inclusion bodies in the lung, liver, and gut (RidauraSanz C: personal communication, 1979),suggest that CMV may be the causative agent in at least some patients. Third, our experience with CMV complement fixation antibody data, as now widely measured in the so-called T O R C H screening method, is inconsistent. The unreliability of the method is well known, and our cases reinforce the lack of diagnostic accuracy of the test even in patients who are actively excreting virus. Proof for the concept that CMV can cause slowly progressive C N S destruction is not yet available because the virus has not been isolated from brain tissue or CSF, nor have typical inclusion bodies been demonstrated in nervous tissue in these cases. Also, the pathogenesis of the changes is not clear. Whether they result from direct viral damage to brain tissue or are secondary to vasculitis or obstructive hydrocephalus due to inflammation and scarring of the aqueduct, basal cisterns, or surface pathways is unknown. The concept of an active and progressive infection i s reinforced by Hanshaw's observation (Hanshaw JB: personal communication, 1979) that parents of children with perinatal CMV infections who were found to be partially deaf at school age reported that these children seemed to hear normally as infants. Supported in part by the Fitch Estate Memorial Fund for Research of Causes, Prevention and Treatment of Mental Retardation, by US Public Health Service Research Grant RR-64 from the Division of Research Resources (Clinical Research Center), and by Grant 5-R01-A 1-1021 7 from the National Institute of Allergy and Intectrous Disease, N I H Presented at tht 104th Annual Meeting of the American Neurological Association, St LOUIS,MO, Ocr 4-6, 1'970 We thank Drs Lowell A Glasgow and James C Overall for their substantial help in studying these patients References 1. Bignami A, Appiatole L: Micropolygyria and cerebral calcification in cytomegalic inclusion discase. Acta Neuropathol (Berl) 4:127-137, 1964 2. Crome L, France NE: Microgyria and cytomegalic inclusion disease of infancy. J Clin Pathol 12:427-434, 1959 3. Halsey JH, Allen N, Chamberlin HR: The morphogenesis of hydranencephaly. J Neurol Sci 12:187-217, 1971 4. Haymaker W, Girdany BR, Stephen J, e t al: Cerebral involvement with advanced periventricular calcification in generalized cytomegalic inclusion disease in the newborn. J Neuropathol Exp Neurol 13:562-586, 1954 5 . Larroche JC: Developmental Pathology o f the Neonate. Amsterdam, Elsevier, 1977, pp 259-281 6. Reynolds D W , Stagno S, Stubbs S, e t al: Inapparent congenital cytomegalovirus infection with elevated cord IgM levels. Causal relation with auditory and mental deficiency. N Engl J Med 290:291-2'96, 1974 7. Smith MG: The salivary gland viruses of man and animal. Prog Med Virol 2:171-202, 195'9 502 8. Weller T H : Cytomegaloviruses: the difficult years. J Infect Dis 122:532-539, 1970 9. Weller T H , Hanshaw JB: Virologic and clinical observations o n cytomegalic inclusion disease. N Engl J Med 266:12331244, 1962 10. Wolf A, Cowens D: Perinatal infections of the central nervous system. J Neuropathol Exp Neurol 18:191-243, 1959 Cerebral Hernodynamics and Metabolism in Postoperative Cerebral Vasospasm and Treatment with Hypertensive Therapy Erwin B. Montgomery, Jr, MD," Robert L. Grubb, Jr, M D , * t and Marcus E. Rachle, M D X t A 24-year-old woman developed subarachnoid hemorrhage from an aneurysm at the bifurcation of the right internal carotid artery. Following successful clipping of the aneurysm she developed a left hemiplegia associated with focal cerebral vasospasm, which markedly improved when systemic blood pressure was raised with intravenous dopamine infusion. Regional cerebral blood flow and oxygen utilization were significantly depressed in both cerebral hemispheres, while blood volume was significantly elevated only on the side with vasospasm. Oxygen extraction was significantly elevated in both hemispheres, indicating a generalized impairment in oxygen delivery to the brain. Montgomery EB Jr. Grubb RL Jr, Raichle ME Cerebral hemodynarnics and metabolism in postoperative cerebral vasospasrn and treatment with hypertensive therapy. Ann Neurol 9.502-506, 1981 Subarachnoid hemorrhage (SAH) from rupture of an intracranial aneurysm may produce severe focal and generalized disturbances in brain function by factors which include ischemia secondary to cerebral vasospasm as well as direct toxic effects of subarachnoid From the 'Department of Neurology and Neurological Surgery and the +Division of Radiation Sciences, The Edward Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, M O 631 10. Received May 28, 1980, and in revised form Oct 27. Accepted for publication Nov 9, 1980. Address reprint requests to D r Montgomery, Department of Neurology and Neurological Surgery, Washington University School of Mcdicine, Barnes Hospital Plaza, St. Louis, M O 63 110. 0364-5 134/8 1/050502-O5$01.25 @ 1980 by the American Neurological Association blood. I n d u c e d systemic hypertension has been used t o treat cerebral ischemia from a variety of causes [ 3 , 41, including cerebral vasospasm [ l , 2, 4 , 5, 81. New quantitative metabolic and h e m o d y n a m i c data rep o r t e d h e r e d e m o n s t r a t e that hypertensive therapy can effectively treat symptomatic cerebral ischemia associated with cerebral vasospasm after ligation of a n intracranial a n e u r y s m and also p r o v i d e evidence of a generalized disturbance i n oxygen delivery t o the brain following SAH. A 24-year-old right-handed woman suddenly developed severe headache and neck stiffness. O n admission three days later her blood pressure was 178/88 mm Hg, and it had decreased to 110170 by the next day. She was lethargic but oriented, with clear speech. Examination otherwise was normal. The cerebrospinal fluid (CSF) was bloody, xanthochromic, and under an opening pressure of 330 mm CSF. Angiography demonstrated an aneurysm at the bifurcation of the right internal carotid artery and no evidence of cerebral vasospasm. O n the day prior to surgery a repeat lumbar puncture revealed an opening pressure of 250 mm CSF. During surgery the aneurysm rebled but was successfully clipped. Immediately afterward the patient developed complete paralysis of the left side of the face and left arm; the remainder of the examination was unremarkable. H e r blood pressure was I20179 mm Hg. Within hours a constant intravenous infusion of dopamine was begun to maintain her systolic blood pressure at 140 to 150 mm Hg. The left-sided paralysis improved within minutes, leaving only moderate weakness of the left arm. By the second postoperative day there was only minimal weakness of her left hand and arm. Postoperatively the patient experienced several episodes when her blood pressure fell below 135195 mm Hg. Each time her mild left hemiparesis increased, often to the point of complete paralysis. In each instance the paralysis resolved promptly when her blood pressure rose with F i g 1 . Continuous EEG recording made during an attempt t o taper the dopamine infusion. A shows the EEG montage. B shows the baseline EEG while bloodpressure was being maintained at 140190 mm Hg. C shows the EEG when blood pressure was reduced t o 100170 mm Hg as dopamine infusion was tapered, associated with marked worsening of the left face and arm weakness. D shows return of the EEG t o baseline as blood pressure was restored by increased dopamine infusion, associated with return of the leftface and arm t o baseline strength. Case Report: Montgomery et al: Cerebral Vasospasm 503 increased dopamine infusion. A critical blood pressure threshold of 135 mm Hg systolic became apparent. O n the seventh postoperative day an attempt was made to taper the dopamine while continuously monitoring the electroencephalogram (EEG). As the rate of dopamine infusion was decreased, the patient's blood pressure fell and the EEG from the right cerebral hemisphere slowed while that from the left hemisphere remained slightly slow and did not change (Fig 1). Simultaneously the previously mild left arm weakness increased markedly, so that at a blood pressure of 85/55 mm H g the patient could not move her left fingers or arm. An increased rate of dopamine infusion restored her blood pressure to 140/90 mm Hg,improved the EEG, and returned left arm strength t o baseline. O n the eighth postoperative day, repeat angiography ckmonstrated severe, diffuse vasospasm involving the distal right internal carotid artery, the A , segment of the right anterior cerebral artery, and the right middle cerebral artery (Fig 2). During angiography the patient's blood pressure was maintained at a level of 140180 mm Hg, and her neurological status remained stable. Measurements of regional cerebral blood flow (rCBF), oxygen utilization (rCMRO,), and blood volume (rCBV) were made in both cerebral hemispheres during angiography, with intracarotid injection of aliquots of the patient's blood tagged with radioactive "0-labeled water, '"0-labeled carboxyhemoglobin, and "0-labeled oxyhemoglobin using techniques described earlier [ l o ] . Then t tests were used to compare differences in rCBF, r C M R 0 2 , and rCBV between the right and left cerebral hemispheres in the patient and to compare these results with previously determined normal values [lo]. rCBF and rCMRO, were significantly depressed throughout both cerebral hemispheres, as shown in Figure 3, while a 504 Annals of Neurology Vol 9 No 5 May 1981 significant increase in rCBV was seen only in the right cerebral hemisphere. T h e depression of rCBF and rCMRO, was most marked in the right posterior frontal and parietal regions. Oxygen extraction, defined as the brain arteriovenous concentration difference for oxygen divided by the arterial oxygen concentration, was significantly increased ( p < lo-') in both cerebral hemispheres. T h e dopamine infusion was gradually tapered over the next several days and was discontinued on the fifteenth postoperative day without any deterioration in the patient's neurological condition. Follow-up examination three months later showed no abnormalities except for mild impairment of fine finger movements of the left hand and moderate left central facial weakness. Discussion We have previously reported decreased rCBF and rCMRO, with increased rCBV in patients with SAH and severe vasospasm causing neurological deficits [ 7 ] , as observed in this case. The large increase in rCBV can be interpreted as a reflection of massive dilation of radiographically inconspicuous intraparenchymal blood vessels (i.e., poststenotic dilatation). The increased oxygen extraction in the hemisphere affected by vasospasm represents failure of the vasculature to meet local metabolic demands. This is F i g 2. Anteraposterior (A) and lutrral(31 rietcs ofthr po3.toperative angiogvam demonstrating .ratiJjartoyy clipping vf the aneurysm. Severe, diff.se vasospa m inr,olm the di.ctal right internal carotid artery (arrows), the A I .tepient of the right anterior cerebrul artery, and t h f right middle cerebral artery. CBF CMR02 m1/100g min m1/100a .min EO, L CBV 1 ml/lOOg 6 r I 00 60 - 40 - 0 l r 2 1 I 131;:I ..... .... P< 10-8 I P P<.02 1 1 CONTROL NS P < I O - ~ NS LEFT HEMISPHERE F i g 3. Measurements o f cerebral bloodjow (CBF), cerebral metabolic rate fur oxygen (CMRO,), cerebral oxygen extraction (E02),and cerebral blood volume (CBV) ohtainedat ihe time qf the angiogranz shown in Figure 2. Datu from each cerebral hemiJphere repreient the mean ( -+ S E M ) of 1.3 regions. Control data were obtained in prez,ious studiej from our Laboratory [121. supported by the direct correlation between the patient's fluctuating neurological signs and the level of arterial blood pressure. The results in this case demonstrated depressed blood flow and oxygen consumption coupled with increased oxygen extraction in the cerebral hemisphere not involved by vasospasm and functionally normal as judged by clinical examination and EEG. In our previous report [7] we did not have occasion to study the uninvolved and presumably normal cerebral hemisphere in a patient with SAH. Although finding depressed rCBF and rCMRO, was not surprising considering the presumed toxic effect of subarachnoid blood [ 9 ] ,the increased oxygen extraction was quite unexpected. O u r tentative conclusion is that oxygen delivery to the hemisphere without evident vasospasm was also compromised. The mechanism and importance of this finding are uncertain. This report emphasizes the efficacy of induced systemic hypertension in the treatment of cerebral ischemia due to postoperative vasospasm. The mechanism of improvement was probably improved rCBF due to increased perfusion pressure across large, stenotic blood vessels. During hypertensive therapy the central venous pressure should be maintained between 8 and 15 cm H,O by infusions of whole blood, albumin, or low-molecular-weight dextran [51. If these methods are unsuccessful, vasopressor agents may be necessary. Levarterenol and phenylephrine NS P