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Stroke
Published in Henry J. Woodford, Essential Geriatrics, 2022
Lacunar events may also disturb the posterior circulation affecting the pons (causing an ataxic hemiparesis by affecting both motor and cerebellar fibres) or thalamus (where they may cause a pure sensory stroke) (seeFigure 10.2). Many lacunar vascular lesions detected on brain imaging are clinically silent.
Control of the Upper Airway during Sleep
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
The remaining five groups of sleep-active neurons are all associated with REM sleep. Among those, a subset of acetylcholine (ACh)-containing neurons of the pedunculopontine and lateral tegmental regions of the pons have activity that distinctly increases during REM sleep only. They are intermixed among other ACh neurons that are activated during both wakefulness and REM sleep (150, 151). Additional ACh cells with activity related to REM sleep are scattered in the medullary reticular formation (152). Some of the pontomedullary ACh cells have efferent projections to the orofacial motor nuclei (153–155) but it remains to be determined whether ACh cells with connections to motoneurons are REM sleep-active.
Anatomy of the head and neck
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
The pons is the upward continuation of the brainstem from the medulla and is divisible into anterior and posterior parts. The anterior part contains the pontocerebellar fibres, which arise from the pontine nuclei. These pass through the middle cerebellar peduncle to the contralateral side of the cerebellum. In the rostral part of the pons, the lateral wall of the fourth ventricle is composed of paired superior cerebellar peduncles, with a thin superior medullary velum connecting them and forming its roof. These peduncles converge towards the midline as they pass into the midbrain and contain cerebellar afferent and efferent fibres.
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
Central neurogenic hyperventilation, a syndrome in which hyperpnea and associated respiratory alkalosis occur during both wakefulness and sleep, is considered a result of a pontine lesion, most commonly secondary to tumors.80,85 The exact pathophysiology beyond stimulation of respiratory control areas in the pons and medulla remains unclear.85 When this syndrome is suspected based on clinical presentation, other causes of hyperventilation, such as pulmonary embolus or respiratory disease, must first be ruled out.80 Lesions to the caudal respiratory neurons can cause an apneustic breathing pattern in which each inspiration is accompanied by a prolonged pause.80 As a FLS, this syndrome can also be caused by lower lesions. There have been five reported cases of such apneustic breathing in patients with achondroplasia, the pathophysiology being cervicomedullary compression rather than vagal or pneumotaxic center lesions.86 The lesion’s severity, location, and reversibility by decompression is variable.86 Central neurogenic hyperventilation can also result from thalamic lesions.85 Diagnosis involves polysomnography sleep studies, measuring somatosensory evoked potentials, and CT and MRI scans of the brain.85,86
The Apnea Test: Requiring Consent for a Test That is a Self-Fulfilling Prophecy, Not Fit for Purpose, and Always Confounded?
Published in The American Journal of Bioethics, 2020
Second, contrary to claims in the article and in guidelines, the apnea test in fact does not evaluate “the functional integrity of the medullary respiratory centers.” Respiratory physiologists have known for years that, when the medulla is isolated from the pons, gasping is the respiratory pattern reproducibly obtained, which is induced by hypoxia, prevented by hyperoxia [which is likely to induce apnea], and not induced by hypercarbia (Abdala et al. 2009; Joffe et al. 2010b; Smith et al. 2009; St-John 2009). Thus, the apnea test, which is done by inducing hypercarbia and hyperoxia, simply cannot test medullary brainstem respiratory function, the exact reason the apnea test is claimed to be required. This means that the apnea test has no diagnostic purpose and only potential harm. For this reason, again, I believe that the apnea test is contraindicated, whether consent is provided or not.
Pseudobulbar affect after stroke: a narrative review
Published in Topics in Stroke Rehabilitation, 2018
Tarun Girotra, Forrest Lowe, Wuwei Feng
Wang et al highlighted the strategic location of the pons when they compared 112 stroke survivors (56 with PBA and 56 without PBA). They observed that patients with PBA are more likely to have pontine lesions than the control group (56.3% vs 17.9%, p < 0.01) and this association was stronger with bilateral pontine lesions (86.7% vs 20%, p < 0.01).15 In the multivariate analysis, pontine lesions with or without other lesions were significantly associated with a greater likelihood for having PBA [odd’s ratio (OR) 12.24, 95% CI: 2.99–58.66].15 This observation is logical as the descending fibers converge at the pons before passing into the cerebellum through the middle cerebellar peduncle. A specific lesion in the pons can have a higher chance for disrupting this network described by Parvizi.