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Encephalitis and Its Mimics in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Differentiating between such encephalopathies and primary brain processes involves two key elements. From the systemic perspective, identification of a specific underlying medical abnormality is key. Neurologically, it is essential to establish whether the observed changes are focal or not—brain disorders resulting from localized damage to the brain cause abnormalities of function related to the site of damage. Damage to the cerebral cortex can cause seizures, an altered level of consciousness and cognitive difficulty. Damage to the deep white matter causes spasticity, ataxia, visual, and sensory problems but not seizures and has a less severe impact on alertness and cognition. Damage to the brainstem can affect level of consciousness, long tracts that pass through the brainstem, and, important diagnostically, cranial nerve function.
Neural Control of Coughing And Sneezing
Published in Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop, Neural Control of the Respiratory Muscles, 2019
Roger Shannon, Donald C. Boiser, Bruce G. Lindsey
The central neuronal network mechanisms that process “cough” and “sneeze” receptor inputs and produce the appropriate changes in respiratory muscle activity are poorly understood. In recent years, there has been renewed interest in these mechanisms because of a better understanding of the brainstem neuronal network that controls breathing. Data from older studies suggest that this network may also be involved in producing the cough and sneeze motor patterns. The main focus of this review will be recent neuronal studies that support this view. All older and recent data were obtained from cats.
The nervous system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
The brainstem, which consists of the medulla, pons and midbrain, is, in evolutionary terms, the oldest and smallest region of the brain. Continuous with the spinal cord, the brainstem receives sensory input and initiates motor output by way of cranial nerves III through XII, which are functionally analogous to the 31 pairs of spinal nerves. Whereas the spinal cord processes sensory and motor activities in the trunk of the body and the limbs, the brainstem processes these activities primarily in the head, neck and face. The brainstem also controls many basic life-sustaining processes, including respiration, circulation, and digestion. Even with the loss of higher cognitive function, this lower level of the brain can sustain bodily functions essential for survival.
Prevalence of hearing loss in COVID-19 patients: a systematic review and meta-analysis
Published in Acta Oto-Laryngologica, 2023
Mi Tang, Jie Wang, Qinxiu Zhang
A growing body of evidence indicates that patients with COVID-19 are at risk of developing hearing loss. However, the pathogenesis of COVID-19-related hearing loss is unclear. According to previous reports, the pathogenesis of hearing loss affected by viruses includes the following: (1) inflammation and oxidative stress mechanisms. Studies have shown that inflammation and oxidative stress can be activated simultaneously under various pathological conditions, including 2019-nCoV-infection [16]. At the same time, it has been pointed out that they can induce acute and chronic inflammation in the occurrence of sudden idiopathic hearing loss, which can be inferred that they may cause indirect damage to the inner ear function of 2019-nCoV-positive patients [17]. (2) the mechanism of brainstem injury. If the SARS-CoV-2 invades and triggers the neuroinflammatory mechanisms, sensory and motor disorders may occur, and even affect advanced human functions [18]. (3) Hematogenous Track. Evidence in humans suggests that SARS-CoV-2 can be transmitted systemically through the circulatory system [19]. The virus can not only destroy the labyrinthine barrier but also invade the inner ear structure, leading to a series of ear symptoms [20].
Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies
Published in Expert Review of Neurotherapeutics, 2023
Bryan Zheng, David D. Liu, Brian B Theyel, Hael Abdulrazeq, Anna R. Kimata, Peter M Lauro, Wael F. Asaad
The thalamus is likely key to the implementation of state transitions between levels or types of cortical arousal and can maintain those states through broad, course regulation of cortical activity[65–69]. This function is evident in various sleep stages and their distinct thalamocortical signatures. For example, the synchronous transition to ‘down’ states across multiple cortical regions during slow-wave sleep is likely mediated by the midline thalamus[70]. Here, the thalamus appears to be the critical link between brainstem regions involved in arousal, primarily the ascending reticular activating system (RAS), and the cortex. This network serves as a synchronous, broad modulator of cortical processing, and a potential regulator of sleep, alertness, and consciousness[71–73]. So, in addition to being the gatekeeper for specific information trying to gain access to cortex, modulatory projections via the thalamus enforce cortical compliance with brainstem-derived state signals.
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Cluster breathing is a respiratory syndrome that has been described with brainstem lesions, particularly low pontine or high medullary, and sometimes midbrain lesions.83 It is characterized by hyperventilation alternating with apnea of varying duration.80,84 Common causes include stroke, cerebellar hemorrhage with brainstem compression, Shy-Drager syndrome, and anoxic encephalophathy.80,83 As a FLS, cluster breathing has also been reported in one patient with bilateral hemispheric lesions and no brainstem lesions.84 The pathophysiology remains unknown, but the existence of this particular case of cluster breathing suggests cortical integration with brainstem control of respiration.84 If the patient is in critical condition due the brain injury, cluster breathing may become evident when a tracheostomy collar is placed and will occur while sleeping, excluding volitional hyperapena as the cause.84 The pattern of breathing itself is repetitive but may not be uniformly periodic.84 Diagnostic criteria also include respiratory alkalosis that is typically found in central neurogenic hyperventilation.84