Dr. Sofie Meyer

The coolest magnetometer is no longer the best one

10:00-11:00 Friday 18th November 2016, Seminar room 4, Main Building

Abstract

Optically Pumped Magnetometers (OPMs) are small (~1cm3) and ultrasensitive devices which measure magnetic fields but do not require cryogenic cooling. They have recently become commercially available and can be placed directly and flexibly on the scalp, increasing sensitivity 5-10-fold relative to conventional Superconducting Quantum Interference Device (SQUID)-based MEG systems. The potential for these sensors to become wearable technology means that the range of possible experimental paradigms, as well as subject and patient groups, will be significantly broadened. I will cover the physical principles underlying their functionality, and discuss both simulation and ongoing empirical work as well as future applications and challenges in relation to their usefulness for basic and clinical MEG research.

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Dr. Velia Cardin

Neural reorganisation as a consequence of congenital deafness

10:00-11:00 Friday 4th November 2016, Seminar room 4, Main Building

Abstract

The extraordinary capacity of the brain for functional and structural reorganisation is known as neural plasticity. Understanding this phenomenon not only provides insights into the capabilities of the brain, but also into its potential for adaptation and enhancement, with applications for sensorimotor substitution, artificial intelligence, policy and education.
In cases of congenital sensory deprivation, it is assumed that cortices of the affected sense process information from other senses. Studies of auditory deprivation and language experience also have a significant social impact, given that they can inform health and educational policies in adults and children. Here, I will present evidence from the study of congenital deafness in humans, showing that plasticity mechanisms result in the auditory cortex not only responding to vision and somatosensation, but also being recruited for higher-order cognitive functions such as working memory. I will discuss the anatomical and functional framework that support these plastic changes, its consequences on behaviour and its implications for interventions.

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Dr. Michael Schmid

Towards delineating perceptual circuits in the primate visual system: rhythmic neuronal activation & cell-specific optogenetics

13:30-14:30 Friday 28th October 2016, Seminar room 4, Main Building

Abstract
How do we see? Research over the past decades has described in detail what brain areas are active in vision and how neurons are modulated in different areas under various contexts. The next frontier is to understand how large-scale neuronal circuits operate, how information is communicated in feedforward and feedback pathways and how these circuit mechanisms are linked to perception. In my talk I will focus on how research in non-human primates can help to address these questions. I will describe our initial steps to apply cell-targeted optogenetics to disentangle thalamo-cortical circuits in the visual system. Using CamKII controlled optogenetics we were able to trace the poorly understood konio-cellular projection from LGN to V1 (Klein et al., Neuron, 2016). These results encourage us to apply cell-target optogenetics to disentangle more complex circuits in cortex. In the second part of my talk, I will present how rhythmic theta spiking in visual cortex emerges during attentional sampling and during perceptual integration under the Kanizsa illusion. I propose theta rhythmic spiking as a dynamic process that arises from receptive-field interactions between neighboring neuronal populations to select an object for visual perception and to suppress alternatives at the same time.

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Dr. Jesper Andersson

Towards a comprehensive framework for movement and distortion correction of diffusion MR images

10:00-11:00 Friday 21st October 2016, Seminar room 4, Main Building

Abstract

MR diffusion imaging is a very important tool for investigating the microstructure of the human brain. It is typically performed by acquiring as set of EPI volumes with diffusion sensitisation along different directions. From this set one can elucidate the directions of more or less hindered diffusion and from that infer on directions of local fibre bundles. Based on these local measures one can perform “tractography” and investigate connections between different parts of the brain. Recent advances in acquisition methodology (i.e. multi-band) has enabled acquisition of data of a previously unimaginable quality.
However, not everything is coming up roses. Diffusion data is plagued by artefacts, possibly more than any other commonly used imaging technique. The poor bandwidth in the phase-encode direction makes EPI very sensitive to off-resonance fields. Additionally, the gradient switching used for the diffusion sensitisation causes strong off-resonance fields. Subject movement is unavoidable and is a particularly difficult problem in diffusion imaging for two reasons i) retrospective registration is difficult because of the different information content in the different diffusion weighted images and ii) movement during the diffusion encoding part of the acquisition leads to signal and resolution loss.
In this talk I will present a framework where I attempt to simultaneously model and correct EPI distortions and the effects of subject movement. I will also discuss the latest developments within this framework. Which is to model and correct also within-volume subject movement. The latter is a particular problem in any population who is less able to collaborate, such as the very young, the very old or subject with certain neurological disorders.

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Assoc. Prof. Steven Chance

Altered senses and excited brains: investigating the neural basis of autism

10:00-11:00 Friday 30th September 2016, Seminar room 4, Main Building

Abstract

In 1943 Leo Kanner first described several of the key characteristics that we still use to diagnose autism today. Research into the neural basis of autism can use these characteristics as clues to identify which brain regions are implicated based on known relationships between brain structure and function. At the UK brain bank for autism research in Oxford, studies of the cellular organisation of specialised brain regions are being combined with multi-modal brain scanning technology (DTI, MEG, MRS) to build a picture of the altered structure-function relationships in the autism brain. Our studies indicate that the microanatomy of primary sensory areas is changed in autism and that altered cortical cytoarchitecture can be detected by a new MRI analysis for in vivo assessment. It is challenging to connect different theories and findings about the neurobiological basis of autism, not only because they reflect the heterogeneity of the autistic spectrum, but also because the methods used are often applied to different populations. Until now, microanatomy has only been assessed in post-mortem or animal models whereas macrostructure and cognition has been assessed in living people. We have found that the changed anatomy also relates to increased cortical excitation, associated with altered cognitive ability in autism. A combination of approaches will enable the development of potential new biomarkers and neuroimaging technology.

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Dr. Michiel Cottaar

Can we predict fiber orientations based on the shape of the gyri?

10:00-11:00 Friday 30th September 2016, IOPPN Boardroom, Main Building

Abstract

In this talk I will present two methods to better characterize the axonal fiber orientations close to the cortex from in-vivo MRI data. First we show that fibers are predominantly radial in the gray matter and tangential in the white matter with respect to a white/gray matter boundary. This allows us to extract with sub-voxel precision the transition boundary, where fibers bend from tangential orientations in the white matter to radial orientations in the cortical gray matter and define new cortical thickness measures based on this transition boundary. This sharp transition in fiber orientations is not captured by traditional diffusion MRI leading to the so-called gyral bias, where most streamlines preferentially terminate at the gyral crown. In the second part of this talk we show a geometric model of how the fibers should transverse through the gyral white matter to avoid this gyral bias and discuss how this model can be validated based on post-mortem human and macaque data.

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Dr. Karen Mullinger

Investigating the oscillatory and haemodynamic responses after stimulation using EEG-fMRI

10:00-11:00 Friday 29th July 2016
Small Lecture Theatre, Main Building, IoPPN

Abstract

Whilst primary brain responses to a stimulus/task onset are well studied, the widely reported fMRI post-stimulus “undershoot” and EEG/MEG “rebound”, which occur after the stimulus stops, are rarely investigated. This is because the origin of these responses are poorly understood and are commonly believed to not hold additional information regarding neuronal activity above that provided by the primary responses. Here I will present a body of work exploring post-stimulus responses, investigating their origin and providing evidence to suggest these responses contain additional information regarding neural responses to that which can derived from the primary response.

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