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Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Brain swelling may lead to herniation of the uncus downwards through the tentorium cerebri and compression of the oculomotor (IIIrd) nerve as it passes over the free edge of the tentorium. This is the cause of a fixed dilated pupil and indicates severe brain swelling requiring immediate treatment. The abducens (VIth) nerve has a long intracranial course and may be compressed or stretched by raised intracranial pressure. Conversely, patients may experience a transient VIth nerve palsy following LP.
Basics of CT Scan Head and Trauma Radiographs
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Ujjwal Gorsi, Chirag Kamal Ahuja
It is reiterated that in any manifestation of head injury, it is a dictum to evaluate for contralateral midline shift and transcompartmental herniations, e.g. uncal herniation, tonsillar herniation and ascending transtentorial herniation along with corresponding vascular ischaemic effects in the anterior and posterior cerebral territories. There may be late effects of head injury in the form of internal carotid artery injury resulting in carotid-cavernous fistula (Figure 29.7) and CSF rhinorrhoea (Figure 29.8).
Head Injury
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Uncal herniation is the syndrome seen when an expanding mass lesion compresses the temporal lobe, pushing the uncus over the free edge of the tentorium cerebelli. This compresses the cerebral peduncle and ipsilateral oculomotor nerve, producing contralateral hemiparesis or hemiplegia and an ipsilateral oculomotor nerve palsy. The latter can present as just pupillary dilatation or progress to include ptosis and a ‘down and out’ pupil secondary to paralysis of the ocular muscles innervated by the third nerve. The Kernohan’s notch phenomenon refers to uncal herniation presenting with weakness ipsilateral to the mass lesion and results from compression of the contralateral cerebral peduncle against the contralateral tentorial edge.
Investigational drugs for the treatment of olfactory dysfunction
Published in Expert Opinion on Investigational Drugs, 2022
Arianna Di Stadio, Cinzia Severini, Andrea Colizza, Marco De Vincentiis, Ignazio La Mantia
The neuroepithelium is connected through the axons of the ORN to the olfactory bulb, which contains glomerulus, mitral cells and tufted relay neurons. The axons converge in the glomerulus to form the first cranial nerve (olfactory nerve). The glomerulus is connected by synapses to the mitral cells; the latter together with the tufted relay neurons forms the olfactory tract. This structure bifurcates in the medial and lateral olfactory stria (y inverted-shaped). The olfactory stimulus is conducted through these structures up to the piriform cortex, the periamygdaloid cortex, the olfactory tuberculosis and the anterior olfactory nucleus. The primary olfactory cortex is formed by the medial and lateral olfactory stria and the anterior perforated substance. The lateral olfactory stria is extended posteriorly giving origin to the entorhinal area which, together with the uncus, forms the secondary olfactory cortex, also known as the orbitofrontal cortex (Figure 2). This area is straightly related to memory. The primary cortex is responsible for the active perception of the sense of smell, while the secondary one is the portion where the smell perception is integrated with emotions and memory.
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
A sign of transtentorial herniation from a supratentorial mass lesion is ipsilateral third nerve palsy with early pupil dilation, but a less commonly reported FLS is contralateral third nerve palsy.65 The supratentorial mass lesion, such as an acute large frontal intraparenchymal hemorrhage may cause a contralateral third nerve palsy, with contralateral pupil dilation and ptosis, that slowly resolves following neurosurgical intervention.65 While the pathophysiological mechanism remains unclear, anomalous anatomy may be involved.65 Contralateral uncal herniation can occur before ipsilateral uncal herniation if the patient has a narrow ipsilateral and wide contralateral tentorial opening.65 Lateral displacement of the midbrain can also cause compression of the opposite third nerve between the posterior cerebral and superior cerebellar arteries. When the hematoma is located inferiorly, initial upward displacement of the brainstem can occur.65 If there is also coronal rotation of the midbrain such that the contralateral side is raised compared with the ipsilateral side, there can be traction on the third nerve as it passes under the posterior cerebral artery, leading to contralateral pupillary dilation.65 It has been experimentally shown that frontal extradural compression produces bilateral uncal herniation, whereas temporal compression causes unilateral herniation.11 Thus, the particular location of lesion should be taken into account in the diagnosis and treatment of such cranial nerve palsies.
Fatal innominate artery hemorrhage in a patient with tetraplegia: Case report and literature review
Published in The Journal of Spinal Cord Medicine, 2018
Before discharge, a small amount of bleeding from the tracheostomy was noted without any other new signs or symptoms. Because the bleeding was minor and spontaneously subsided, it was attributed to abrasion at the stoma site following forceful coughing. The next day, 5–10 ml of bleeding was found during tracheostomy suctioning. His vital signs remained stable, and his oxygen saturation was normal on room air. The ENT Department was informed, and the patient remained under close observation. Frequent suctioning was required for excessive secretions. Minor bleeding continued over next 3 hours followed by sudden profuse bleeding from the tracheostomy. During life support measures, he was unable to maintain oxygenation, became hypotensive, and lost consciousness. An emergency median sternotomy was performed, and repair of the innominate artery by primary closure was conducted to maintain blood flow in the main trunk. Postoperatively, the patient was transferred to the ICU and given inotropic support and mechanical ventilation without sedation, but remained in a coma. Computed tomography scanning of the brain suggested a poor prognosis due to potentially irreversible uncal herniation. After discussion with the family, the patient’s status was changed to do not resuscitate and inotropes were withheld. He had a cardiac arrest and died on the third postoperative day.