[Bilateral diaphragmatic palsy due to Lyme neuroborreliosis]. / Une paralysie diaphragmatique bilatérale révélant une neuroborréliose de Lyme.

INTRODUCTION: Lyme disease is not uncommon and can sometimes progress to neurological complications. We report here an unusual case of bilateral diaphragmatic paralysis secondary to Lyme neuroborreliosis. CASE REPORT: A 79-year-old man was admitted to the intensive care unit for acute respiratory distress requiring intubation and the long-term use of nocturnal non-invasive ventilation. Three months beforehand he had been bitten by a tick and developed erythema migrans which was treated with Doxycycline for 10 days. This clinical presentation became complicated a few days later by the progressive onset of severe dyspnoea. At admission, chest radiography revealed bilateral elevation of the diaphragm. Pulmonary function tests revealed a severe restrictive disorder aggravated by decubitus. A diaphragmatic electromyogram showed bilateral axonal polyneuropathy of the phrenic nerves. IgG and IgM antibodies to Borrelia burgdorferi were detectable in serum and cerebrospinal fluid, leading to the diagnosis of Lyme disease. He was treated with intravenous ceftriaxone 2g per day for 21 days, leading to a substantial improvement in symptoms. CONCLUSION: In the presence of unilateral or bilateral diaphragmatic paralysis of undetermined aetiology, it seems relevant to perform Lyme serology in the blood and, in positive cases, to follow up with a lumbar puncture in order to detect intrathecal IgG synthesis.

[Functional exercise testing in idiopathic inflammatory myopathies with pulmonary involvement]. / Intérêt de l'épreuve fonctionnelle d'exercice au cours des myopathies inflammatoires avec atteinte pulmonaire.

INTRODUCTION: Dyspnoea occurring during inflammatory myopathy associated with interstitial lung disease (ILD) can be ascribed to several physiopathological pathways. The purpose of this study was to analyse cardiopulmonary exercise testing (CPET) abnormalities in these patients in order to precise mechanisms responsible for decreased aerobic capacity. METHODS: Ten patients (52 +/- 12 years) were diagnosed as having inflammatory myopathy with interstitial lung disease. Exercise dyspnoea was found in 9 patients. All of them had a restrictive pattern associated to and impairment of the transfer factor for carbon monoxide. CPET was performed with a bicycle ergometer using a standard protocol of incremental increasing work load. RESULTS: Two patients had a normal exercise capacity while eight patients had abnormal VO2 associated with hyperventilation, abnormal gas exchange, as well as and abnormal dead space. Five patients also exhibited decreased oxygen pulse (<80% expected value) at peak exercise; 4 out of 5 had persistence of ventilatory reserve. In addition DeltaFC/DeltaVO2 was increased (>50) in 7 cases. CONCLUSION: CPET provides useful information in the understanding of mechanisms of dyspnoea and might be an effective tool in treatment decision making: in patients with inflammatory myopathy and associated ILD abnormal oxygen pulse may reflect cardiac disorder or muscular abnormalities (inflammatory or steroid myopathy).