Jorge R.E.,One Baylor Plaza
CONTINUUM Lifelong Learning in Neurology | Year: 2015
The objectives of this article are to update the reader on the current definition and diagnostic assessment of posttraumatic stress disorder (PTSD) and to describe its clinical characteristics, discuss its epidemiology and pathophysiologic aspects, as well as to summarize the current therapeutic options for PTSD. Recent Findings: The new nomenclature of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) includes 20 PTSD symptoms clustered into four symptomatic domains: intrusive symptoms, active avoidance, disturbed emotional states, and alterations of arousal and reactivity. Diagnostic structured interviews and severity scales have been updated in order to address this recent revision. It is also recognized that the neural circuits whose disruption might explain the genesis of PTSD symptoms, although overlapping, may be different between these four domains, a fact that may inform new biologically based phenotypes with prognostic and therapeutic implications. During the past years, there has been active research into the different factors influencing vulnerability and resilience to stress, including the effect of genetic and epigenetic variations. The neural circuits involved in the processing of threatening stimuli have been studied in patients with PTSD through paradigms inspired in animal research. These studies suggest that patients with PTSD have difficulty discriminating danger from safety cues and have problems suppressing fear in the presence of safety cues. Functional MRI (fMRI) studies suggest that the increased amygdala activation observed in these patients results from abnormal modulatory input from the ventromedial prefrontal cortex. Structural brain abnormalities, on the other hand, have been more consistently identified in the hippocampus. Prolonged exposure therapy and cognitive reprocessing are the interventions that have the more extensive validation of their psychotherapeutic efficacy. Medications are modestly more effective than placebo to treat PTSD symptoms, and selective serotonin reuptake inhibitors (SSRIs) are considered a safe initial choice. Use of combined strategies including pharmacologic modulation of fear processing is an area of active research. Summary: PTSD is a frequent psychopathologic condition with a lifetime prevalence that is close to 10%. In the past few years, there have been significant advances in the definition of the disorder, in elucidating the neurobiology of vulnerability and resilience, and in developing new treatment alternatives. © 2015 by the American Academy of Neurology.
Hannawi Y.,One Baylor Plaza |
Goldsmith C.E.,One Baylor Plaza |
Kass J.S.,One Baylor Plaza |
Olar A.,Baylor College of Medicine |
And 2 more authors.
Journal of Clinical Neuromuscular Disease | Year: 2013
Objectives: The involvement of the peripheral nervous system by anti-CV2/CRMP5 paraneoplastic antibodies is typically encountered as a mixed sensorimotor polyneuropathy. We report a fatal case of severe chronic progressive axonal polyradiculoneuropathy in association with this antibody. Methods: Review of the patient's chart, nerve conduction/electromyographic studies, and nerve biopsy. Results: A 51-year-old man presented with a progressive quadriparesis over a 4-month period. Extensive evaluation for potential etiologies was significant only for positive anti-CV2/CRMP5 antibodies without detection of an underlying neoplasm. Despite multiple immunomodulatory therapies, the patient progressed and demonstrated electrodiagnostic evidence for a chronic axonal polyradiculoneuropathy with ongoing denervation. The patient eventually died of respiratory failure. Conclusions: This case adds to the clinical spectrum of the peripheral nervous system involvement in patients with paraneoplastic anti-CV2/CRMP5 antibodies. © 2013 by Lippincott Williams and Wilkins.
Haeri M.,One Baylor Plaza |
Haeri M.,Baylor College of Medicine |
Gelowani V.,One Baylor Plaza |
Beaudet A.L.,One Baylor Plaza
MethodsX | Year: 2016
Pathological copy number variants (CNVs) and point mutations are major genetic causes of hundreds of disorders. Comparative genomic hybridization (CGH) also known as chromosomal microarray analysis (CMA) is the best available tool to detect copy number variations in chromosomal make up. We have optimized several different protocols and introduce a high-throughput approach to perform a cost-effective, fast, high-throughput and high-quality CMA. We managed to reach to high quality arrays with 17 ± 0.04 (mean ± SD, n = 90) Derivative Log Ratio (DLR) spread, a measure of array quality (<0.20 considered as excellent) for our arrays. High-throughput and high-quality arrays are gaining more attention and the current manuscript is a step forward to this increasing demand.This manuscript introduces a low cost, fast, efficient, high throughput and high-quality aCGH protocol;This protocol provides specific instructions and crucial detail for processing up to 24 slides which is equal to 48, 96, or 192 arrays by only one person in one day;This manuscript is accompanied with a step-by-step video. © 2015 The Authors.
El Sahly H.M.,One Baylor Plaza |
El Sahly H.M.,Baylor College of Medicine |
Davis C.,University of Maryland, Baltimore |
Kotloff K.,University of Maryland, Baltimore |
And 11 more authors.
Journal of Infectious Diseases | Year: 2012
(See the editorial commentary by Overton, on pages 697-9.)Background. The immunogenicity of a high hemagglutinin (HA) dose or a second dose of influenza vaccine in human immunodeficiency virus (HIV)-infected individuals has not been fully explored.Methods.One hundered ninety-two HIV-infected individuals aged 18-64 years were stratified by CD4 cell count (<200 cells/mL or ≥200 cells/mL) and randomized to receive 2 doses of 15 μg or 30 μg HA 2009 H1N1 vaccine 21 days apart. Hemagglutination inhibition (HAI) and microneutralization (MN) antibodies were measured on days 0, 10, 21, 31, 42, and 201.Results.Recipients of 30 μg HA had significantly higher HAI geometric mean titers (GMTs), compared with recipients of 15 μg HA on days 10 (139.0 vs 51.9; P =. 01), 21 (106.7 vs 51.9; P =. 001), and 31 (130.0 vs 73.7; P =. 03) but not on days 42 (91.8 vs 61.6; P =. 11) and 201 (43.0 vs 27.0; P =. 08). When analyzed by CD4 cell count stratum, HAI GMTs were significantly higher among 30 μg HA recipients than among 15 μg HA in the CD4 cell count <200 cells/mL stratum on days 21 and 31 and the MN GMTs on days 10, 21, 31, and 42 (P <. 05). In the CD4 cell count ≥200 cells/mL stratum, MN GMTs were significantly higher among recipients of 30 μg HA than among recipients of 15 μg HA on day 10 (P =. 03).Conclusion.Increasing the HA dose of the 2009 H1N1 vaccine improves the vaccine's immunogenicity in HIV-infected individuals.Clinical Trials Registration. NCT00992433. © 2012 The Author. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.
Smith K.D.B.,One Baylor Plaza |
Paylor R.,Baylor College of Medicine |
Pautler R.G.,One Baylor Plaza |
Pautler R.G.,Baylor College of Medicine
Magnetic Resonance in Medicine | Year: 2011
Axonal pathology is a prevalent feature of Alzheimer's disease (AD) and is thought to occur predominantly due to the accumulation of amyloid beta (Aβ). However, it remains unclear whether therapeutics geared toward reducing Aβ improves axonal deficits. We have previously used Manganese Enhanced MRI to demonstrate that axonal transport deficits occur before plaque formation in the Tg2576 mouse model of Alzheimer's disease. Here we tested whether axonal transport deficits in the Tg2576 mouse model improve in response to the Aβ42 selective lowering agent R-Flurbiprofen (R-F). We demonstrated that in young animals (before Aβ plaque formation), R-F treatment reduced Aβ42 levels and coincided with a significant improvement in axonal transport (P = 0.0186). However, in older animals (after plaque formation had occurred), we observed that R-F treatment did not reduce Aβ42 levels although we still observed a significant improvement in axonal transport as assessed with MEMRI (P = 0.0329). We then determined that R-F treatment reduced tau hyper-phosphorylation in the older animals. These data indicate that both Aβ42 and tau comprise a role in axonal transport rate deficits in the Tg2576 model of Alzheimer's Disease. Magn Reson Med, 2011. © 2010 Wiley-Liss, Inc.