Hemodynamics of subarachnoid hemorrhage arrest.

Subarachnoid hemorrhage (SAH) causes a spectrum of clinical syndromes from mild discomfort to rapid brain death. The reason for these heterogeneous consequences is poorly understood. A canine autologous shunt model of SAH was used to study this problem. The duration and volume of hemorrhage into the suprasellar cistern at each animal's mean arterial blood pressure were measured at variable hemorrhage flow rates. At high rates of bleeding in seven dogs (18.7 +/- 2.2 ml/min, mean +/- standard deviation), hemorrhage duration was significantly less (191 +/- 116 seconds, p < 0.03) and hemorrhage volume was significantly greater (15.1 +/- 7.0 ml, p < 0.05) than at low flow rates. At low flow rates of bleeding in nine dogs (4.4 +/- 2.2 ml/min), hemorrhage duration was 394 +/- 202 seconds and volume was 10.9 +/- 6.5 ml. Cerebral perfusion pressure (CPP) decreased at all hemorrhage rates but never to 0 mm Hg (perfusion arrest). No correlation between a decrease in CPP and SAH volume or duration was identified. The initial flow rate of SAH had a positive linear correlation with the volume of hemorrhage (23 dogs, r = 0.64, p < 0.01). The data suggest that initial SAH flow rate, and not CPP, has a primary influence on hemorrhage arrest. This finding may influence the clinical rationale for acute management of SAH-induced brain injury.

Cerebral oxygen metabolism during hypothermic circulatory arrest in humans.

Profound hypothermia with circulatory arrest is an important surgical adjuvant that allows protected cessation of cerebral blood flow for a brief period. In seven patients undergoing this procedure, continuous spectroscopic measurement of cerebral hemoglobin oxygen saturation was performed. Circulatory arrest at 18 degrees C was associated with a significant progressive desaturation (p < 0.01) of residual cerebral hemoglobin. Arrest time varied based on operative complexity (range 10 to 65 minutes), and a negative linear correlation between arrest time (y) and oxygen saturation (x) was noted (y = -0.87 x + 64). Five patients whose saturation remained above 35% had no neurological injury attributable to hypoxia. One patient (Hunt and Hess Grade 0) whose saturation fell below 35% had evidence of a global hypoxic injury at postmortem examination. Spectroscopically measured cerebral hemoglobin saturation (cerebral oximetry) may be used to monitor metabolic activity during circulatory arrest. Although the clinical utility of such monitoring cannot be established at this time, the potential may exist to prolong the safe duration of induced circulatory arrest for cerebral protection.

Pigmented villonodular synovitis of the spine. Case report.

Pigmented villonodular synovitis commonly occurs in synovial joints of the appendicular skeleton, but rarely affects the synovial joints of the spine. It has both neoplastic and benign features, and the etiology is thought to be posttraumatic. The case of a young man presenting with paraparesis and a large thoracic lesion is reported.

Cerebellar hemorrhage associated with capillary telangiectasia and venous angioma: a case report.

We report a case of recurrent cerebellar hemorrhage from a capillary telangiectasia associated with a venous angioma. Based on the findings in this case and a review of the literature, we concluded that the hemorrhage was from the telangiectasia and not from the associated venous angioma. The association between capillary telangiectasias and cavernous malformations and the established association of the latter with venous angiomas are reviewed. This case illustrates the complex interrelationship between these histologically distinct malformations and its influence on their potential to hemorrhage.

Intracranial pressure reduction by a central alpha-2 adrenoreceptor agonist after subarachnoid hemorrhage.

Pharmacological manipulation of cerebral venous blood volume is a theoretical approach to reduce elevated intracranial pressure (ICP). Microapplication of alpha-2 adrenoreceptor agonists has been shown to constrict pial veins selectively. This report explores the physiological effects of the intravenous alpha-2 agonist xylazine in a canine model of raised ICP after subarachnoid hemorrhage (mean arterial pressure, heart rate, and ICP were measured and compared in five groups: normal saline [n = 4], xylazine [0.05-1.00 mg/kg] [n = 28], tolazoline [a semiselective alpha-2 antagonist, 5 mg/kg] [n = 6], tolazoline [5 mg/kg] plus xylazine [1.0 mg/kg] [n = 7], and phenylephrine [0.008 mg/kg], a selective alpha-1 agonist [n = 3]). Treatment with xylazine produced a significant (P < 0.01), transient, dose-dependent reduction in ICP that was blocked by pretreatment with tolazoline. Treatment with tolazoline alone produced significant (P < 0.01) increases in ICP and mean arterial pressure. Treatment with phenylephrine produced significant (P < 0.01) increases in mean arterial pressure but had no affect on ICP. These results raise the possibility of using an alpha-2 adrenoreceptor agonist for the treatment of elevated ICP after brain injury.

Relationship of perfusion pressure and size to risk of hemorrhage from arteriovenous malformations.

The relationship between the size of an arteriovenous malformation (AVM) and its propensity to hemorrhage is unclear. Although nidus volume increases geometrically with respect to AVM diameter, hemorrhages are at least as common, in small AVM's compared to large AVM's. The authors prospectively evaluated 92 AVM's for nidus size, hematoma size, and arterial feeding pressure to determine if these variables influence the tendency to hemorrhage. Small AVM's (diameter less than or equal to 3 cm) presented with hemorrhage significantly more often (p less than 0.001) than large AVM's (diameter greater than 6 cm), the incidence being 82% versus 21%. Intraoperative arterial pressures were recorded from the main feeding vessel(s) in 24 of the 92 patients in this series: 10 presented with hemorrhage and 14 presented with other neurological symptoms. In the AVM's that had hemorrhaged, the mean difference between mean arterial blood pressure and the feeding artery pressure was 6.5 mm Hg (range 2 to 15 mm Hg). In the AVM's that did not rupture, this difference was 40 mm Hg (range 17 to 63 mm Hg). Smaller AVM's had significantly higher feeding artery pressures (p less than 0.05) than did larger AVM's, and they were associated with large hemorrhages. It is suggested that differences in arterial feeding pressure may be responsible for the observed relationship between the size of AVM's and the frequency and severity of hemorrhage.

Thromboendarterectomy of the symptomatic occluded internal carotid artery.

A retrospective review of 42 patients (mean age 61.4 years) with surgically managed symptomatic internal carotid artery occlusion is reported. A standardized surgical protocol aimed at restoration of flow in the vessel was used. Presenting symptoms included hemispheric transient ischemic attacks in 68% of patients, new fixed neurological deficits in 28%, amaurosis fugax in 28%, and stroke-in-evolution in 9%. Twenty-four arteries were successfully reopened. A proximal remnant angioplasty (stumpectomy) was performed alone in nine patients or in combination with an external carotid endarterectomy in nine. In four patients with persisting symptoms who failed to achieve primary restoration of flow, a superficial temporal-to-middle cerebral artery bypass procedure was performed. The permanent surgical morbidity rate was 2% and the surgical mortality rate was 0%. Transient postoperative deficits were present in three patients (7%). Follow-up review at a mean of 40 months was obtained in 39 patients (93%). Following surgical intervention, five patients died of unrelated causes, two had neurological events consistent with a transient cerebral ischemic attack, and two had vertebrobasilar insufficiency. No patient suffered from stroke. Of the 24 successfully reopened vessels, follow-up ultrasound evaluations were obtained in 17 (73%) at a mean of 28 months after surgery. In 15 patients (88%) the vessels were widely patent, one (5.8%) had stenosis greater than 70%, and one (5.8%) showed asymptomatic reocclusion. Reopening occluded internal carotid arteries in selected patients is associated with low surgical morbidity and mortality rates. Further studies are necessary to determine the impact of this surgical therapy on the natural history of this condition.

Intracerebral penetration of infrared light. Technical note.

Near infrared transmission spectroscopy of the human cerebrum may allow noninvasive evaluation of cerebral hemoglobin saturation in humans. The emerging spectroscopy configuration for this application is a side-by-side source-receiver construct. The ability of this spectroscopy paradigm to detect changes in intracerebral attenuation by selective injection of the infrared tracer indocyanine green into the internal and external carotid arteries during endarterectomy is evaluated in five adult patients. In all five, simultaneous two-channel infrared transmission spectroscopy over the ipsilateral hemisphere documented tracer bolus transit with a signal-to-noise ratio greater than 100:1. In addition, the two channels could be configured to achieve depth resolution of the collected spectra.

Disabling cerebral transient ischemic attacks.

The surgical management of an emerging clinical entity, namely disabling transient cerebral ischemic attacks, is described. A series of 19 patients treated in a 2-year period (12 with anterior circulation dysfunction and seven with posterior insufficiency) met the following criteria: 1) stereotypical recurrent episodes of transient neurological dysfunction related to the anterior or posterior circulation distribution; 2) failure of maximum medical therapy to control the transient neurological dysfunction; 3) four-vessel cerebral angiography demonstrating an isolated vascular territory corresponding to patient symptoms; 4) inhalation xenon cerebral blood flow studies with at least three of eight probe-pairs showing significant asymmetries in the initial slope index, localizing an area of relative oligemia to the symptomatic hemisphere (anterior circulation only); and 5) severe restriction of lifestyle due to transient ischemic attacks (TIA's). Seventeen patients underwent surgical bypass therapy: deep sylvian superficial temporal artery (STA)-middle cerebral artery (MCA) bypass in nine; surface STA-MCA bypass in three; STA-superior cerebellar artery bypass in three; STA-posterior cerebral artery bypass in one; and aorta-carotid artery bypass in one. There was one perioperative death and four perioperative strokes (two ipsilateral and two contralateral to the operated side). The average follow-up period was 14 months. Of the 16 surviving surgically treated patients, 13 (81%) have had an excellent to good outcome with complete resolution of TIA's and minimal neurological deficits. Three patients had a poor outcome with either a significant persistent neurological deficit or continued TIA's. The two patients not treated surgically continue to have vertebrobasilar insufficiency episodes while receiving oral anticoagulation medication. The overall mortality rate (5.5%) and stroke morbidity rate (22.2%) of surgical therapy for disabling TIA's are high in this neurologically unstable group of patients, but are associated with an 81% excellent to good response. Although the natural history of disabling TIA's is not known, these patients present with significant to total disability due to their symptoms. It is concluded that disabling TIA's respond to surgical revascularization and may represent an indication for cerebral revascularization surgery.

Cerebral oxygen metabolism measured during hypothermic circulatory arrest: a case report.

Infrared transmission spectroscopy was used to detect changes in cerebral oxy- and deoxyhemoglobin attenuation of infrared light in a patient undergoing circulatory arrest at 15 degrees C. Wavelength specific attenuation was used to determine hemoglobin oxygen saturation in the cerebral vasculature using a previously described paradigm. The fate of the residual oxygenated hemoglobin in the cerebrovascular compartment was followed during 15 min of circulatory arrest at 15 degrees C, and cerebral oxygen metabolism was identified as the progressive desaturation of this hemoglobin. The aggregate arterial and venous saturation fell from a normal value of 70% to an abnormally low value of 50%. Reperfusion resulted in near normalization of cerebrovascular oxygen saturation over 5 min, but evidence of persistent mild desaturation below prearrest baseline followed reperfusion. This case demonstrates both continued cerebral oxygen metabolism under hypothermic, circulatory arrest conditions and a cerebral oxygen delivery-consumption mismatch during reperfusion.

Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans.

Regional cerebrovascular oxygen saturation, a quantitative measure of hemoglobin saturation in the combined arterial, venous, and microcirculatory compartments of the brain, can be measured noninvasively with near infrared spectroscopy. We assessed the sensitivity of this aggregate saturation to cerebral hypoxia during transient cerebral hypoxic hypoxia in seven human subjects. Regional cerebrovascular oxygen saturation measured over the middle frontal gyrus and analog electroencephalogram were recorded. We compared the time to achieve two end points: the earliest paroxysmal burst of theta-delta background slowing and a cerebrovascular oxygen saturation of less than 55%. Saturation fell below 55% prior to the electroencephalographic change (p less than 0.05). In a related effort, we also compared spectroscopically measured regional cerebrovascular oxygen saturation with an estimate of this value calculated from arterial and cerebral mixed venous saturation in nine patients. A positive linear relation (n = 68, R2 = 0.55, s = 4.2) was noted.

Measurement of regional cerebrovascular haemoglobin oxygen saturation in cats using optical spectroscopy.

We describe the use of optical spectroscopy in the near infra-red light range to non-invasively measure regional cerebral haemoglobin oxygen saturation (rSHbO2) in cats during progressive cerebral hypoxia. This technique differs from spectroscopic techniques previously described in that the concentration ratio--percentage haemoglobin: oxygen saturation--is quantified. This saturation is the weighted summation of saturation in the cerebrovascular system: arterial, venous, and capillary beds. In a cat model of progressive cerebral hypoxia, a positive linear correlation between this regional measurement of cerebral saturation and actual saturation, calculated from cerebral arterial and mixed venous blood, was noted (n = 20, r = 0.88, p less than 0.01). The spectroscopic measurement rSHbO2 is also used to index cerebral oxygen extraction. During hypoxia spectroscopic indexed oxygen extraction (iOE) and cerebral arterial-venous difference in oxygen content were simultaneously measured. A least-squares positive linear correlation between these two parameters was noted [AVDO2 = iOE (0.05) + 4.4] (n = 40, r = 0.6, s = 1.2). Objective measurement of 'regional cerebrovascular haemoglobin saturation' and an index of cerebral oxygen extraction are possible using optical spectroscopy.

Noninvasive cerebral optical spectroscopy for monitoring cerebral oxygen delivery and hemodynamics.

OBJECTIVE: To present an algorithm for noninvasive measurement of cerebral oxygen saturation (cerebral oximetry) and cerebral hemodynamics with near infrared spectroscopy. DESIGN: In vitro correlation of oximetry measurements with reference measurements; illustrative cases of hemodynamic and oximetric recordings. SETTING: Tertiary care neuroscience ICU. PATIENTS: Brain-injured patients with a prolonged, decreased level of consciousness chosen as illustrative examples. INTERVENTIONS: Two-channel multiple wavelength diffuse infrared transmission spectroscopy was interfaced with the scalp using adhesive. Transmission data were collected with gross superficial-to-deep spatial resolution. Saturation calculation based on the deep signal was observed longitudinally in the patient. With the same technology, arterial input and cerebral response functions, generated by iv tracer bolus, were deconvoluted to measure mean cerebral transit time. MEASUREMENTS AND MAIN RESULTS: A positive linear regression fit between diffuse transmission oximetry and measured blood oxygen saturation over the range 23% to 99% (r2 = .98, p less than .001) was noted. CONCLUSIONS: The approach used overcomes previously identified difficulties with cerebral oximetry, and demonstrates excellent in vitro correlation. The technique can be performed clinically without difficulty. A simultaneous measure of mean cortical transit time is possible.

Management of cerebral aneurysms: further facts and additional myths.

In 1985 we reviewed 17 misconceptions or myths surrounding the treatment of aneurysmal subarachnoid hemorrhage that may contribute to the dismal outcome from these lesions. Since that time, significant new data, or facts, have become available regarding the influence of early aneurysm surgery on rebleeding, the efficacy of treatments for symptomatic arterial narrowing, improvements in surgical techniques such as temporary arterial clipping, and measures to protect the brain from ischemic injury. However, additional myths have become apparent which continue to limit our ability to improve the outcome of these patients. We review these facts and myths and discuss management of the patient with aneurysmal subarachnoid hemorrhage.

Hemodynamic vertebrobasilar insufficiency as an adverse effect of antihypertensive therapy.

A 63-year-old white male with a 25-year history of hypertension experienced the onset of intermittent diplopia and gait disturbance 24 hours after a change in antihypertensive medication from atenolol 50 mg/d to enalapril 5 mg bid. Three weeks later, the patient was admitted with a worsening of symptoms. Cerebral arteriography revealed significant bilateral vertebral artery stenosis. Symptoms continued to progress in the hospital, and at the time of posterior circulation revascularization the patient had a persistent bilateral internuclear ophthalmoplegia and right ptosis. The need for a neurovascular workup and adjustment of therapy in patients with antihypertensive-associated cerebral ischemia is discussed.

(Na+ + K+)-dependent adenosine triphosphatase. Regulation of inorganic phosphate, magnesium ion, and calcium ion interactions with the enzyme by ouabain.

1. (Na+ + K+)-dependent adenosine triphosphatase was phosphorylated on the alpha-subunit by Pi in the presence of Mg2+. Phosphorylation was stimulated by ouabain. The interactions of Pi, Mg2+, and ouabain with the enzyme could be explained by a random terreactant scheme in which the binding of each ligand to the enzyme increased the affinities for the other two. Dissociation constants of all steps of this scheme were estimated. 2. In the presence of Pi and ouabain and without added Mg2+, the phosphoenzyme was formed. Because this could be prevented by ethylenediaminetetraacetic acid, but not ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, phosphoenzyme formation under these conditions was probably dependent on traces of endogenous Mg2+. The ability of this Mg2+ to support phosphorylation could be explained by the large increase in the enzyme's affinity for Mg2+ by ouabain. 3. In the absence of ouabain, Ca2+ did not support phosphorylation and inhibited Mg2+-dependent phosphorylation. At lower concentrations, Ca2+ was competitive with Mg2+. With increasing Ca2+ concentration, negative cooperativity was observed, suggesting the existence of multiple divalent cation sites with equivalent affinities for Mg2+, but varying affinities for Ca2+. 4. In the presence of ouabain, the maximum inhibition of Mg2+-dependent phosphorylation by Ca2+ was 50%. With saturating Pi, Mg2+, and ouabain, the number of sites binding ouabain was equal to the number of sites phosphorylated. Although Ca2+ halved phosphorylation and reduced the affinity for ouabain about 100-fold, it did not affect the number of ouabain sites. 5. We suggest that the enzyme is an alpha-oligomer and that the half-of-the-sites reactivity for phosphorylation in the presence of Pi, Mg2+, ouabain, and optimal Ca2+ is caused by (a) ouabain-induced increase in the affinities of both protomers for Mg2+ and (b) the inability of Ca2+ to replace Mg2+ on one of the protomers.

Immediate care after aspiration of vomit.

The diagnosis of aspiration can be made from the characteristic clinical features. Management is then based on the measurement of the pH of the gastric contents, blood gases and acid-base values, the serial measurement of pulse blood pressure and central venous pressure, and the haemoglobin and haematocrit. If available measurement of the plasma or blood volume, pulmonary artery and wedge pressure and cardiac output may also be of value in diagnosis and guiding treatment. The following treatment should be carried out: Head down in right lateral position to drain vomit from airway. Suction. Laryngoscopy to clear the airway. Bronchoscophy if asphyxiated by solid material. Endotracheal intubation if liquid. High inspired oxygen. Artificial ventilation if the PO2 is low. Steroids Hydrocortisone 200 mg intravenously and 100 mg intramuscularly every 6 hours; or Dexamethasone 10 mg intravenously and 5 mg intramuscularly every 6 hours. Aminophylline if bronchospasm is severe. Plasma or plasma substitute for hypotension and hypovolaemia. Correct acidosis.