Autonomic Dysreflexia

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Andrei V Krassioukov - One of the best experts on this subject based on the ideXlab platform.

  • prediction of Autonomic Dysreflexia during urodynamics a prospective cohort study
    BMC Medicine, 2018
    Co-Authors: Matthias Walter, S Knupfer, Jacquelyn J Cragg, Lorenz Leitner, Marc P Schneider, Ulrich Mehnert, Andrei V Krassioukov, Martin Schubert
    Abstract:

    Autonomic Dysreflexia is a severe and potentially life-threatening condition in patients with spinal cord injury, as it can lead to myocardial ischemia, brain hemorrhage, or even death. Urodynamic investigation is the gold standard to assess neurogenic lower urinary tract dysfunction due to spinal cord injury and reveal crucial pathological findings, such as neurogenic detrusor overactivity. However, neurogenic detrusor overactivity and urodynamic investigation are known to be leading triggers of Autonomic Dysreflexia. Therefore, we aimed to determine predictors of Autonomic Dysreflexia in individuals with spinal cord injury during urodynamic investigation. This prospective cohort study included 300 patients with spinal cord injuries and complete datasets of continuous non-invasive cardiovascular monitoring, recorded during same session repeat urodynamic investigation. We used logistic regression to reveal predictors of Autonomic Dysreflexia during urodynamic investigation. We found that level of injury and presence of neurogenic detrusor overactivity were the only two independent significant predictors for Autonomic Dysreflexia during urodynamic investigation. A lesion at spinal segment T6 or above (odds ratio (OR) 5.5, 95% CI 3.2–9.4) compared to one at T7 or below, and presence of neurogenic detrusor overactivity (OR 2.7, 95% confidence interval (CI) 1.4–4.9) were associated with a significant increased odds of Autonomic Dysreflexia during urodynamic investigation. Both odds persisted after adjustment for age, sex, and completeness and stage of injury (adjusted OR (AOR) 6.6, 95% CI 3.8–11.7, and AOR 2.2, 95% CI 1.1–4.5, respectively). Further stratification by lesion level showed level-dependent significantly increased adjusted odds of Autonomic Dysreflexia, i.e., from C1–C4 (AOR 16.2, 95% CI 5.9–57.9) to T4–T6 (AOR 2.6, 95% CI 1.3–5.2), compared to lesions at T7 or below. In patients with neurogenic lower urinary tract dysfunction due to spinal cord injury, Autonomic Dysreflexia is independently predicted by lesion level and presence of neurogenic detrusor overactivity. Considering the health risks associated with Autonomic Dysreflexia, such as seizures, stroke, retinal bleeding, or even death, we recommend both continuous cardiovascular monitoring during urodynamic investigation in all spinal cord-injured patients with emphasis on those with cervical lesions, and appropriate neurogenic detrusor overactivity treatment to reduce the probability of potentially life-threatening complications. ClinicalTrials.gov, NCT01293110 .

  • Reduction in Bladder-Related Autonomic Dysreflexia after OnabotulinumtoxinA Treatment in Spinal Cord Injury.
    Journal of Neurotrauma, 2016
    Co-Authors: Renee J. Fougere, Katharine D. Currie, Mark Nigro, Lynn Stothers, Daniel Rapoport, Andrei V Krassioukov
    Abstract:

    Abstract Bladder-related events, including neurogenic detrusor overactivity, are the leading cause of Autonomic Dysreflexia in spinal cord injured individuals. Self-reported Autonomic Dysreflexia is reduced following onabotulinumtoxinA treatment for neurogenic detrusor overactivity; however, none of these trials have assessed Autonomic Dysreflexia events using the clinical cutoff of an increase in systolic blood pressure ≥20 mm Hg. This study used a prospective, open-labelled design from 2013 to 2014 to quantitatively assess the efficacy of one cycle 200 U intradetrusor-injected onabotulinumtoxinA (20 sites) on reducing the severity and frequency of bladder-related Autonomic Dysreflexia events and improving quality of life. Twelve men and five women with chronic, traumatic spinal cord injuries at or above the sixth thoracic level, and concomitant Autonomic Dysreflexia and neurogenic detrusor overactivity, underwent blood pressure monitoring during urodynamics and over a 24 h period using ambulatory blood ...

  • Online training improves paramedics' knowledge of Autonomic Dysreflexia management guidelines.
    Spinal Cord, 2016
    Co-Authors: K A Martin Ginis, Jennifer R Tomasone, Michelle Welsford, Karen Ethans, Adrienne R. Sinden, M Longeway, Andrei V Krassioukov
    Abstract:

    Online training improves paramedics’ knowledge of Autonomic Dysreflexia management guidelines

  • Cardiac Consequences of Autonomic Dysreflexia in Spinal Cord Injury.
    Hypertension, 2016
    Co-Authors: Christopher R. West, Katharine D. Currie, Jordan W. Squair, Laura A. Mccracken, Rishi K. Somvanshi, Violet G. Yuen, Aaron A. Phillips, Ujendra Kumar, John H. Mcneill, Andrei V Krassioukov
    Abstract:

    Autonomic Dysreflexia (AD), which describes episodic hypertension, is highly prevalent in people with spinal cord injury (SCI). In non-SCI, primary hypertension depresses cardiac contractile reserv...

  • Autonomic Dysreflexia severity during urodynamics and cystoscopy in individuals with spinal cord injury
    Spinal Cord, 2013
    Co-Authors: Renee J. Fougere, Andrei V Krassioukov, Mark Nigro, M W Zhou
    Abstract:

    Autonomic Dysreflexia severity during urodynamics and cystoscopy in individuals with spinal cord injury

Jacquelyn J Cragg - One of the best experts on this subject based on the ideXlab platform.

  • prediction of Autonomic Dysreflexia during urodynamics a prospective cohort study
    BMC Medicine, 2018
    Co-Authors: Matthias Walter, S Knupfer, Jacquelyn J Cragg, Lorenz Leitner, Marc P Schneider, Ulrich Mehnert, Andrei V Krassioukov, Martin Schubert
    Abstract:

    Autonomic Dysreflexia is a severe and potentially life-threatening condition in patients with spinal cord injury, as it can lead to myocardial ischemia, brain hemorrhage, or even death. Urodynamic investigation is the gold standard to assess neurogenic lower urinary tract dysfunction due to spinal cord injury and reveal crucial pathological findings, such as neurogenic detrusor overactivity. However, neurogenic detrusor overactivity and urodynamic investigation are known to be leading triggers of Autonomic Dysreflexia. Therefore, we aimed to determine predictors of Autonomic Dysreflexia in individuals with spinal cord injury during urodynamic investigation. This prospective cohort study included 300 patients with spinal cord injuries and complete datasets of continuous non-invasive cardiovascular monitoring, recorded during same session repeat urodynamic investigation. We used logistic regression to reveal predictors of Autonomic Dysreflexia during urodynamic investigation. We found that level of injury and presence of neurogenic detrusor overactivity were the only two independent significant predictors for Autonomic Dysreflexia during urodynamic investigation. A lesion at spinal segment T6 or above (odds ratio (OR) 5.5, 95% CI 3.2–9.4) compared to one at T7 or below, and presence of neurogenic detrusor overactivity (OR 2.7, 95% confidence interval (CI) 1.4–4.9) were associated with a significant increased odds of Autonomic Dysreflexia during urodynamic investigation. Both odds persisted after adjustment for age, sex, and completeness and stage of injury (adjusted OR (AOR) 6.6, 95% CI 3.8–11.7, and AOR 2.2, 95% CI 1.1–4.5, respectively). Further stratification by lesion level showed level-dependent significantly increased adjusted odds of Autonomic Dysreflexia, i.e., from C1–C4 (AOR 16.2, 95% CI 5.9–57.9) to T4–T6 (AOR 2.6, 95% CI 1.3–5.2), compared to lesions at T7 or below. In patients with neurogenic lower urinary tract dysfunction due to spinal cord injury, Autonomic Dysreflexia is independently predicted by lesion level and presence of neurogenic detrusor overactivity. Considering the health risks associated with Autonomic Dysreflexia, such as seizures, stroke, retinal bleeding, or even death, we recommend both continuous cardiovascular monitoring during urodynamic investigation in all spinal cord-injured patients with emphasis on those with cervical lesions, and appropriate neurogenic detrusor overactivity treatment to reduce the probability of potentially life-threatening complications. ClinicalTrials.gov, NCT01293110 .

  • pearls oy sters transient horner syndrome associated with Autonomic Dysreflexia
    Neurology, 2013
    Co-Authors: Jacquelyn J Cragg, Andrei V Krassioukov
    Abstract:

    Autonomic Dysreflexia is a potentially life-threatening condition that occurs in individuals with high thoracic and cervical spinal cord injuries (SCIs) and is characterized by severe episodic hypertension.

  • Pearls & Oy-sters: Transient Horner syndrome associated with Autonomic Dysreflexia
    Neurology, 2013
    Co-Authors: Jacquelyn J Cragg, Andrei V Krassioukov
    Abstract:

    Autonomic Dysreflexia is a potentially life-threatening condition that occurs in individuals with high thoracic and cervical spinal cord injuries (SCIs) and is characterized by severe episodic hypertension.

Inder Perkash - One of the best experts on this subject based on the ideXlab platform.

  • transurethral sphincterotomy provides significant relief in Autonomic Dysreflexia in spinal cord injured male patients long term followup results
    The Journal of Urology, 2007
    Co-Authors: Inder Perkash
    Abstract:

    Purpose: An evaluation of the results of transurethral sphincterotomy in spinal cord injured patients for the relief of Autonomic Dysreflexia is presented.Materials and Methods: The study describes experience with the treatment of 46 consecutive spinal cord injured males presenting with frequent symptoms of Autonomic Dysreflexia and inadequate voiding. The selection criteria include patients injured above the thoracic 6 level with subjective symptoms of Autonomic Dysreflexia who did not want to be catheterized or were unable to perform intermittent catheterization. Patients were studied with complex urodynamics before and at least 3 months after undergoing transurethral sphincterotomy. During cystometrogram the maximum increase in systolic and diastolic blood pressure was recorded. After transurethral sphincterotomy patients were followed for a mean of 5.4 ± 3.1 years (range 1 to 12).Results: There was subjective relief in Autonomic Dysreflexia following transurethral sphincterotomy in all patients, which...

Lynne C. Weaver - One of the best experts on this subject based on the ideXlab platform.

  • Autonomic Dysreflexia after spinal cord injury: central mechanisms and strategies for prevention.
    Autonomic Dysfunction After Spinal Cord Injury, 2006
    Co-Authors: Lynne C. Weaver, Arthur Brown, Daniel R. Marsh, Denis Gris, Gregory A. Dekaban
    Abstract:

    Spinal reflexes dominate cardiovascular control after spinal cord injury (SCI). These reflexes are no longer restrained by descending control and they can be impacted by degenerative and plastic changes within the injured cord. Autonomic Dysreflexia is a condition of episodic hypertension that stems from spinal reflexes initiated by sensory input entering the spinal cord caudal to the site of injury. This hypertension greatly detracts from the quality of life for people with cord injury and can be life-threatening. Changes in the spinal cord contribute substantially to the development of this condition. Rodent models are ideal for investigating these changes. Within the spinal cord, injury-induced plasticity leads to nerve growth factor (NGF)-dependent enlargement of the central arbor of a sub-population of sensory neurons. This enlarged arbor can provide increased afferent input to the spinal reflex, intensifying Autonomic Dysreflexia. Treatments such as antibodies against NGF can limit this afferent sprouting, and diminish the magnitude of Dysreflexia. To assess treatments, a compression model of SCI that leads to progressive secondary damage, and also to some white matter sparing, is very useful. The types of spinal reflexes that likely mediate Autonomic Dysreflexia are highly susceptible to inhibitory influences of bulbospinal pathways traversing the white matter. Compression models of cord injury reveal that treatments that spare white matter axons also markedly reduce Autonomic Dysreflexia. One such treatment is an antibody to the integrin CD11d expressed by inflammatory leukocytes that enter the cord acutely after injury and cause significant secondary damage. This antibody blocks integrin-mediated leukocyte entry, resulting in greatly reduced white-matter damage and decreased Autonomic Dysreflexia after cord injury. Understanding the mechanisms for Autonomic Dysreflexia will provide us with strategies for treatments that, if given early after cord injury, can prevent this serious disorder from developing.

  • Chapter 7 Central mechanisms for Autonomic Dysreflexia after spinal cord injury
    Progress in Brain Research, 2002
    Co-Authors: Lynne C. Weaver, Daniel R. Marsh, Denis Gris, Susan O. Meakin, Gregory A. Dekaban
    Abstract:

    Publisher Summary This chapter discusses the central mechanisms for Autonomic Dysreflexia after spinal cord injury. Mechanisms for Autonomic Dysreflexia include upregulation of vascular catecholamine receptors, increased neural release of catecholamines, loss of the baroreceptor reflex, and loss of tonic bulbospinal inhibitory input to spinal neurons. Spinal cord injury leads to a host of changes within the injured cord that promote pathological secondary outcomes, such as Autonomic Dysreflexia. Studies show that neurotrophic factors are useful and probably necessary for the process of regeneration of injured tracts and neurons whereas nerve growth factor (NGF) does not appear to be a good candidate for this task as it clearly contributes to secondary disorders. Likewise, inflammation is a necessary part of healing but, in the central nervous system (CNS), inflammation can cause great damage that is not readily reversed. Therefore, the inflammatory response to cord injury also is an ideal target for manipulation to maintain its useful functions while limiting its capacity to cause destructive or maladaptive responses. Autonomic Dysreflexia is one of many secondary consequences of cord injury such as bladder and sexual dysfunction, chronic pain, muscle spasticity. Understanding the mechanisms of Autonomic Dysreflexia and development of treatments to prevent its development may influence many of these disabling secondary disorders.

  • Autonomic Dysreflexia in a mouse model of spinal cord injury.
    Neuroscience, 2001
    Co-Authors: J.e. Jacob, Lynne C. Weaver, A Pniak, Arthur Brown
    Abstract:

    Abstract Most experimental studies of spinal cord injury have centered on the rat as an experimental model. A shift toward a mouse model has occurred in recent years because of its usefulness as a genetic tool. While many studies have concentrated on motor function and the inflammatory response following spinal cord injury in the mouse, the development of Autonomic Dysreflexia after injury has yet to be described. Autonomic Dysreflexia is a condition in which episodic hypertension develops after injuries above the mid-thoracic segment of the spinal cord. In this study 129Sv mice received a spinal cord transection at the second thoracic segment. The presence of Autonomic Dysreflexia was assessed 2 weeks later. Blood pressure responses to stimulation were as follows: moderate cutaneous pinch caudal to the injury (35±6 mm Hg), tail pinch (25±7 mm Hg), and a 0.3 ml balloon distension of the colon (37±4 mm Hg). Previous reports have suggested that small diameter primary afferent fiber sprouting after spinal cord injury may be responsible for the development of Autonomic Dysreflexia. In order to determine whether Autonomic Dysreflexia in the mouse may be caused by a similar mechanism, the size of the small diameter primary afferent arbor in spinal cord-injured and sham-operated animals was assessed by measuring the area occupied by calcitonin gene-related peptide-immunoreactive fibers. The percentage increase in the area of the small diameter primary afferent arbor in transected over sham-operated spinal cords was 46%, 45% and 80% at spinal segments thoracic T5–8, thoracic T9–12 and thoracic T13–lumbar L2 respectively. This study demonstrates the development of Autonomic dysfunction in a mouse model of spinal cord injury that is associated with sprouting of calcitonin gene-related peptide fibers. These results provide strong support for the use of this mouse model of spinal cord injury in the study of Autonomic Dysreflexia.

  • Autonomic Dysreflexia and Primary Afferent Sprouting after Clip-Compression Injury of the Rat Spinal Cord
    Journal of Neurotrauma, 2001
    Co-Authors: Lynne C. Weaver, P. Verghese, Jamie C. Bruce, Michael G. Fehlings, Natalie R. Krenz, Daniel R. Marsh
    Abstract:

    Spinal cord injury leads to many forms of Autonomic dysfunction including Autonomic Dysreflexia, a condition involving recurrent episodes of paroxysmal hypertension and associated bradycardia. This hypertension may reach intensities that are life-threatening. We investigated Autonomic Dysreflexia and the sprouting of central processes of primary afferent neurons (a potential mechanism for Autonomic Dysreflexia) in a clinically-relevant calibrated clip-compression model of spinal cord injury in the rat. Autonomic Dysreflexia was induced by colon distension in the conscious rats 2 weeks after severe (50-g) clip compression injury of the spinal cord at the 4th thoracic segment. The central arbor of small-diameter primary afferent fibers in laminae III-VII of the spinal cord dorsal horn was also assessed at 2 weeks after cord injury by quantitative morphometry, using calcitonin gene-related peptide as a marker. In response to colon distension, arterial pressure increased by 41 ± 3 mmHg from a resting value of...

  • neutralizing intraspinal nerve growth factor blocks Autonomic Dysreflexia caused by spinal cord injury
    The Journal of Neuroscience, 1999
    Co-Authors: Andrei V Krassioukov, Lynne C. Weaver, Susan O. Meakin, Natalie R. Krenz
    Abstract:

    Autonomic Dysreflexia is a condition that develops after spinal cord injury in which potentially life-threatening episodic hypertension is triggered by stimulation of sensory nerves in the body below the site of injury. Central sprouting of small-diameter primary afferent fibers in the dorsal horn of the spinal cord occurs concurrently with the development of this condition. We propose a model for the development of Autonomic Dysreflexia in which increased nerve growth factor (NGF) in the injured cord stimulates small-diameter primary afferent fiber sprouting, thereby magnifying spinal sympathetic reflexes and promoting Dysreflexia. We identified this population of afferent neurons using immunocytochemistry for calcitonin gene-related peptide. Blocking intraspinal NGF with an intrathecally-delivered neutralizing antibody to NGF prevented small-diameter afferent sprouting in rats 2 weeks after a high thoracic spinal cord transection. In the same rats, this anti-NGF antibody treatment significantly decreased (by 43%) the hypertension induced by colon stimulation. The extent of small-diameter afferent sprouting after cord transection correlated significantly with the magnitude of increases in arterial pressure during the Autonomic Dysreflexia. Neutralizing NGF in the spinal cord is a promising strategy to minimize the life-threatening Autonomic Dysreflexia that develops after spinal cord injury.

Kessler, Thomas M - One of the best experts on this subject based on the ideXlab platform.

  • Prediction of Autonomic Dysreflexia during urodynamics: a prospective cohort study
    BioMed Central, 2018
    Co-Authors: Walter Matthias, Knüpfer, Stephanie C, Cragg, Jacquelyn J, Leitner Lorenz, Schneider, Marc P, Mehnert Ulrich, Krassioukov Andrei, Schubert Martin, Curt Armin, Kessler, Thomas M
    Abstract:

    BACKGROUND Autonomic Dysreflexia is a severe and potentially life-threatening condition in patients with spinal cord injury, as it can lead to myocardial ischemia, brain hemorrhage, or even death. Urodynamic investigation is the gold standard to assess neurogenic lower urinary tract dysfunction due to spinal cord injury and reveal crucial pathological findings, such as neurogenic detrusor overactivity. However, neurogenic detrusor overactivity and urodynamic investigation are known to be leading triggers of Autonomic Dysreflexia. Therefore, we aimed to determine predictors of Autonomic Dysreflexia in individuals with spinal cord injury during urodynamic investigation. METHODS This prospective cohort study included 300 patients with spinal cord injuries and complete datasets of continuous non-invasive cardiovascular monitoring, recorded during same session repeat urodynamic investigation. We used logistic regression to reveal predictors of Autonomic Dysreflexia during urodynamic investigation. RESULTS We found that level of injury and presence of neurogenic detrusor overactivity were the only two independent significant predictors for Autonomic Dysreflexia during urodynamic investigation. A lesion at spinal segment T6 or above (odds ratio (OR) 5.5, 95% CI 3.2-9.4) compared to one at T7 or below, and presence of neurogenic detrusor overactivity (OR 2.7, 95% confidence interval (CI) 1.4-4.9) were associated with a significant increased odds of Autonomic Dysreflexia during urodynamic investigation. Both odds persisted after adjustment for age, sex, and completeness and stage of injury (adjusted OR (AOR) 6.6, 95% CI 3.8-11.7, and AOR 2.2, 95% CI 1.1-4.5, respectively). Further stratification by lesion level showed level-dependent significantly increased adjusted odds of Autonomic Dysreflexia, i.e., from C1-C4 (AOR 16.2, 95% CI 5.9-57.9) to T4-T6 (AOR 2.6, 95% CI 1.3-5.2), compared to lesions at T7 or below. CONCLUSIONS In patients with neurogenic lower urinary tract dysfunction due to spinal cord injury, Autonomic Dysreflexia is independently predicted by lesion level and presence of neurogenic detrusor overactivity. Considering the health risks associated with Autonomic Dysreflexia, such as seizures, stroke, retinal bleeding, or even death, we recommend both continuous cardiovascular monitoring during urodynamic investigation in all spinal cord-injured patients with emphasis on those with cervical lesions, and appropriate neurogenic detrusor overactivity treatment to reduce the probability of potentially life-threatening complications. TRIAL REGISTRATION ClinicalTrials.gov, NCT01293110

  • Prediction of Autonomic Dysreflexia during urodynamics: a prospective cohort study
    'Springer Science and Business Media LLC', 2018
    Co-Authors: Walter Matthias, Knüpfer, Stephanie C, Cragg, Jacquelyn J, Leitner Lorenz, Schneider, Marc P, Mehnert Ulrich, Krassioukov Andrei, Schubert Martin, Curt Armin, Kessler, Thomas M
    Abstract:

    Background: Autonomic Dysreflexia is a severe and potentially life-threatening condition in patients with spinal cord injury, as it can lead to myocardial ischemia, brain hemorrhage, or even death. Urodynamic investigation is the gold standard to assess neurogenic lower urinary tract dysfunction due to spinal cord injury and reveal crucial pathological findings, such as neurogenic detrusor overactivity. However, neurogenic detrusor overactivity and urodynamic investigation are known to be leading triggers of Autonomic Dysreflexia. Therefore, we aimed to determine predictors of Autonomic Dysreflexia in individuals with spinal cord injury during urodynamic investigation. Methods: This prospective cohort study included 300 patients with spinal cord injuries and complete datasets of continuous non-invasive cardiovascular monitoring, recorded during same session repeat urodynamic investigation. We used logistic regression to reveal predictors of Autonomic Dysreflexia during urodynamic investigation. Results: We found that level of injury and presence of neurogenic detrusor overactivity were the only two independent significant predictors for Autonomic Dysreflexia during urodynamic investigation. A lesion at spinal segment T6 or above (odds ratio (OR) 5.5, 95% CI 3.2–9.4) compared to one at T7 or below, and presence of neurogenic detrusor overactivity (OR 2.7, 95% confidence interval (CI) 1.4–4.9) were associated with a significant increased odds of Autonomic Dysreflexia during urodynamic investigation. Both odds persisted after adjustment for age, sex, and completeness and stage of injury (adjusted OR (AOR) 6.6, 95% CI 3.8–11.7, and AOR 2.2, 95% CI 1.1–4.5, respectively). Further stratification by lesion level showed level-dependent significantly increased adjusted odds of Autonomic Dysreflexia, i.e., from C1–C4 (AOR 16.2, 95% CI 5.9–57.9) to T4–T6 (AOR 2.6, 95% CI 1.3–5.2), compared to lesions at T7 or below. Conclusions: In patients with neurogenic lower urinary tract dysfunction due to spinal cord injury, Autonomic Dysreflexia is independently predicted by lesion level and presence of neurogenic detrusor overactivity. Considering the health risks associated with Autonomic Dysreflexia, such as seizures, stroke, retinal bleeding, or even death, we recommend both continuous cardiovascular monitoring during urodynamic investigation in all spinal cord-injured patients with emphasis on those with cervical lesions, and appropriate neurogenic detrusor overactivity treatment to reduce the probability of potentially life-threatening complications. Trial registration ClinicalTrials.gov, NCT01293110 .Medicine, Faculty ofOther UBCNon UBCReviewedFacult