8,204 research outputs found

    Functional anatomy of the masking level difference, an fMRI study

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    Introduction: Masking level differences (MLDs) are differences in the hearing threshold for the detection of a signal presented in a noise background, where either the phase of the signal or noise is reversed between ears. We use N0/Nπ to denote noise presented in-phase/out-of-phase between ears and S0/Sπ to denote a 500 Hz sine wave signal as in/out-of-phase. Signal detection level for the noise/signal combinations N0Sπ and NπS0 is typically 10-20 dB better than for N0S0. All combinations have the same spectrum, level, and duration of both the signal and the noise. Methods: Ten participants (5 female), age: 22-43, with N0Sπ-N0S0 MLDs greater than 10 dB, were imaged using a sparse BOLD fMRI sequence, with a 9 second gap (1 second quiet preceding stimuli). Band-pass (400-600 Hz) noise and an enveloped signal (.25 second tone burst, 50% duty-cycle) were used to create the stimuli. Brain maps of statistically significant regions were formed from a second-level analysis using SPM5. Results: The contrast NπS0- N0Sπ had significant regions of activation in the right pulvinar, corpus callosum, and insula bilaterally. The left inferior frontal gyrus had significant activation for contrasts N0Sπ-N0S0 and NπS0-N0S0. The contrast N0S0-N0Sπ revealed a region in the right insula, and the contrast N0S0-NπS0 had a region of significance in the left insula. Conclusion: Our results extend the view that the thalamus acts as a gating mechanism to enable dichotic listening, and suggest that MLD processing is accomplished through thalamic communication with the insula, which communicate across the corpus callosum to either enhance or diminish the binaural signal (depending on the MLD condition). The audibility improvement of the signal with both MLD conditions is likely reflected by activation in the left inferior frontal gyrus, a late stage in the what/where model of auditory processing. © 2012 Wack et al

    Reduced structural connectivity between left auditory thalamus and the motion-sensitive planum temporale in developmental dyslexia

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    Developmental dyslexia is characterized by the inability to acquire typical reading and writing skills. Dyslexia has been frequently linked to cerebral cortex alterations; however recent evidence also points towards sensory thalamus dysfunctions: dyslexics showed reduced responses in the left auditory thalamus (medial geniculate body, MGB) during speech processing in contrast to neurotypical readers. In addition, in the visual modality, dyslexics have reduced structural connectivity between the left visual thalamus (lateral geniculate nucleus, LGN) and V5/MT, a cerebral cortex region involved in visual movement processing. Higher LGN-V5/MT connectivity in dyslexics was associated with the faster rapid naming of letters and numbers (RANln), a measure that is highly correlated with reading proficiency. We here tested two hypotheses that were directly derived from these previous findings. First, we tested the hypothesis that dyslexics have reduced structural connectivity between the left MGB and the auditory motion-sensitive part of the left planum temporale (mPT). Second, we hypothesized that the amount of left mPT-MGB connectivity correlates with dyslexics RANln scores. Using diffusion tensor imaging based probabilistic tracking we show that male adults with developmental dyslexia have reduced structural connectivity between the left MGB and the left mPT, confirming the first hypothesis. Stronger left mPT-MGB connectivity was not associated with faster RANnl scores in dyslexics, but in neurotypical readers. Our findings provide first evidence that reduced cortico-thalamic connectivity in the auditory modality is a feature of developmental dyslexia, and that it may also impact on reading related cognitive abilities in neurotypical readers

    Articulating: the neural mechanisms of speech production

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    Speech production is a highly complex sensorimotor task involving tightly coordinated processing across large expanses of the cerebral cortex. Historically, the study of the neural underpinnings of speech suffered from the lack of an animal model. The development of non-invasive structural and functional neuroimaging techniques in the late 20th century has dramatically improved our understanding of the speech network. Techniques for measuring regional cerebral blood flow have illuminated the neural regions involved in various aspects of speech, including feedforward and feedback control mechanisms. In parallel, we have designed, experimentally tested, and refined a neural network model detailing the neural computations performed by specific neuroanatomical regions during speech. Computer simulations of the model account for a wide range of experimental findings, including data on articulatory kinematics and brain activity during normal and perturbed speech. Furthermore, the model is being used to investigate a wide range of communication disorders.R01 DC002852 - NIDCD NIH HHS; R01 DC007683 - NIDCD NIH HHS; R01 DC016270 - NIDCD NIH HHSAccepted manuscrip

    Developmental disorders of vision

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    This review of developmental disorders of vision focuses on a few of the many disorders that disrupt visual development. Given the enormity of the human visual system in the primate brain and complexity of visual development, however, there are likely hundreds or thousands of potential types of disorders affecting high-level vision. The rapid progress seen in developmental dyslexia and Williams syndrome demonstrates the possibilities and difficulties inherent in researching such disorders, and the authors hope that similar progress will be made for congenital prosopagnosia and other disorders in the near future

    Neural responses to facial and vocal expressions of fear and disgust

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    Neuropsychological studies report more impaired responses to facial expressions of fear than disgust in people with amygdala lesions, and vice versa in people with Huntington's disease. Experiments using functional magnetic resonance imaging (fMRI) have confirmed the role of the amygdala in the response to fearful faces and have implicated the anterior insula in the response to facial expressions of disgust. We used fMRI to extend these studies to the perception of fear and disgust from both facial and vocal expressions. Consistent with neuropsychological findings, both types of fearful stimuli activated the amygdala. Facial expressions of disgust activated the anterior insula and the caudate-putamen; vocal expressions of disgust did not significantly activate either of these regions. All four types of stimuli activated the superior temporal gyrus. Our findings therefore (i) support the differential localization of the neural substrates of fear and disgust; (ii) confirm the involvement of the amygdala in the emotion of fear, whether evoked by facial or vocal expressions; (iii) confirm the involvement of the anterior insula and the striatum in reactions to facial expressions of disgust; and (iv) suggest a possible general role for the perception of emotional expressions for the superior temporal gyrus

    In praise of tedious anatomy

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    Functional neuroimaging is fundamentally a tool for mapping function to structure, and its success consequently requires neuroanatomical precision and accuracy. Here we review the various means by which functional activation can be localized to neuroanatomy and suggest that the gold standard should be localization to the individual’s or group’s own anatomy through the use of neuroanatomical knowledge and atlases of neuroanatomy. While automated means of localization may be useful, they cannot provide the necessary accuracy, given variability between individuals. We also suggest that the field of functional neuroimaging needs to converge on a common set of methods for reporting functional localization including a common “standard” space and criteria for what constitutes sufficient evidence to report activation in terms of Brodmann’s areas

    Age differences in fMRI adaptation for sound identity and location

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    We explored age differences in auditory perception by measuring fMRI adaptation of brain activity to repetitions of sound identity (what) and location (where), using meaningful environmental sounds. In one condition, both sound identity and location were repeated allowing us to assess non-specific adaptation. In other conditions, only one feature was repeated (identity or location) to assess domain-specific adaptation. Both young and older adults showed comparable non-specific adaptation (identity and location) in bilateral temporal lobes, medial parietal cortex, and subcortical regions. However, older adults showed reduced domain-specific adaptation to location repetitions in a distributed set of regions, including frontal and parietal areas, and to identity repetition in anterior temporal cortex. We also re-analyzed data from a previously published 1-back fMRI study, in which participants responded to infrequent repetition of the identity or location of meaningful sounds. This analysis revealed age differences in domain-specific adaptation in a set of brain regions that overlapped substantially with those identified in the adaptation experiment. This converging evidence of reductions in the degree of auditory fMRI adaptation in older adults suggests that the processing of specific auditory “what” and “where” information is altered with age, which may influence cognitive functions that depend on this processing

    Review of various intraoperative neurophysiologic monitoring techniques

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    IONM is use to monitoring nervous tissues (including brain, spinal cord, cranial nerves and peripheral nerves) in real-time during surgeries, alert neurological injuries and corrective measures and prevent disability. There are various IONM monitoring techniques including evoke potentials (SSEP, BAEP, MEP), EMG (Free-running and triggered), NAP (Nerve action potential) and Electroencephalography (EEG) to monitor the functional integrity of neural structures. SSEP evaluates integrity of posterior column-medial lemniscus pathway. SSEP is clinical use in spinal cord surgeries, vascular surgeries (carotid endarterectomy, cerebral aneurysm surgery etc), and localization of sensor motor cortex. BAEP evaluates integrity of peripheral and central auditory pathway. BAEP is clinical use in CP angle tumors surgery (acoustic neuroma ,meningioma), microvascular decompression of CN-VII for hemifacial spasm, CN-V for trigeminal neuralgia, CN-IX for glossopharyngeal neuralgia, skull base surgery, Suboccipital decompression (e.g. fractures/dislocation C-1vertebra, chiari malformation). MEP evaluates integrity of motor pathway. MEP is sensitive to neuromuscular blocker anesthetic medications. Clinical utility of MEP including any surgery risking motor pathway injury include tumor near the motor cortex or corticospinal tract, intracranial aneurysm clipping, posterior fossa surgery, tethered cord or cauda equina surgeries, spinal deformity or fracture surgery, vertebral tumor resections, and anterior cervical discectomy, descending aortic procedures, spinal arteriovenous malformation interventions and carotid endarterectomy. EMG (free running and triggered) evaluates integrity of innervating nerves and electrical activity of muscles. Clinical utility of facial and other cranial nerve monitoring in posterior fossa surgery (eg, acoustic neuroma), selective dorsal rhizotomy, tethered cord release , Pedicle screw placement and Anal or urinary sphincter function monitoring

    Sound recognition and localization in man: specialized cortical networks and effects of acute circumscribed lesions

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    Functional imaging studies have shown that information relevant to sound recognition and sound localization are processed in anatomically distinct cortical networks. We have investigated the functional organization of these specialized networks by evaluating acute effects of circumscribed hemispheric lesions. Thirty patients with a primary unilateral hemispheric lesion, 15 with right-hemispheric damage (RHD) and 15 with left-hemispheric damage (LHD), were evaluated for their capacity to recognise environmental sounds, to localize sounds in space and to perceive sound motion. One patient with RHD and 2 with LHD had a selective deficit in sound recognition; 3 with RHD a selective deficit in sound localization; 2 with LHD a selective deficit in sound motion perception; 4 with RHD and 3 with LHD a combined deficit of sound localization and motion perception; 2 with RHD and 1 with LHD a combined deficit of sound recognition and motion perception; and 1 with LHD a combined deficit of sound recognition, localization and motion perception. Five patients with RHD and 6 with LHD had normal performance in all three domains. Deficient performance in sound recognition, sound localization and/or sound motion perception was always associated with a lesion that involved the shared auditory structures and the specialized What and/or Where networks, while normal performance was associated with lesions within or outside these territories. Thus, damage to regions known to be involved in auditory processing in normal subjects is necessary, but not sufficient for a deficit to occur. Lesions of a specialized network was not always associated with the corresponding deficit. Conversely, specific deficits tended not be associated predominantly with lesions of the corresponding network; e.g. deficits in auditory spatial tasks were observed in patients whose lesions involved to a larger extent the shared auditory structures and the specialized What network than the specialized Where network, and deficits in sound recognition in patients whose lesions involved mostly the shared auditory structures and to a varying degree the specialized What network. The human auditory cortex consists of functionally defined auditory areas, whose intrinsic organization is currently not understood. In particular, areas involved in the What and Where pathways can be conceived as: (1) specialized regions, in which lesions cause dysfunction limited to the damaged part; observed deficits should be then related to the specialization of the damaged region and their magnitude to the extent of the damage; or (2) specialized networks, in which lesions cause dysfunction that may spread over the two specialized networks; observed deficits may then not be related to the damaged region and their magnitude not proportional to the extent of the damage. Our results support strongly the network hypothesi
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