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Vartanian and de la Monte,
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Although their use was in favor during the 1980s, bacterial-antigen tests have been shown to be insensitive and nonspecific and to have little, if any, effect on the care of patients with suspected bacterial meningitis.2,3 Gram's staining in such patients is highly sensitive and much more specific.4 The Venereal Disease Research Laboratory test performed on cerebrospinal fluid, although highly specific, is insensitive and should only be performed in patients with serologic (i.e., serum) evidence of syphilis.5 Finally, a cold-agglutinin test, although simple to perform, is insensitive and nonspecific for mycoplasma infection.6
Irving Nachamkin, Dr.P.H.
University of Pennsylvania
Philadelphia, PA 19104-4283
References
Bernhard Zünkeler, M.D.
St. Joseph's Medical Center
Baltimore, MD 21204
References
In our view, cerebral endothelial cells are the main target in primary demyelinating diseases1 and highlight the role of the blood–brain barrier in the pathogenesis of these disorders.
Abhijit Chaudhuri, D.M., M.D.
Peter O. Behan, D.Sc., M.D.
Southern General Hospital
Glasgow G51 4TF, United Kingdom
References
To the Editor: Zünkeler's comments on lumbar puncture are certainly well taken. Unfortunately, the clinical synopsis was inaccurate. Figure 1, which was cited on page 127, should have been cited on page 128 in the discussion of the third hospital day. The initial CT scan (which was not shown) showed bifrontoparietal edema, with obliterated sulci and diffuse hypodensity of white matter underlying the same regions, intact sulci in the occipital lobe, mild effacement of the third and lateral ventricles, a normal fourth ventricle, and no obliteration of the basilar cisterns. There was also no midline shift. Under these conditions and considering the critical importance of making a prompt and proper diagnosis of a presumed meningitis or encephalitis (or both), we believed that the lumbar puncture was necessary. Although it was not mentioned, an intracranial-pressure monitor was placed the day after admission. The lateral ventricles were not amenable to a ventriculostomy. The patient did have intermittent decerebrate posturing 10 hours after the lumbar puncture, but at that time brain-stem function was clinically intact, with small, reactive pupils and intact doll's-eye maneuvers. The results of the repeated CT performed at that time (also not shown) were unchanged from the previous ones, suggesting that the neurologic signs were secondary to the bilateral hemispheric edema and not to herniation or brain-stem compromise. A CT scan obtained on the third hospital day (which was shown as Figure 1 of the article), 72 hours after the lumbar puncture, did show transtentorial herniation and distortion of the brain stem. This massive swelling was considered to be due to bihemispheric parenchymal disease and not to herniation. Although lumbar puncture in the presence of known cerebral edema is risky, studies have shown that in the absence of obstruction of cerebrospinal fluid flow or a clinically significant midline shift (or both), it rarely precipitates herniation.1,2,3 In this case, the risk of delayed diagnosis or misdiagnosis outweighed the risk of herniation.
Anne B. Young, M.D., Ph.D.
Massachusetts General Hospital
Boston, MA 02114
References
To the Editor: The pathophysiology of necrotizing angiitis in patients with acute hemorrhagic leukoencephalitis is poorly understood. Although necrotizing angiitis is a distinguishing feature of this disorder, an individual patient may have some lesions at autopsy that resemble acute hemorrhagic leukoencephalitis and others that resemble acute disseminated encephalomyelitis (i.e., inflammatory demyelinating lesions with and without necrotizing angiitis). This fact, along with data from animals showing that acute and hyperacute experimental allergic encephalitis can be elicited by the same antigen, favors the argument that these diseases are part of a spectrum.
Does the necrotizing angiitis of acute hemorrhagic leukoencephalitis result from a specific insult to the cerebral microvasculature, or is it the result of an intense inflammatory response in the brain parenchyma, with secondary destruction of endothelial cells? Destruction of the cerebral vasculature by the inflammatory response, perhaps due to the generation of reactive oxygen intermediates, would help explain the lack of clinically significant involvement of blood vessels in other organs. However, endothelial cells within the central nervous system, in contrast to most other organs, have unique molecular components that contribute to the function of the blood–brain barrier. Thus, it is possible that they are uniquely susceptible or specifically targeted in acute hemorrhagic leukoencephalitis. This important question of whether there is a primary insult to the blood–brain barrier in demyelinating diseases, which has been considered by many investigators throughout the century, has yet to be answered.
Timothy Vartanian, M.D., Ph.D.
Harvard Institutes of Medicine
Boston, MA 02115
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