Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by repeated episodes of upper airways collapse during the sleep. The following intermittent hypoxia triggers a state of chronic inflammation, which also interests the nervous system leading to neuronal damage and increased risk of cognitive impairment. Brain derived neurotrophic factor (BDNF) is a growth factor often associated with neuroplasticity and neuroprotection whose levels increase in several condition associated with neuronal damage. However, whether patients affected by OSAS have altered BDNF levels and whether such alteration may be reflective of their cognitive impairment is still controversial. Here we show that, when compared to healthy control volunteers, OSAS patients have increased serum levels of BDNF. Moreover, OSAS patients with the higher levels of BDNF also have reduced neurocognitive impairment as measured by The Montreal Cognitive Assessment (MoCA) questionnaire. Treatment with standard non-invasive mechanical ventilation (CPAP) also was able to ameliorate the level of cognitive impairment. Altogether our results indicate that BDNF levels represent a neuroprotective response to intermittent hypoxia in OSAS patients.

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Introduction. Bilateral paralysis of the diaphragm may be an idiopathic clinical condition or associated with several diseases such as trauma, surgery, viral infections, neurologic disorders. The diaphragm is the main respiratory muscle. It is a cupoliform muscle-tendon structure, innervated bilaterally by phrenic nerve, which originates from C3-C5 nerve roots. Diaphragmatic paralysis is a clinical disorder that generates hypoventilation and basal pulmonary atelectasis, predisposing to hypercapnic respiratory failure. The clinic manifestations mimic cardio-respiratory pathologies, therefore often misdiagnosticated. Case presentation. A 55-year-old man with a previous C6-7 traumatic fracture, referred multiple accesses to the emergency room for acute nocturnal dyspnoea, treated with antibiotic therapy, diuretic therapy and long-term oxygen therapy, without beneficial effects. He referred to our pulmonary clinic for evaluation of persistent and worsening orthopnoea due to unknown cause for about 2 years. Clinical examination, respiratory functional tests and diaphragm ultrasound revealed a strong suspicion of diaphragmatic deficit, confirmed by electromyography. Conclusions. The patient accesses to the emergency room numerous times and the clinical frame have been always oriented towards a cardio-respiratory origin. From the onset of the symptom to the respiratory evaluation, about 2.5 years have passed. The manifestation of clear orthopnoea has addressed the functional respiratory study towards a more thorough diaphragmatic evaluation assessed by ultrasound.

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