Prior to surgery, these investigators verified the fact that the phantosmia disappeared after occlusion of the left nostril as well as after cocainization of the left olfactory epithelium. The phantosmia was eliminated by excising a section of the left olfactory epithelium. (1991) reported the case of a woman whose 8-year-long phantosmia germinated within the left side of the nose. Taking a different approach to the surgical treatment of long-term phantosmia, Leopold et al. study, no olfactory function was preserved. (1993) reported a case in which bilateral resection of the olfactory bulbs successfully treated a bilateral phantosmia, although unlike the Kaufman et al. After complete resection of this bulb, her phantosmia episodes disappeared. An enlarged pale left olfactory bulb was found during the operation. Her olfactory dysfunction was not responsive to phenobarbital, carbamazepine, thioridazine, baclofen, or haloperidol. A year before symptom onset, she had suffered a nonconcussive head injury that was followed by a severe headache that lasted for several days. The patient was a 31-year-old woman with an 11-year history of an intermittent unpleasant phantosmia that arose from the left side of the nose. The first report in which a phantosmia was eliminated by olfactory bulb resection was that of Kaufman et al. In some such cases, removal of either the olfactory bulbs via an anterior craniotomy or intranasal lesioning of the olfactory epithelium has proved efficacious. Although such aberrations commonly resolve spontaneously over time, some remain intractable and unresponsive to medical therapies. Doty, in Handbook of Clinical Neurology, 2019 Surgical excision of olfactory bulbs or olfactory mucosaĪmong the most debilitating chemosensory disorders is the presence of disturbing smell sensations in the absence of any apparent stimulus (phantosmia). These findings are in agreement with other prospective studies reporting that the use of levodopa or dopamine agonists, and LED did not increase the risk of PD psychosis ( De la Riva, Smith, Xie, & Weintraub, 2014 Gibson et al., 2013 Goetz, Stebbins, & Ouyang, 2011 Zhu, Van Hilten, Putter, & Marinus, 2013). In contrast, there was no difference in LED between PD patients with and without psychosis in several cross-sectional studies ( Aarsland, Larsen, Cummins, & Laake, 1999 Papapetropoulos, Argyriou, & Ellul, 2005 Sanchez-Ramos, Ortoll, & Paulson, 1996). One proposed mechanism to explain their relationship is that chronic dopaminergic therapy leads to overstimulation or hypersensitivity of the mesocorticolimbic D 2/D 3 receptors ( Wolters, 1999). (2012) reported that the prescription of dopamine agonist at baseline was associated with the development of PD psychosis over a 24-month period. A prospective cohort study of 230 patients with PD who were followed up for 12 years identified higher LED at baseline as a risk factor for PD psychosis (odds ratio: 1.26 per 100 mg, P = 0.01) ( Forsaa et al., 2010). Possible mechanisms of PD psychosis include sleep, cognition, changes in visual function, and medication effects ( Ffytche et al., 2017).Īlthough clinical experience suggests a strong link between dopaminergic treatment and PD psychosis, evidence is lacking to support their direct causality. A large-scale study of 250 patients with PD described that 26% had psychotic symptoms with 52.3% of those having hallucinations and/or delusions ( Mack et al., 2012). Ryul Kim, Beomseok Jeon, in International Review of Neurobiology, 2017 3.1.3 PsychosisĪlthough visual hallucinations are the most common psychotic symptom in PD, auditory, tactile, and olfactory hallucinations are also relatively common ( Fenelon, Soulas, Zenasni, & Cleret de Langavant, 2010). Multiple sclerosis (before the age of 40) -Īlzheimer's disease (after the age of 40).
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