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Correspondence: When an article is eligible for submission of Correspondence, a link to the response form is available within the full-text article. You must be a current subscriber who has activated the online portion of your subscription in order to send a Correspondence. Any reader can read published Correspondence.
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Correspondence:Correspondence published:
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Brainstem involvement in hypertensive encephalopathy: Clinical and radiological findings
- Valerie Biousse, Nancy J. Newman (8 June 2004)
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Reply from the authors
- Salvador Cruz-Flores, Francisco de Assis Aquino Gondim, Enrique C Leira (8 June 2004)
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Brainstem involvement in hypertensive encephalopathy: Clinical and radiological findings
- Gregory Y Chang, APO AP 96205-0017 (8 June 2004)
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Valerie Biousse, Emory University Neuro-ophthalmology Unit, 1365-B Clifton Rd, Atlanta, GA 30322, Nancy J. Newman
Send Correspondence to journal:
vbiouss{at}emory.edu Valerie Biousse, et al.
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In their article, Cruz-Flores et al describe two original cases and reviewed the literature. In their methods, the authors stated that they excluded most of previously published articles because of lack of adequate data. Only 15 reports met their inclusion criteria. Because of the limitation of the number of allowed references to 10 for a “Brief Communication” in Neurology, the authors referenced only 9 articles, none of which included selected patients with brainstem hypertensive encephalopathy. The readers have to login to the Neurology Web site to consult the appendix in order to see which studies have been selected. Although it may be convenient to post additional material such as large tables on the Neurology Web site, the list of references used in a review of the literature should be immediately available to the reader of printed articles. Indeed a quick review of this article is misleading and would suggest that these two cases are unique and that brainstem involvement of hypertensive encephalopathy was never well documented in the past. As detailed by the authors in appendix E1, at least 15 good studies (usually with more than two cases) have reported similar clinical and radiological findings, most of which were published with in the past few years, including in Neurology. Reference 1.)Cruz-Flores S, de Assis Aquino Gondim F, Leira EC. Brainstem involvement in hypertensive encephalopathy. Neurology 2004; 62: 1417-1419 |
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Salvador Cruz-Flores, Saint Louis University School of Medicine 3635 Vista Ave Department of Neurology, St. Louis, MO, 63110, Francisco de Assis Aquino Gondim, Enrique C Leira
Send Correspondence to journal:
salvador.cruz-flores{at}tenethealth.com Salvador Cruz-Flores, et al.
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We appreciate Dr. Chang’s comments regarding our article [1]. He makes a valid clinical observation of neurogenic hypertension caused by a cystic schwannoma resulting in hypertensive encephalopathy. However, he addresses the “clinical radiological dissociation” in the context of a patient with a known tumor causing distortion of the brainstem and presenting with hypertensive encephalopathy with no brainstem involvement. We think the concept of clinical radiological dissociation might be better applied in presence of severe parenchymal abnormalities as he initially described [2], and as it is seen in all cases included in our review [1]. It is with the parenchymal abnormalities and minimal clinical signs that the concept becomes helpful in differentiating this condition from infarction. Drs. Biousse and Newman also make a valid point. They are correct that the number of allowed references for a “Brief Communication” is ten. Although we agree that the references used in a review like ours should be readily available to the reader, the complete list in the printed version would not have been possible given the limit of the format. Therefore, we decided to keep the included studies together in an Appendix in the Neurology Web site rather than providing an incomplete set of references. No portion of the presentation states our cases were unique, they were meant to be illustrative. Moreover, the “Results” section of our paper is very explicit about the available and included studies. [1] Thus, we fail to see how our article might be misleading or might be suggesting the uniqueness of our report. The purpose of the review was to provide a summary description of this entity based on the reported cases, including those reported by them. [3] References 1. Cruz-Flores S, Gondim F, Leira E. Brainstem involvement in hypertensive encephalopathy. Clinical and radiological findings. Neurology 2004; 62: 1417-1419 2. Chang GY, Keane JR. Hypertensive brainstem encephalopathy. Neurology. 1999; 53: 652-654. 3. Thambisetty M, Biousse V, Newman NJ. Hypertensive brainstem encephalopathy:clinical and radiographic features. J Neurol Sci 2003; 208: 93-99 |
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Gregory Y Chang, 121st US Army Gen Hosp HHC 121st US Army Gen Hosp, Box #277, APO AP 96205-0017
Send Correspondence to journal:
gychang{at}operamail.com Gregory Y Chang, et al.
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Cruz-Flores et al 1 reported two additional cases of brainstem edema as a manifestation of hypertensive encephalopathy (HTE). They emphasized minimal clinical brainstem dysfunction despite the marked brainstem edema seen on MRI as a diagnostic clue as we suggested in 1999. [2] I recently encountered a patient with a progressive left brainstem distortion from an extrinsic tumor resulting in a neurogenic hypertension but without additional brainstem signs. Transient HTE manifested by bilateral occipital lobe involvement was documented. A 75-year-old man with previously well-controlled hypertension of 20 years and known cystic schwannoma of 3 years was admitted with worsening headache, blurry vision and unsteadiness. Admission blood pressure was 211/156 mm Hg. Previously documented Horner's, deafness, facial myokymia and hemi-lingual atrophy, all on the left side, and hoarseness were unchanged. Serial MRI documented progression of the left brainstem distortion. Additionally, bilateral occipital lobe changes typical of HTE were seen. (Figure) Treatment starting with intravenous nitroprusside followed by adjustment of his oral antihypertensive medications resulted in prompt resolution of his symptoms. This case illustrates left brainstem lesion may result in a neurogenic hypertension and subsequently manifest clinical symptoms and MRI signs of HTE. Importance of left cranial nerve IX-X root entry zone in producing hypertension has been repeatedly demonstrated in human neurovascular compressive cases [3] and experimental observations in primates. Additionally, clinico-radiologic dissociation was also demonstrated with easily reversible HTE as the primary clinical manifestation despite the impressive brainstem distortion on the MRI. LEGEND Figure
References 1.) Cruz-Flores S, Gondim F, Leira E. Brainstem involvement in hypertensive encephalopathy. Clinical and radiological findings. Neurology 1004; 62:1417-1419. 2.) Chang GY, Keane JR. Hypertensive brainstem encephalopathy. Neurology 1999;53:652-654. 3.Hohenbleicher H, Schmitz SA, Koennecke HC, et al. Neurovascular Contact of Cranial Nerve IX and X Root-Entry Zone in Hypertensive Patients. Hypertension 2001;37:176-181. Note: The opinions or assertions contained herein are the private views of the author (GYC) and are not to be construded as representing the views of the Department of Defense, the Department of the Army, or the Uniformed Services University of the Health Sciences. |
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(A) An axial T2-weighted image shows left cystic schwannoma causing
shift and distortion of the caudal pons. Distortion progressed over the 3-year period. (B) An axial FLAIR image shows midbrain distortion from
the tumor extension and patchy bilateral occipital lobe lesions.
Diffusion-weighted image of the occipital lobe is normal (not shown).
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