Diaschisis with cerebral infarction. R Slater, M Reivich, H Goldberg, R Banka and J Greenberg Stroke. 1977;8:684-690 doi: 10.1161/01.STR.8.6.684 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1977 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/8/6/684
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/ at UNIVERSITY OF NEWCASTLE on March 17, 2014
684
Diaschisis with Cerebral Infarction ROBERT SLATER, M.D.,
MARTIN REIVICH, M.D.,
REENA BANKA, M.D.,
HERBERT GOLDBERG,
M.D.,
AND JOEL GREENBERG, P H . D .
SUMMARY Fifteen patients admitted to Philadelphia General Hospital with acute strokes had repeated measurements of cerebral blood flow measured by the "'Xenon inhalation method. A progressive decline in cerebral blood flow in both hemispheres was observed during the first week after infarction in twelve of these patients. This decline could be partially explained by loss of autoregulation, but could not be correlated with level of consciousness,
clinical status or Pco 2 . This progressive decline in flow in the nonischemic hemisphere indicates a process more complex than a simple destruction of axonal afferants to neurons as implied by the term diaschisis. The flow changes in the non-ischemic hemisphere are likely caused by a combination of the immediate effects of decreased neuronal stimulation modified by loss of autoregulation, release of vasoactive substances, cerebral edema, and other factors.
CHANGES IN CEREBRAL blood flow on the side opposite an infarction had been demonstrated repeatedly since first described by Kempinsky, et al., in 1961* and HottRasmussen and Skinhoj in 1964.2 Several theories were proposed to explain this bilateral reduction in blood flow postulating neurogenic, vasogenic and chemical mechanisms.1"8 Most past observations of this phenomenon, called diaschisis, had been limited, since the method used to measure cerebral blood flow was invasive, requiring either an injection into the carotid artery or jugular vein catheterization, thereby exposing the patient to risk and prohibiting repeated measurements. Patients therefore were usually only studied once or twice and interpretations were made by comparing blood flow in the two hemispheres in separate patients at variable intervals following a stroke. These previous studies left unanswered the question as to whether these flow reductions preceded the onset of a stroke, or were the consequence of it. Since development of the Xenon inhalation method for determining regional cerebral blood flow, serial studies have been possible without exposing patients to risk.9-l0> " This study, using this technique, has for the first time examined in detail the time course of flow changes in the "non-ischemic" hemisphere in the immediate post stroke period. These data showed a previously unrecognized progressive decline in blood flow in the "nonischemic" hemisphere over a period of five to ten days. This decline in flow did not correlate with clinical status but was related in part to loss of autoregulation. These findings help in the development of hypotheses to explain diaschisis.
showed increasing neurologic deficit for 1 week prior to being admitted to the study and the other patient had progressive symptoms over a 3-month period. This last patient had a focal stenosis of the rolandic artery, demonstrated at angiography, as the cause of his neurologic syndrome. Angiography was not routinely performed on these patients; however, all patients had lumbar punctures which showed normal pressure and no signs of hemorrhage. Cerebral blood flow was determined using a Xenon inhalation method described by Obrist.9 Patients breathed a mixture of air containing Xenon in concentration of 5 to 7 mCi/L for 1 minute. Cephalic clearance curves were monitored with a series of 4 to 5 scintillation detectors placed over the affected hemisphere and 2 to 3 over the opposite hemisphere. Harshaw probes within collimators 11 mm in diameter and 2.5 cm long were used. An automated end-tidal sampler measured end expiratory Xenon concentration following each breath. This measurement was used as an estimate of the arterial Xenon concentration. The data from each probe and the end-tidal detector was processed on a PDP 10 computer using programs designed by Obrist to perform a 2 compartmental analysis. 9 ' 10 The data were further analyzed by the method described by Risberg,12 which takes the 2 compartmental solution and calculates an initial slope index (ISIR) based upon the slope of the reconstructed curve during the second to third minute interval of desaturation.* A coefficient of variation of 7.5% was determined for ISIR in our laboratory for variation between sequential studies in both normal volunteers and patients with cerebrovascular disease.13 The ISIR determination as described by Risberg12 was chosen for analysis rather than the fast compartment flow because of marked variations in fast flow rates that were accompanied by equally marked opposite changes in the weight of this compartment in repeated studies. These changes were felt to be an artifact of the method of analysis and not a reflection of true alterations in flow. ISIR determinations appeared to be more stabile than fast flow in our experience as well as that of Risberg.12 Patients had flow studies repeated 2 to 6 times, with 2 patients having only 2 flows. The period of observation ranged from a minimum of 7 to a maximum of 90 days. End-tidal CO 2 was measured with a infrared CO 2 analyzer
Methods Studies were performed on 15 patients admitted to Philadelphia General Hospital with the diagnosis of acute stroke. Informed consent was obtained in each case. The ages of patients varied from 47 to 85 and averaged 66 years for the entire group. All patients, except I, were black. There were 6 women and 9 men. Seven patients were studied within 48 hours of the onset of their neurologic deficit and an additional 4 patients within 72 hours. One patient was studied 3 days and one 4 days following onset. Two patients were seen over 4 days after the onset of symptoms. One
From the Cerebrovascular Research Center, Department of Neurology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. Supported by USPHS Program Project Grant No. 10939-05.
•Data from Patient 415 was not used for analysis and does not appear in the graphs because failure of the end-tidal sampler prohibited determination of ISIR. The fast compartmental flow estimates from cephalic clearance curves, not corrected by recirculation, are presented in table 1.
Downloaded from http://stroke.ahajournals.org/ at UNIVERSITY OF NEWCASTLE on March 17, 2014
TABLE 1 Data on Fifteen Patients I.D. number Age/Sex
Clinical
Angio
338
73/M
Left hemiparesis One year ago right hemiparesis
346
46/F
20% stenosis left Right hemiparesis carotid artery Right hand weakness demonstrated 5 5 months prior months prior
352
75/F
Right hemiparesis Aphasia
399
70
402
85
404
51/M
Stenosis left Left hemiplegia but ACA artery bilateral 'hemiplegia' initially Left hemiparesis and inattention LMCA BR Aphasia Occlusion
415
60/F
Left hemiparesis Previous stroke same side, 1971
416
65/F
Left hemiparesis
417
63/M
Right hemiparesis Somnolence
425
67/M
Dementia Left hemiparesis and fieldcut Previous stroke, 1972, left arm
426
65/M
Progressive left hemiparesis for 3 months
Focal stenosis rolandic artery
428
54/M
One week progressive left hemiparesis
RMCA branch occlusion plaque in carotid in neck
353
67/F
354
73/M
370
75/M
Days post stroke
Flow ISIR
BP mean
Clinical score
Level of consciousness
0 2 5 10 33 1 11
24 19 18 21 19
193 141 125 115 138
81 42 96 106 15
20 2 20 20 1
47 37
107 113
135 140
20 20
1 2 10 4 7 11 2 7 2 5 7 13
165 165 104 113 94 110 106 106 110 101 92 92
145 155 150 39 53 41 201 201
20 20 20 20 20 20 20 20 20 20 20 20
128 134
195 —
Lenticulostriate Disease
3 4
31 34 18 40 34 47 37 26 53 41 41 57 29* 47*
20 — (records insufficient) 10 22* 11 142 131 •fast
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/8/6/684
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/ at UNIVERSITY OF NEWCASTLE on March 17, 2014
684
Diaschisis with Cerebral Infarction ROBERT SLATER, M.D.,
MARTIN REIVICH, M.D.,
REENA BANKA, M.D.,
HERBERT GOLDBERG,
M.D.,
AND JOEL GREENBERG, P H . D .
SUMMARY Fifteen patients admitted to Philadelphia General Hospital with acute strokes had repeated measurements of cerebral blood flow measured by the "'Xenon inhalation method. A progressive decline in cerebral blood flow in both hemispheres was observed during the first week after infarction in twelve of these patients. This decline could be partially explained by loss of autoregulation, but could not be correlated with level of consciousness,
clinical status or Pco 2 . This progressive decline in flow in the nonischemic hemisphere indicates a process more complex than a simple destruction of axonal afferants to neurons as implied by the term diaschisis. The flow changes in the non-ischemic hemisphere are likely caused by a combination of the immediate effects of decreased neuronal stimulation modified by loss of autoregulation, release of vasoactive substances, cerebral edema, and other factors.
CHANGES IN CEREBRAL blood flow on the side opposite an infarction had been demonstrated repeatedly since first described by Kempinsky, et al., in 1961* and HottRasmussen and Skinhoj in 1964.2 Several theories were proposed to explain this bilateral reduction in blood flow postulating neurogenic, vasogenic and chemical mechanisms.1"8 Most past observations of this phenomenon, called diaschisis, had been limited, since the method used to measure cerebral blood flow was invasive, requiring either an injection into the carotid artery or jugular vein catheterization, thereby exposing the patient to risk and prohibiting repeated measurements. Patients therefore were usually only studied once or twice and interpretations were made by comparing blood flow in the two hemispheres in separate patients at variable intervals following a stroke. These previous studies left unanswered the question as to whether these flow reductions preceded the onset of a stroke, or were the consequence of it. Since development of the Xenon inhalation method for determining regional cerebral blood flow, serial studies have been possible without exposing patients to risk.9-l0> " This study, using this technique, has for the first time examined in detail the time course of flow changes in the "non-ischemic" hemisphere in the immediate post stroke period. These data showed a previously unrecognized progressive decline in blood flow in the "nonischemic" hemisphere over a period of five to ten days. This decline in flow did not correlate with clinical status but was related in part to loss of autoregulation. These findings help in the development of hypotheses to explain diaschisis.
showed increasing neurologic deficit for 1 week prior to being admitted to the study and the other patient had progressive symptoms over a 3-month period. This last patient had a focal stenosis of the rolandic artery, demonstrated at angiography, as the cause of his neurologic syndrome. Angiography was not routinely performed on these patients; however, all patients had lumbar punctures which showed normal pressure and no signs of hemorrhage. Cerebral blood flow was determined using a Xenon inhalation method described by Obrist.9 Patients breathed a mixture of air containing Xenon in concentration of 5 to 7 mCi/L for 1 minute. Cephalic clearance curves were monitored with a series of 4 to 5 scintillation detectors placed over the affected hemisphere and 2 to 3 over the opposite hemisphere. Harshaw probes within collimators 11 mm in diameter and 2.5 cm long were used. An automated end-tidal sampler measured end expiratory Xenon concentration following each breath. This measurement was used as an estimate of the arterial Xenon concentration. The data from each probe and the end-tidal detector was processed on a PDP 10 computer using programs designed by Obrist to perform a 2 compartmental analysis. 9 ' 10 The data were further analyzed by the method described by Risberg,12 which takes the 2 compartmental solution and calculates an initial slope index (ISIR) based upon the slope of the reconstructed curve during the second to third minute interval of desaturation.* A coefficient of variation of 7.5% was determined for ISIR in our laboratory for variation between sequential studies in both normal volunteers and patients with cerebrovascular disease.13 The ISIR determination as described by Risberg12 was chosen for analysis rather than the fast compartment flow because of marked variations in fast flow rates that were accompanied by equally marked opposite changes in the weight of this compartment in repeated studies. These changes were felt to be an artifact of the method of analysis and not a reflection of true alterations in flow. ISIR determinations appeared to be more stabile than fast flow in our experience as well as that of Risberg.12 Patients had flow studies repeated 2 to 6 times, with 2 patients having only 2 flows. The period of observation ranged from a minimum of 7 to a maximum of 90 days. End-tidal CO 2 was measured with a infrared CO 2 analyzer
Methods Studies were performed on 15 patients admitted to Philadelphia General Hospital with the diagnosis of acute stroke. Informed consent was obtained in each case. The ages of patients varied from 47 to 85 and averaged 66 years for the entire group. All patients, except I, were black. There were 6 women and 9 men. Seven patients were studied within 48 hours of the onset of their neurologic deficit and an additional 4 patients within 72 hours. One patient was studied 3 days and one 4 days following onset. Two patients were seen over 4 days after the onset of symptoms. One
From the Cerebrovascular Research Center, Department of Neurology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. Supported by USPHS Program Project Grant No. 10939-05.
•Data from Patient 415 was not used for analysis and does not appear in the graphs because failure of the end-tidal sampler prohibited determination of ISIR. The fast compartmental flow estimates from cephalic clearance curves, not corrected by recirculation, are presented in table 1.
Downloaded from http://stroke.ahajournals.org/ at UNIVERSITY OF NEWCASTLE on March 17, 2014
TABLE 1 Data on Fifteen Patients I.D. number Age/Sex
Clinical
Angio
338
73/M
Left hemiparesis One year ago right hemiparesis
346
46/F
20% stenosis left Right hemiparesis carotid artery Right hand weakness demonstrated 5 5 months prior months prior
352
75/F
Right hemiparesis Aphasia
399
70
402
85
404
51/M
Stenosis left Left hemiplegia but ACA artery bilateral 'hemiplegia' initially Left hemiparesis and inattention LMCA BR Aphasia Occlusion
415
60/F
Left hemiparesis Previous stroke same side, 1971
416
65/F
Left hemiparesis
417
63/M
Right hemiparesis Somnolence
425
67/M
Dementia Left hemiparesis and fieldcut Previous stroke, 1972, left arm
426
65/M
Progressive left hemiparesis for 3 months
Focal stenosis rolandic artery
428
54/M
One week progressive left hemiparesis
RMCA branch occlusion plaque in carotid in neck
353
67/F
354
73/M
370
75/M
Days post stroke
Flow ISIR
BP mean
Clinical score
Level of consciousness
0 2 5 10 33 1 11
24 19 18 21 19
193 141 125 115 138
81 42 96 106 15
20 2 20 20 1
47 37
107 113
135 140
20 20
1 2 10 4 7 11 2 7 2 5 7 13
165 165 104 113 94 110 106 106 110 101 92 92
145 155 150 39 53 41 201 201
20 20 20 20 20 20 20 20 20 20 20 20
128 134
195 —
Lenticulostriate Disease
3 4
31 34 18 40 34 47 37 26 53 41 41 57 29* 47*
20 — (records insufficient) 10 22* 11 142 131 •fast
