Transcranial optical monitoring for detecting intracranial pressure alterations in children with benign external hydrocephalus: a proof-of-concept study

Hydrocephalus; Optical techniques; PathophysiologyHidrocefalia; Técnicas ópticas; FisiopatologíaHidrocefàlia; Tècniques òptiques; FisiopatologiaSignificance Benign external hydrocephalus (BEH) is considered a self-limiting pathology with a good prognosis. However, some children present a pathological intracranial pressure (ICP) characterized by quantitative and qualitative alterations (the so-called B-waves) that can lead to neurological sequelae. Aim Our purpose was to evaluate whether there were cerebral hemodynamic changes associated with ICP B-waves that could be evaluated with noninvasive neuromonitoring. Approach We recruited eleven patients (median age 16 months, range 7 to 55 months) with BEH and an unfavorable evolution requiring ICP monitoring. Bedside, nocturnal monitoring using near-infrared time-resolved and diffuse correlation spectroscopies synchronized to the clinical monitoring was performed. Results By focusing on the timing of different ICP patterns that were identified manually by clinicians, we detected significant tissue oxygen saturation (StO2) changes (p = 0.002) and blood flow index (BFI) variability (p = 0.005) between regular and high-amplitude B-wave patterns. A blinded analysis looking for analogs of ICP patterns in BFI time traces achieved 90% sensitivity in identifying B-waves and 76% specificity in detecting the regular patterns. Conclusions We revealed the presence of StO2 and BFI variations—detectable with optical techniques—during ICP B-waves in BEH children. Finally, the feasibility of detecting ICP B-waves in hemodynamic time traces obtained noninvasively was shown.This work was realized with the support of the Department of Cirugía and Ciencias Morfológicas of the Universitat Autònoma de Barcelona. The work was supported by the European Union’s Horizon 2020 Research and Innovation Program under the Marie Sklodowska-Curie (Grant No. 675332) (BitMap: brain injury and trauma monitoring using advanced photonics) and the European Union’s Horizon 2020 Research and Innovation Program [Grant No. 101017113 (TinyBrains) and Grant No. 101016087 (VASCOVID)]; Fondo de Investigación Sanitaria (Instituto de Salud Carlos III) (Grant No. PI18/00468); Fundació CELLEX Barcelona, Fundació Mir Puig, Agencia Estatal de Investigación (PHOTOMETABO, Grant No. PID2019106481RBC31); the “Severo Ochoa” Program for Centers of Excelence in R&D (Grant No. CEX2019-000910-S); the Obra social “La Caixa” Foundation (LlumMedBcn), Generalitat de Catalunya (CERCA, AGAUR-2017-SGR-1380, RIS3CAT-001-P-001682 CECH), FEDER EC and LASERLAB EUROPE V (EC H2020 No. 871124); KidsBrainIT (ERANET NEURON); Fundació La Marató de TV3 (Grant Nos. 201724.31 and 201709.31)

Hypogonadism in Systemic Diseases

Serum testosterone is often lower than normal in patients with acute or chronic systemic diseases. The underlying mechanisms involved in the reduced testosterone secretion depend on the type of systemic disease; thus, many pathogenetic mechanisms might be involved. These mechanisms involve the hypothalamus and the pituitary (secondary hypogonadism), the testis (primary hypogonadism), or both. The resulting low-serum testosterone could be reversible or not depending on the pathogenetic mechanism. Furthermore, the relationships between hypogonadism and the systemic disease are complex since these two clinical conditions may interact with each other in a bidirectional interplay. How to interpret low-serum testosterone in systemic diseases is not easy and univocal. Biochemical hypogonadism should be differentiated into overt clinical hypogonadism and functional hypogonadism, and testosterone treatment should be offered taking into account the primary systemic disease and the possible beneficial or harmful effect on it, as well as the presence of signs and symptoms of hypogonadism. In this chapter the main systemic illnesses associated with hypogonadism will be discussed together with their underlying pathogenetic mechanisms, clinical significance, relevance, and clinical and practical implications

Rivaroxaban with or without aspirin in stable cardiovascular disease

BACKGROUND: We evaluated whether rivaroxaban alone or in combination with aspirin would be more effective than aspirin alone for secondary cardiovascular prevention. METHODS: In this double-blind trial, we randomly assigned 27,395 participants with stable atherosclerotic vascular disease to receive rivaroxaban (2.5 mg twice daily) plus aspirin (100 mg once daily), rivaroxaban (5 mg twice daily), or aspirin (100 mg once daily). The primary outcome was a composite of cardiovascular death, stroke, or myocardial infarction. The study was stopped for superiority of the rivaroxaban-plus-aspirin group after a mean follow-up of 23 months. RESULTS: The primary outcome occurred in fewer patients in the rivaroxaban-plus-aspirin group than in the aspirin-alone group (379 patients [4.1%] vs. 496 patients [5.4%]; hazard ratio, 0.76; 95% confidence interval [CI], 0.66 to 0.86; P<0.001; z=−4.126), but major bleeding events occurred in more patients in the rivaroxaban-plus-aspirin group (288 patients [3.1%] vs. 170 patients [1.9%]; hazard ratio, 1.70; 95% CI, 1.40 to 2.05; P<0.001). There was no significant difference in intracranial or fatal bleeding between these two groups. There were 313 deaths (3.4%) in the rivaroxaban-plus-aspirin group as compared with 378 (4.1%) in the aspirin-alone group (hazard ratio, 0.82; 95% CI, 0.71 to 0.96; P=0.01; threshold P value for significance, 0.0025). The primary outcome did not occur in significantly fewer patients in the rivaroxaban-alone group than in the aspirin-alone group, but major bleeding events occurred in more patients in the rivaroxaban-alone group. CONCLUSIONS: Among patients with stable atherosclerotic vascular disease, those assigned to rivaroxaban (2.5 mg twice daily) plus aspirin had better cardiovascular outcomes and more major bleeding events than those assigned to aspirin alone. Rivaroxaban (5 mg twice daily) alone did not result in better cardiovascular outcomes than aspirin alone and resulted in more major bleeding events