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El sueño es un estado de conciencia fisiológico y reversible, de desconexión parcial y temporal del entorno, con un aumento del umbral de respuestas a estímulos externos. A lo largo de la vida del ser humano se pasa 1/3 en el estado de sueño. Se han descrito múltiples funciones y se conoce que la falta de sueño conlleva consecuencias perjudiciales a la salud. Neurofisiológicamente se describen 2 grandes estados de sueño, el sueño sin movimientos oculares rápidos (dividido en tres estadios denominados N1, N2 y N3) y el sueño con movimientos oculares rápidos. Existen múltiples centros generadores de la vigilia, generadores del sueño, y dentro del sueño promotores o inhibidores del sueño MOR, estos sistemas utilizan diversos neurotransmisores, entre ellos la orexina, que promueven o inhiben los estados de conciencia. La transición entre estadios está regulada por modelos de interruptores flip-flop que permite una transición sutil y rápida sin que se presenten intrusiones de un estadio en otro. A su vez la transición entre la vigilia y el sueño está regulado por un proceso homeostático (proceso S) que está en relación con las horas de vigilia y un proceso circadiano (proceso C) que está regulado por el núcleo supraquiasmático (reloj biológico). El adecuado conocimiento de la neuroanatomía y neurofisiología del sueño es necesario para la comprensión de la fisiopatología y tratamiento de los trastornos del sueño.

La cefalea por abuso de medicamentos corresponde a un fenómeno de cronificación y agravamiento de los síntomas en pacientes con cefaleas primarias, principalmente, migrañosa o tensional, quienes consumen con alta frecuencia, medicación para el alivio de las crisis dolorosas. Esta entidad alcanza una prevalencia del 1 al 2 % en la población general. A continuación, se expone una revisión clínica de la etiología, fisiopatología, epidemiología, diagnóstico y manejo de este cuadro, altamente frecuente en la consulta médica general y especializada

La epilepsia de ausencias juveniles (EAJ) es parte del espectro de las epilepsias genéticas generalizadas; su prevalencia se estima entre 0,2 y 2,4% de los pacientes con epilepsia. A continuación, se expone el caso de una paciente de 20 años quien fue evaluada por inicio en la adolescencia de una epilepsia de ausencias que asoció un deterioro cognitivo leve. Se discuten los principales determinantes del deterioro cognitivo en personas con epilepsia y se revisan las generalidades de la EAJ.

Background: Differentiating between nontuberculous mycobacterial lung disease (NTM-LD) and pulmonary NTM colonization (NTM-Col) is difficult. Compared with healthy controls, patients with NTM-LD generally present immune tolerance along with increased expressions of T-cell immunoglobulin mucin domain-3 (TIM-3) and programmed cell death-1 (PD-1) on T lymphocytes. However, the role of soluble TIM-3 (sTIM-3) and soluble PD-1 (sPD-1) in differentiating NTM-LD from NTM colonization (NTM-Col) remains unclear., Methods: Patients with NTM-positive respiratory samples and controls were enrolled from 2016 to 2019. Patients were classified into NTM-Col and NTM-LD groups. Levels of sTIM-3, sPD-1, soluble PD-ligand-1 (sPD-L1), and TIM-3 expression were measured. Factors associated with NTM-LD were analyzed by logistical regression., Results: TIM-3 expression on CD4 + and CD8 + T lymphocytes were highest in NTM-LD group, followed by NTM-Col, and control (P=.017 and P=.011 for trend). sTIM-3 elevated in the NTM-Col group compared with the NTM-LD and control groups (856.3±518.7 vs. 595.3±352.6pg/mL, P=.009; vs. 437.0±267.4pg/mL, P<.001). Levels of soluble PD-1 and its ligand were similar among groups. Among the 79 NTM-positive patients, sTIM-3 was associated with NTM-LD (100-pg/mL increase, adjusted odds ratio (aOR) 0.658 [95% CI, 0.502-0.864], P=.003). Patients with ≥2 risk factors (sTIM-3≤530pg/mL, BMI≤22.5, and radiographic score ≥5) were 13 times more likely to exhibit NTM-LD than those without (aOR 13.234 [2.983-58.709], P=.001)., Conclusions: sTIM-3 was an independent factor for differentiating NTM-LD from NTM-Col, suggesting the immunologic role of sTIM-3 in NTM-LD pathogenesis. By assessing sTIM-3 levels and other risk factors, physicians may be able to identify NTM-LD cases in a simplified manner., (Copyright © 2022 SEPAR. Published by Elsevier España, S.L.U. All rights reserved.)

Background: Differentiating between nontuberculous mycobacterial lung disease (NTM-LD) and pulmonary NTM colonization (NTM-Col) is difficult. Compared with healthy controls, patients with NTM-LD generally present immune tolerance along with increased expressions of T-cell immunoglobulin mucin domain-3 (TIM-3) and programmed cell death-1 (PD-1) on T lymphocytes. However, the role of soluble TIM-3 (sTIM-3) and soluble PD-1 (sPD-1) in differentiating NTM-LD from NTM colonization (NTM-Col) remains unclear., Methods: Patients with NTM-positive respiratory samples and controls were enrolled from 2016 to 2019. Patients were classified into NTM-Col and NTM-LD groups. Levels of sTIM-3, sPD-1, soluble PD-ligand-1 (sPD-L1), and TIM-3 expression were measured. Factors associated with NTM-LD were analyzed by logistical regression., Results: TIM-3 expression on CD4 + and CD8 + T lymphocytes were highest in NTM-LD group, followed by NTM-Col, and control (P=.017 and P=.011 for trend). sTIM-3 elevated in the NTM-Col group compared with the NTM-LD and control groups (856.3±518.7 vs. 595.3±352.6pg/mL, P=.009; vs. 437.0±267.4pg/mL, P<.001). Levels of sPD-1 and sPD-L1 were similar among groups. Among the 79 NTM-positive patients, sTIM-3 was associated with NTM-LD (100-pg/mL increase, adjusted odds ratio (aOR) 0.658 [95% CI, 0.502-0.864], P=.003). Patients with ≥2 risk factors (sTIM-3≤530pg/mL, BMI≤22.5, and radiographic score ≥5) were 13 times more likely to exhibit NTM-LD than those without (aOR 13.234 [2.983-58.709], P=.001)., Conclusions: sTIM-3 was an independent factor for differentiating NTM-LD from NTM-Col, suggesting the immunologic role of sTIM-3 in NTM-LD pathogenesis. By assessing sTIM-3 levels and other risk factors, physicians may be able to identify NTM-LD cases in a simplified manner., (Copyright © 2021. Publicado por Elsevier España, S.L.U.)

Introduction: The association between GOLD categorizations and future exacerbations has not been fully investigated. This study elucidates whether the GOLD 2017 classification is associated with different future exacerbation risk in patients with chronic obstructive pulmonary disease (COPD) compared with the previous GOLD categorization. Another objective was to investigate the impacts of the symptoms and FEV1 on the predicted future exacerbation independently of previous exacerbation history., Methods: We analyzed patients from three prospective COPD cohorts (SNUH, KOCOSS, and KOLD) and evaluated the risk of moderate to severe exacerbation among different models, including GOLD grade (FEV1), GOLD 2011, and GOLD 2017., Results: In total, 611 COPD patients were included (36 from SNUH, 257 from KOCOSS, and 318 from KOLD). GOLD 2017 classification, excluding FEV1% for categorization criteria, showed no differences in future exacerbation risk compared with GOLD grade and GOLD 2011 based on c-statistics. Among those with no frequent exacerbation history and FEV1 ≥50%, the group with more symptoms was significantly associated with future exacerbations than the group with less symptoms. A lower FEV1 (FEV1 <50%) was not associated with a higher future exacerbation risk than a higher FEV1 (FEV1 ≥50%), regardless of prior exacerbation history and symptom group., Conclusion: The GOLD 2017 classification was not different from GOLD grade and GOLD 2011 regarding the association with future exacerbation risk, and there were no significant differences in exacerbation risk according to FEV1%. This suggests that FEV1 might not be an important factor in future exacerbation risk. These results partly support the GOLD 2017 assessment tool., (Copyright © 2019 SEPAR. Publicado por Elsevier España, S.L.U. All rights reserved.)