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Related Concept Videos

Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

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Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...
763

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Hypertensive encephalopathy and cerebral infarction.

Bengt Edvardsson1

  • 1Department of Clinical Sciences, Lund, Neurology, Skane University Hospital, Lund University, S-221 85 Lund, Sweden.

Springerplus
|May 2, 2015
PubMed
Summary

Hypertensive encephalopathy can cause posterior reversible encephalopathy syndrome (PRES). Prompt treatment is crucial to prevent cerebral damage, as imaging revealed partial resolution with subsequent small infarcts.

Keywords:
Cerebral infarctionHypertensive encephalopathyIschemiaMagnetic resonance imagingPosterior reversible encephalopathy syndrome

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Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
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Area of Science:

  • Neurology
  • Radiology

Background:

  • Posterior reversible encephalopathy syndrome (PRES) can be caused by hypertensive encephalopathy.
  • The co-occurrence of hypertensive encephalopathy and cerebral infarction is rarely reported.

Purpose of the Study:

  • To present a case of hypertensive encephalopathy leading to PRES.
  • To illustrate the imaging findings and evolution of the condition.

Main Methods:

  • A 51-year-old woman with hypertensive encephalopathy underwent magnetic resonance imaging (MRI).
  • MRI sequences included T2-weighted, diffusion-weighted, and perfusion imaging.
  • Follow-up MRI was performed 5 months later.

Main Results:

  • Initial MRI showed bilateral occipital and parietal lobe hyperintense lesions, indicative of cytotoxic edema.
  • Perfusion imaging revealed reduced blood volume and flow.
  • Follow-up MRI demonstrated subtotal regression of T2 hyperintensity but revealed small bilateral infarcts.

Conclusions:

  • Hypertensive encephalopathy can cause PRES with imaging evidence of cytotoxic edema and subsequent infarcts.
  • Early recognition and treatment of hypertensive encephalopathy are vital to prevent irreversible brain damage.