Surg Neurol 1991;36:315-6

315

Letters to the Editor

To the Editor: Perhaps I did not make it clear that I agree that the operation of MVD for hemifacial spasm is the best one available and, indeed, one that I perform myself. What I do wish to question, however, is the mechanism of hemifacial spasm and the mechanism of microvascular decompression. My view is that the operation works by trauma, and, if one looks at the results of MVD for trigeminal neuralgia, these are no better or worse than those obtained by Gardner and Miklos and Taarnhof, who performed a nerve rubbing procedure and no more. The point of this is that there may be a safer way of "traumatizing" the nerve than microvascular decompression, which does demand a considerable degree of retraction.

C.B.T. Adams, M. Chir., F.R.C.S.

Oxford. United Kingdom

To the Editor: We read with the greatest interest the article by Wagle et al (Surgical Neurology 1990;34:435-8), in which a case of a pencil glioma of the cerebral aqueduct that presented with neurogenic pulmonary edema was reported. We would like to make the following comments. (1) The presentation of an aqueduct glioma with neurogenic pulmonary edema and a ringlike lesion at the tectum in the computed tomography (CT) scan is indeed very interesting. Apparently, this is the first description of a pencil glioma of the aqueduct demonstrated by CT scan. In this regard, we would consider, in the differential diagnosis of this lesion, the existence of a tumor, an arteriovenous malformation, and encephalitis, in addition to cysticercosis and abscess. (2) The authors' statement regarding that all cases, except the one reported by Sandford et al, were diagnosed at autopsy seems to be incorrect. Pool [2] described two cases of aqueductal tumors that had long survival times. In 1987 we documented the case of a 9-year-old girl with hydrocephalus due to aqueduct occlusion that evolved with intermittent changes in the level of consciousness, obesity, and hirsutism. Computed tomography and ventriculography failed to detect the cause of the obstruction of the iter. Cerebrospinal fluid (CSF) cytology was positive for tumor cells of astrocytic origin, and, accordingly, a presumptive diagnosis of aqueductal glioma was made while the patient was alive [3]. The patient died while awaiting cobalt therapy. Postmortem study confirmed the existence of a pilocytic astrocytoma of the sylvian aqueduct. (3) The diagnostic difficulties in assessing these tumors are well recognized in current literature. In most reports neurora© 1991 by Elsevier Science Publishing Co., Inc.

diological investigations, including high-resolution CT, failed to show the cause of the aqueductal occlusion. Even macroscopic inspection at autopsy may miss the neoplasm that is only diagnosed in microscopic slices. Perhaps some of the published instances of"gliosis" of the aqueduct may belong to low-grade gliomas, taking into account the difficulties encountered in distinguishing gliosis and low-grade astrocytomas, as suggested by Ho [1]. (4) We have recently experienced three additional cases of "occult" tumors that had been discovered during the routine follow-up study in instances of aqueduct stenosis hydrocephalus investigated by magnetic resonance imaging (MRI). Therefore, it seems that with the advent of MRI, aqueductal tumors will be discovered more readily. (5) Finally, we would like to suggest that cases of aqueduct stenosis presenting at unusual ages or evolving with unusual features should be evaluated by MRI and/or CSF cytology. Juan F. Martinez-Lage, M.D. Joaquin Sola, M.D.

Murcia, Spain References 1. Ho K-L. Tumors of the cerebral aqueduct. Cancer 1982;49:154-62. 2. Pool JL. Gliomas of the region of the brain stem. J Neurosurg 1968;29: 164-7. 3. Sola J, Areas l, Martinez-Lage JF, Martinez Perez M, Esteban JA, Poza M. Astrocytoma of the cerebral aqueduct. Childs Nerv Syst 1987;3:294-6.

To the Editor: Cerebral vasospasm has continued to be an elusive problem. There have been many clinical regimens suggested to combat or prevent the effects of cerebral vasospasm [5]. The current use of Nimotop (Miles Pharmaceuticals, West Haven, Conn.) has certainly advanced the treatment of this problem. However, cerebral vasospasm and its treatment still remain a part of the "Art of Medicine." A 56-year-old man, who weighed 75 kg, suffered a subarachnoid hemorrhage on April 3, 1989. The presentation was one of a subfrontal headache accompanied by posterior cervical discomfort. A computed tomography (CT) scan was performed by a neurologist and showed diffuse subarachnoid hemorrhage extending from the circle of Willis out into both sylvian cisterns. The patient was awake without gross neurologic deficits on admission. The day after subarachnoid hemorrhage, he underwent cerebral angiogram, revealing a 9-mm bulbusappearing aneurysm of the anterior communicating artery complex. A craniotomy with uneventful clipping of the aneurysm was performed on April 5, 1989. He was given nimodipine postoperatively, 30 mg, two tablets every 4 hours. Following 0090-~019/9I/$3.50

Pencil glioma of the cerebral aqueduct that presented with neurogenic pulmonary edema.

Surg Neurol 1991;36:315-6 315 Letters to the Editor To the Editor: Perhaps I did not make it clear that I agree that the operation of MVD for hemif...
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