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NEUROLOGY 2005;65:E5
© 2005 American Academy of Neurology
Resident and Fellow Page

The triumvirate of acute hypertension

Michael L. Bell, MD and Eelco F.M. Wijdicks, MD

From the Mayo Clinic College of Medicine, Division of Critical Care Neurology Department of Neurology, Rochester, MN.

Address correspondence and reprint requests to Dr. Eelco F.M. Wijdicks, Mayo Clinic College of Medicine, Division of Critical Care Neurology, Department of Neurology, W8B, 200 First Street SW, Rochester, MN 55905; e-mail: wijde{at}mayo.edu

A 52-year-old man acutely developed delirium and seizures associated with hypertension. MRI showed left hemispheric and brainstem lesions (figure). Profound agitation precluded visualization of the fundi, however an acute hypertensive retinopathy became apparent after pupillary dilatation (see figure). EKG (figure) and echocardiography showed left ventricular hypertrophy. With antihypertensive treatment, most lesions resolved within 2 weeks.



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  		Figure. Flair MRI of the brain shows unilateral left hemispheric and bilateral pontine lesions. These lesions are absent on diffusion weighted images (not shown) and consistent with cytotoxic edema. Fundus shows hemorrhages and cotton wool spots consistent with malignant hypertension.2 EKG shows left ventricular hypertrophy.

 

Hypertensive encephalopathy typically causes symmetric, posterior predominant cortical and subcortical lesions. Frontotemporal, corona radiata, pontine, or cerebellar lesions or strictly unilateral lesions occur less commonly.1 In any patient with unexplained MRI abnormalities and hypertension, attention should be directed toward other organ damage particularly the retina.

Footnotes

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References

  1. Schwartz RB, Mulkern RV, Gudbjartsson H, et al. Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis. Am J Neuroradiol 1998;19:859–862.[Abstract]
  2. McGregor E, Isles CG, Jay JL, et al. Retinal changes in malignant hypertension. BMJ 1986;292:233–234.[Medline]




This Article
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