PeerJ Preprints: Cognitive Disordershttps://peerj.com/preprints/index.atom?journal=peerj&subject=3650Cognitive Disorders articles published in PeerJ PreprintsVocal emotion recognition in school-age children: normative data for the EmoHI testhttps://peerj.com/preprints/279212019-08-282019-08-28Leanne NagelsEtienne GaudrainDebi VickersMarta Matos LopesPetra HendriksDeniz Başkent
Traditionally, emotion recognition research has primarily used pictures and videos while audio test materials have received less attention and are not always readily available. Particularly for testing vocal emotion recognition in hearing-impaired listeners, the audio quality of assessment materials may becrucial. Here, we present a vocal emotion recognition test with non-language specific pseudospeech productions of multiple speakers expressing three core emotions (happy, angry, and sad): the EmoHI test. Recorded with high sound quality, the test is suitable to use with populations of children and adults with normal or impaired hearing, and across different languages. In the present study, we obtained normative data for vocal emotion recognition development in normal-hearing school-age (4-12 years) children using the EmoHI test. In addition, we tested Dutch and English children to investigate cross-language effects. Our results show that children’s emotion recognition accuracy scores improved significantly with age from the youngest group tested on (mean accuracy 4-6 years: 48.9%), but children’s performance did not reach adult-like values (mean accuracy adults: 94.1%) even for the oldest age group tested (mean accuracy 10-12 years: 81.1%). Furthermore, the effect of age on children’s development did not differ across languages. The strong but slow development in children’s ability to recognize vocal emotions emphasizes the role of auditory experience in forming robust representations of vocal emotions. The wide range of age-related performances that are captured and the lack of significant differences across the tested languages affirm the usability and versatility of the EmoHI test.
Traditionally, emotion recognition research has primarily used pictures and videos while audio test materials have received less attention and are not always readily available. Particularly for testing vocal emotion recognition in hearing-impaired listeners, the audio quality of assessment materials may becrucial. Here, we present a vocal emotion recognition test with non-language specific pseudospeech productions of multiple speakers expressing three core emotions (happy, angry, and sad): the EmoHI test. Recorded with high sound quality, the test is suitable to use with populations of children and adults with normal or impaired hearing, and across different languages. In the present study, we obtained normative data for vocal emotion recognition development in normal-hearing school-age (4-12 years) children using the EmoHI test. In addition, we tested Dutch and English children to investigate cross-language effects. Our results show that children’s emotion recognition accuracy scores improved significantly with age from the youngest group tested on (mean accuracy 4-6 years: 48.9%), but children’s performance did not reach adult-like values (mean accuracy adults: 94.1%) even for the oldest age group tested (mean accuracy 10-12 years: 81.1%). Furthermore, the effect of age on children’s development did not differ across languages. The strong but slow development in children’s ability to recognize vocal emotions emphasizes the role of auditory experience in forming robust representations of vocal emotions. The wide range of age-related performances that are captured and the lack of significant differences across the tested languages affirm the usability and versatility of the EmoHI test.Presumptive spontaneous brain microhemorrhages in geriatric dogs: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunctionhttps://peerj.com/preprints/278682019-07-192019-07-19Curtis W DeweyMark RishniwPhilippa J JohnsonEmma S DaviesJoseph J SackmanMarissa O'Donnell
The objective of this study was to compare specific brain MRI anatomic measurements between three groups of geriatric ( > 8yrs) dogs: 1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of canine cognitive dysfunction 2) dogs with canine cognitive dysfunction 3) dogs without clinical evidence of cognitive impairment or abnormalities on neurologic examination (control dogs). MR images from 46 geriatric dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. All interthalamic adhesion measurement parameters were significantly (p<0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/13; 92 %) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/19; 16%). Affected dogs without cognitive dysfunction had more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct diseasecategory.
The objective of this study was to compare specific brain MRI anatomic measurements between three groups of geriatric ( > 8yrs) dogs: 1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of canine cognitive dysfunction 2) dogs with canine cognitive dysfunction 3) dogs without clinical evidence of cognitive impairment or abnormalities on neurologic examination (control dogs). MR images from 46 geriatric dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. All interthalamic adhesion measurement parameters were significantly (p<0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/13; 92 %) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/19; 16%). Affected dogs without cognitive dysfunction had more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct diseasecategory.The lateral habenula in depression: a mini-reviewhttps://peerj.com/preprints/276592019-04-172019-04-17Sterling Street
Although much remains unknown about this once-obscure structure, the lateral habenula is receiving increasing attention as a component of the circuitry of many conditions including mood disorders, anxiety disorders, pain disorders, substance use disorders, psychosis spectrum disorders, and neurodegenerative diseases. In depression research, there is growing interest in this structure as a component of the brain’s “anti-reward system”, since it can inhibit the release of monoamines into regions involved in the expectation, pursuit, and receival of rewards. This mini-review covers the basics of lateral habenula structure and function, and discusses recent advances made in understanding habenular dysfunction in depression.
Although much remains unknown about this once-obscure structure, the lateral habenula is receiving increasing attention as a component of the circuitry of many conditions including mood disorders, anxiety disorders, pain disorders, substance use disorders, psychosis spectrum disorders, and neurodegenerative diseases. In depression research, there is growing interest in this structure as a component of the brain’s “anti-reward system”, since it can inhibit the release of monoamines into regions involved in the expectation, pursuit, and receival of rewards. This mini-review covers the basics of lateral habenula structure and function, and discusses recent advances made in understanding habenular dysfunction in depression.Brasilia Parkinson Cohort: assessing clinical, neuropsychological and imaging predictors of cognitive decline in Parkinson's diseasehttps://peerj.com/preprints/276392019-04-052019-04-05Pedro Renato de Paula BrandãoFernando Bisinoto MalufTalyta GrippeIngrid FaberDanilo Assis PereiraNasser AllamFrancisco E.C. CardosoCarlos TomazMaria Clotilde H Tavares
The following study protocol describes the rationale and methods of a cohort with a nested case-control study, which aims to identify risk factors and predictors of cognitive dysfunction in Parkinson's disease (PD). It is a study that will follow PD every 18 months with a comprehensive neuropsychological, clinical (motor and non-motor symptoms) and imaging (Magnetic Resonance Imaging) data collection. The criteria for diagnosing mild cognitive impairment (MCI) and dementia will respect the parameters previously published by the International Working Group on Mild Cognitive Impairment, and compared with those recommended by the Fifth edition of the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM-5) and the International Parkinson's and Movement Disorders Society (MDS) criteria. We will also evaluate the neural substrate and underpinnings of PD non-motor symptoms, using advanced neuroimaging techniques, such as diffusion tensor imaging (DTI) and gray matter and white matter volumetric measurements.
The following study protocol describes the rationale and methods of a cohort with a nested case-control study, which aims to identify risk factors and predictors of cognitive dysfunction in Parkinson's disease (PD). It is a study that will follow PD every 18 months with a comprehensive neuropsychological, clinical (motor and non-motor symptoms) and imaging (Magnetic Resonance Imaging) data collection. The criteria for diagnosing mild cognitive impairment (MCI) and dementia will respect the parameters previously published by the International Working Group on Mild Cognitive Impairment, and compared with those recommended by the Fifth edition of the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM-5) and the International Parkinson's and Movement Disorders Society (MDS) criteria. We will also evaluate the neural substrate and underpinnings of PD non-motor symptoms, using advanced neuroimaging techniques, such as diffusion tensor imaging (DTI) and gray matter and white matter volumetric measurements.The extreme degeneracy of inputs in firing a neuron leads to loss of information when neuronal firing is examinedhttps://peerj.com/preprints/272282019-01-192019-01-19Kunjumon I Vadakkan
Possible combinations of inputs in the order of 10100 can fire (axonal spike or action potential) a neuron that has nearly 104 inputs (dendritic spines). This extreme degeneracy of inputs that can fire a neuron is associated with significant loss of information when examination is limited to neuronal firing. Excitatory postsynaptic potentials (EPSPs) propagating from remote locations on the dendritic tree attenuate as they arrive at the axon hillock, depending on the distance they propagate. Moreover, some EPSPs from remote locations will not even reach the axonal hillock. In this context, an operational mechanism at the location of origin of these EPSPs is necessary to preserve information for efficient storage. Evidence for information storage or retrieval can be observed only as the tip of an iceberg of operational mechanisms occurring at a narrow window when sub-threshold activated (before learning) neurons fire during these events. Even firing of a set of neurons does not identify the location where information is stored due to the extreme degeneracy of inputs that can contribute potentials to cross the threshold and fire those neurons. In summary, it is necessary to identify initial locations where specific inputs to a neuron arrive where information is expected to make retrieval-efficient changes.
Possible combinations of inputs in the order of 10100 can fire (axonal spike or action potential) a neuron that has nearly 104 inputs (dendritic spines). This extreme degeneracy of inputs that can fire a neuron is associated with significant loss of information when examination is limited to neuronal firing. Excitatory postsynaptic potentials (EPSPs) propagating from remote locations on the dendritic tree attenuate as they arrive at the axon hillock, depending on the distance they propagate. Moreover, some EPSPs from remote locations will not even reach the axonal hillock. In this context, an operational mechanism at the location of origin of these EPSPs is necessary to preserve information for efficient storage. Evidence for information storage or retrieval can be observed only as the tip of an iceberg of operational mechanisms occurring at a narrow window when sub-threshold activated (before learning) neurons fire during these events. Even firing of a set of neurons does not identify the location where information is stored due to the extreme degeneracy of inputs that can contribute potentials to cross the threshold and fire those neurons. In summary, it is necessary to identify initial locations where specific inputs to a neuron arrive where information is expected to make retrieval-efficient changes.A learning mechanism completed in milliseconds capable of transitioning to stabilizable forms can generate working, short and long-term memories - A verifiable mechanismhttps://peerj.com/preprints/273432018-11-122018-11-12Kunjumon I Vadakkan
Multiple associative learning events can take place within sub-second time and the "completed" mechanism can then be used for specific memory retrieval without any lapse of time. This indicates that a biological process is completed within the matching time-scales of milliseconds that can be used for retrieving specific memory. Since qualia of working, short-term and long-term memories are same except for degradation of features in long-term memory and since every long-term memory had the capability to induce working memory immediately after learning, all memories are anticipated to get induced from a mechanism formed at the time of learning. When memories are viewed as first-person internal sensations, a derived mechanism fulfills the "completion" requirement within milliseconds that can be used to induce working memory and can be transitioned to stabilizable forms to induce short-term and long-term memories.
Multiple associative learning events can take place within sub-second time and the "completed" mechanism can then be used for specific memory retrieval without any lapse of time. This indicates that a biological process is completed within the matching time-scales of milliseconds that can be used for retrieving specific memory. Since qualia of working, short-term and long-term memories are same except for degradation of features in long-term memory and since every long-term memory had the capability to induce working memory immediately after learning, all memories are anticipated to get induced from a mechanism formed at the time of learning. When memories are viewed as first-person internal sensations, a derived mechanism fulfills the "completion" requirement within milliseconds that can be used to induce working memory and can be transitioned to stabilizable forms to induce short-term and long-term memories.Towards a new understanding of fear generalization and its neural originhttps://peerj.com/preprints/273112018-10-312018-10-31Selim Onat
Forming generalizations from previous experiences is a complex skill, which requires a delicate coordination between several basic cognitive abilities. In menacing situations, this ability is called “fear generalization”. It allows humans to predict harmful events and is necessary for survival. Impairments of this ability may lead to overgeneralizations – a phenomenon we know from anxiety disorders. By and large, fear generalization has been studied with one type of experimental paradigm. Stimuli forming a carefully controlled perceptual similarity gradient have been the basis to quantify behavioral and neuronal “fear generalization profiles”. This paradigm has provided fruitful insights into how learnt fear generalizes to perceptually similar events. Yet, a number of findings suggest that fear generalization is more adaptive than predicted by a mechanism which is solely based on perceptual similarity. This is a proposal that aims to bring new perspectives onto fear generalization as a complex, adaptive process. I will investigate the following major hypotheses: (1) Fear generalization can be understood as the optimal result of a Bayesian inference problem. (2) In real-world conditions, fear generalization builds on conceptual knowledge rather than perceptual similarity alone. (3) Brain structures involved in fear generalization can be causally linked to modulate fear responses adaptively. To test these hypotheses, I propose use of tools including fMRI, EEG as well as intracranial electrical stimulation and LFP recordings in presurgical epilepsy patients. With the combination of these tools, the expected findings have the potential to revolutionize our understanding of fear generalization and anxiety disorders.
Forming generalizations from previous experiences is a complex skill, which requires a delicate coordination between several basic cognitive abilities. In menacing situations, this ability is called “fear generalization”. It allows humans to predict harmful events and is necessary for survival. Impairments of this ability may lead to overgeneralizations – a phenomenon we know from anxiety disorders. By and large, fear generalization has been studied with one type of experimental paradigm. Stimuli forming a carefully controlled perceptual similarity gradient have been the basis to quantify behavioral and neuronal “fear generalization profiles”. This paradigm has provided fruitful insights into how learnt fear generalizes to perceptually similar events. Yet, a number of findings suggest that fear generalization is more adaptive than predicted by a mechanism which is solely based on perceptual similarity. This is a proposal that aims to bring new perspectives onto fear generalization as a complex, adaptive process. I will investigate the following major hypotheses: (1) Fear generalization can be understood as the optimal result of a Bayesian inference problem. (2) In real-world conditions, fear generalization builds on conceptual knowledge rather than perceptual similarity alone. (3) Brain structures involved in fear generalization can be causally linked to modulate fear responses adaptively. To test these hypotheses, I propose use of tools including fMRI, EEG as well as intracranial electrical stimulation and LFP recordings in presurgical epilepsy patients. With the combination of these tools, the expected findings have the potential to revolutionize our understanding of fear generalization and anxiety disorders.Multiple object categorization and effect of spatial frequencieshttps://peerj.com/preprints/266662018-03-132018-03-13Alvydas SoliunasAleksandras PleskaciauskasAlgis Daktariunas
A process of interaction between objects and scene is widely investigated but much less attention is paid to the interaction between objects in multiple objects stimuli. In psychophysical experiment, we presented one, two, or three visual objects simultaneously for 100 ms and then asked subjects to answer whether objects belong to the same category (Experiments 1 and 2), or whether afterwards presented probe-word signify an object that was presented (Experiments 3 and 4). Interestingly, performance accuracy and reaction time did not depend on the number of objects if they belonged to the same category, but performance deteriorated when more categories were presented. Filtering out high or low spatial frequencies did not affect performance peculiarities of the objects of the same or different categories. The findings support assumption that visual objects of the same category could be identified simultaneously but the different categories are identified successively.
A process of interaction between objects and scene is widely investigated but much less attention is paid to the interaction between objects in multiple objects stimuli. In psychophysical experiment, we presented one, two, or three visual objects simultaneously for 100 ms and then asked subjects to answer whether objects belong to the same category (Experiments 1 and 2), or whether afterwards presented probe-word signify an object that was presented (Experiments 3 and 4). Interestingly, performance accuracy and reaction time did not depend on the number of objects if they belonged to the same category, but performance deteriorated when more categories were presented. Filtering out high or low spatial frequencies did not affect performance peculiarities of the objects of the same or different categories. The findings support assumption that visual objects of the same category could be identified simultaneously but the different categories are identified successively.Why is nonword reading so variable in adult skilled readers?https://peerj.com/preprints/266472018-03-092018-03-09Max ColtheartAnastasia Ulicheva
When the task is reading nonwords aloud, skilled adult readers are very variable in the responses they produce: a nonword can evoke as many as 24 different responses in a group of such readers. Why is nonword reading so variable? We analysed a large database of reading responses to nonwords, and identified two factors responsible for this variability. The first factor is variability in graphemic parsing (the parsing of a letter string into its constituent graphemes): the same nonword can be graphemically parsed in different ways by different readers. The second factor is phoneme assignment: even when all subjects produce the same graphemic parsing of a nonword, they vary in what phonemes they assign to the resulting set of graphemes. We consider the implications of these results for the computational modelling of reading, for the assessment of impairments of nonword reading, and for the study of reading aloud in other alphabetically-written languages and in nonalphabetic writing systems.
When the task is reading nonwords aloud, skilled adult readers are very variable in the responses they produce: a nonword can evoke as many as 24 different responses in a group of such readers. Why is nonword reading so variable? We analysed a large database of reading responses to nonwords, and identified two factors responsible for this variability. The first factor is variability in graphemic parsing (the parsing of a letter string into its constituent graphemes): the same nonword can be graphemically parsed in different ways by different readers. The second factor is phoneme assignment: even when all subjects produce the same graphemic parsing of a nonword, they vary in what phonemes they assign to the resulting set of graphemes. We consider the implications of these results for the computational modelling of reading, for the assessment of impairments of nonword reading, and for the study of reading aloud in other alphabetically-written languages and in nonalphabetic writing systems.The neuronal migration hypothesis of dyslexia: a critical evaluation thirty years onhttps://peerj.com/preprints/266372018-03-072018-03-07Luiz G GuidiAntonio Velayos-BaezaIsabel Martinez-GarayAnthony P MonacoSilvia ParacchiniDorothy V M BishopZoltan Molnar
The capacity for language is one of the key features underlying the complexity of human cognition and its evolution. However, little is known about the neurobiological mechanisms that mediate normal or impaired linguistic ability. For developmental dyslexia, early post-mortem studies conducted in the 1980s linked the disorder to subtle defects in the migration of neurons in the developing neocortex. These early studies were reinforced by human genetic analyses that identified dyslexia susceptibility genes and subsequent evidence of their involvement in neuronal migration. In this review, we examine recent experimental evidence that does not support the link between dyslexia and neuronal migration. We critically evaluate gene function studies conducted in rodent models and draw attention to the lack of robust evidence from histopathological and imaging studies in humans. Our review suggests that the neuronal migration hypothesis of dyslexia should be reconsidered, and the anatomical and genetic basis of dyslexia should be approached with a fresh start.
The capacity for language is one of the key features underlying the complexity of human cognition and its evolution. However, little is known about the neurobiological mechanisms that mediate normal or impaired linguistic ability. For developmental dyslexia, early post-mortem studies conducted in the 1980s linked the disorder to subtle defects in the migration of neurons in the developing neocortex. These early studies were reinforced by human genetic analyses that identified dyslexia susceptibility genes and subsequent evidence of their involvement in neuronal migration. In this review, we examine recent experimental evidence that does not support the link between dyslexia and neuronal migration. We critically evaluate gene function studies conducted in rodent models and draw attention to the lack of robust evidence from histopathological and imaging studies in humans. Our review suggests that the neuronal migration hypothesis of dyslexia should be reconsidered, and the anatomical and genetic basis of dyslexia should be approached with a fresh start.