Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2016 Oct 18;188(15):1100-1103.
doi: 10.1503/cmaj.151311. Epub 2016 May 24.

Emergency management of autonomic dysreflexia with neurologic complications

Jordan W Squair  1 , Aaron A Phillips  1 , Mark Harmon  1 , Andrei V Krassioukov  2
Affiliations
Case Reports

Emergency management of autonomic dysreflexia with neurologic complications

Jordan W Squair et al. CMAJ. .
No abstract available

PubMed Disclaimer

Figures

Figure 1:
Figure 1:
Magnetic resonance imaging consistent with posterior reversible encephalopathy syndrome. (A) Transverse imaging (T2, top; fluid-attenuated inversion recovery, middle; and diffusion-weighted imaging, bottom) shows cortical edema in the left parietal lobe (red arrows). The normal findings on diffusion-weighted imaging (bottom) suggest vasogenic rather than cytotoxic edema. (B) Contiguous sagittal fluid-attenuated inversion recovery images confirmed vasogenic edema in cortical (red arrows) and subcortical (white arrows) areas. Further areas of cortical and subcortical edema were present throughout the parietal and occipital lobes bilaterally (not shown). Given the patient’s acute, severe hypertension, the imaging findings were consistent with mild but evolving posterior reversible encephalopathy syndrome.
Figure 2:
Figure 2:
Theoretical framework underlying cerebrovascular events induced by autonomic dysreflexia. In this case, the level of the patient’s injury may have played a role in the development of autonomic dysreflexia–induced posterior reversible encephalopathy syndrome. Specifically, hyperexcitation of the sympathetic preganglionic neurons below the level of injury and a subsequent increase in blood pressure would result in dilatation of the cerebral blood vessels because of intact supraspinal regulation of the superior cervical ganglion (SCG). Paradoxic baroreflex-mediated relaxation of the cerebral arteries would impair autoregulation of the increasing blood pressure and expose the delicate cerebral microvasculature to insulting elevation in cerebral blood flow, potentially compromising the integrity of the blood–brain barrier. CG = celiac ganglion, IMG = inferior mesenteric ganglion, SMG = superior mesenteric ganglion.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Phillips AA, Krassioukov AV. Contemporary cardiovascular concerns after spinal cord injury: mechanisms, maladaptations and management. J Neurotrauma 2015;32:1927–42. - PubMed
    1. Cragg JJ, Noonan VK, Krassioukov AV, et al. Cardiovascular disease and spinal cord injury: results from a national population health survey. Neurology 2013;81:723–8. - PMC - PubMed
    1. Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494–500. - PubMed
    1. Hefzy HM, Bartynski WS, Boardman JF, et al. Hemorrhage in posterior reversible encephalopathy syndrome: imaging and clinical features. AJNR Am J Neuroradiol 2009;30:1371–9. - PMC - PubMed
    1. Consortium for Spinal Cord Medicine. Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities. J Spinal Cord Med 2002;25 Suppl 1:S67–88. - PubMed

Publication types

MeSH terms