RESUMEN
Most reported neurological symptoms that happen after exposure to microgravity could be originated from alterations in cerebral hemodynamics. The complicated mechanisms involved in the process of hemodynamics and the disparate experimental protocols designed to study the process may have contributed to the discrepancies in results between studies and the lack of consensus among researchers. This literature review examines spaceflight and ground-based studies of cerebral hemodynamics and aims to summarize the underlying physiological mechanisms that are altered in cerebral hemodynamics during microgravity. We reviewed studies that were published before July 2020 and sought to provide a comprehensive summary of the physiological or pathological theories of hemodynamics and to arrive at firm conclusions from incongruous results that were reported in those related articles. We give plausible explanations of inconsistent results on factors including intracranial pressure, cerebral blood flow, and cerebrovascular autoregulation. Although there are no definitive data to confirm how cerebral hemodynamics changes during microgravity, every discrepancy in results was interpreted by existing theories, which were derived from physiological and pathological processes. We conclude that microgravity-induced alterations of hemodynamics at the brain level are multifaceted. Factors including duration, partial pressures of carbon dioxide, and individual adaptability contribute to this process and are unpredictable. With a growing understanding of this hemodynamics model, additional factors will likely be considered. Aiming for a full understanding of the physiological and/or pathological changes of hemodynamics will enable researchers to investigate its cellular and molecular mechanisms in future studies, which are desperately needed.
Asunto(s)
Circulación Cerebrovascular , Ingravidez/efectos adversos , Animales , Hemodinámica , Humanos , Presión IntracranealRESUMEN
INTRODUCTION: : Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) is a subtype of glutamate receptor that mediates most of the fast excitatory neurotransmission in the brain. Anti-AMPAR encephalitis is an autoimmune-mediated neurological disorder, frequently accompanied by the presence of neoplasms, comprising a spectrum of paraneoplastic syndrome. PATIENT CONCERNS: A 56-year-old man was admitted for deterioration in memory and aberrant psychological behaviors, which lasted for at least 20âdays. DIAGNOSIS: The patient was diagnosed as anti-AMPAR encephalitis and 4 months later, he was diagnosed with small cell lung cancer. INTERVENTIONS: Once diagnosis for anti-AMPAR encephalitis was confirmed, methylprednisolone was prescribed with initial dose 500âmg/d for 14âdays until the patient returned to pre-illness state. Then he was discharged with oral treatment with corticosteroids. Following the diagnosis of small cell lung cancer, he received 5 rounds of chemotherapy, including carboplatin and etoposide. OUTCOMES: After taken the prescription of Methylprednisolone for anti-AMPAR encephalitis, he returned to pre-illness state and was discharged. In April 21, 2017, after symptoms of respiratory system showed up, he was diagnosed with small cell lung cancer and he eventually died of respiratory failure. CONCLUSION: Though progress has been made in recent years in diagnosis and treatment for autoimmune encephalitis, it is challenging to diagnose due to the similarity in clinical findings with other autoimmune or infectious encephalitis. In addition, it is necessary for these patients to regularly have tumor screening, considering AMPAR antibody encephalitis is closely associated with neoplasm, and the incidence of paraneoplastic syndrome is 63% to 70%.