectively, and they presented to our institution over the course of four years. Both the patients in our study were right-handed with involvement of the dominant hand in one and the non-dominant hand in the other. No correlation could be inferred between handedness and involvement in the present report, and no correlation has been described to date in the literature [
6,
8,
9]. Bilateral involvement has been reported in up to one-third of cases in strikingly asymmetrical fashion [
9]. The disease typically starts suddenly, with severe pain followed by flaccid paralysis of the shoulder muscles when the pain abates. Usually, atrophy of one or more of the involved muscles develops, and the weakness commonly resolves spontaneously over a period of 6 to 18 months [
5]. This classical chronology was followed in only one of our two patients (patient 1); the other patient (patient 2) presented with insidious onset pain during the course of two to three months with progressive muscle weakness over this period. Atypical presentation complicates the diagnosis. There have been reports of cranial nerve and phrenic nerve involvement. These cases have been misunderstood as diaphragmatic rupture or palsy, and often patients underwent extensive investigations to procure evidence of such misdiagnosis [
3]. PTS most commonly involves suprascapular, axillary and long thoracic nerves individually or in combination [
6]. In our study, both the cases revealed isolated suprascapular nerve involvement, and the supraspinatus and infraspinatus muscles were affected in both cases. These muscles have almost invariably been affected in most studies [
9]. MRI findings in PTS usually reflect acute denervation edema or chronic atrophy with fatty infiltration. MRI remains the single most useful modality for diagnosis, with most cases being first suspected when a patient is referred for shoulder MRI after a likely sports injury. Acute changes are depicted best by bright signal intensity on T2 sequences with fat saturation within two weeks after denervation and may concur without any T1-weighted signal intensity change. These changes are thought to result from increased extracellular water content or increased capillary blood volume in the affected muscles. T1 sequences best depict chronic loss of muscle bulk and bright intramuscular intensity consistent with fatty infiltration [
6,
11]. Patient 1 in our report presented with acute-onset symptoms, and MRI revealed increased T2-weighted signal intensity without fatty atrophy on T1 sequences, which is consistent with acute denervation changes. Of note, however, were the MRI findings in patient 2, who presented with an insidious case history but showed acute T2-weighted signal hyperintensity without any evidence of fatty atrophy of muscles, as was expected on the basis of our current understanding of the pathophysiology of this disease. The treatment is conservative and based on physical therapy and treatment with analgesics and corticosteroids [
5].