BACKGROUNDParsonage-Turner syndrome (PTS), also known as neuralgic amyotrophy or idiopathic brachial plexopathy, is a rare peripheral multifocal inflammatory neuropathy that usually affects the upper limbs. 1 However, it is widely misdiagnosed because of its heterogeneous clinical appearance. 2 The classic presentation is a patient with subacute-onset of asymmetric shoulder pain, followed several days later by weakness and amyotrophy. 3 Although its exact cause is still unknown, multiple factors have been identified such as immunological (infection, vaccination, surgery, pregnancy, physical, or mental stress), mechanical (trauma, sports, or heavy labor), and genetic factors. 4 In the last years, PTS has been associated with severe COVID-19 infection as well as its vaccination. 5 Therefore, we report a rare case of a subacute-onset of PTS as a result of COVID-19 vaccine. | CASE DESCRIPTIONWe represent the case of a 50-year-old right-handed male patient, admitted to the neurology department of the Military Hospital of Tunis-Tunisia. He has no medical history of chronic diseases or medication use. He had a mild COVID-19 infection confirmed by RT-PCR on April 2021. The COVID-19 infection did not require hospitalization, nor oxygen therapy, neither other medication. He had a complete immunization schedule with no history of vaccine

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Background: Pulmonary alveolar proteinosis is a very rare diffuse lung disease characterized by the accumulation of amorphous and periodic acid Schiff-positive lipoproteinaceous material in the alveolar spaces due to impaired surfactant clearance by alveolar macrophages. Three main types were identified: Autoimmune, secondary and congenital. Pulmonary alveolar proteinosis has been previously reported to be associated with several systemic auto-immune diseases. Accordingly, we present the first case report of pulmonary alveolar proteinosis associated with myasthenia gravis. Case: A 27-year-old female patient, ex-smoker, developed a dyspnea on exertion in 2020. The chest X-ray detected diffuse symmetric alveolar opacities. Pulmonary infection was ruled out, particularly COVID-19 infection. The chest scan revealed the “crazy paving” pattern. The bronchoalveolar lavage showed a rosy liquid with granular acellular eosinophilic material Periodic acid-Schiff positive. According to the lung biopsy results, she was diagnosed with pulmonary alveolar proteinosis. The granulocyte macrophage colony-stimulating factor autoantibodies were negative. Nine months later, she was diagnosed with bulbar seronegative myasthenia gravis, confirmed with the electroneuromyography with repetitive nerve stimulation showing significant amplitude decrement of the trapezius and spinal muscles. She was treated with pyridostigmine, oral corticosteroids and azathioprine. Given the worsening respiratory condition of the patient, a bilateral whole lung lavage was performed with a partial resolution of symptoms. Thus, this previously unreported association was treated successfully with rituximab, including improvement of dyspnea, diplopia and muscle fatigability at six months of follow-up. Conclusions: This case emphasizes on the possible association of auto-immune disease to PAP, which could worsen the disease course, as the specific treatment does not exist yet. Hence, further studies are needed to establish clear-cut guidelines for PAP management, particularly when associated to auto-immune diseases.