Introduction: Dysphagia is a frequent problem in various neurological disorders. However, knowledge on swallowing function in patients with cerebral hypoxia is sparse. The objective of this study is to report the development of swallowing function in a series of adolescent and young-adult patients with cerebral hypoxia.
Methods: We recruited eight patients (1 male) who were admitted to our institution after the acute phase following cerebral hypoxia. Each patient underwent detailed neurological evaluation, magnetic resonance imaging (MRI), standardized neurophysiological assessment and repeated clinical and fiber-endoscopic evaluation of swallowing. Furthermore, all patients received daily physical and occupational therapy and intensive logopedic therapy for swallowing.
Results: Mean age in this case series was 19.9±3.6 years (range 16-25). All eight patients initially displayed severe swallowing dysfunction, but the reflexive components of swallowing were intact in seven patients without brainstem lesions. The only patient with additional brainstem involvement initially suffered from absence of an intact swallowing reflex and developed silent aspiration. However, follow-up examinations revealed intact swallowing reflexes in all eight patients.
Discussion: Dysphagia is common in patients with cerebral hypoxia, mainly resulting in a delayed oral phase consistent with impaired volitional execution of swallowing. Additional lesions in the brainstem may affect the integrity of the central pattern-generating circuitry for swallowing, resulting in additional dysfunction of the non-volitional reflexive component. In conclusion, dysphagia in patients with cerebral hypoxia is a common complication particularly in the early stages of remission, while long-term prognosis with respect to swallowing is often good. Swallowing function should be closely monitored in patients with acquired brain injury.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3233/NRE-182437 | DOI Listing |
Heliyon
January 2025
Department of Neurosurgery, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, 210029, China.
Background: Emerging perspectives on tumor metabolism reveal its heterogeneity, a characteristic yet to be fully explored in gliomas. To advance therapies targeting metabolic processes, it is crucial to uncover metabolic differences and identify distinct metabolic subtypes. Therefore, we aimed to develop a classification system for gliomas based on the enrichment levels of four key metabolic pathways: glutaminolysis, glycolysis, the pentose phosphate pathway, and fatty acid oxidation.
View Article and Find Full Text PDFACS Biomater Sci Eng
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.
Mitochondrial dysfunction contributes to the pathology of hypoxia-ischemia (HI) brain damage by aberrant production of ROS. Hydrogen sulfide (HS) has been demonstrated to exert neuroprotective effects through antioxidant mechanisms. However, the diffusion of HS is not specifically targeted and may even be systemically toxic.
View Article and Find Full Text PDFActa Neuropathol
January 2025
Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Objective: Ischemia-reperfusion of the abdominal aorta often results in damage to distant organs, such as the heart and brain. This cellular heterogeneity within affected tissues complicates the roles of specific cell subsets in abdominal aorta occlusion model (AAO) injury. However, cell type-specific molecular pathology in the hippocampus after ischemia is poorly understood.
View Article and Find Full Text PDFExp Neurol
January 2025
Department of Neurosurgery, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi 214000, China; Wuxi Medical Center of Nanjing Medical University, Wuxi 214000, China. Electronic address:
Ischemic stroke, resulting from the blockage or narrowing of cerebral vessels, causes brain tissue damage due to ischemia and hypoxia. Although reperfusion therapy is essential to restore blood flow, it may also result in reperfusion injury, causing secondary damage through mechanisms like oxidative stress, inflammation, and excitotoxicity. These effects significantly impact astrocytes, neurons, and endothelial cells, aggravating brain injury and disrupting the blood-brain barrier.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!