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Goldfine A.M.,New York Medical College | Goldfine A.M.,Burke Medical Research Institute | Victor J.D.,New York Medical College | Conte M.M.,New York Medical College | And 2 more authors.
Clinical Neurophysiology | Year: 2011

Objective: To determine whether EEG spectral analysis could be used to demonstrate awareness in patients with severe brain injury. Methods: We recorded EEG from healthy controls and three patients with severe brain injury, ranging from minimally conscious state (MCS) to locked-in-state (LIS), while they were asked to imagine motor and spatial navigation tasks. We assessed EEG spectral differences from 4 to 24. Hz with univariate comparisons (individual frequencies) and multivariate comparisons (patterns across the frequency range). Results: In controls, EEG spectral power differed at multiple frequency bands and channels during performance of both tasks compared to a resting baseline. As patterns of signal change were inconsistent between controls, we defined a positive response in patient subjects as consistent spectral changes across task performances. One patient in MCS and one in LIS showed evidence of motor imagery task performance, though with patterns of spectral change different from the controls. Conclusions: EEG power spectral analysis demonstrates evidence for performance of mental imagery tasks in healthy controls and patients with severe brain injury. Significance: EEG power spectral analysis can be used as a flexible bedside tool to demonstrate awareness in brain-injured patients who are otherwise unable to communicate. © 2011 International Federation of Clinical Neurophysiology.

Cave J.W.,Cornell College | Cave J.W.,Burke Medical Research Institute
Developmental Biology | Year: 2011

The Notch signaling pathway regulates metazoan development, in part, by directly controlling the transcription of target genes. For a given cellular context, however, only subsets of the known target genes are transcribed when the pathway is activated. Thus, there are context-dependent mechanisms that selectively maintain repression of target gene transcription when the Notch pathway is activated. This review focuses on molecular mechanisms that have been recently reported to mediate selective repression of Notch pathway target gene transcription. These mechanisms are essential for generating the complex spatial and temporal expression patterns of Notch target genes during development. © 2011 Elsevier Inc.

Zhong J.,Burke Medical Research Institute | Zhong J.,Cornell University | Zou H.,Mount Sinai School of Medicine
Current Opinion in Neurobiology | Year: 2014

Neuronal competence to re-extend axons and a permissive environment that allows growth cone navigation are two major determinants for successful axon regeneration. Here, we review the roles of bone morphogenetic protein (BMP) signaling in mediating both neuronal and glial injury responses after CNS injury. BMPs can activate a pro-regenerative transcription program in neurons through Smad-mediated canonical pathway, or act locally on cytoskeleton assembly at distal axons via non-canonical pathways. Emerging evidence implicates retrograde BMP signalosomes in connecting the cytoskeletal and nuclear responses. In addition, BMP/Smad signaling modulates neurotrophin-mediated axonal outgrowth, and interacts with the epigenetic machinery to initiate epigenetic reprogramming for axon regeneration. Besides their influences on neurons, BMPs also regulate astrogliosis, inflammatory processes, and neural progenitor cell differentiation at the injury site, all of which can either positively or negatively modify the injury microenvironment. Lastly, an increasing number of BMP signaling partners, sensitizers, and downstream effectors collectively fine-tune the signaling intensity and spatiotemporal dynamics of BMP activity in an integrated signaling network during axon regeneration. © 2014 Elsevier Ltd.

Goldfine A.M.,Burke Medical Research Institute | Goldfine A.M.,New York Medical College | Schiff N.D.,New York Medical College
Current Opinion in Neurology | Year: 2011

Purpose of Review: Standard neurorehabilitation approaches have limited impact on motor recovery in patients with severe brain injuries. Consideration of the contributions of impaired arousal offers a novel approach to understand and enhance recovery. Recent Findings: Animal and human neuroimaging studies are elucidating the neuroanatomical bases of arousal and of arousal regulation, the process by which the cerebrum mobilizes resources. Studies of patients with disorders of consciousness have revealed that recovery of these processes is associated with marked improvements in motor performance. Recent studies have also demonstrated that patients with less severe brain injuries also have impaired arousal, manifesting as diminished sustained attention, fatigue, and apathy. In these less severely injured patients, it is difficult to connect disorders of arousal with motor recovery because of a lack of measures of arousal that are independent of motor function. Summary: Arousal impairment is common after brain injury and likely plays a significant role in recovery of motor function. A more detailed understanding of this connection will help to develop new therapeutic strategies applicable for a wide range of patients. This requires new tools that continuously and objectively measure arousal in patients with brain injury, to correlate with detailed measures of motor performance and recovery. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Hollis E.R.,Burke Medical Research Institute | Hollis E.R.,New York Medical College
Neurotherapeutics | Year: 2016

…once the development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably.Santiago Ramón y Cajal Cajal’s neurotropic theory postulates that the complexity of the nervous system arises from the collaboration of neurotropic signals from neuronal and non-neuronal cells and that once development has ended, a paucity of neurotropic signals means that the pathways of the central nervous system are “fixed, ended, immutable”. While the capacity for regeneration and plasticity of the central nervous system may not be quite as paltry as Cajal proposed, regeneration is severely limited in scope as there is no spontaneous regeneration of long-distance projections in mammals and therefore limited opportunity for functional recovery following spinal cord injury. It is not a far stretch from Cajal to hypothesize that reappropriation of the neurotropic programs of development may be an appropriate strategy for reconstitution of injured circuits. It has become clear, however, that a significant number of the molecular cues governing circuit development become re-active after injury and many assume roles that paradoxically obstruct the functional re-wiring of severed neural connections. Therefore, the problem to address is how individual neural circuits respond to specific molecular cues following injury, and what strategies will be necessary for instigating functional repair or remodeling of the injured spinal cord. © 2015, The American Society for Experimental NeuroTherapeutics, Inc.

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