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Traumatic brain injury (TBI) as a major public health problem may lead to olfactory dysfunction. However, little is known about brain responses to odors in TBI olfactory loss patients. Nineteen healthy controls and forty TBI olfactory dysfunctional patients (19 with hyposmia and 21 with anosmia) underwent a functional magnetic resonance imaging scan when two odors (peach and coffee) were presented intranasally using a computerized olfactometer. Olfactory performance was measured using the "Sniffin' Sticks" test. TBI patients with hyposmia or anosmia showed decreased odor-induced brain activations in the primary olfactory area and insular cortex as compared to healthy controls (FWE-corrected peak p < 0.05). In addition, negative correlations were found between the time since injury (in month) and odor-induced brain responses in the right primary olfactory area for patients with hyposmia. Similar correlations were seen in the insula and orbitofrontal cortex for patients with anosmia. In conclusion, results from the current study are evidences for the impairment of central nervous processing of odor perception at all levels of the olfactory system among TBI patients with olfactory loss. In addition, the duration after the initial injury may have an impact on the severity of olfactory dysfunction.

There is a large inter-individual variation for umami taste perception. However the neural mechanism for this variability is not well understood. This study investigated brain responses to umami and salty taste among individuals with different umami identification abilities and the effect of repeated oral umami exposure on umami identification and neural processing of taste perceptions. Fifteen participants with high umami identification ability ("High Tasters, HT) and fifteen with low umami identification ability ("Low Tasters", LT) underwent three weeks of controlled exposure to umami taste (umami training). Prior to and after the training, participants underwent fMRI scans during which the umami taste solution and a control taste (salty) solution were delivered to their mouth using a gustometer. Taste intensity and pleasantness were rated after each scan. Umami taste identification was assessed before and after the umami training using "Taste Strips" test. Neuroimaging results showed different central processing of umami and salty taste based on umami identification ability, in which the umami LT had stronger activation in the thalamus and hippocampus while the umami HT showed stronger activation in the primary gustatory cortex. In addition, umami identification was significantly improved after umami training for LT. However, it was not reflected in changes in neural activation. The current study shows that attention and association/memory related brain structures play a significant role in the perception of umami taste; and with reference to the results of repeated umami exposure, the presence of very subtle changes regarding the neural processing., (Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.)

Odors are typically bimodal in nature, interacting with the olfactory and trigeminal systems. The trigeminal component may be noticed (e.g. menthol) or perceptually ignored, leading to different neural substrates being recruited during odor encoding. Therefore, the current study was designed to explore the perceptual and central-nervous activations in response to pleasant bimodal odors using functional magnetic resonance imaging (fMRI). In this study, healthy subjects were exposed to odorants alone (unimodal) or with a "cooling" trigeminal component (bimodal) at sub- and suprathreshold concentrations with a portable olfactometer in a 3T fMRI scanner. Within the scanner, subjects reported all odorants as pleasant and intensity increasing with trigeminal concentration. Many of the regions of interest [orbital frontal cortex (OFC), insula, thalamus, cerebellum, postcentral gyrus and cingulate cortex] were activated during bimodal odor conditions when contrasted with unimodal, and interestingly, most of these activations were seen prior to trigeminal perception (e.g. at a sub-threshold level). This includes large bilateral activations within the OFC, insula, cerebellum and parts of the cingulate cortex. Additionally, activation of the thalamus was seen early in the stages of bimodal odor encoding suggesting its role of mediating attention toward the presence of two stimuli. Lastly, intensity encoding during bimodal processing shows overlap of previously demonstrated simple trigeminal encoding areas (medial cingulate cortex) and the more complex olfactory encoding areas (bilateral insula, superior temporal gyrus, OFC, and cerebellum), but not the amygdala., (Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.)

Background: Individuals with hyposmia, or the partial loss of smell, represent a large sector (15 %) of the population that is likely to grow with the current aging population; however, our understanding to how hyposmics centrally process odors is still not clear. One popular non-invasive tool for in vivo imaging of biological activity among human brains has been function magnetic resonance imaging (fMRI) which uses blood-oxygenation level dependent (BOLD) signal as an indirect measurement. Therefore, the aim of this study was to understand differences in olfaction processing between patients with hyposmia and healthy controls using functional magnetic resonance imaging (fMRI)., Methodology: Eleven hyposmic and 12 healthy, normosmic subjects were exposed to two different food-related odors (coffee and peach) during a block-designed fMRI session. Additionally, odor perception qualities were rated for each odor throughout the scanning session., Results: The activations of the normosmic group were localized in typical olfactory areas (insula, orbitofrontal cortex [OFC], limbic system and amygdala). The hyposmic group showed similar regions of activation (insula, OFC, limbic system), however, less activation was found in the amygdala, left anterior cingulate and right OFC, but higher activation was shown in the right parahippocampal and both the left and right posterior cingulate gyrus which are assumed to play an important role in the processing and remembrance of memories., Conclusions: These results indicate similar central olfactory processing among groups, yet subjects with partial loss may attempt to compensate smell impairment with odor memory or higher motivation to smell.

Rats are able to lateralize odors. This ability involves specialized neurons in the orbitofrontal cortex which are able to process the left, right and bilateral presentation of stimuli. However, it is not clear whether this function is preserved in humans. Humans are in general not able to differentiate whether a selective olfactory stimulant has been applied to the left or right nostril; however exceptions have been reported. Following a screening of 152 individuals with an olfactory lateralization test, we identified 19 who could lateralize odors above chance level. 15 of these "lateralizers" underwent olfactory fMRI scanning in a block design and were compared to 15 controls matched for age and sex distribution. As a result, both groups showed comparable activation of olfactory eloquent brain areas. However, subjects with lateralization ability had a significantly enhanced activation of cerebral trigeminal processing areas (somatosensory cortex, intraparietal sulcus). In contrast to controls, lateralizers furthermore exhibited no suppression in the area of the trigeminal principal sensory nucleus. An exploratory study with an olfactory change detection paradigm furthermore showed that lateralizers oriented faster towards changes in the olfactory environment. Taken together, our study suggests that the trigeminal system is activated to a higher degree by the odorous stimuli in the group of "lateralizers". We conclude that humans are not able to lateralize odors based on the olfactory input alone, but vary in the degree to which the trigeminal system is recruited., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Cerebral activations during olfactory mental imagery are fairly well investigated in healthy participants but little attention has been given to olfactory imagery in patients with olfactory loss. To explore whether olfactory loss leads to deficits in olfactory imagery, neural responses using functional magnetic resonance imaging (fMRI) and self-report measures were investigated in 16 participants with acquired olfactory loss and 19 control participants. Participants imagined both pleasant and unpleasant odors and their visual representations. Patients reported less vivid olfactory but not visual images than controls. Results from neuroimaging revealed that activation patterns differed between patients and controls. While the control group showed stronger activation in olfactory brain regions for unpleasant compared to pleasant odors, the patient group did not. Also, activation in critical areas for olfactory imagery was correlated with the duration of olfactory dysfunction, indicating that the longer the duration of dysfunction, the more the attentional resources were employed. This indicates that participants with olfactory loss have difficulties to perform olfactory imagery in the conventional way. Regular exposure to olfactory information may be necessary to maintain an olfactory imagery capacity., (Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.)

Aim was to investigate differences in the central-nervous processing of gustatory stimuli between normogeusic subjects and patients with taste disorders. Twelve subjects with normal gustatory function and eight patients suffering from hypo- to ageusia underwent one fMRI run each in a 1.5 T scanner where they received liquid gustatory stimuli. fMRI analyses were performed by means of SPM2. Across all participants clusters of activated voxels were mainly found in orbitofrontal and insular regions of interest. Even those patients who did not perceive any stimuli showed some activation of gustatory centers. Group comparisons revealed higher activation of the insular and orbitofrontal cortices in patients compared to the group of healthy subjects. While further studies are needed, this finding may be interpreted in terms of enhanced neuronal recruitment due to functional impairment in patients with gustatory loss. It may ultimately prove useful in terms of the prognostic evaluation of individual patients.

Is MEG source analysis able to precisely locate the primary focal epileptic activity? 22 patients with pharmacoresistant temporal lobe epilepsy were recorded during presurgical evaluation simultaneously with multichannel MEG/EEG and invasive (subdural) electrodes to evaluate the increase of information gained by MEG concerning the localization of focal epileptic activity and lesions. With this systematic study it should become clearer how often MEG can establish a diagnostic bridge between function and morphology. In addition, MEG localization accuracy of focal epileptic activity was to be validated empirically by invasive EEG recordings and postsurgical outcome. Spikes in the MEG were used for magnetic source localization, and the result was combined with magnetic resonance imaging (MRI). All patients definitely suffered from temporal lobe epilepsy and revealed a structural abnormality in MRI. 17 patients with lesions in the temporal lobe were operated meanwhile and became markedly improved or seizure free. In 7 of 8 patients with a tumor and validated operation outcome, a very close correlation of the 3D-magnetic source localization and the border of the tumor in the brain was found (distance less than 10 mm). In 8 of 9 patients with a temporal/hippocampal atrophy and validated operation outcome, dipoles of epileptiform activity were located within the atrophic lobe.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to investigate the topographical distribution of chemosensory event-related potentials in relation to stimulation with nicotine. The recognition thresholds of 3 different sensations elicited by nicotine (odor, burning, stinging) were determined. Subsequently, 3 concentrations of nicotine were applied which were just above mean threshold for each of the 3 sensations. Subjects rated the intensity of odor, burning, and stinging. Additionally, they tracked the time course of these sensations. Odor and stinging appeared immediately after stimulus onset. Burning started after several seconds. Intensity ratings of burning and stinging increased with rising stimulus concentrations, whereas the odorous sensation was strongest at medium concentrations. After low and medium stimuli largest mean amplitudes were parietally obtained, whereas following stimulation with the highest concentration, amplitudes peaked at Cz.

A stimulation method was employed by which chemosensory evoked potentials were recorded without tactile somatosensory contamination. The purpose of the study was to determine whether potential components evoked by stimulation of the chemoreceptors of the trigeminal nerve can be distinguished from those of the olfactory nerve. The stimulants (vanillin, phenylethyl alcohol, limonene, menthol, anethol, benzaldehyde, carbon dioxide and a mixture of vanillin and carbon dioxide) were presented in a randomized order to 13 volunteers. Chemosensory evoked potentials to substances which anosmics are unable to perceive (vanillin, phenylethyl alcohol) were termed olfactory evoked potentials; potentials to CO2, which effected no olfactory sensations were termed chemo-somatosensory potentials. Analysis of variance revealed that the different substances resulted in statistically significant changes in the amplitudes and latencies of the evoked potentials, and also in the subjective estimates of intensity. An increased excitation of the somatosensory system resulted in reduced latencies and enhanced amplitudes of the evoked potentials. Responses to the mixture of carbon dioxide and vanillin appeared significantly earlier (50-150 msec) than responses to either substance alone.