The picture was compatible with bilateral neuralgic amyotrophy. viral illness being the most common associated trigger [4]. To our knowledge, only 3 case reports have documented neuralgic amyotrophy in association with SARS-CoV-2 infection in the literature [5C7]. Herein, we present a case of severe, bilateral asymmetric neuralgic amyotrophy in a 32-year-old male, in association with laboratory-confirmed infection with SARS-CoV-2. This represents the first case from the Middle East and North Africa (MENA) region, to the best of our knowledge, expanding the spectrum of neurological involvement in association with COVID-19 infection. Case report A 32-year-old right-handed male with no relevant past medical history developed fever, cough, and generalized body pain in November 2020. He tested positive for SARS-CoV-2 via a nasopharyngeal swab CGP 57380 reverse transcription-polymerase chain reaction (RT-PCR). He was hospitalized in a specialized institution for COVID-19 and received oxygen, antibiotics, vitamins, and anticoagulants and was discharged after 7 days. During hospital stay, he experienced severe pain at the left shoulder, aggravated?by touch and movement, for which he received acetaminophen with minimal relief. The pain involved the right shoulder one week later. After discharge, the pain intensified and progressed to involve both forearms and hands. Two weeks from the onset, he started to develop progressive proximal weakness of both upper limbs, more on the left side, in addition to developing bilateral hand numbness, and an area of sensory loss over his left shoulder and radial forearm. He was initially evaluated by general physician and orthopedic surgeon and received pregabalin 300 mg/day, tramadol hydrochloride 50 mg twice daily, and local injection of steroids and lidocaine in both shoulders. He showed little improvement and was referred to our neurology outpatient clinic after 5 weeks of onset. He reported having severe pain ranging from 7 to 10 out of 10 on numerical rating scale (NRS), where 0 is no pain and 10 is the most severe pain. Findings of his systemic examination were normal. On neurological examination, he was alert, conscious, and oriented with normal speech and higher mental functions. Cranial nerve assessment was normal. Motor examination on the left side showed winging of scapula, weakness of shoulder abduction and flexion of Medical Research Council (MRC) grade 1/5, CGP 57380 weakness of shoulder external rotation and elbow flexion of MRC grade 2/5, and weakness of flexion of the distal interphalangeal joints of the thumb and index finger OK sign of MRC grade 4/5. On the right side, he had weakness of shoulder abduction, shoulder flexion, and elbow flexion of MRC grade 4/5. Minimal atrophy was observed on both shoulders, more on the left side. Motor examination of CGP 57380 both lower limbs was normal. Deep tendon reflexes were absent all over the body, except for right triceps and brachioradialis reflexes. Sensory assessment showed reduced sensation over the right and left shoulders, and left forearm. Planter response was downgoing bilaterally. Electrophysiological studies (nerve conduction tests and electromyography) were performed 5 weeks after initial presentation. It revealed sensory and motor axonal involvement, in the form of low amplitude of compound motor action potentials of musculocutaneous, axillary, and suprascapular nerves on both sides, and long thoracic and anterior interosseous nerve on the Rabbit Polyclonal to IKK-gamma left side, with patchy denervation. The picture was compatible with bilateral neuralgic amyotrophy. A magnetic resonance imaging (MRI) showed hyperintense T2-weighted signal of supra- and infraspinatus muscles, indicating intramuscular edema, with normal cervical spine and both brachial plexuses, further confirming the diagnosis (Fig. ?(Fig.11). Open in a separate window Fig. 1 Magnetic resonance imaging (MRI) of cervical spine and both brachial plexuses in a 32-year-old male. a Coronal 3D T2-weighted images with fat suppression using sampling perfection with application-optimized contrasts by using flip angle evolution (SPACE) sequence, showing abnormal signal that involved the rotator cuff muscles bilaterally (arrows); b coronal 3D T2-weighted image through the brachial plexus showing no pathological changes; and c sagittal T2-weighted image of the cervical spine showing no myelopathy or compressing masses An extensive blood workup showed normal complete blood count; renal and liver functions; serum electrolytes; creatine kinase; inflammatory markers (erythrocyte sedimentation rate, C-reactive protein); serum vitamins B1, B6, B12, and folate; protein electrophoresis; immunoglobulin essay; thyroid function; and antithyroid autoantibodies. There was no serological evidence of infection with hepatitis B, C, and E; herpes simplex virus (HSV); human immunodeficiency virus (HIV); Lyme; syphilis; or toxoplasma. A panel for vasculitis and autoimmune antibodies yielded negative results. Cerebrospinal fluid (CSF) analysis showed normal protein and glucose levels, with.