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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
This reinforces the observations by Landis and Burkhard of the association of phantosmias and PD and response to medications used for parkinsonism. It also highlights the need for chemosensory testing in those without complaints of olfactory deficits. The described patient denied a reduced ability to smell, but testing demonstrated hyposmia. Lack of self-recognition of olfactory loss is common in PD—in a study by Doty et al (Doty, Deems, and Stellar 1988), 72% of those with olfactory deficits were unaware of their deficit.
History Stations
Published in Peter Kullar, Joseph Manjaly, Livy Kenyon, Joseph Manjaly, Peter Kullar, Joseph Manjaly, Peter Kullar, ENT OSCEs, 2023
Peter Kullar, Joseph Manjaly, Livy Kenyon, Joseph Manjaly, Peter Kullar, Joseph Manjaly, Peter Kullar
The most common causes of anosmia/hyposmia you will be expected to know areSinonasal diseasePost-viral anosmia (rhinovirus, coronavirus including COVID-19, parainfluenza virus)Head traumaOther, rarer causes (intracranial neoplasia; Turner's, Cushing's or Kallmann's syndrome)
Diagnosis and Management of Facial Pain
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Caroline P. Smith, Tim Woolford, Rajiv K. Bhalla
Pain in sinusitis that is not acute or associated with a complication is rare (Table 45.1). Patients may complain of pressure, fullness or throbbing in the distribution of the paranasal sinuses or at the vertex of the head. Symptoms may be bilateral or unilateral depending on which sinuses are affected. Exacerbation of these symptoms on bending forward is not diagnostic of rhinosinusitis. Symptoms may be acute, recurrent acute (moderated by repeated short courses of antibiotics) or chronic. There may be associated nasal congestion and/or hyposmia. There should be endoscopic signs of oedema and/or polyposis causing obstruction of outflow drainage pathways, and mucosal disease. Over 80% of patients with endoscopic evidence of purulent secretions have no headache or facial pain. If surgery is performed in cases where facial pain is the dominant symptom without firm clinical evidence of rhinosinusitis, patients largely continue to complain of facial pain postoperatively.
Analyses on the influence of normal nasal morphological variations on odorant transport to the olfactory cleft
Published in Inhalation Toxicology, 2022
Ryan M. Sicard, Reanna Shah, Dennis O. Frank-Ito
Olfaction is the sensation arising from the nasal cavity following stimulation of the olfactory receptors by odorant molecules. Olfactory dysfunction is characterized by reduced or absent sense of smell, ranging from hyposmia to anosmia (Guss et al. 2009). While olfactory perception is effective when the combination of sensorineural components and conductive factors function properly, the role of conductive factors (respiratory effort and nasal anatomical structure) in olfaction has been given less attention. The nasal cavity plays an essential role in odor perception, which consists of the transportation of volatile chemical molecules via airflow to the olfactory receptors (Zhao et al. 2004). In order to completely understand human olfaction, it is crucial to gain knowledge of the airflow patterns in the human nasal cavity and quantify the transport of odorant-laden air to the olfactory region.
Olfactory function and findings on chest computed tomography in COVID-19: is there any correlation?
Published in Acta Oto-Laryngologica, 2021
Lucas Resende Lucinda Mangia, Marcelly Botelho Soares, Thiago Sasso Carmona de Souza, Patrícia Cristina Scarabotto, Roberta David João De Masi, Gabriel Lucca de Oliveira Salvador, Rogério Hamerschmidt
Current knowledge on the molecular mechanisms of infectivity and virulence of the SARS-CoV-2 are also consistent with those obtained from clinical studies on smell disorders in COVID-19. The angiotensin-converting enzyme 2 (ACE2) has been identified as the cell receptor for SARS-CoV-2. The spike S1 glycoprotein in the viral surface binds to the ACE2 and ultimately leads to receptor-dependent endocytosis [12]. The expression of ACE2 in human neurons remains a controversial topic in the literature. Studies in vitro or with animal models have suggested that it might occur [16]. Also, this enzyme has also shown a correlation with neurodegeneration [17]. These findings could therefore support a theory that SARS-CoV-2 would directly invade and damage olfactory neurons. Other authors, however, argue that only non-neuronal cells would express ACE2 and thus be able to be infected by SARS-CoV-2. In this case, olfactory disorders would occur in COVID-19 due to the invasion of the surrounding support cells, stem cells and perivascular cells in the neuroepithelium, rather than as a consequence of neuronal damage [18]. Regardless of the underlying mechanisms, it appears to be clear that the molecular studies on olfactory dysfunction in the disease point to a very different pathogenic pathway from that of the lung involvement. The considerable number of individuals with COVID-19 and hyposmia as the only manifestation seems also to be consistent with this theory.
Berg adder (Bitis atropos) envenoming: an analysis of 14 cases
Published in Clinical Toxicology, 2019
Andrew John van der Walt, Gert Jacobus Muller
Hyposmia was a symptom featured in all the patients in whom this modality was assessed (10/10 patients; 100%). Unfortunately this component was not tested in three paediatric patients. Hyposmia manifested early, within 1–2 hours, and resolved slowly and variably, ranging from days to years. A diminished sense of smell was present for more than 10 years after envenoming in two patients. Similarly, loss of taste was a complaint in eight cases. In all these cases hyposmia was noted as a concomitant complaint. As with hyposmia loss of taste was an early manifestation. Furthermore, the time of onset of loss of taste generally correlated with the time of onset of hyposmia. In only one case, a discrepancy between the onset of loss of taste (occurring at 2 hours) and the onset of hyposmia (occurring at 24 hours) was observed. Loss of taste resolved slowly and variably, ranging from 6 days to 1 year. Expert neurological assessment was performed in one of the patients with hyposmia and loss of taste. This assessment took place at 14 days post-envenoming and showed that the basic modalities of taste (sour, salt, sweet and bitter) were intact, but sense of smell was almost absent.