(1) Background: The aim of this review is to map research into the molecular mechanisms linking sleep-related breathing disorders (SRBDs) and acute stroke and their clinical and therapeutic implications and to identify existing knowledge gaps to suggest new areas of research. (2) Methods: This review was conducted according to the PRISMA extension for scoping reviews (PRISMA-ScR) and a predetermined protocol shared among all authors. (3) Results: The review of the thirteen studies analyzed provides a focused view of the molecular features about interaction between obstructive sleep apnea (OSA) and acute stroke. Our review identifies and highlights the biomarkers most frequently found to be associated with acute stroke, SRBDs, and their clinical repercussions. (4) Conclusions: The association between the presence of sleep apnea, especially in its severe form, and elevated levels of inflammatory markers in patients with acute stroke is highlighted and new research topics in this area are proposed.

Background: Obstructive sleep apnea (OSA) is highly prevalent in the early stages of Alzheimer’s disease (AD), and its hallmark, sleep fragmentation, may accelerate cognitive decline. Continuous positive airway pressure (CPAP) improves OSA-related hypoxia during slow-wave sleep, but its cognitive benefits in AD remain unclear. Methods: We performed a 12-month sub-analysis of a prospective, longitudinal pilot study that enrolled 21 adults (median age = 77 yr; 71% women) with Mild Cognitive Impairment (MCI) with AD confirmed biomarkers and polysomnography-diagnosed OSA. All participants underwent baseline overnight polysomnography (PSG) and neuropsychological testing (Clinical Dementia Rating (CDR), Mini-Mental State Examination (MMSE), Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)) that were repeated after 12 months. Twelve participants were CPAP-compliant (moderate/severe OSA) and nine were non-users (mild OSA/intolerance). Cognitive change scores (Δ = 12 months -baseline) were compared with Generalized Linear Models (GLM) adjusted for baseline cognition and Apnea–Hypopnea Index (AHI); associations between baseline sleep parameters and cognitive trajectories were examined. And the association of sleep variables with the use of CPAP was also evaluated. Results: Compared with non-users, CPAP users showed significantly slower global decline (Δ MMSE: p = 0.016) and improvements in overall cognition (Δ RBANS Total: p = 0.028) and RBANS sub-domains (Δ RBANS FC: p = 0.010; Δ RBANS SF: p = 0.045). Longer baseline non-rapid eye movement (NREM) stage 3 and rapid eye movement (REM) sleep, greater total sleep time and sleep efficiency, and right-side sleeping were each linked to better cognitive outcomes, whereas extended NREM stage 2, wakefulness, and supine sleeping were associated with poorer trajectories. Conclusions: Twelve months of CPAP use was associated with attenuated cognitive decline and domain-specific gains in AD-related MCI with OSA. Sleep architecture and body position during sleep predicted cognitive outcomes, underscoring the therapeutic relevance of optimizing breathing and sleep quality. Larger, longer-term trials are warranted to confirm CPAP’s disease-modifying potential and to clarify the mechanistic role of sleep in AD progression.

Background Obstructive sleep apnea (OSA) is highly prevalent in the early stages of Alzheimer’s disease (AD), and its hallmark, sleep fragmentation, may accelerate cognitive decline. Continuous positive airway pressure (CPAP) improves OSA-related hypoxia during slow-wave sleep, but its cognitive benefits in AD remain unclear. Methods We performed a 12-month sub-analysis of a prospective, longitudinal pilot study that enrolled 21 adults (median age = 77 yr; 71% women) with MCI with AD confirmed biomarkers and polysomnography-diagnosed OSA. All participants underwent baseline overnight PSG and neuropsychological testing (CDR, MMSE, RBANS) that were repeated after 12 months. Twelve participants were CPAP-compliant (moderate/severe OSA) and nine were non-users (mild OSA/intolerance). Cognitive change scores (Δ = 12 months – baseline) were compared with generalized linear models adjusted for baseline cognition and apnea-hypopnea index; associations between baseline sleep parameters and cognitive trajectories were examined. And the association of sleep variables with the use of CPAP was also evaluated. Results Compared with non-users, CPAP users showed significantly slower global decline (Δ MMSE: p = 1.60e-02) and improvements in overall cognition (Δ RBANS Total: p = 2.80e-02), and RBANS subdomains (Δ RBANS FC: p = 1.06e-02; Δ RBANS SF: p = 4.53e-02). Longer baseline NREM stage 3 and REM sleep, greater total sleep time and sleep efficiency, and right-side sleeping were each linked to better cognitive outcomes, whereas extended NREM stage 2, wakefulness, and supine sleeping were associated with poorer trajectories. Conclusions Twelve months of CPAP use was associated with attenuated cognitive decline and domain-specific gains in AD-related MCI with OSA. Sleep architecture and body position during sleep predicted cognitive outcomes, underscoring the therapeutic relevance of optimizing breathing and sleep quality. Larger, longer-term trials are warranted to confirm CPAP’s disease-modifying potential and to clarify the mechanistic role of sleep in AD progression.

Background and Clinical Significance: Intracerebral hemorrhage (ICH) is a very rare complication following endovascular closure of direct carotid-cavernous fistulas (CCFs). When reported, ICH typically appears within the first 48 h after CCF closure. We performed an extensive literature review, starting from the case of a 48-year-old patient presenting with an intracerebral hemorrhage after CCF closure. Case Presentation: A 48-year-old woman with arterial hypertension developed an intracerebral hemorrhage in the right frontal lobe 12 days after successful closure of a traumatic CCF. The patient exhibited acute neurological deterioration in a previously hypoperfused territory. A narrative review identifies the classical molecular theory of hemodynamic dysregulation, known as Normal Perfusion Pressure Breakthrough (NPPB), as the principal pathophysiological mechanism. Other mechanisms such as oxidative stress, microglial activation, blood–brain barrier disruption, metalloproteinase expression, and possible genetic alterations such as ICA1L variants are also implicated. Conclusions: This case underscores the importance of considering molecular mechanisms in the pathophysiology of delayed post-endovascular treatment of ICH, as well as the need for hemodynamic monitoring and follow-up in patients with vascular comorbidities.

Background: Central sleep apnea (CSA) syndromes and acute ischemic stroke are linked by a complex, bidirectional relationship. After ischemic stroke, CSA prevalence rises markedly compared with the general population, in which it is usually below 1%. In stroke cohorts, CSA frequencies of around 8%–12% have been reported, although estimates are heterogeneous owing to differing diagnostic criteria. In this scoping review we map the evidence on CSA syndromes during sleep in patients with stroke, summarizing prevalence, mechanisms, clinical correlates, and prognostic implications. Methods: The Medline (PubMed), Scopus, Cochrane Reviews, and Web of Science databases were searched for observational and interventional studies published from inception to August 31 2025 in English and Spanish assessing CSA syndromes in adults with ischemic stroke. Two reviewers independently screened records, selected studies, and extracted data on study design, stroke characteristics, CSA definitions, comorbidities, and clinical outcomes; disagreements were resolved by consensus with a third reviewer. Results: Fifty-five studies including several thousand patients with ischemic stroke were identified. Across studies, post-stroke CSA prevalence ranged from approximately 8% to 12%, clearly exceeding rates in the general population. CSA was often reported in the absence of overt cardiac comorbidities, and patients with CSA tended to have lower body mass index and fewer classic cardiovascular risk factors than those typically described with obstructive sleep apnea. Pathophysiological analyses emphasized disturbed central ventilatory control after cerebral ischemia; however, several studies did not show a consistent association between specific lesion locations and CSA occurrence, suggesting that stroke may unmask CSA in predisposed individuals rather than cause it solely through focal damage. In older adults, CSA appeared as an independent correlate of ischemic stroke and a potential marker of silent cerebral injury or impaired central respiratory regulation. Conclusions: Available evidence indicates that CSA syndromes during sleep are substantially more frequent in patients with ischemic stroke than in the general population and may be associated with increased cerebrovascular risk and subclinical brain injury. Heterogeneity in CSA definitions, diagnostic protocols, and outcome measures limits firm conclusions. Standardized criteria and adequately powered prospective studies are needed to clarify the mechanistic and prognostic role of CSA in stroke.