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Chemosensory Disorders and Nutrition
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
Carl M. Wahlstrom, Alan R. Hirsch, Bradley W. Whitman
Head injury is a common cause of olfactory defects and can occur from trauma as minimal as “heading” a soccer ball (Custer, Raudenbush, Robinson, Schlegel, and Moore 2014). Many possible mechanisms have been suggested (Hirsch and Wyse 1993). One is that acceleration injury produces shearing forces on the olfactory nerves as they pass through the cribriform plate of the ethmoid bone. Fracture of the cribriform plate may compress the olfactory nerves or a hematoma may compress them, thereby impairing olfaction. Another theory suggests that the primary insult in trauma is the destruction of central connection pathways of olfaction (Levin, High, and Eisenberg 1985).
Rhinolaryngoscopy for the Allergist
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Jerald W Koepke, William K Dolen
With the endoscope approximately 1 cm into the nose, the nasal vestibule with its hairs (vibrissae) will be encountered and often a medial protrusion on the floor of the nose (the lateral feet of the medial crura) will be noted. The inferior turbinate, floor of the nose and septum will be in view (Fig. 11.12). If the endoscope tip is flexed slightly upward, the middle turbinate will be seen in the distance; with upward flexion to 60–90 degrees, the superior portion of the anterior nose can be evaluated. If the inferior turbinate is large or swollen, it may be necessary to advance the tip of the endoscope over the anterior margin of the inferior turbinate in order to view the middle turbinate. A large maxillary ridge or displaced septal cartilage may similarly impede advancement of the endoscope. With the endoscope placed in the middle portion of the nasal cavity, the roof of the nose may be viewed by directing the endoscope upwards; this is the region of the cribriform plate. It is not usually possible to advance the endoscope towards the superior turbinate from this position.
Traumatic CSF rhinorrhea
Published in Jyotirmay S. Hegde, Hemanth Vamanshankar, CSF Rhinorrhea, 2020
Hemanth Vamanshankar, Jyotirmay S Hegde
Surgical management is particularly required in fractures where spontaneous closures are not possible, such as a fracture with complications like tension pneumocephalus, cranial nerve deficits, a large depressed fracture, or in cases of pathologies requiring acute intervention.11,12 Rocchi et al. suggest that surgical intervention is needed in compound, depressed, comminuted, or craniofacial fractures larger than 1 cm, fractures involving cribriform plate, or those in midline, and those injuries associated with a meningocele or encephalocele.25
Olfactory nerve schwannoma: how human anatomy and electron microscopy can help to solve an intriguing scientific puzzle
Published in Ultrastructural Pathology, 2022
Fabbri Vp, Valentina Papa, Tonon C, Agati R, Toni F, Zoli M, Mazzatenta D, Fioravanti A, Badaloni F, Cenacchi G, Foschini Mp, Asioli S
Another intriguing anatomic theory about the origin of OGS is related to the presence of the nervus terminalis (recognized as cranial pair zero, CN0).8 Originally discovered in 1878 by Fritsch in the brain of the sharks and then described also in humans (1913), this nerve originates in the olfactory placode. It is observed in human embryos and less recognizable in adults. Fibers originating in the nasal cavity passes into the cranium through the middle area of the cribriform plate of the ethmoid bone. The nervus terminalis shows ganglion cells, that sometimes form clusters, normally one or two located at the base of the crista Galli, the so-called ganglion of the nervus terminalis. Its function is uncertain. Despite some studies that did not find Schwann cells in CN0 of mice9 other authors have shown that the migrating GnRH cells of the nervus terminalis are accompanied by the presumptive Schwann cells precursors in the Odontocetes.10
Spontaneous sphenoid meningoencephalocele with sepsis
Published in Baylor University Medical Center Proceedings, 2020
Monica Shah, Marco A. Tadeo Bermúdez Borjas, Karen Brust
CSF rhinorrhea is a symptom caused by leakage of CSF into the nasal sinus, resulting from a defect in the skull base. The most frequent cause is head trauma, followed by idiopathic, congenital, and neoplastic lesions.2 This case is unique because it led to streptococci bacteremia from spontaneous CSF leak due to sphenoid meningoencephalocele. The patient denied any history of trauma that could lead to such an insult. The common sites of origin for CSF rhinorrhea after anterior skull base trauma include the cribriform plate, the roof of the sphenoid sinus, and the posterior wall of the frontal sinus.3,4 In this case, it was the left sphenoid sinus likely herniating the temporal lobe, causing CSF leakage. The patient also had positive beta-2-transferrin, which exists exclusively in the CSF. His transesophageal echocardiogram was negative for any vegetation.
Assessment of olfactory function after traumatic brain injury: comparison of single odour tool with detailed assessment tool
Published in Brain Injury, 2018
OD is common within clinical practice. It may be due to several different clinical conditions including Parkinson’s disease, hypertension, diabetes mellitus and idiopathic changes with age (3). However, up to 60% of OD cases are due to traumatic brain injury (TBI) and upper respiratory tract infection (URTI) including nasal and paranasal sinus disease (4). The relationship between OD and TBI is well understood, as the olfactory system is at risk of damage following TBI. The peripheral olfactory pathways may be damaged owing to blunt force trauma to the nose and olfactory epithelium or owing to shearing forces acting on the nerves in the cribriform plate. Alternatively, compression of the secondary olfactory centres within the basal frontal and temporal lobes can occur against the skull base of the anterior cranial fossa because of contrecoup damage following blunt force trauma to the occipital aspect of the skull (5). The incidence of OD following TBI increases with TBI severity (6–9).