Circulation. 2007;115:e310-e311
doi: 10.1161/CIRCULATIONAHA.106.653618
(Circulation. 2007;115:e310-e311.)
© 2007 American Heart Association, Inc.
Images in Cardiovascular Medicine |
Hypertensive Brainstem Encephalopathy
Raymond C.S. Seet;
Erle C.H. Lim
From the Department of Medicine, Yong Loo Lin School of Medicine, National University, Singapore, and the Division of Neurology, National University Hospital, Singapore.
Correspondence to Dr Raymond Chee-Seong Seet, Department of Medicine, National University Hospital, 5 Lower Kent Ridge Road, Singapore. E-mail raymond_seet{at}nus.edu.sg
A 34-year-old man, previously in good health with no past history of hypertension, presented with a 2-day history of bitemporal headaches and a sudden onset of left-sided weakness 4 days after ingesting traditional Chinese medications for nonspecific abdominal pain. He was afebrile, drowsy, disoriented, and dysarthric, with a blood pressure of 270/170 mm Hg. Clinical examination revealed mild left facial weakness and strength of Medical Research Council grade 4/5 in the left upper and lower limbs. Deep tendon reflexes were brisk, and he demonstrated bilateral extensor plantar responses. Fundoscopy revealed grade 4 hypertensive retinopathy changes (Figure 1). ECG was consistent with left ventricular hypertrophy. Treatment with intravenous glyceryl trinitrate was commenced to achieve normotension. Blood tests suggested rhabdomyolysis with 127 µmol/L (42–112) creatinine, 11231 U/L (30–350) of creatine kinase, >1000 ng/mL (16–96) of serum myoglobin, and 31.4 U/L (<7.6) of aldolase.
View larger version (55K):
[in this window]
[in a new window]
|
Figure 1. Fundoscopic appearance of grade IV hypertensive retinopathy, with papilloedema (1), arteriovenous nipping (2), flame-shaped hemorrhages (3), and soft (4) and hard (5) exudates.
|
|
Computed tomography of the brain showed low-attenuation abnormalities in the brain stem and white matter of both cerebral hemispheres, consistent with edema (Figure 2). Likewise, fluid-attenuated inversion recovery sequence of the magnetic resonance brain image revealed asymmetrical hyperintensities within the brain stem, dentate nuclei, inferior cerebellar peduncles, and white matter of the cerebrum (Figure 2). Diffusion-weighted imaging was normal, indicating the absence of infarction. There was no enhancement with the administration of gadolinium contrast. Twenty-four hour urinary total protein was 3.45 g/d (normal, <0.30), and creatinine clearance was measured at 49 mL/min (75–135). Ultrasound and Doppler studies of the kidney were unremarkable. Urinary metanerphrine, normetanephrine, and vanillyl mandelic acid were within normal ranges, excluding phaeochromocytoma as a cause of the patient’s malignant hypertension. Toxicological and microbiological studies of the blood and urine to investigate the cause of rhabdomyolysis were negative. With judicious fluid management, creatine kinase and myoglobin normalized 5 days later. The patient’s neurological deficits and magnetic resonance imaging changes also normalized with achievement of normal blood pressure. He was discharged 10 days later, with residual hyperreflexia in the limbs, but no neurological deficits.
View larger version (62K):
[in this window]
[in a new window]
|
Figure 2. Computed tomography image of the brain. A, Hypodensities in the brain stem (BS) and cerebral white matter (CWM), consistent with cerebral edema. Axial (B) and coronal (C) fluid-attenuated inversion recovery sequenced magnetic resonance image showing hyperintensities in the brain stem, cerebellar peduncles (CP), and cerebral white matter.
|
|
Hypertensive crises are important medical emergencies that can result in acute end-organ injuries such as stroke, pulmonary edema, congestive heart failure, aortic dissection, acute myocardial infarction, unstable angina, acute renal failure, and hypertensive encephalopathy.1 Up to 16% of patients with hypertensive crisis have hypertensive encephalopathy, which is characterized by severe hypertension, confusion, visual complaints, headache, stupor, and seizures.2 Brain-stem and cerebellar involvement in hypertensive encephalopathy are rarely reported. These occur more frequently in younger patients (ie, younger than 40 years) with secondary hypertension.2 Hypertensive encephalopathy is believed to arise from the breakdown of autoregulation, resulting in dilatation of cerebral arterioles and disruption of the blood–brain barrier, causing vasogenic edema.3,4 The posterior circulation (vertebrobasilar and posterior cerebral arteries) is sparsely innervated by sympathetic nerves, accounting for the susceptibility of the occipital lobes, brain stem, and cerebellum to this breakdown of autoregulation.4 Despite the wide availability of antihypertensive therapies, hypertensive crisis remains an important reversible medical emergency that requires immediate reduction of blood pressure.
 |
Disclosures
|
|---|
None.
|
References
|
|---|
- The fifth report of the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure (JNC V). Arch Intern Med. 1993; 153: 154–183.[CrossRef][Medline]
[Order article via Infotrieve]
- Cruz-Flores S, de Assis Aquino Gondim F, Leira EC. Brainstem involvement in hypertensive encephalopathy: clinical and radiological findings. Neurology. 2004; 62: 1417–1419.[Abstract/Free Full Text]
- Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, Pessin MS, Lamy C, Mas JL, Caplan LR. A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996; 334: 494–500.[Abstract/Free Full Text]
- de Seze J, Mastain B, Stojkovic T, Ferriby D, Pruvo JP, Destee A, Vermersch P. Unusual MR findings of the brain stem in arterial hypertension. AJNR Am J Neuroradiol. 2000; 21: 391–394.[Abstract/Free Full Text]
Related Article:
-
Issue Highlights
Circulation 2007 115: 1059.
[Full Text]
Top
Disclosures
References