Olfactory Deficits in Frontotemporal Dementia as Measured by the Alberta Smell Test

Heyanka, Daniel J.; Golden, Charles J.; McCue, Robert; Scarisbrick, D; Linck, John; Zlatkin, Nancy I.

doi:10.1080/09084282.2013.782031

Cited by 18 publications

(17 citation statements)

References 25 publications

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“…Olfaction deteriorates in neurodegenerative conditions such as Alzheimer's and Parkinson's disease (Mesholam et al, 1998), and has been called into question in bvFTD. Prior work has largely shown that patients with bvFTD have difficulty identifying odours (McLaughlin and Westervelt, 2008;Pardini et al, 2009;Omar et al, 2013;Heyanka et al, 2014;Magerova et al, 2014), possibly related to anomia or semantic problems, but have intact odour discrimination (Luzzi et al, 2007;Rami et al, 2007;Orasji et al, 2016). While patients with bvFTD in this study did not discriminate odours as well as the control subjects did, those with high discrimination scores rated valence no differently from those with low scores, and adding discrimination score as a covariate did not alter the significance of the diagnosis by odour valence interaction for subjective pleasantness ratings.…”

Section: Discussioncontrasting

confidence: 61%

Reward deficits in behavioural variant frontotemporal dementia include insensitivity to negative stimuli

Perry

Datta

Sturm

et al. 2017

Brain

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During reward processing individuals weigh positive and negative features of a stimulus to determine whether they will pursue or avoid it. Though patients with behavioural variant frontotemporal dementia display changes in their pursuit of rewards, such as food, alcohol, money, and sex, the basis for these shifts is not clearly established. In particular, it is unknown whether patients' behaviour results from excessive focus on rewards, insensitivity to punishment, or to dysfunction in a particular stage of reward processing, such as anticipation, consumption, or action selection. Our goal was to determine the nature of the reward deficit in behavioural variant frontotemporal dementia and its underlying anatomy. We devised a series of tasks involving pleasant, unpleasant, and neutral olfactory stimuli, designed to separate distinct phases of reward processing. In a group of 25 patients with behavioural variant frontotemporal dementia and 21 control subjects, diagnosis by valence interactions revealed that patients with behavioural variant frontotemporal dementia rated unpleasant odours as less aversive than did controls and displayed lower skin conductance responses when anticipating an upcoming aversive odour. Subjective pleasantness ratings and skin conductance responses did not differ between behavioural variant frontotemporal dementia and controls for pleasant or neutral smells. In a task designed to measure the effort subjects would expend to smell or avoid smelling a stimulus, patients with behavioural variant frontotemporal dementia were less motivated, and therefore less successful than control subjects, at avoiding what they preferred not to smell, but had equivalent success at obtaining stimuli they found rewarding. Voxel-based morphometry of patients with behavioural variant frontotemporal dementia revealed that the inability to subjectively differentiate the valence of pleasant and unpleasant odours correlated with atrophy in right ventral mid-insula and right amygdala. High pleasantness ratings of unpleasant stimuli correlated with left dorsal anterior insula and frontal pole atrophy. These findings indicate that insensitivity to negative information may be a key component of the reward-seeking behaviours in behavioural variant frontotemporal dementia, and may relate to degeneration of structures that are involved in representing the emotional salience of sensory information.

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Section: Discussioncontrasting

confidence: 61%

Reward deficits in behavioural variant frontotemporal dementia include insensitivity to negative stimuli

Perry

Datta

Sturm

et al. 2017

Brain

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“…28 , 29 Moreover, damage to these regions, whether from brain trauma, stroke, or through neurodegenerative processes (e.g., premotor Parkinson disease, Alzheimer disease, multiple sclerosis, frontotemporal dementia), has been demonstrated to significantly impair memory and thereby the ability of the brain to correctly match up and link common inhalational odorant molecules to past learning and experience. 30 – 34 …”

Section: Discussionmentioning

confidence: 99%

Olfactory impairment and traumatic brain injury in blast-injured combat troops

et al. 2015

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Objective:To determine whether a structured and quantitative assessment of differential olfactory performance—recognized between a blast-injured traumatic brain injury (TBI) group and a demographically comparable blast-injured control group—can serve as a reliable antecedent marker for preclinical detection of intracranial neurotrauma.Methods:We prospectively and consecutively enrolled 231 polytrauma inpatients, acutely injured from explosions during combat operations in either Afghanistan or Iraq and requiring immediate stateside evacuation and sequential admission to our tertiary care medical center over a 2½-year period. This study correlates olfactometric scores with both contemporaneous neuroimaging findings as well as the clinical diagnosis of TBI, tabulates population-specific incidence data, and investigates return of olfactory function.Results:Olfactometric score predicted abnormal neuroimaging significantly better than chance alone (area under the curve = 0.78, 95% confidence interval [CI] 0.70–0.87). Normosmia was present in all troops with mild TBI (i.e., concussion) and all control subjects. Troops with radiographic evidence of frontal lobe injuries were 3 times more likely to have olfactory impairment than troops with injuries to other brain regions (relative risk 3.0, 95% CI 0.98–9.14). Normalization of scores occurred in all anosmic troops available for follow-up testing.Conclusion:Quantitative identification olfactometry has limited sensitivity but high specificity as a marker for detecting acute structural neuropathology from trauma. When considering whether to order advanced neuroimaging, a functional disturbance with central olfactory impairment should be regarded as an important tool to inform the decision process.Classification of evidence:This study provides Class III evidence that central olfactory dysfunction identifies patients with TBI who have intracranial radiographic abnormalities with a sensitivity of 35% (95% CI 20.6%–51.7%) and specificity of 100% (95% CI 97.7%–100.0%).

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“…Numerous non-parkinsonian neurodegenerative diseases exhibit mild to severe olfactory dysfunction. Odor identification is impaired in the frontal variant of FTD (prevalence 96%) ( Heyanka et al, 2014 ; Luzzi et al, 2007 ; McLaughlin and Westervelt, 2008 ; Pardini et al, 2009 ), in ALS (prevalence 75%) ( Ahlskog et al, 1998 ; Elian, 1991 ; Hawkes et al, 1998 ; Takeda et al, 2015 ), in some patients with multiple sclerosis ( Lucassen et al, 2016 ), and in Huntington’s disease ( Bylsma et al, 1997 ; Hamilton et al, 1999 ; Lazic et al, 2007 ). Other olfactory abilities have not been systematically assessed, but deficits in odor recognition and memory odor detection are described in HD ( Barrios et al, 2007 ; Hamilton et al, 1999 ; Nordin et al, 1995 ; Pirogovsky et al, 2007 ), in a new variant of CJD ( Reuber et al, 2001 ), and in multiple sclerosis (depending on the location of the demyelinating lesions) ( Bartosik-Psujek et al, 2004 ; Constantinescu et al, 1994 ; Doty et al, 1998 ; L.-M. Li et al, 2016 ; Lucassen et al, 2016 ; Lutterotti et al, 2011 ).…”

Section: Olfactory Dysfunction Is Common In Many Neurodegenerativementioning

confidence: 99%

The olfactory bulb as the entry site for prion-like propagation in neurodegenerative diseases

Rey

Wesson

Brundin

2018

Neurobiology of Disease

212

181

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Olfactory deficits are present in numerous neurodegenerative disorders and are accompanied by pathology in related brain regions. In several of these disorders, olfactory disturbances appear early and are considered as prodromal symptoms of the disease. In addition, pathological protein aggregates affect olfactory regions prior to other regions, suggesting that the olfactory system might be particularly vulnerable to neurodegenerative diseases. Exposed to the external environment, the olfactory epithelium and olfactory bulb allow pathogen and toxin penetration into the brain, a process that has been proposed to play a role in neurodegenerative diseases. Determining whether the olfactory bulb could be a starting point of pathology and of pathology spread is crucial to understanding how neurodegenerative diseases evolve. We argue that pathological changes following environmental insults contribute to the initiation of protein aggregation in the olfactory bulb, which then triggers the spread of the pathology within the brain by a templating mechanism in a prion-like manner.We review the evidence for the early involvement of olfactory structures in neurodegenerative diseases and the relationship between neuropathology and olfactory function. We discuss the vulnerability and putative underlying mechanisms by which pathology could be initiated in the olfactory bulb, from the entry of pathogens (promoted by increased permeability of the olfactory epithelium with aging or inflammation) to the sensitivity of the olfactory system to oxidative stress and inflammation. Finally, we review changes in protein expression and neural excitability triggered by pathogenic proteins that can promote pathogenesis in the olfactory bulb and beyond.

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Olfactory Deficits in Frontotemporal Dementia as Measured by the Alberta Smell Test

Cited by 18 publications

References 25 publications

Reward deficits in behavioural variant frontotemporal dementia include insensitivity to negative stimuli

Reward deficits in behavioural variant frontotemporal dementia include insensitivity to negative stimuli

Olfactory impairment and traumatic brain injury in blast-injured combat troops

The olfactory bulb as the entry site for prion-like propagation in neurodegenerative diseases

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