Neuromagnetic evidence of impaired cortical auditory processing in pediatric intractable epilepsy
Division of Neurology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. Epilepsy research
(Impact Factor: 2.02).
11/2010; 92(1):63-73. DOI: 10.1016/j.eplepsyres.2010.08.008
We aimed to determine the changes in neural correlates of auditory information processing such as auditory detection, encoding, and sensory discrimination in pediatric patients with intractable epilepsy.
In this magnetoencephalography (MEG) study, 10 patients and 10 age- and gender-matched healthy controls were investigated with the multi-feature mismatch negativity (MMN) paradigm. Latencies and amplitudes of M100, M150, M200, and MMN event-related fields were evaluated.
All event-related fields in response to standard stimuli (M100, M150 and M200) and responses to occasional five deviant sounds, deviating from the standard stimuli either in duration, frequency, intensity, location, or by including a silent gap were reduced in amplitude in epilepsy patients compared with healthy controls.
Our study suggests that auditory information processing is impaired in patients with drug-resistant epilepsy, being evident both in stimulus feature encoding (as reflected by changes of early event-related components, e.g., M100) and in cortical sound discrimination (as reflected by MMNm). The neural changes involving diminished M100 as well as MMNms for all five deviant sound types suggest wide-spread auditory information processing impairments in these patients.
Available from: Elyse Sussman
- "However, there has been some discrepancy as to the nature of the poorer auditory function, in particular regarding whether deficits are specific to speech input (Boatman et al. 2008; Rosburg et al. 2005). MMN has also been used to assess specific post-treatment recovery of function (Borghetti et al. 2007), as well as to assess the nature of the deficits (Korostenskaja et al. 2010). Consistent with this, Lin et al. (2007) reported that MMNm was temporally overlapped by a phase-locking response of alpha and theta rhythms, which was especially pronounced in the five patients who subsequently became seizure-free after the successful surgical removal of right temporal epileptic focus. "
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ABSTRACT: Cognition is often affected in a variety of neuropsychiatric, neurological, and neurodevelopmental disorders. The neural discriminative response, reflected in mismatch negativity (MMN) and its magnetoencephalographic equivalent (MMNm), has been used as a tool to study a variety of disorders involving auditory cognition. MMN/MMNm is an involuntary brain response to auditory change or, more generally, to pattern regularity violation. For a number of disorders, MMN/MMNm amplitude to sound deviance has been shown to be attenuated or the peak-latency of the component prolonged compared to controls. This general finding suggests that while not serving as a specific marker to any particular disorder, MMN may be useful for understanding factors of cognition in various disorders, and has potential to serve as an indicator of risk. This review presents a brief history of the MMN, followed by a description of how MMN has been used to index auditory processing capability in a range of neuropsychiatric, neurological, and neurodevelopmental disorders. Finally, we suggest future directions for research to further enhance our understanding of the neural substrate of deviance detection that could lead to improvements in the use of MMN as a clinical tool.
Available from: Milena Korostenskaja
- "The tones were delivered binaurally through plastic tubes with ER-3A ear inserts with an intensity of 70-dB nHL. BrainX software was used for stimulus generation and delivery (Korostenskaja et al., 2010a; 2010b; Xiang et al., 2001). BrainX generated an inter-stimulus interval with a consistent time (600 ms) period and a randomized time period, which was 507 50 milliseconds (0–100 ms). "
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ABSTRACT: Patients with obsessive-compulsive disorder (OCD) often report sensory intolerances which may lead to significant functional impairment. This study used auditory evoked fields (AEFs) to address the question of whether neural correlates of sensory auditory information processing differ in youth with OCD compared with healthy comparison subjects (HCS). AEFs, recorded with a whole head 275-channel magnetoencephalography system, were elicited in response to binaural auditory stimuli from 10 pediatric subjects with OCD (ages 8-13, mean 11 years, 6 males) and 10 age- and gender-matched HCS. Three major neuromagnetic responses were studied: M70 (60-80ms), M100 (90-120ms), and M150 (130-190ms). When compared with HCS, subjects with OCD demonstrated delayed latency of the M100 response. In subjects with OCD the amplitude of the M100 and M150 responses was significantly greater in the right hemisphere compared with the left hemisphere. Current results suggest that when compared with HCS, subjects with OCD have altered auditory information processing, evident from the delayed latency of the M100 response, which is thought to be associated with the encoding of physical stimulus characteristics. Interhemispheric asymmetry with increased M100 and M150 amplitudes over the right hemisphere compared with the left hemisphere was found in young OCD subjects. These results should be interpreted with caution due to the high variability rate of responses in both HCS and OCD subjects, as well as the possible effect of medication in OCD subjects.
Available from: Dasuni Alwis
- "In many cases of brain disorders, sensory processing deficits may contribute significantly to the overall morbidity of the condition , , , , , , , , , , . In the present study we examine the sensory cortical changes occurring in traumatic brain injury (TBI) which, in the US, affects approximately 1.7 million people annually, is a contributing factor in 30% of all injury-related deaths, and accounts for significant long-term hospitalizations across a range of populations . "
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ABSTRACT: Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits including long-term altered sensory processing. The few animal models of sensory cortical processing effects of TBI have been limited to examination of effects immediately after TBI and only in some layers of cortex. We have now used the rat whisker tactile system and the cortex processing whisker-derived input to provide a highly detailed description of TBI-induced long-term changes in neuronal responses across the entire columnar network in primary sensory cortex. Brain injury (n = 19) was induced using an impact acceleration method and sham controls received surgery only (n = 15). Animals were tested in a range of sensorimotor behaviour tasks prior to and up to 6 weeks post-injury when there were still significant sensorimotor behaviour deficits. At 8-10 weeks post-trauma, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including motion that mimicked whisker motion observed in awake animals undertaking different tasks. In cortex, there were lamina-specific neuronal response alterations that appeared to reflect local circuit changes. Hyper-excitation was found only in supragranular layers involved in intra-areal processing and long-range integration, and only for stimulation with complex, naturalistic whisker motion patterns and not for stimulation with simple trapezoidal whisker motion. Thus TBI induces long-term directional changes in integrative sensory cortical layers that depend on the complexity of the incoming sensory information. The nature of these changes allow predictions as to what types of sensory processes may be affected in TBI and contribute to post-trauma sensorimotor deficits.
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