Neurologia medico-chirurgica

Cerebral Blood Flow and the Response to Acetazolamide during the Acute, Subacute, and Chronic Stages of Aneurysmal Subarachnoid Hemorrhage

Akira TANAKA, Shinya YOSHINAGA, Yoshiya NAKAYAMA, Masamichi TOMONAGA

1998 Volume 38 Issue 10 Pages 623-632
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.623

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Cerebral blood flow (CBF) and response to acetazolamide were measured during the acute, subacute, and chronic stages after aneurysmal subarachnoid hemorrhage and correlated with symptomatic vasospasm and clinical outcome in 45 patients who underwent early clipping of ruptured cerebral aneurysms, of whom 18 had symptomatic vasospasm and 27 did not. Xenon-enhanced computed tomography was used to measure CBF in both groups during the acute, subacute, and chronic stages, defined as days 0-4, 5-20, and ≥ 21, respectively. Vasoresponse was assessed by the CBF increase in response to 1 g of acetazolamide administered after the baseline CBF study, except in the subacute stage of patients with symptomatic vasospasm. Outcome was scored based on activities of daily living 2-3 months after subarachnoid hemorrhage. CBF values and the response to acetazolamide were preserved during the acute stage but CBF values fell considerably below control values during the subacute stage in patients with vasospasm. The regions with flow values below 15 ml/100 g/min subsequently converted to infarction and the regions with those above 19 ml/100 g/min remained intact without infarction. During the chronic stage, low CBF persisted, but the response to acetazolamide was higher than that of the control group. Outcome scores were good and fair. CBF values were normal during all stages in patients without vasospasm. The response to acetazolamide fell transiently during the subacute stage. All outcome scores were excellent. In conclusion, the CBF informations soon after the onset of symptomatic vasospasm are useful to predict a reversibility of ischemic brain tissue and a final outcome. We suggest that vasospasm may cause a pathological or ischemic insult to brain tissue during the subacute stage, and the brain may remain metabolically depressed thereafter, leading to a poor outcome. Even clinically asymptomatic patients may suffer mildly vasospastic or ischemic conditions during the subacute stage.

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Effect of Dexamethasone on Cell Proliferation of Neuroepithelial Tumor Cell Lines

Atsufumi KAWAMURA, Norihiko TAMAKI, Takashi KOKUNAI

1998 Volume 38 Issue 10 Pages 633-640
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.633

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The effect of glucocorticoid on cell proliferation, the expression of glucocorticoid receptor, and the relationship between inhibition of cell growth and apoptosis were investigated in four established neuroepithelial tumor cell lines (KNS42, T98G, A172, and U251MG). Glucocorticoid receptor expression was located in the cytoplasm of untreated cells, but translocated into nuclei after treatment with dexamethasone in KNS42, T98G, and A172 cells. U251MG did not express glucocorticoid receptors. Dexamethasone significantly inhibited the growth of KNS42 and T98G cell lines, at high concentrations in contrast to growth stimulation at low concentration. Dexamethasone inhibited proliferation of A172 cell line at all concentrations from 10^-4M to 10^-7M. These were prevented by RU38486, a specific glucocorticoid antagonist. Apoptosis did not occur in any cell lines after dexamethasone treatment. There was no response to glucocorticoid by U251MG cells. Dexamethasone treatment of neuroepithelial tumor cells expressing glucocorticoid receptors causes translocation into the nucleus to modulate cell proliferation upon binding of different concentrations of dexamethasone in vitro. Dexamethasone inhibits proliferation of some neuroepithelial cell lines, not by glucocorticoid-induced apoptosis. The bimodal potential of glucocorticoid to stimulate or suppress proliferation of neuroepithelial tumor cells expressing glucocorticoid receptor must be considered in clinical trials.

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Cervical Fast Spin Echo Three-dimensional Magnetic Resonance Myelography

Masami ISHII, Nobuhito ODA, Shusaku TAKAHAGI, Seiko SHIBATA, Takeshi Y ...

1998 Volume 38 Issue 10 Pages 641-647
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.641

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A technique of fast spin echo three-dimensional magnetic resonance (MR) myelography with flow compensation was developed for the evaluation of the cervical spinal lesions. The whole spinal cord and roots in the spinal canal can be visualized non-invasively on voxel images by the maximum intensity projection process to achieve the best static contrast of the cerebrospinal fluid. This method of MR myelography is applicable as a screening test for the patients with cervical spinal lesions.

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Cavernous Angioma Associated with Venous Angioma —Two Case Reports—

Toshihiko KUROIWA, Tomio OHTA

1998 Volume 38 Issue 10 Pages 648-653
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.648

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A 17-year-old male and a 28-year-old female presented with cavernous angioma and venous angioma colocated in the same region, and manifesting as convulsions. The cavernous angiomas were extirpated without damage to the venous angioma. No postoperative neurological deficits were observed. The patients have been free of convulsions without anticonvulsant medication for 2 years. Early extirpation of cavernous angioma with presentation of venous angioma is recommended, preferably before bleeding occurs.

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Fatal Epistaxis Caused by Rupture of an Intratumoral Aneurysm Enclosed by a Large Prolactinoma —Case Report—

Junichi IMAMURA, Tatuya OKUZONO, Yoshiko OKUZONO

1998 Volume 38 Issue 10 Pages 654-656
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.654

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A 72-year-old female presented with episodes of epistaxis. Neuroimaging demonstrated a large prolactinoma totally enclosing a large intracavernous aneurysm of the internal carotid artery. Adjacent bony structures were eroded and destroyed by tumor invasion and extension. Rupture of the intratumoral aneurysm caused fatal epistaxis rather than subarachnoid hemorrhage before surgery. Intratumoral aneurysm is rare and epistaxis caused by rupture of it is extremely rare. Lack of bony protection apparently have contributed to the aneurysmal growth and rupture.

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Cerebral Mycotic Aneurysm Treated with Endovascular Occlusion —Case Report—

Akira WATANABE, Kazuhiro HIRANO, Ryoji ISHII

1998 Volume 38 Issue 10 Pages 657-660
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.657

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A 56-year-old male with two mycotic aneurysms associated with infective endocarditis was treated by endovascular surgery before mitral valve replacement. Angiography revealed a ruptured proximal aneurysm and an unruptured distal aneurysm on the right middle cerebral artery. The ruptured aneurysm was successfully treated with an interlocking detachable coil, and patency of the parent artery was preserved. The unruptured distal aneurysm disappeared as a result of antibiotic therapy. Endovascular surgery of the mycotic aneurysm is less invasive and more effective than craniotomy under general anesthesia for patients with infective endocarditis.

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Transient Neurological Deficits Simulating Transient Ischemic Attacks in a Patient with Meningioma —Case Report—

Yasushi UENO, Akira TANAKA, Yoshiya NAKAYAMA

1998 Volume 38 Issue 10 Pages 661-665
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.661

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A 67-year-old female had a history of transient neurological deficits involving fainting and right-sided hemiparesis. Magnetic resonance imaging showed a sphenoid ridge meningioma on the left, which had encased the internal carotid and middle cerebral arteries. Carotid angiography showed occlusion of the left internal carotid artery, a tumor stain, and engorgement of the surrounding cortical veins. Xenon-enhanced computed tomography showed reduced cerebral blood flow and poor response to acetazolamide in the surrounding brain tissue. The tumor was totally removed. Postoperatively, the patient had no more transient neurological deficts, and the response to acetazolamide was fully restored. An intracranial tumor may cause transient neurological deficits by reducing the cerebral perfusion pressure. This vascular insufficiency may occur when the tumor occludes major cerebral arteries, steals flow from the surrounding tissue, increases focal tissue pressure, and impedes regional venous outflow. The latter two factors were probably responsible in this patient.

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Symptomatic Vessel Narrowing Caused by Spontaneous Rupture of Craniopharyngioma Cyst —Case Report—

Naoki SHIDA, Nobukazu NAKASATO, Kazuo MIZOI, Masaya KANAKI, Takashi YO ...

1998 Volume 38 Issue 10 Pages 666-668
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.666

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A 36-year-old female presented with cerebral infarction due to severe vessel stenosis after spontaneous rupture of a craniopharyngioma, manifesting as aphasia and drowsiness. Neuroimaging showed the suprasellar cystic tumor with wall enhancement and cerebral infarction in the left temporoparietal region, and also enhancement of the left sylvian fissure and prepontine cistern. Angiography showed severe narrowing at the C₁ portion of the left internal carotid artery (ICA) and the M₁ portion of the left middle cerebral artery (MCA). The tumor was subtotally removed via a bifrontal craniotomy. There was accumulated milky-white debris around the left ICA and MCA. She became alert within a few days postoperatively. Repeat angiography 1 month after surgery demonstrated slight improvement of vessel narrowing. The neuroimaging and intraoperative findings suggested that the stenosis was due to vasospasm induced by chemical meningitis resulting from cyst rupture.

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Shock Syndrome Induced by Bromocriptine Test in a Patient with Prolactinoma —Case Report—

Yoko NAKASU, Akihiko SHIINO, Satoshi NAKASU, Jyoji HANDA

1998 Volume 38 Issue 10 Pages 669-671
Published: 1998
Released on J-STAGE: March 30, 2006

DOIhttps://doi.org/10.2176/nmc.38.669

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A 72-year-old male developed shock syndrome after a single dose of bromocriptine. He had undergone uncomplicated subtotal removal of an invasive prolactinoma in our department. The patient had normal ranges of pituitary hormones apart from hyperprolactinemia (167.7 ng/ml) after surgery. An acute suppression test with bromocriptine (2.5 mg per os) was done in the supine position 6 days following surgery. Three and a half hours after bromocriptine administration, he suddenly complained of anterior chest discomfort in bed. Cyanosis and profuse diaphoresis were noted. His blood pressure was 80/60 mmHg. Electrocardiography revealed sporadic premature contractions and slight depression in the ST segments. He recovered in about 10 hours after a rapid infusion of corticosteroid and lactic Ringer solution, and was discharged without sequelae. This is a very rare complication of bromocriptine, but the cardiovascular function of patients taking bromocriptine for therapeutic and diagnostic purpose should be monitored carefully.

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