Journal of the Neurological Sciences, 1979, 43 : 301-311 © Elsevier/North-Holland Biomedical Press
301
NONINVAS1VE M E A S U R E M E N T OF CEREBRAL VASOPASM IN PATIENTS W I T H S U B A R A C H N O I D H E M O R R H A G E
MASAHIRO YAMAMOTO, JOHN MEYER, HIROAKI NARITOMI, FUMIHIKO SAKAI, FUMIE YAMAGUCHI and TERRY SHAW Department o f Neurology, Baylor College of Medicine, the Cerebral Blood Flow Laboratory, Veterans Administration Hospital, and the Baylor Center for Cerebrovascular Research, Houston, TX (U.S.A.)
(Received 26 March, 1979) (Accepted 9 April, 1979)
SUMMARY Regional cerebral blood flow (rCBF) was measured as fast flow clearance (F1) and the initial slope index (ISI2) after inhalation of 133Xe in 30 patients with subarachnoid hemorrhage (SAH). Vasomotor responsiveness to reduction in end-tidal PECO2 was examined in those patients who could carry out this procedure satisfactorily as a test for the presence or absence of vasospasm. F1 and ISb. were significantly reduced in patients with recent SAH compared to 35 age-matched normal volunteers. The degree of reduction of F1 and ISI2 correlated directly with severity of the neurological deficit graded according to the Hunt and Hess rating scale. Topographic reductions o f r C B F correlated with angiographically demonstrated vasospasm or intracerebral hematoma. The degree of impairment of cerebral vasomotor responsiveness to reduction of PECO2 by hyperventilation also correlated with the severity of vasospasm demonstrated angiographically in 16 patients. The reductions of rCBF values were maximal during the first week after SAH but returned gradually toward normal by the 5th week. Individual patients with SAH whose lowest F1 values were above 50 ml/100 g bram/min tolerated surgical intervention best. Non-invasive measurements of rCBF after SAH appear to be helpful in estimating the presence and time course ofvasospasm, in recognizing the development of normal pressure hydrocephalus, and in planning medical and surgical management.
INTRODUCTION For the past 25 years, clinical studies have consistently reported that the graded This work was supported by Grant NS-09287 of the U.S. Public Health Service. Address reprint requests and correspondence to Dr. John S. Meyer, Director Cerebrovascular Research, Veterans Administration Hospital, 2002 Holcombe, Houston, TX 77211, U.S.A.
302 neurological status of a patient at the time of surgical treatment of a ruptured intracranial aneurysm or arteriovenous malformation (AVM) is a reliable indicator of the mortality rate and quality of survival. Patients with impaired consciousness and severe neurological deficit have a grave prognosis and do not tolerate surgical intervention, while alert patients with little or no neurological deficit have better prognosis and are ideal candidates for surgical intervention (Hunt and Hess 1968). It seems possible that decreased cerebral perfusion, as a result of cerebral vasospasm, may be responsible for many of the neurological deficits and be an important factor influencing the natural history, prognosis and results of surgical treatments in patients with SAH. The role of vasospasm has been controversial and requires documentation by measurement of cerebral perfusion in a manner that will not endanger the patient. Regional cerebral blood flow (rCBF) measurements using the intracarotid injection method have been reported from several laboratories, including this one, to show that rCBF is reduced in patients with subarachnoid hemorrhage (SAH), particularly in those with impaired states of consciousness and severe neurological deficits whether they are caused by cerebral edema, intracerebral hematoma, hydrocephalus, or vasospasm (James 1968; Zingesser and Scheinberg 1968; Heilbrun et al. 1972; Mathew et al. 1974; Grubb et al. 1977). The present investigation was designed to test the hypothesis that measurements of rCBF after inhalation of 13ZXe may be utilized as a non-invasive indicator of cerebral perfusion in patients with subarachnoid hemorrhage and may prove useful in planning medical management and the optimal time for surgical intervention. The 133Xe inhalation metl~d for measuring rCBF was selected as the measure of cerebral perfusion because it carries minimum risk or discomfort and makes serial estimations o f r C B F possible. Measurements or rCBF might also prove useful for estimating the time course of major complications of SAH such as vasospasm, intracerebral hematoma and hydrocephalus by plotting the time interval after the SAH of single or multiple rCBF measurements, correlated with the neurological status at that time, and with the eventual clinical outcome. CASE MATERIAL Regional CBF measurements were made after 133Xe inhalation in a total of 30 patients with either recent SAH (N = 24, 4-41 days after onset), or remote SAH (N ----6. 3 months to 6 years after onset). Diagnosis was established by detailed history, neurological examination, cerebrospinal fluid examination, aortocranial 4-vessel angiography (carried out within 6 days of rCBF measurements) EEG and computerized tomography (CT scan). Sex, diagnosis, neurological status, interval between the onset of SAH and first rCBF measurement, presence or absence of vasospasm demonstrated by angiography, or intracerebral hematoma (shown by CT scan within 4 days of rCBF measurements) are listed in Table 1. Patients with recent S A H (N = 24)
The diagnosis of recent SAH was confirmed by lumbar puncture (showing con-
303 TABLE 1 CLINICAL SUMMARIES OF PATIENTS WITH SUBARACHNOID HEMORRHAGE CORRELATED WITH THE TIME OF INITIAL rCBF MEASUREMENT Case No.
Age/ Sex
Arteriographic diagnosis
Interval after onset* o f S A H a n d 1st rCBF
Arteriographically d e m o n s t r a t e d v a s o s p a s m within 6 days o f r C B F
Intracerebral hematoma by C T within 4 days o f rCBF
Neurological status • at time o f rCBF
4 days 5 days 5 days 6 days 7 days 8 days 8 days 9 days
+ + ---+ -r --
---+ --+ --
III IV I III II IV I II
10 days 10 days 10 days 11 days 12 days 14 days 14 days 16 days 17 days 18 days 19 days 23 days 21 days 25 days 31 days 41 days
---+ + + --5 + -+ + + + + +
----+ + --+ + + -+ ----
I I II II IV I III III Ili IV III II III III 1II III
-------
-------
seizures headaches headaches headaches headaches seizures
Recent subarachnoid hemorrhage 1 2 3 4 5 6 7 8 9
49 F 33 M 47 M 36 M 43 F 54 F 51 F 42 F 15 M
10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
47 F 65 F 43 F 50 F 47 F 47 M 35 M 49 M 19 M 64 M 42 M 46 F 64 M 52 F 65 M
RACA aneurysm LMCA aneurysm A. C o m . A. a n e u r y s m A V M L parietooccipital LACA aneurysm RMCA aneurysm RMCA aneurysm A. C o m . A. a n e u r y s m S A H etiology u n k n o w n (suspected a n e u r y s m ) RICA aneurysm LPCA aneurysm LMCA aneurysm RPCA anemysm LMCA aneurysm RACA aneurysm RPCA aneurysm A. C o m . A. a n e u r y s m A V M left h e m i s p h e r e LMCA aneurysm LMCA aneurysm RMCA aneurysm BA aneurysm RMCA aneurysm A. C o m . A. a n e u r y s m
Remote subarachnoid hemorrhage 25 26 27 28 29 30
41 M S A H etiology u n k n o w n (suspected a n e u r y s m ) 58 F L P C A a n e u r y s m 54 M L M C A a n e u r y s m 48 F R I C A a n e u r y s m 63 F R M C A a n e u r y s m 22 M L frontal A V M
3 months 4 months 1 year 2 years 2 years 6 years
a Neurological status after recent s u b a r a c h n o i d h e m o r r h a g e classified according to H u n t a n d Hess (1967). S A H = s u b a r a c h n o i d h e m o r r h a g e ; A V M = arteriovenous m a l f o r m a t i o n ; L = left; R = right; I C A , A C A , M C A , P C A , B A a n d A. C o m . A. = internal carotid, anterior cerebral, middle cerebral, posterior cerebral, basilar a n d anterior c o m m u n i c a t i n g arteries.
sistently bloody CSF in 3 separate tubes) in 24 patients plus the presence of subarachnoid blood shown by CT scan. As summarized
i n T a b l e 1, a r t e r i o g r a p h y
demonstrated
304 intracranial aneurysm in 21 cases, or AVM in 2 and in the remaining case the arteriograms were normal. In this case, where SAH was confirmed by CT scan a small aneurysm of the anterior circle of Willis was suspected, but was not demonstrated. Arteriography showed vasospasm in 15 patients and CT scan showed an intracerebral hematoma in 8. The aneurysms were located on the anterior circle of Willis and its main hemispheric branches in all cases except one, which was located on the distal basilar artery. The neurological status of the 24 patients at the time of the initial rCBF measurements was graded according to the classification of Hunt and Hess as follows: Grade I (N = 5), Grade II (N -- 5), Grade III (N = 10), Grade IV (N ~ 4). Grade I cases were asymptomatic with minimal headache and nuchal rigidity. Grade II cases had moderate to severe headache with nuchal rigidity but no neurological deficit other than cranial nerve palsy. Grade III cases showed drowsiness, confusion, or mild focal neurological deficit. Grade IV cases showed stupor, moderate to severe hemiparesis, early decerebrate rigidity in some cases and vegetative disturbances. Grade V cases showing deep coma, decerebrate rigidity and moribund appearance, were excluded since transportation to the laboratory was contraindicated. Eleven patients underwent surgery, 4 shortly before the rCBF measurements and 7 after the measurements. Of the 11 cases undergoing surgery, all except 3 had intracranial clipping or obliteration of the aneurysm. The 3 exceptions had progressive clamping of the carotid artery in the neck with monitoring of rCBF F1 values, which did not decrease below 50 ml/100 g brain/min. The remainder, (including all patients with AVMs or normal arteriogram) were treated conservatively without surgical intervention. The mean interval between the time of angiography and the first measurement of rCBF was 4 :~ 2 days. Patients with remote S A H (N -- 6)
Comparable measurements were made for purposes of comparison in 6 patients who had been hospitalized for SAH 3 months to 6 years prior to the rCBF measurement. As listed in Table 1, 4 had SAH from arteriographically demonstrated intracranial aneurysms and one from an AVM. In the remaining patient the etiology of SAH was never determined despite 4 vessel cerebral angiography. These patients were admitted to hospital to exclude recurrent SAH as a cause of seizures or severe headache. None had nuchal rigidity. Recurrent SAH was excluded by clinical examination, CT scan and lumbar puncture. Normative data
For comparison with these patients, rCBF was also measured in 35 age-matched normal volunteers (mean age 41.9 ± 12.2 years). The measurements were made under similar laboratory conditions. Cerebral vasomotor responsiveness to changes in PECO2 by hyperventilation was also tested (N ~ 17, mean age 37 ± 14 years) during a second rCBF measurement. METHOD Regional CBF was measured by our modification of the la3Xe inhalation method
305 originally described by Obrist et al. (1975), details of which has been reported in previous publications (Meyer et al. 1978a, b). In brief, a mixture of 133Xe gas mixed with room air (5-7 mCi/l) was inhaled via a close-fitting face mask for one minute. Clearance curves for 133Xe derived from 16 regions of the head and the end-tidal air were recorded throughout the ensuing 11 min by an on line PDP 11-5 computer programmed for this purpose. Collimated thallium-activated NaI crystal scintillation detectors were mounted by means of a helmet over both cerebral hemispheres and brain stem-cerebellum regions as a radial array. Each probe maintained firm pressure on the scalp perpendicular to the underlying skull and were placed over both frontal, temporal, parietal and occipital regions. The output discrimination for each detector was set to accept pulses between 67.5 and 94.5 KEV (gamma activity). The arterial concentration of 138Xe, as an input function, was estimated from the end-tidal air. This was used to deconvolute the head curves using Obrist's two-compartmental model for analysis. By multiplying K1 with 2 gray (Veall and Mallet 1965) the blood flow of fast component (F1 value) was estimated. ISI2 (introduced by Risberg et al. 1975) which obviates the use of 2 since this may be altered in ischemic brain was also calculated simultaneously by the computer. End-tidal partial pressure for carbon dioxide (PECO2), oxygen (PEO2) and 133Xe activity were all recorded from the face mask during the rCBF measurement together with the blood pressure, EEG and skin temperature on a polygraph. Cerebral vasomotor responsiveness to lowered PECO2 was tested during voluntary hyperventilation in 11 patients (mean age 45 -+- 14 years) that were able to cooperate. CO2 responsiveness was expressed as percentage change oflSI2 per mm Hg change in PECO2. Results of the hyperventilation tests in the SAH patients were compared with 17 aged-matched normal volunteers (mean age 37 ± 14 years) serving as controls. RESULTS
Mean hemispheric Fx and 1SI2 values in patients with SAH Table 2 displays the results of the initial mean hemispheric F~ and ISI2 measurements made at the time of admission to the study together with the corresponding mean TABLE 2 MEAN HEMISPHERIC F1 AND ISI2 VALUES COMPARED BETWEEN NORMAL VOLUNTEERS AND PATIENTS WITH RECENT AND REMOTE SUBARACHNOID HEMORRHAGE Values are mean ~ SD. Classification of subjects measured
No. of Age (yr) cases
Mean heMeanheMABP mispheric F1 mispheric (mm Hg) (ml/100 g 1SI2(× 100) brain/min)
PECO2 (mm Hg)
Normal volunteers N = 35 44.8 -t- •4.7 76.4 -4- 10.3 52.0 :k 9.4 92.4 ~ 5.5 37.5± 2.7 Patients with recent SAH (4-41 days) N -- 24 46.0 d_ 12.6 70.1 ~ 10.0a 42.6 ± 7.6 a 96.2 d- 10.4 35.8 zk 4.4 Patients with remote hemorrhage (3 months-6 years) N = 6 47.6 ± 14.7 83.2 i 9.2 49.5 zk 4.6 99.0 ± 14.1 36.0 ± 2.2 a Significantly decreased compared to normal volunteers and patients with remote SAH (P < 0.05, Student's t-test). MABP = mean arterial pressure; PECO2 = end-tidal COo..
306 Remote SAH Neurological Status
0 N=6
Recent SAH
Grade I&ll N=IO
Grade III N=IO
Grade IV N=4
100 --
90
°--
~= 80
~
-
70 -
~. 60
Ib 8o
-
-.q-P
301
NONINVAS1VE M E A S U R E M E N T OF CEREBRAL VASOPASM IN PATIENTS W I T H S U B A R A C H N O I D H E M O R R H A G E
MASAHIRO YAMAMOTO, JOHN MEYER, HIROAKI NARITOMI, FUMIHIKO SAKAI, FUMIE YAMAGUCHI and TERRY SHAW Department o f Neurology, Baylor College of Medicine, the Cerebral Blood Flow Laboratory, Veterans Administration Hospital, and the Baylor Center for Cerebrovascular Research, Houston, TX (U.S.A.)
(Received 26 March, 1979) (Accepted 9 April, 1979)
SUMMARY Regional cerebral blood flow (rCBF) was measured as fast flow clearance (F1) and the initial slope index (ISI2) after inhalation of 133Xe in 30 patients with subarachnoid hemorrhage (SAH). Vasomotor responsiveness to reduction in end-tidal PECO2 was examined in those patients who could carry out this procedure satisfactorily as a test for the presence or absence of vasospasm. F1 and ISb. were significantly reduced in patients with recent SAH compared to 35 age-matched normal volunteers. The degree of reduction of F1 and ISI2 correlated directly with severity of the neurological deficit graded according to the Hunt and Hess rating scale. Topographic reductions o f r C B F correlated with angiographically demonstrated vasospasm or intracerebral hematoma. The degree of impairment of cerebral vasomotor responsiveness to reduction of PECO2 by hyperventilation also correlated with the severity of vasospasm demonstrated angiographically in 16 patients. The reductions of rCBF values were maximal during the first week after SAH but returned gradually toward normal by the 5th week. Individual patients with SAH whose lowest F1 values were above 50 ml/100 g bram/min tolerated surgical intervention best. Non-invasive measurements of rCBF after SAH appear to be helpful in estimating the presence and time course ofvasospasm, in recognizing the development of normal pressure hydrocephalus, and in planning medical and surgical management.
INTRODUCTION For the past 25 years, clinical studies have consistently reported that the graded This work was supported by Grant NS-09287 of the U.S. Public Health Service. Address reprint requests and correspondence to Dr. John S. Meyer, Director Cerebrovascular Research, Veterans Administration Hospital, 2002 Holcombe, Houston, TX 77211, U.S.A.
302 neurological status of a patient at the time of surgical treatment of a ruptured intracranial aneurysm or arteriovenous malformation (AVM) is a reliable indicator of the mortality rate and quality of survival. Patients with impaired consciousness and severe neurological deficit have a grave prognosis and do not tolerate surgical intervention, while alert patients with little or no neurological deficit have better prognosis and are ideal candidates for surgical intervention (Hunt and Hess 1968). It seems possible that decreased cerebral perfusion, as a result of cerebral vasospasm, may be responsible for many of the neurological deficits and be an important factor influencing the natural history, prognosis and results of surgical treatments in patients with SAH. The role of vasospasm has been controversial and requires documentation by measurement of cerebral perfusion in a manner that will not endanger the patient. Regional cerebral blood flow (rCBF) measurements using the intracarotid injection method have been reported from several laboratories, including this one, to show that rCBF is reduced in patients with subarachnoid hemorrhage (SAH), particularly in those with impaired states of consciousness and severe neurological deficits whether they are caused by cerebral edema, intracerebral hematoma, hydrocephalus, or vasospasm (James 1968; Zingesser and Scheinberg 1968; Heilbrun et al. 1972; Mathew et al. 1974; Grubb et al. 1977). The present investigation was designed to test the hypothesis that measurements of rCBF after inhalation of 13ZXe may be utilized as a non-invasive indicator of cerebral perfusion in patients with subarachnoid hemorrhage and may prove useful in planning medical management and the optimal time for surgical intervention. The 133Xe inhalation metl~d for measuring rCBF was selected as the measure of cerebral perfusion because it carries minimum risk or discomfort and makes serial estimations o f r C B F possible. Measurements or rCBF might also prove useful for estimating the time course of major complications of SAH such as vasospasm, intracerebral hematoma and hydrocephalus by plotting the time interval after the SAH of single or multiple rCBF measurements, correlated with the neurological status at that time, and with the eventual clinical outcome. CASE MATERIAL Regional CBF measurements were made after 133Xe inhalation in a total of 30 patients with either recent SAH (N = 24, 4-41 days after onset), or remote SAH (N ----6. 3 months to 6 years after onset). Diagnosis was established by detailed history, neurological examination, cerebrospinal fluid examination, aortocranial 4-vessel angiography (carried out within 6 days of rCBF measurements) EEG and computerized tomography (CT scan). Sex, diagnosis, neurological status, interval between the onset of SAH and first rCBF measurement, presence or absence of vasospasm demonstrated by angiography, or intracerebral hematoma (shown by CT scan within 4 days of rCBF measurements) are listed in Table 1. Patients with recent S A H (N = 24)
The diagnosis of recent SAH was confirmed by lumbar puncture (showing con-
303 TABLE 1 CLINICAL SUMMARIES OF PATIENTS WITH SUBARACHNOID HEMORRHAGE CORRELATED WITH THE TIME OF INITIAL rCBF MEASUREMENT Case No.
Age/ Sex
Arteriographic diagnosis
Interval after onset* o f S A H a n d 1st rCBF
Arteriographically d e m o n s t r a t e d v a s o s p a s m within 6 days o f r C B F
Intracerebral hematoma by C T within 4 days o f rCBF
Neurological status • at time o f rCBF
4 days 5 days 5 days 6 days 7 days 8 days 8 days 9 days
+ + ---+ -r --
---+ --+ --
III IV I III II IV I II
10 days 10 days 10 days 11 days 12 days 14 days 14 days 16 days 17 days 18 days 19 days 23 days 21 days 25 days 31 days 41 days
---+ + + --5 + -+ + + + + +
----+ + --+ + + -+ ----
I I II II IV I III III Ili IV III II III III 1II III
-------
-------
seizures headaches headaches headaches headaches seizures
Recent subarachnoid hemorrhage 1 2 3 4 5 6 7 8 9
49 F 33 M 47 M 36 M 43 F 54 F 51 F 42 F 15 M
10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
47 F 65 F 43 F 50 F 47 F 47 M 35 M 49 M 19 M 64 M 42 M 46 F 64 M 52 F 65 M
RACA aneurysm LMCA aneurysm A. C o m . A. a n e u r y s m A V M L parietooccipital LACA aneurysm RMCA aneurysm RMCA aneurysm A. C o m . A. a n e u r y s m S A H etiology u n k n o w n (suspected a n e u r y s m ) RICA aneurysm LPCA aneurysm LMCA aneurysm RPCA anemysm LMCA aneurysm RACA aneurysm RPCA aneurysm A. C o m . A. a n e u r y s m A V M left h e m i s p h e r e LMCA aneurysm LMCA aneurysm RMCA aneurysm BA aneurysm RMCA aneurysm A. C o m . A. a n e u r y s m
Remote subarachnoid hemorrhage 25 26 27 28 29 30
41 M S A H etiology u n k n o w n (suspected a n e u r y s m ) 58 F L P C A a n e u r y s m 54 M L M C A a n e u r y s m 48 F R I C A a n e u r y s m 63 F R M C A a n e u r y s m 22 M L frontal A V M
3 months 4 months 1 year 2 years 2 years 6 years
a Neurological status after recent s u b a r a c h n o i d h e m o r r h a g e classified according to H u n t a n d Hess (1967). S A H = s u b a r a c h n o i d h e m o r r h a g e ; A V M = arteriovenous m a l f o r m a t i o n ; L = left; R = right; I C A , A C A , M C A , P C A , B A a n d A. C o m . A. = internal carotid, anterior cerebral, middle cerebral, posterior cerebral, basilar a n d anterior c o m m u n i c a t i n g arteries.
sistently bloody CSF in 3 separate tubes) in 24 patients plus the presence of subarachnoid blood shown by CT scan. As summarized
i n T a b l e 1, a r t e r i o g r a p h y
demonstrated
304 intracranial aneurysm in 21 cases, or AVM in 2 and in the remaining case the arteriograms were normal. In this case, where SAH was confirmed by CT scan a small aneurysm of the anterior circle of Willis was suspected, but was not demonstrated. Arteriography showed vasospasm in 15 patients and CT scan showed an intracerebral hematoma in 8. The aneurysms were located on the anterior circle of Willis and its main hemispheric branches in all cases except one, which was located on the distal basilar artery. The neurological status of the 24 patients at the time of the initial rCBF measurements was graded according to the classification of Hunt and Hess as follows: Grade I (N = 5), Grade II (N -- 5), Grade III (N = 10), Grade IV (N ~ 4). Grade I cases were asymptomatic with minimal headache and nuchal rigidity. Grade II cases had moderate to severe headache with nuchal rigidity but no neurological deficit other than cranial nerve palsy. Grade III cases showed drowsiness, confusion, or mild focal neurological deficit. Grade IV cases showed stupor, moderate to severe hemiparesis, early decerebrate rigidity in some cases and vegetative disturbances. Grade V cases showing deep coma, decerebrate rigidity and moribund appearance, were excluded since transportation to the laboratory was contraindicated. Eleven patients underwent surgery, 4 shortly before the rCBF measurements and 7 after the measurements. Of the 11 cases undergoing surgery, all except 3 had intracranial clipping or obliteration of the aneurysm. The 3 exceptions had progressive clamping of the carotid artery in the neck with monitoring of rCBF F1 values, which did not decrease below 50 ml/100 g brain/min. The remainder, (including all patients with AVMs or normal arteriogram) were treated conservatively without surgical intervention. The mean interval between the time of angiography and the first measurement of rCBF was 4 :~ 2 days. Patients with remote S A H (N -- 6)
Comparable measurements were made for purposes of comparison in 6 patients who had been hospitalized for SAH 3 months to 6 years prior to the rCBF measurement. As listed in Table 1, 4 had SAH from arteriographically demonstrated intracranial aneurysms and one from an AVM. In the remaining patient the etiology of SAH was never determined despite 4 vessel cerebral angiography. These patients were admitted to hospital to exclude recurrent SAH as a cause of seizures or severe headache. None had nuchal rigidity. Recurrent SAH was excluded by clinical examination, CT scan and lumbar puncture. Normative data
For comparison with these patients, rCBF was also measured in 35 age-matched normal volunteers (mean age 41.9 ± 12.2 years). The measurements were made under similar laboratory conditions. Cerebral vasomotor responsiveness to changes in PECO2 by hyperventilation was also tested (N ~ 17, mean age 37 ± 14 years) during a second rCBF measurement. METHOD Regional CBF was measured by our modification of the la3Xe inhalation method
305 originally described by Obrist et al. (1975), details of which has been reported in previous publications (Meyer et al. 1978a, b). In brief, a mixture of 133Xe gas mixed with room air (5-7 mCi/l) was inhaled via a close-fitting face mask for one minute. Clearance curves for 133Xe derived from 16 regions of the head and the end-tidal air were recorded throughout the ensuing 11 min by an on line PDP 11-5 computer programmed for this purpose. Collimated thallium-activated NaI crystal scintillation detectors were mounted by means of a helmet over both cerebral hemispheres and brain stem-cerebellum regions as a radial array. Each probe maintained firm pressure on the scalp perpendicular to the underlying skull and were placed over both frontal, temporal, parietal and occipital regions. The output discrimination for each detector was set to accept pulses between 67.5 and 94.5 KEV (gamma activity). The arterial concentration of 138Xe, as an input function, was estimated from the end-tidal air. This was used to deconvolute the head curves using Obrist's two-compartmental model for analysis. By multiplying K1 with 2 gray (Veall and Mallet 1965) the blood flow of fast component (F1 value) was estimated. ISI2 (introduced by Risberg et al. 1975) which obviates the use of 2 since this may be altered in ischemic brain was also calculated simultaneously by the computer. End-tidal partial pressure for carbon dioxide (PECO2), oxygen (PEO2) and 133Xe activity were all recorded from the face mask during the rCBF measurement together with the blood pressure, EEG and skin temperature on a polygraph. Cerebral vasomotor responsiveness to lowered PECO2 was tested during voluntary hyperventilation in 11 patients (mean age 45 -+- 14 years) that were able to cooperate. CO2 responsiveness was expressed as percentage change oflSI2 per mm Hg change in PECO2. Results of the hyperventilation tests in the SAH patients were compared with 17 aged-matched normal volunteers (mean age 37 ± 14 years) serving as controls. RESULTS
Mean hemispheric Fx and 1SI2 values in patients with SAH Table 2 displays the results of the initial mean hemispheric F~ and ISI2 measurements made at the time of admission to the study together with the corresponding mean TABLE 2 MEAN HEMISPHERIC F1 AND ISI2 VALUES COMPARED BETWEEN NORMAL VOLUNTEERS AND PATIENTS WITH RECENT AND REMOTE SUBARACHNOID HEMORRHAGE Values are mean ~ SD. Classification of subjects measured
No. of Age (yr) cases
Mean heMeanheMABP mispheric F1 mispheric (mm Hg) (ml/100 g 1SI2(× 100) brain/min)
PECO2 (mm Hg)
Normal volunteers N = 35 44.8 -t- •4.7 76.4 -4- 10.3 52.0 :k 9.4 92.4 ~ 5.5 37.5± 2.7 Patients with recent SAH (4-41 days) N -- 24 46.0 d_ 12.6 70.1 ~ 10.0a 42.6 ± 7.6 a 96.2 d- 10.4 35.8 zk 4.4 Patients with remote hemorrhage (3 months-6 years) N = 6 47.6 ± 14.7 83.2 i 9.2 49.5 zk 4.6 99.0 ± 14.1 36.0 ± 2.2 a Significantly decreased compared to normal volunteers and patients with remote SAH (P < 0.05, Student's t-test). MABP = mean arterial pressure; PECO2 = end-tidal COo..
306 Remote SAH Neurological Status
0 N=6
Recent SAH
Grade I&ll N=IO
Grade III N=IO
Grade IV N=4
100 --
90
°--
~= 80
~
-
70 -
~. 60
Ib 8o
-
-.q-P
