Letters to the Editor
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M
c/Boi, . 0036 c :0044 r c.i.D. FIGURE 1. Saggital Tl -weighted magnetic resonance imaging scan (TR 500 msec, TE 40 msec) performed 24 hours after admission. A hyperintense tubular signal enhanced with gadolinium at the level of intracranial left vertebral artery is noted
(arrow). extremities. Past medical history and review of the systems was unremarkable except for a 1-2 pack-per-day smoking history for 20 years. Upon examination, the patient appeared ill. Blood pressure, pulse, respirations, and temperature were normal. He was fully oriented, without neck rigidity or meningeal signs. Fundi appeared normal. A left Horner syndrome and bilateral rotatory nystagmus in all directions were observed. Remaining cranial nerve functions were intact. A moderate right hemiparesis, right hyperreflexia, right extensor plantar response, and dissociated hemihypesthesia was observed. In the left extremities, moderate dysmetria, dysdiadochokinesis, and hypotonia were seen. Blood chemistry, hematologic, coagulation, and immunologic studies, as well as an electrocardiogram and an echocardiogram were normal. Anticardiolipin antibodies, syphilis, and human immunodeficiency virus (HIV) tests were negative. Cerebrospinal fluid was clear, with an opening pressure of 210 mm H2O. There were 8 WBC/mm3 (all mononuclear), glucose was 79 mg/dl, and protein 55 mg/dl (immunoglobulin G 12.1 and oligoclonal bands 14.9%). Cerebrospinal fluid culture and mycobacterial, fungus, viral, syphilis, brucella and HIV tests were negative. A computed tomography (CT) scan without and with contrast material reveal no abnormalities. An enhanced CT of the head was normal. Cranial MRI scan was performed 20 hours after the onset of the acute symptoms using a 0.5-T superconducting magnet unit with and without gadolinium. On plain MRI and on Tl-weighted images, a small signal hyperintensity at the level of the intracranial left VA was observed. This signal was enhanced on the postcontrast MRI scan, suggesting slow flow through the artery (Figure 1). Digital subtraction angiography was performed 36 hours after the onset of acute symptoms and showed a nondominant (hypoplastic) left VA, with an irregularly narrowed segment at the intracranial portion extending to the beginning of the basilar artery. The patient was treated with heparin and developed no further deficits. One week later, a plain MRI scan was performed. Tl-weighted images disclosed a tubular hyperintense signal at the level of the intracranial left VA. No signal abnormalities were found on the brain stem, either on Tlor T2-weighted sequences. He was discharged on coumadin. Three months after admission, the patient was well and only minor
1607
neurological signs could be detected. A repeat cranial MRI examination with and without Gd-DPTA was normal. A digital subtraction angiography was performed and showed resolution of the previous angiographic abnormalities. Magnetic resonance imaging is more sensitive than CT for detection of strokes, particularly in the vertebrobasilar system.3"5 Only a few reports of MRI imaging of vertebrobasilar artery occlusions have been made.1-4 In two of them,2-3 nonenhanced MRI was performed in the acute stage, within 24 hours of the ictal event, and showed absence of a flow void in the affected vessel on axial T2-weighted images and areas of iso- or mild hyperintensity signal relative to brain parenchyma on Tl-weighted or proton density images. None of them used a contrast-enhanced MRI scan. In our patient, gadolinium demonstrated contrast enhancement of the abnormal signal over the left VA, suggesting slow flow within this artery, and thus aided the diagnosis of dissection. Although changes in signal intensity within the vessel may be attributed to thrombus formation, altered (i.e., slow) flow dynamics is the more likely possibility in this case because of the hyperintense signal on Tl-weighted imaging enhanced with gadolinium. This phenomenon occurs more frequently in vessels with slow flow, usually in the venous system, probably because of the enhancement of the hydrogen nuclei within the slowly flowing vertebral artery.67 This case supports the usefulness of enhanced MRI as a noninvasive method for early diagnosis of patients with suspected acute intracranial vertebral artery dissection, a situation in which plain MRI may not show conclusive abnormalities. S. Arroyo, MD
A. Munoz, MD A. Vazquez, MD A. Hernandez, MD E. Varela de Seijas, MD Servicio de Neurologia y Servicio de Radiologia Hospital Cllnico Universitario de San Carlos Madrid, Spain
References 1. Chen J, Smith R, Keller A, Kucharczyk W: Spontaneous dissection of the vertebral artery: MR findings. J Comput Assist Tomogr 1989;13:326-329 2. Uchino A, Ohnazi N, Ohno M: MR imaging of intracranial vertebral artery occlusion. Neuroradiology 1989;31:403-407 3. Knepper L, Biller J, Adams HP, Yuh W, Ryals T, Godersky J: MR imaging of basilar artery occlusion. J Comput Assist Tomogr 1990; 14:32-35 4. Schwainghofer BW, Klein MV, Lyden PD, Hesselink JR: MR imaging of vertebrobasilar vascular disease. / Comput Assist Tomogr 1990;14:895-904 5. Han JS, Bonstelle CT, Kaufman B, Benson JE, AJfid RJ, Clampitt M, Van Dyke C, Huss R: Magnetic resonance imaging in the evaluation of the brainstem. Neuroradiology 1984;150: 705-712 6. Harris TM, Smith RR, Koch KJ: Gadolinium-DTPA enhanced MR imaging of septic dural sinus thrombosis. / Comput Assist Tomogr 1989;13:682-684 7. Bradley WG, Waluch V: Blood flow: Magnetic resonance imaging. Radiology 1985;154:443-450
Platelet Aggregation in Patients With Parkinson's Disease To the Editor: In their article, Struck et al1 commented on the lower incidence of ischemic stroke in patients with Parkinson's disease as compared with controls and attributed it to decreased tobacco intake, decrease in generalized atherosclerosis, and dopamine deficiency.
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
1608
Stroke
Vol 22, No 12 December 1991
We would like to suggest another factor, namely, that of decreased platelet aggregation, which may contribute to their observation. We studied platelet aggregation in 25 newly diagnosed patients with Parkinson's disease and 25 age- and sex-matched controls. None were diabetic, hypertensive, smokers, or on any treatment. Citrated blood was collected by venipuncture and centrifuged at 20Qg for 10 minutes, and the supernatant platelet-rich plasma was obtained. Platelet counts were measured using a platelet counter (Contraves, Switzerland). No patient had a low platelet count. Platelet aggregation was measured by the Born method 2 using a four-channel aggrerecorder (Daiichi-PA 3220, Kyoto, Japan). Adenosine diphosphate (2.5 ^.M/ml), collagen (2.5 /iM/ml), and epinephrine (3 /xMJ ml) were used as inducers. The stock solution was diluted with 0.85% saline. The aggregation was studied at fixed intervals of 5 minutes for collagen and 10 minutes each for adenosine diphosphate and epinephrine. The absorbance was measured as % aggregation. The results were analyzed statistically using Student's 1 test. Platelet aggregation induced by adenosine diphosphate and epinephrine was significantly decreased (32% and 60%, respectively) in Parkinson's disease cases, while collagen-induced aggregation was unchanged. To the best of our knowledge, these findings have not been recorded elsewhere. We hypothesize that decreased platelet aggregation in Parkinson's patients may be a significant contributory factor for the reduced incidence of ischemic stroke. P. Sharma, MD D. Nag, MD Department of Neurology V. Atam, MD Department of Medicine KG's Medical College
20 -
0
2
4
6
8
10
(0)
(D
(2)
(3)
(4)
(5)
% of glycerol + (X of fructose) during primary exposure
FIGURE 1.
Graph showing percentage of lysed red blood
cells from two subjects after resuspension in normal saline following primary exposure in varying concentrations of glycerol in saline only ( ) and glycerol plus fructose in saline (—). Red blood cells from three other subjects yielded similar findings. Primary exposure in the presence of fructose mitigates against saline resuspension hemolysis. Thus, regardless of the possible benefits before embarking on further studies to evaluate the value of more rapid glycerol infusions in managing acute stroke, it is important to address this anticipated and alarming degree of intravascular hemolysis. C.R. Kumana, FRCP Y.L. Yu, FRCP CM. Chang, MRCP M. Kou, HV Department of Medicine
P.K. Seth, PhD V.K. Khanna, PhD ITRC Lucknow, India
D. Wei, FRCPA Department of Pathology University of Hong Kong Queen Mary Hospital Hong Kong
References 1. Struck LK, Rodnitzky RL, Dobson JK: Stroke and its modification in Parkinson's disease. Stroke 1990;21:1395-1399 2. Born GVR: Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-929
References Glycerol Infusion Rates Warrant Caution To the Editor: We wish to comment on the assertion by Nau and colleagues1 that very high intravenous infusion rates of glycerol (>500 ml of 10% solutions given over 4 hours) are required to exert any significant osmotic effect on cerebral edema associated with acute stroke. The most important side effect of such dosages is intravascular hemolysis.2 We conducted a critical evaluation of the latter adverse effect and its possible mechanism in the course of a large, randomized, double-blind clinical trial of intravenous glycerol treatment in patients with acute stroke. This in vivo and in vitro study 3 suggested that hemolysis resulted from glycerol at the site of infusion rapidly entering red cells and from destruction of the latter in more central veins due to osmotically induced swelling beyond a critical limit. Moreover, so long as the infusion rate was not allowed to exceed 125 ml/hr, even temporarily, clinically significant hemolysis was avoidable. Japanese investigators and clinicians have reported that use of glycerol solutions containing small amounts of fructose can overcome this problem associated with more rapid infusion rates.4-5 Moreover, in vitro studies in our institution (Figure 1) are also consistent with such a possibility.
1. Nau R, Prin F, Prange HW: Serum concentrations of glycerol with continuous or discontinuous intravenous administration. Stroke 1991;22:693-694 2. Frank MSB, Nahata MC, Hilty MD: Glycerol: A review of its pharmacology, pharmacokinetics, adverse reactions and clinical use. Pharmacotherapy 1981;l:147-160 3. Kumana CR, Chan GT, Yu YL, Lauder IJ, Chan TKP, Kou M: Investigation of intravascular haemolysis during treatment of acute stroke with intravenous glycerol. BrJ Clin Pharmacol 1990; 29:347-353 4. Arakawa M, Kondo T, Mitsui H, Suzuki S, Shiba M: Glycerolinduced haemolysis of mammalian erythrocytes and inhibition of the lysis by fructose. Folia Pharmacol Japon 1977;73:541-547 5. Tsubokawa T, Katayama Y, Ishii S: Fructose-added glycerol (GlyceolR) for therapy of elevated intracranial pressure: Analysis of the side effects of long-term administration in a multiinstitutional trial. Neurol Res 1989;ll:249-252
Multiple Aneurysms Caused by Hemodynamic Stress and Hypertension To the Editor: Increased hemodynamic stress is possibly a factor in the development of cerebral aneurysms. The clinical basis for this possibility includes the development of aneurysms in feeders of arteriovenous
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
Platelet aggregation in patients with Parkinson's disease. P Sharma, D Nag, V Atam, P K Seth and V K Khanna Stroke. 1991;22:1607-1608 doi: 10.1161/01.STR.22.12.1607 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1991 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://stroke.ahajournals.org/content/22/12/1607.citation
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Stroke is online at: http://stroke.ahajournals.org//subscriptions/
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
1» /
M
c/Boi, . 0036 c :0044 r c.i.D. FIGURE 1. Saggital Tl -weighted magnetic resonance imaging scan (TR 500 msec, TE 40 msec) performed 24 hours after admission. A hyperintense tubular signal enhanced with gadolinium at the level of intracranial left vertebral artery is noted
(arrow). extremities. Past medical history and review of the systems was unremarkable except for a 1-2 pack-per-day smoking history for 20 years. Upon examination, the patient appeared ill. Blood pressure, pulse, respirations, and temperature were normal. He was fully oriented, without neck rigidity or meningeal signs. Fundi appeared normal. A left Horner syndrome and bilateral rotatory nystagmus in all directions were observed. Remaining cranial nerve functions were intact. A moderate right hemiparesis, right hyperreflexia, right extensor plantar response, and dissociated hemihypesthesia was observed. In the left extremities, moderate dysmetria, dysdiadochokinesis, and hypotonia were seen. Blood chemistry, hematologic, coagulation, and immunologic studies, as well as an electrocardiogram and an echocardiogram were normal. Anticardiolipin antibodies, syphilis, and human immunodeficiency virus (HIV) tests were negative. Cerebrospinal fluid was clear, with an opening pressure of 210 mm H2O. There were 8 WBC/mm3 (all mononuclear), glucose was 79 mg/dl, and protein 55 mg/dl (immunoglobulin G 12.1 and oligoclonal bands 14.9%). Cerebrospinal fluid culture and mycobacterial, fungus, viral, syphilis, brucella and HIV tests were negative. A computed tomography (CT) scan without and with contrast material reveal no abnormalities. An enhanced CT of the head was normal. Cranial MRI scan was performed 20 hours after the onset of the acute symptoms using a 0.5-T superconducting magnet unit with and without gadolinium. On plain MRI and on Tl-weighted images, a small signal hyperintensity at the level of the intracranial left VA was observed. This signal was enhanced on the postcontrast MRI scan, suggesting slow flow through the artery (Figure 1). Digital subtraction angiography was performed 36 hours after the onset of acute symptoms and showed a nondominant (hypoplastic) left VA, with an irregularly narrowed segment at the intracranial portion extending to the beginning of the basilar artery. The patient was treated with heparin and developed no further deficits. One week later, a plain MRI scan was performed. Tl-weighted images disclosed a tubular hyperintense signal at the level of the intracranial left VA. No signal abnormalities were found on the brain stem, either on Tlor T2-weighted sequences. He was discharged on coumadin. Three months after admission, the patient was well and only minor
1607
neurological signs could be detected. A repeat cranial MRI examination with and without Gd-DPTA was normal. A digital subtraction angiography was performed and showed resolution of the previous angiographic abnormalities. Magnetic resonance imaging is more sensitive than CT for detection of strokes, particularly in the vertebrobasilar system.3"5 Only a few reports of MRI imaging of vertebrobasilar artery occlusions have been made.1-4 In two of them,2-3 nonenhanced MRI was performed in the acute stage, within 24 hours of the ictal event, and showed absence of a flow void in the affected vessel on axial T2-weighted images and areas of iso- or mild hyperintensity signal relative to brain parenchyma on Tl-weighted or proton density images. None of them used a contrast-enhanced MRI scan. In our patient, gadolinium demonstrated contrast enhancement of the abnormal signal over the left VA, suggesting slow flow within this artery, and thus aided the diagnosis of dissection. Although changes in signal intensity within the vessel may be attributed to thrombus formation, altered (i.e., slow) flow dynamics is the more likely possibility in this case because of the hyperintense signal on Tl-weighted imaging enhanced with gadolinium. This phenomenon occurs more frequently in vessels with slow flow, usually in the venous system, probably because of the enhancement of the hydrogen nuclei within the slowly flowing vertebral artery.67 This case supports the usefulness of enhanced MRI as a noninvasive method for early diagnosis of patients with suspected acute intracranial vertebral artery dissection, a situation in which plain MRI may not show conclusive abnormalities. S. Arroyo, MD
A. Munoz, MD A. Vazquez, MD A. Hernandez, MD E. Varela de Seijas, MD Servicio de Neurologia y Servicio de Radiologia Hospital Cllnico Universitario de San Carlos Madrid, Spain
References 1. Chen J, Smith R, Keller A, Kucharczyk W: Spontaneous dissection of the vertebral artery: MR findings. J Comput Assist Tomogr 1989;13:326-329 2. Uchino A, Ohnazi N, Ohno M: MR imaging of intracranial vertebral artery occlusion. Neuroradiology 1989;31:403-407 3. Knepper L, Biller J, Adams HP, Yuh W, Ryals T, Godersky J: MR imaging of basilar artery occlusion. J Comput Assist Tomogr 1990; 14:32-35 4. Schwainghofer BW, Klein MV, Lyden PD, Hesselink JR: MR imaging of vertebrobasilar vascular disease. / Comput Assist Tomogr 1990;14:895-904 5. Han JS, Bonstelle CT, Kaufman B, Benson JE, AJfid RJ, Clampitt M, Van Dyke C, Huss R: Magnetic resonance imaging in the evaluation of the brainstem. Neuroradiology 1984;150: 705-712 6. Harris TM, Smith RR, Koch KJ: Gadolinium-DTPA enhanced MR imaging of septic dural sinus thrombosis. / Comput Assist Tomogr 1989;13:682-684 7. Bradley WG, Waluch V: Blood flow: Magnetic resonance imaging. Radiology 1985;154:443-450
Platelet Aggregation in Patients With Parkinson's Disease To the Editor: In their article, Struck et al1 commented on the lower incidence of ischemic stroke in patients with Parkinson's disease as compared with controls and attributed it to decreased tobacco intake, decrease in generalized atherosclerosis, and dopamine deficiency.
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
1608
Stroke
Vol 22, No 12 December 1991
We would like to suggest another factor, namely, that of decreased platelet aggregation, which may contribute to their observation. We studied platelet aggregation in 25 newly diagnosed patients with Parkinson's disease and 25 age- and sex-matched controls. None were diabetic, hypertensive, smokers, or on any treatment. Citrated blood was collected by venipuncture and centrifuged at 20Qg for 10 minutes, and the supernatant platelet-rich plasma was obtained. Platelet counts were measured using a platelet counter (Contraves, Switzerland). No patient had a low platelet count. Platelet aggregation was measured by the Born method 2 using a four-channel aggrerecorder (Daiichi-PA 3220, Kyoto, Japan). Adenosine diphosphate (2.5 ^.M/ml), collagen (2.5 /iM/ml), and epinephrine (3 /xMJ ml) were used as inducers. The stock solution was diluted with 0.85% saline. The aggregation was studied at fixed intervals of 5 minutes for collagen and 10 minutes each for adenosine diphosphate and epinephrine. The absorbance was measured as % aggregation. The results were analyzed statistically using Student's 1 test. Platelet aggregation induced by adenosine diphosphate and epinephrine was significantly decreased (32% and 60%, respectively) in Parkinson's disease cases, while collagen-induced aggregation was unchanged. To the best of our knowledge, these findings have not been recorded elsewhere. We hypothesize that decreased platelet aggregation in Parkinson's patients may be a significant contributory factor for the reduced incidence of ischemic stroke. P. Sharma, MD D. Nag, MD Department of Neurology V. Atam, MD Department of Medicine KG's Medical College
20 -
0
2
4
6
8
10
(0)
(D
(2)
(3)
(4)
(5)
% of glycerol + (X of fructose) during primary exposure
FIGURE 1.
Graph showing percentage of lysed red blood
cells from two subjects after resuspension in normal saline following primary exposure in varying concentrations of glycerol in saline only ( ) and glycerol plus fructose in saline (—). Red blood cells from three other subjects yielded similar findings. Primary exposure in the presence of fructose mitigates against saline resuspension hemolysis. Thus, regardless of the possible benefits before embarking on further studies to evaluate the value of more rapid glycerol infusions in managing acute stroke, it is important to address this anticipated and alarming degree of intravascular hemolysis. C.R. Kumana, FRCP Y.L. Yu, FRCP CM. Chang, MRCP M. Kou, HV Department of Medicine
P.K. Seth, PhD V.K. Khanna, PhD ITRC Lucknow, India
D. Wei, FRCPA Department of Pathology University of Hong Kong Queen Mary Hospital Hong Kong
References 1. Struck LK, Rodnitzky RL, Dobson JK: Stroke and its modification in Parkinson's disease. Stroke 1990;21:1395-1399 2. Born GVR: Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-929
References Glycerol Infusion Rates Warrant Caution To the Editor: We wish to comment on the assertion by Nau and colleagues1 that very high intravenous infusion rates of glycerol (>500 ml of 10% solutions given over 4 hours) are required to exert any significant osmotic effect on cerebral edema associated with acute stroke. The most important side effect of such dosages is intravascular hemolysis.2 We conducted a critical evaluation of the latter adverse effect and its possible mechanism in the course of a large, randomized, double-blind clinical trial of intravenous glycerol treatment in patients with acute stroke. This in vivo and in vitro study 3 suggested that hemolysis resulted from glycerol at the site of infusion rapidly entering red cells and from destruction of the latter in more central veins due to osmotically induced swelling beyond a critical limit. Moreover, so long as the infusion rate was not allowed to exceed 125 ml/hr, even temporarily, clinically significant hemolysis was avoidable. Japanese investigators and clinicians have reported that use of glycerol solutions containing small amounts of fructose can overcome this problem associated with more rapid infusion rates.4-5 Moreover, in vitro studies in our institution (Figure 1) are also consistent with such a possibility.
1. Nau R, Prin F, Prange HW: Serum concentrations of glycerol with continuous or discontinuous intravenous administration. Stroke 1991;22:693-694 2. Frank MSB, Nahata MC, Hilty MD: Glycerol: A review of its pharmacology, pharmacokinetics, adverse reactions and clinical use. Pharmacotherapy 1981;l:147-160 3. Kumana CR, Chan GT, Yu YL, Lauder IJ, Chan TKP, Kou M: Investigation of intravascular haemolysis during treatment of acute stroke with intravenous glycerol. BrJ Clin Pharmacol 1990; 29:347-353 4. Arakawa M, Kondo T, Mitsui H, Suzuki S, Shiba M: Glycerolinduced haemolysis of mammalian erythrocytes and inhibition of the lysis by fructose. Folia Pharmacol Japon 1977;73:541-547 5. Tsubokawa T, Katayama Y, Ishii S: Fructose-added glycerol (GlyceolR) for therapy of elevated intracranial pressure: Analysis of the side effects of long-term administration in a multiinstitutional trial. Neurol Res 1989;ll:249-252
Multiple Aneurysms Caused by Hemodynamic Stress and Hypertension To the Editor: Increased hemodynamic stress is possibly a factor in the development of cerebral aneurysms. The clinical basis for this possibility includes the development of aneurysms in feeders of arteriovenous
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
Platelet aggregation in patients with Parkinson's disease. P Sharma, D Nag, V Atam, P K Seth and V K Khanna Stroke. 1991;22:1607-1608 doi: 10.1161/01.STR.22.12.1607 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1991 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://stroke.ahajournals.org/content/22/12/1607.citation
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Stroke is online at: http://stroke.ahajournals.org//subscriptions/
Downloaded from http://stroke.ahajournals.org/ by guest on June 29, 2016
