From blindsight to blindsmell: a mini review

Zucco, Gesualdo M.; Priftis, Konstantinos; Stevenson, Richard J.

doi:10.1515/tnsci-2015-0002

Cited by 13 publications

(10 citation statements)

References 30 publications

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“…It is striking that the odor‐specific piriform cortex activation was not only present in hyposmic, but also in anosmic patients. Since the anosmic patients had no functional olfactory perception based on their Sniffin’ Sticks score, the observed piriform cortex activation in anosmics might be in line with evidence that odors can alter behavior and brain activity even if they are not consciously perceived (Arzi et al, ; Lorig, ; Smeets & Dijksterhuis, ; Sobel et al, ; Zucco et al, ). This finding suggests that the pathway from the olfactory epithelium to the piriform cortex might still be intact in these patients and that the olfactory dysfunction occurs after piriform processing.…”

Section: Discussionsupporting

confidence: 67%

Severity of olfactory deficits is reflected in functional brain networks—An fMRI study

Reichert

Postma

Smeets

et al. 2018

Human Brain Mapping

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Even though deficits in olfactory function affect a considerable part of the population, the neuronal basis of olfactory deficits remains scarcely investigated. To achieve a better understanding of how smell loss affects neural activation patterns and functional networks, we set out to investigate patients with olfactory dysfunction using functional magnetic resonance imaging (fMRI) and olfactory stimulation. We used patients' scores on a standardized olfactory test as continuous measure of olfactory function. 48 patients (mean olfactory threshold discrimination identification (TDI) score = 16.33, SD = 6.4, range 6 - 28.5) were investigated. Overall, patients showed piriform cortex activation during odor stimulation compared to pure sniffing. Group independent component analysis indicated that the recruitment of three networks during odor stimulation was correlated with olfactory function: a sensory processing network (including regions such as insula, thalamus and piriform cortex), a cerebellar network and an occipital network. Interestingly, recruitment of these networks during pure sniffing was related to olfactory function as well. Our results support previous findings that sniffing alone can activate olfactory regions. Extending this, we found that the severity of olfactory deficits is related to the extent to which neural networks are recruited both during olfactory stimulation and pure sniffing. This indicates that olfactory deficits are not only reflected in changes in specific olfactory areas but also in the recruitment of occipital and cerebellar networks. These findings pave the way for future investigations on whether characteristics of these networks might be of use for the prediction of disease prognosis or of treatment success.

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Section: Discussionsupporting

confidence: 67%

Severity of olfactory deficits is reflected in functional brain networks—An fMRI study

Reichert

Postma

Smeets

et al. 2018

Human Brain Mapping

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“…Earlier studies from our group suggested that the MBT, which detects subtle motor behaviors missed by the CRS-R, can clinically discriminate patients with potential [19,20] Cranial nerve palsies Imaging (MRI)-brain-stem nuclear or nerve lesions Non convulsive status epilepticus Staring, eye deviations, neglect, myoclonus EEG-epileptic potentials Cortical blindness [12,13] Absence of visual interaction, absence of menace reflex, absence of visual pursuit Imaging (MRI)-bilateral occipital lesions Akinetic (frontal) Syndrome [18] Marked reduction of spontaneous movement and speech production with inconstant visual fixation and tracking, inconstant commandfollowing and vocalization…”

Section: Discussionmentioning

confidence: 99%

“…Lesions in frontal, temporal, parietal, occipital, basal ganglia, thalamus, hypothalamus, mesencephalon, pons, and cerebellum regions were identified bilaterally and recorded. Special attention was given to score lesions in areas strategic for vision (calcarine cortex [ 12 , 13 ]), language (dominant fronto-temporo-parietal cortices involved in language [ 14 , 15 ]), arousal control (thalamic involvement [ 16 , 17 ]), motor planification and execution (frontal–subcortical circuitry [ 18 ]), and cranial nerve nuclei in the brain stem [ 19 , 20 ].…”

Section: Methodsmentioning

confidence: 99%

Early discrimination of cognitive motor dissociation from disorders of consciousness: pitfalls and clues

et al. 2020

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Bedside assessment of consciousness and awareness after a severe brain injury might be hampered by confounding clinical factors (i.e., pitfalls) interfering with the production of behavioral or motor responses to external stimuli. Despite the use of validated clinical scales, a high misdiagnosis rate is indeed observed. We retrospectively analyzed a cohort of 49 patients with severe brain injury admitted to an acute neuro-rehabilitation program. Patients' behavior was assessed using the Motor Behavior Tool and Coma Recovery Scale Revised. All patients underwent systematic assessment for pitfalls including polyneuropathy and/or myopathy and/or myelopathy, major cranial nerve palsies, non-convulsive status epilepticus, aphasia (expressive or comprehensive), cortical blindness, thalamic involvement and frontal akinetic syndrome. A high prevalence (75%) of pitfalls potentially interfering with sensory afference (polyneuropathy, myopathy, myelopathy, and sensory aphasia), motor efference (polyneuropathy, myopathy, motor aphasia, and frontal akinetic syndrome), and intrinsic brain activity (thalamic involvement and epilepsy) was found. Nonetheless, the motor behavior tool identified residual cognition (i.e. a cognitive motor dissociation condition) regardless of the presence of these pitfalls in 70% of the patients diagnosed as unresponsive using the Coma Recovery Scale Revised. On one hand, pitfalls might contribute to misdiagnosis. On the other, it could be argued that they are clues for diagnosing cognitive motor dissociation rather than true disorders of consciousness given their prominent effect on the sensory-motor input-output balance.

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“…In principle, this strategy could be extended to non-mammals, based on identifying homologues or analogues of V1 in those animals. While blindsight solely concerns vision, there is some evidence for parallel phenomena in hearing and olfaction [ 20 , 21 ]. The drawback to this neurological route is that it is invasive and difficult.…”

Section: P-richnessmentioning

confidence: 99%

Dimensions of Animal Consciousness

Birch

Schnell

Clayton

2020

Trends in Cognitive Sciences

189

137

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How does consciousness vary across the animal kingdom? Are some animals ‘more conscious’ than others? This article presents a multidimensional framework for understanding interspecies variation in states of consciousness. The framework distinguishes five key dimensions of variation: perceptual richness, evaluative richness, integration at a time, integration across time, and selfconsciousness. For each dimension, existing experiments that bear on it are reviewed and future experiments are suggested. By assessing a given species against each dimension, we can construct a consciousness profile for that species. On this framework, there is no single scale along which species can be ranked as more or less conscious. Rather, each species has its own distinctive consciousness profile.

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From blindsight to blindsmell: a mini review

Cited by 13 publications

References 30 publications

Severity of olfactory deficits is reflected in functional brain networks—An fMRI study

Severity of olfactory deficits is reflected in functional brain networks—An fMRI study

Early discrimination of cognitive motor dissociation from disorders of consciousness: pitfalls and clues

Dimensions of Animal Consciousness

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