A new perspective on the relationship between communication impairment and disempowerment following head injury in information exchanges

Transcranial doppler sonography is a diagnostic tool that allows the noninvasive study of intracranial circulation. In patients with aneurysmal subarachnoid hemorrhage, cerebral vasospasm is promptly diagnosed, even before clinical related symptoms. Feeding arteries of an arteriovenous cerebral malformation can be detected and their variations can be correlated to the treatment (neurosurgical and/or neuroradiological). When raised intracranial pressure (namely in head trauma), transcranial doppler sonography depicts vasospasm and/or typical variations of the waveforms, suggesting intracranial circulatory arrest.     

Transcranial Doppler for early identification of potential organ transplant donors

BACKGROUND: Encouraging results in transplant medicine create a growing demand for organ transplant donors. Transcranial Doppler (TCD) has been used by several investigators to assess arrest of the cerebral circulation in brain dead patients. We report on TCD as a monitoring tool for early identification of potential organ transplant donors. DESIGN: A prospective clinical study. SETTING: Intensive care unit (ICU) of a 900-bed community hospital (primary and tertiary care center) in Vienna, Austria. SUBJECTS AND METHODS: All patients with acute intracranial lesions admitted to our intensive care unit underwent TCD examination at least once daily. In patients with Glasgow Coma Scores < 7, TCD waveforms with high resistance profiles unchanged by therapeutic attempts to lower intracranial pressure indicated the need for repeated TCD up to four times a day. TCD waveform abnormality consisting of absent or reversed diastolic flow or small early systolic spikes in at least two intracranial arteries was considered to constitute intracranial circulatory arrest. Brain death was confirmed by clinical criteria, an isoelectric electroencephalography (EEG) or non filling of the intracerebral arteries on arteriography. RESULTS: From January 1994 to July 1996 we identified 11 comatose patients as potential organ transplant donors with typical TCD findings indicating intracranial circulatory arrest. Diagnosis was subarachnoid hemorrhage in 7 and intracerebral hemorrhage in 4 patients. Brain death diagnosis according to the criteria of Austrian law was initiated immediately after the TCD findings suggested intracranial circulatory arrest. Confirmation of brain death was obtained by clinical criteria and either EEG (6 patients) or cerebral angiography (5 patients). CONCLUSION: TCD examinations on a daily routine basis offer a noninvasive monitoring method for early assessment of intracranial circulatory arrest. TCD enables quick identification and further diagnosis of candidates for organ transplant donation.     

Effects of induced hypertension on transcranial Doppler ultrasound velocities in patients after subarachnoid hemorrhage

BACKGROUND AND PURPOSE: Transcranial doppler ultrasound (TCD) is used after subarachnoid hemorrhage to detect cerebral vasospasm and is often treated with induced hypertension. Cerebral autoregulation, however, may be disturbed in this population, raising the possibility that TCD velocities may be elevated by induced hypertension. To study this possibility, we performed continuous TCD monitoring of the middle cerebral artery during the induction and withdrawal of induced hypertension in patients after subarachnoid hemorrhage. METHODS: Twenty-eight patients were studied during the induction and withdrawal of hypertension using primarily phenylephrine. Continuous monitoring was performed on the middle cerebral artery with the highest flow velocity. Treatment was based on rising TCD velocities or clinical evidence for cerebral vasospasm. Mean arterial pressure and mean TCD velocities were recorded every minute. A change of > 15% from starting TCD values was considered significant. Cerebral autoregulation was calculated as a percentage of intact autoregulation. Patients were subsequently divided into groups of disturbed and intact autoregulation. RESULTS: In 10 of 19 patients (53%), TCD velocities changed by > 15% and paralleled changes in mean arterial pressure. This directly altered the TCD interpretation of the grade of vasospasm in 7 of 19 patients (36%). Three additional patients had smaller absolute changes in TCD velocities. No clinical difference could be identified between patients with disturbed and intact autoregulation. CONCLUSIONS: In patients with disturbed autoregulation after subarachnoid hemorrhage, induced hypertension can alter cerebral blood flow velocities. The level of autoregulation needs to be considered when interpreting TCD velocities in patients after subarachnoid hemorrhage.     

Cerebrovascular reserve capacity many years after vasospasm due to aneurysmal subarachnoid hemorrhage. A transcranial Doppler study with acetazolamide test

BACKGROUND AND PURPOSE: Vasospasm in aneurysmal subarachnoid hemorrhage results in proliferative vasculopathy. Systemic hypertension also causes vascular hypertrophy. Both of these histological changes can lead to rigidity of the cerebrovascular system, reducing its autoregulatory capacity. METHODS: Blood flow velocity (BFV) in the middle cerebral artery at rest and cerebrovascular reserve capacity (CVRC) (percent rise in BFV after acetazolamide stimulation) measured by means of transcranial Doppler sonography were studied many years after aneurysmal subarachnoid hemorrhage in patients with proven cerebral vasospasm (mean BFV > 160 cm/s). The BFV under resting conditions and the CVRC values of the ipsilateral and the contralateral hemispheres were measured in 29 patients (mean age, 43 years; mean follow-up, 4.6 years) and compared with those of control subjects. RESULTS: Persistent high BFV (> 120 cm/s) was found in three patients in the peripheral branch of the ipsilateral middle cerebral artery. In the main trunks of the arteries of the anterior circle of Willis, BFV was normal in all cases. CVRC was normal in all patients (ipsilateral, 52 +/- 21%; contralateral, 56 +/- 17%); values did not differ significantly from each other or from the control value (45 +/- 18%). The higher value of CVRC on the contralateral side was found to be statistically significant in selected groups (hypertensive patients and patients with residual infarct on late CT). CONCLUSIONS: Proliferative vasculopathy developed at the time of vasospasm must have resolved and did not reduce late vasoreactivity. Comorbidity with hypertension also did not seem to influence the late vasoreactivity toward normalization.     

Slow rhythmic oscillations of blood pressure, intracranial pressure, microcirculation, and cerebral oxygenation. Dynamic interrelation and time course in humans

BACKGROUND AND PURPOSE: Various biological signals show nonpulsatile, slow rhythmic oscillations. These include arterial blood pressure (aBP), blood flow velocity in cerebral arteries, intracranial pressure (ICP), cerebral microflow, and cerebral tissue PO2. Generation and interrelations between these rhythmic fluctuations remained unclear. The aim of this study was to analyze whether stable dynamic interrelations in the low-frequency range exist between these different variables, and if they do, to analyze their exact time delay. METHODS: In a clinical study, 16 comatose patients with either higher-grade subarachnoid hemorrhage or severe traumatic brain injury were examined. A multimodal digital data acquisition system was used to simultaneously monitor aBP, flow velocity in the middle cerebral artery (FVMCA), ICP, cerebral microflow, and oxygen saturation in the jugular bulb (SjO2). Cross-correlation as a means to analyze time delay and correlation between two periodic signals was applied to a time series of 30 minutes' duration divided into four segments of 2048 data points (approximately 436 seconds) each. This resulted in four cross-correlations for each 30-minute time series. If the four cross-correlations were consistent and reproducible, averaging of the original cross-correlations was performed, resulting in a representative time delay and correlation for the complete 30-minute interval. RESULTS: Reproducible cross-correlations and stable dynamic interrelations were found between aBP, FVMCA, ICP, and SjO2. The mean time delay between aBP and ICP was 6.89 +/- 1.90 seconds, with a negative correlation in 81%. A mean time delay of 1.50 +/- 1.29 seconds (median, 0.85 seconds) was found between FVMCA and ICP, with a positive correlation in 94%. The mean delay between ICP and SjO2 was 9.47 +/- 2.21 seconds, with a positive correlation in 77%. Mean values of aBP and ICP did not influence the time delay and dynamic interrelation between the different parameters. CONCLUSIONS: These results strongly support Rosner's theory that ICP B-waves are the autoregulatory response of spontaneous fluctuations of cerebral perfusion pressure. There is casuistic evidence that failure of autoregulation significantly modifies time delay and the correlation between aBP and ICP.     

Long-term follow-up study of unruptured intracranial aneurysms

OBJECTIVE: The purpose of this study was to clarify the risk of rupture of unruptured intracranial aneurysms among large groups of patients with various underlying diseases or conditions. METHODS: A long-term follow-up study of unruptured intracranial aneurysms was performed with 360 patients who were treated conservatively during the period from April 1969 to December 1992. RESULTS: Follow-up evaluation (between February and June 1994) could be performed for 234 (65%) of the patients. The underlying diseases included multiple aneurysms with subarachnoid hemorrhage for 60 patients, cerebral infarction for 108, intracerebral hemorrhage for 27, and other diseases for 39. Single aneurysms were present in 171 patients and multiple aneurysms in 63. The mean follow-up period was 75 months (range, 3-270 mo). Of the 234 patients, 132 (56.4%) survived, 59 (25.2%) died because of other diseases, 9 (3.8%) underwent surgery, and 34 (14.5%) showed bleeding from unruptured aneurysms, which was fatal for 18 of the patients. The average annual rupture rate for all patients was 2.3% (subarachnoid hemorrhage, 3.2%; cerebral infarction, 2.2%; intracerebral hemorrhage, 3.2%; other diseases, 3.6%). There were no significant differences among the patients according to underlying disease or aneurysm site. The cumulative rate of bleeding for all patients was 20% at 10 years after diagnosis and 35% at 15 years. The cumulative probability of rupture was significantly higher for the multiple aneurysms than the single aneurysms (P < 0.001). CONCLUSION: The risk of rupture of unruptured aneurysms is high, especially for multiple aneurysms, but there are no significant differences in the risk of rupture according to the underlying disease or the aneurysm location. Radical treatment should be considered for patients with unruptured intracranial aneurysms.     

Cerebral circulation dysfunction and hemodynamic abnormalities in syncope during upright tilt test

OBJECTIVE: To assess the hemodynamic features, including monitoring of cerebral circulation, blood pressure and heart rate, in syncope patients during upright tilt test. DESIGN: Nonrandomized sequential patients with history of syncope of uncertain etiology compared with healthy subjects. SETTING: Noninvasive hemodynamic laboratory of a tertiary referral centre. PATIENTS: Twenty patients with history of syncope and 10 controls without syncope. PROCEDURES: Transcranial Doppler measurement or middle cerebral artery flow velocity, noninvasive and invasive blood pressure monitoring, electrocardiography and pulse oximetry monitoring during upright tilt testing. Measurements were taken in patients at the height of symptoms in supine and upright posture. MAIN RESULTS: Ten patients, while still normotensive, had a drop of 53 +/- 10% (mean +/- SD) in cerebral bloodflow velocity (P = 0.0001) and an increase in heart rate by 58 +/- 35%. The remaining 10 patients had a 58 +/- 15% reduction in cerebral bloodflow velocity (P = 0.0001), a drop in blood pressure of 33 +/- 8% (P = 0.0001) and no change in heart rate. The controls showed no significant changes in cerebral bloodflow velocity and a 25 +/- 12% increase in heart rate (P = 0.0002). CONCLUSIONS: Transcranial Doppler monitoring of cerebral bloodflow velocity during upright tilt testing may improve insight into the complex physiology of syncope.     

Changes in cerebral perfusion pressure in puerperal women with preeclampsia

OBJECTIVE: To determine the variation in the estimated maternal cerebral perfusion and cerebrovascular resistance (the resistance area product) in the puerperium. METHODS: The maternal middle cerebral artery was evaluated by transcranial Doppler ultrasound in ten women 2 days before labor, in 21 women in early labor and at 24 and 48 hours postpartum, and in 6 women at 1 week postpartum. Cerebral blood flow velocities were determined. Women were diagnosed initially with mild preeclampsia. Estimated cerebral perfusion pressure was Vmean/[Vmean - Vdiastolic] [BPmean - BPdiastolic]. Because the diameter of the vessels could not be measured directly, an index of resistance was calculated: the resistance area product = BPmean/velocitymean. We calculated an index of cerebral blood flow to be estimated cerebral perfusion pressure divided by resistance area product. Our study had a power of 80% to detect a 16-cm/second increase in middle cerebral blood flow velocity. RESULTS: Estimated maternal cerebral perfusion was maintained for up to 1 week postpartum. Cerebrovascular resistance did not change in the puerperium. Cerebral blood flow index (+/-standard deviation) was significantly increased at 1 week postpartum compared with early labor levels (28.3 +/-6.9 versus 46.7+/-15.6, respectively) (P < .05). CONCLUSION: Cerebral blood flow 1 week postpartum increased significantly over early labor values. These persistent changes in the cerebral vasculature might put patients at risk for seizures up to 1 week postpartum.     

Prevalence of risk factors in spontaneous intracerebral hemorrhage and aneurysmal subarachnoid hemorrhage

OBJECTIVE: To evaluate whether differences exist in the occurrence of modifiable risk factors between aneurysmal subarachnoid hemorrhage and spontaneous intracerebral hemorrhage, since these stroke subtypes have frequently been combined in epidemiological studies and labeled hemorrhagic stroke. DESIGN: Cross-sectional survey. SETTING: Helsinki University Central Hospital in Helsinki, Finland. PATIENTS: One hundred fifty-six consecutive patients with spontaneous intracerebral hemorrhage aged 16 to 60 years (96 males and 60 females) and 281 patients with aneurysmal subarachnoid hemorrhage (145 males and 136 females) who were admitted to an emergency department. MAIN OUTCOME MEASURES: Prevalence of several health habits, previous diseases, and medication of patients with spontaneous intracerebral hemorrhage were compared with that of patients with subarachnoid hemorrhage using multiple logistic regression. RESULTS: Hypertension (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.6-4.3), diabetes mellitus (OR, 26.4; 95% CI, 3.1-221.6), alcohol intake within the preceding week (for 1-150 g of alcohol: OR, 2.0; 95% CI, 1.1-3.6; for 151-300 g of alcohol: OR, 1.7; 95% CI, 0.8-3.8; and for > 300 g of alcohol: OR, 4.4; 95% CI, 2.1-9.1), and anticoagulant treatment (OR, 21.8; 95% CI, 2.3-207.3) were all significantly more common, but current cigarette smoking (OR, 0.3; 95% CI, 0.2-0.5) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage simultaneously after adjustment for sex, age, and body mass index. In males, hypertension (OR, 2.3; 95% CI, 1.1-4.5) and alcohol intake (for > 300 g/wk: OR, 5.8; 95% CI, 2.2-15.7) were more common, but current smoking (OR, 0.2; 95% CI, 0.1-0.4) was less common in patients with intracerebral hemorrhage than in those with subarachnoid hemorrhage after adjustment for age, body mass index, and diabetes mellitus. In females, hypertension (OR, 2.9; 95% CI, 1.4-5.8) and anticoagulant treatment (OR, 10.0; 95% CI, 1.0-100.2) were more common in patients with intracerebral hemorrhage after adjustment for age and body mass index. In univariate statistics, patients with intracerebral hemorrhage were also older, more often had previous symptoms of cerebral ischemia, and had higher values for body mass index and gamma-glutamyltransferase than did those with subarachnoid hemorrhage. CONCLUSIONS: Hypertension, diabetes mellitus, anticoagulant treatment, and amount of alcohol taken within 1 week seem more commonly to be associated with intracerebral hemorrhage than with subarachnoid hemorrhage, which is, however, associated more frequently with cigarette smoking.     

Anatomical and biomechanical similarity in intracranial environment in identical twins with external hydrocephalus

Identical twins who both presented with progressively enlarging heads in their first year of life are reported. Neuroimaging demonstrated morphological similarities in the cerebral cortex. The CSF space, including ventricular system, and subarachnoid space were dilated, suggesting external hydrocephalus. Cerebral blood flow velocity in the anterior cerebral artery monitored by Doppler sonogram indicated the two had similar flow patterns and velocities. Simultaneous recording of ICP waves and intracranial biomechanical properties, that is, pressure buffering capacity (pressure volume index: PVI) and CSF outflow resistance (Ro) measured by the bolus saline injection technique, objectively indicated that all these biomechanical factors were also quite similar in the twins. These results indicate that identical twins with external hydrocephalus have very similar intracranial environments, both anatomically and biomechanically.     

Epidemiology, appropriateness, and cost of vancomycin use

OBJECTIVE: Our purpose was to compare the estimated maternal cerebral perfusion pressure and an index of vascular resistance, the resistance area product, in nonpregnant women with hypertensive pregnant women. STUDY DESIGN: The maternal middle cerebral artery was evaluated by transcranial Doppler ultrasonography in 17 nonpregnant women, 17 pregnant normotensive patients, 20 pregnant patients with chronic hypertension, and 21 pregnant patients with pre-eclampsia (defined by The American College of Obstetricians and Gynecologists criteria) and cerebral blood flow velocities were determined. We calculated estimated cerebral perfusion pressure as [Estimated cerebral perfusion pressure = V mean/(V mean = V diastolic) (Mean blood pressure - Diastolic blood pressure)] modified from Aaslid et al, 1986. Because the diameter of the vessels could not be measured directly, an index of resistance, the resistance area product, was calculated. Resistance area product = Mean blood pressure/mean velocity (Evans et al, 1988). We calculated an index of cerebral blood flow (Cerebral blood flow index) = Estimated cerebral perfusion pressure/resistance area product. RESULTS: Women who were chronically hypertensive and those with pre-eclampsia showed a significant increase in estimated cerebral perfusion pressure and resistance area product compared with nonpregnant and pregnant normotensive women. An estimate of cerebral blood flow (cerebral blood flow index) in nonpregnant women showed that pregnancy resulted in a nonsignificant 18% increase in cerebral blood flow. CONCLUSIONS: Women with chronic hypertension and pre-eclampsia behave similarly by demonstrating significant increases in cerebral perfusion pressure (estimated cerebral perfusion pressure) and cerebrovascular resistance (resistance area product) compared with normotensive and nonpregnant women. Pregnant patients have a minimal increase in cerebral blood flow (18%).     

Paracentesis-induced circulatory dysfunction: mechanism and effect on hepatic hemodynamics in cirrhosis

BACKGROUND & AIMS: Therapeutic paracentesis may be associated with a circulatory dysfunction, manifested by a marked increase of the plasma renin activity and plasma norepinephrine. The aim of the study was to characterize the systemic and hepatic hemodynamic changes associated with paracentesis-induced circulatory dysfunction. METHODS: Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hepatic hemodynamics were assessed 1 hour and 6 days after complete mobilization of ascites in 37 patients treated by total paracentesis plus intravenous dextran-70 infusion. RESULTS: Paracentesis-induced circulatory dysfunction occurred in 10 patients (renin and norepinephrine increased from 9.0 +/- 10.5 to 28.8 +/- 19.0 ng.mL-1.h-1 and from 752.0 +/- 364.0 to 1223.0 +/- 294.0 pg/mL, respectively) and was associated with significant reduction in systemic vascular resistance (-13.0% +/- 2.6%; P < 0.05) and increase in hepatic venous pressure gradient (from 19.5 +/- 1.5 to 22.5 +/- 2.4 mm Hg; P < 0.01). In the remaining 27 patients, mobilization of ascites also induced a significant but smaller reduction in systemic vascular resistance (-5.0% +/- 1.6%; P < 0.05) without significant changes in renin, norepinephrine, and hepatic venous pressure gradient. CONCLUSIONS: Paracentesis-induced circulatory dysfunction is predominantly caused by an accentuation of the arteriolar vasodilation already present in untreated cirrhotic patients with ascites. The homeostatic activation of endogenous vasoactive systems may account for the increased intrahepatic vascular resistance associated with this condition.     

Effect of coat on rate of temperature increase in muscle during ultrasound treatment of dogs

BACKGROUND AND PURPOSE: The vasomotor response can be tested by means of transcranial Doppler sonography. If a constant vessel diameter is assumed, the flow velocity changes will reflect blood flow volume changes. This hypothesis is difficult to verify. Simultaneous assessment of intracranial flow velocity and extracranial flow volume changes may solve this problem. METHODS: We tested vasomotor response in 32 volunteers (age, 42+/-18 years) with 5% CO2. Acetazolamide (1 g) was tested in 15 volunteers (age, 28+/-8 years). To evaluate drug-dependent flow changes in the external carotid artery territory, acetazolamide was administered in 7 patients with unilateral occlusion of the internal carotid artery without evidence of collateralization through the ophthalmic artery (age, 67+/-12 years). Simultaneous recording included measurements of flow volume in the common carotid arteries (M-mode color duplex system) and flow velocity in the middle cerebral arteries. RESULTS: With CO2 and acetazolamide, intracranial flow velocity increased by 31% and 39%, respectively, with a simultaneous increase of common carotid artery flow volume of 47% and 50%, respectively. No change in extracranial flow volume was observed in patients with an occluded internal carotid artery. CONCLUSIONS: These data show not only the expected increase of flow velocity in the middle cerebral artery but also suggest an increase in cross-sectional vessel diameter of 6% and 4% with CO2 and acetazolamide, respectively. It remains unresolved whether this observation is due to a direct effect of the drug on the vessel walls or is simply pressure dependent.     

Effects of sufentanil on cerebral hemodynamics and intracranial pressure in patients with brain injury

BACKGROUND: The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). METHODS: Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. RESULTS: Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. CONCLUSIONS: The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.     

Application of transcranial Doppler sonography to evaluate cerebral hemodynamics in carotid artery disease. Comparative analysis of different hemodynamic variables

BACKGROUND AND PURPOSE: Transcranial Doppler sonography in combination with manipulation of cerebral resistance vessels is widely used to screen patients with suspected intracranial hemodynamic disturbances. Maximal flow velocity (Vmax), mean flow velocity (Vmean), cerebral pulsatility index (CPi), and cerebral resistance index (CRi) have all been used to describe cerebral hemodynamics. The present study examined CO2 reactivity of the above hemodynamic variables with respect to its variability between different age groups and its capability to discriminate between normal and abnormal findings. METHODS: Absolute and relative CO2 reactivity of Vmax, Vmean, CRi, and CPi were determined in both hemispheres in 30 young and 37 elderly control subjects and in 245 consecutive patients with strictly unilateral symptomatic (n = 101) or asymptomatic (n = 144) carotid artery disease (> 80% stenosis or occlusion). RESULTS: Hemispheric reactivities of Vmean, CRi, and CPi were significantly age dependent. Hemispheric Vmax reactivity and interhemispheric differences of individual reactivities (except absolute CPi reactivity) did not vary with age and could therefore be used to define normal values. Patient classification according to these values revealed different frequencies of subjects with pathological findings (3% for hemispheric Vmax reactivity, 5% to 7% for interhemispheric differences of Vmax or Vmean reactivity, 39% and 45% for interhemispheric differences of relative CRi and CPi reactivity, respectively). CONCLUSIONS: Hemispheric reactivities are less suitable to evaluate cerebral hemodynamics than interhemispheric differences, since most of the latter do not vary with age. However, interhemispheric differences vary with respect to their discriminatory power. Power is low for interhemispheric differences of Vmax and Vmean reactivity, since the corresponding frequencies of abnormal findings do not differ from the 5% frequency expected in the reference population (reference range defined as mean +/- 2 SD). With respect to the discriminatory power, interhemispheric differences of relative CRi and CPi reactivity may be superior to other parameters.     

Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain

OBJECTIVE: To determine the effect of continuous hypertonic (3%) saline/acetate infusion on intracranial pressure (ICP) and lateral displacement of the brain in patients with cerebral edema. DESIGN: Retrospective chart review. SETTINGS: Neurocritical care unit of a university hospital. PATIENTS: Twenty-seven consecutive patients with cerebral edema (30 episodes), including patients with head trauma (n = 8), postoperative edema (n = 5), nontraumatic intracranial hemorrhage (n = 8), and cerebral infarction (n = 6). INTERVENTION: Intravenous infusion of 3% saline/acetate to increase serum sodium concentrations to 145 to 155 mmol/L. MEASUREMENTS AND MAIN RESULTS: A reduction in mean ICP within the first 12 hrs correlating with an increase in the serum sodium concentration was observed in patients with head trauma (r2 = .91, p = .03), and postoperative edema (r2 = .82, p = .06), but not in patients with nontraumatic intracranial hemorrhage or cerebral infarction. In patients with head trauma, the beneficial effect of hypertonic saline on ICP was short-lasting, and after 72 hrs of infusion, four patients required intravenous pentobarbital due to poor ICP control. Among the 21 patients who had a repeat computed tomographic scan within 72 hrs of initiating hypertonic saline, lateral displacement of the brain was reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SEM]) and in patients with postoperative edema (3.1 +/- 1.6 to 1.1 +/- 0.7). This effect was not observed in patients with nontraumatic intracranial bleeding or cerebral infarction. The treatment was terminated in three patients due to the development of pulmonary edema, and was terminated in another three patients due to development of diabetes insipidus. CONCLUSIONS: Hypertonic saline administration as a 3% infusion appears to be a promising therapy for cerebral edema in patients with head trauma or postoperative edema. Further studies are required to determine the optimal duration of benefit and the specific patient population that is most likely to benefit from this treatment.     

Role of transcranial Doppler and stump pressure during carotid endarterectomy

BACKGROUND AND PURPOSE: The aim of our study was to clarify the pathophysiology of perioperative cerebral complications during carotid endarterectomy in our series. METHODS: By means of transcranial Doppler ultrasonography and stump pressure measurement, we monitored 112 patients who underwent carotid endarterectomy under general anesthesia for symptomatic or asymptomatic severe carotid stenosis. RESULTS: Of 18 patients who underwent carotid endarterectomy with intra-arterial shunt, 2 (11.1%) developed an ischemic stroke. Of the other 94 patients, one suffered a nucleocapsular hemorrhage and 5 had cerebral ischemic complications. In these 5 patients, the duration of clamping was significantly longer (mean +/- SD, 16.4 +/- 1.1 versus 12.7 +/- 2.6 minutes; P = .0019), and the decrease of middle cerebral artery mean velocity on clamping was significantly greater (mean +/- SD, 56.4 +/- 4.9% versus 28.8 +/- 20.2%; P = .0031), while stump pressure was not significantly different. Microembolic signals were recorded in 70 patients (62.5%) and were not associated with cerebral ischemic complications. The 7 patients who developed cerebral ischemic complications had a significantly higher percentage of stenosis in the contralateral internal carotid artery (mean +/- SD, 82.0 +/- 17.8% versus 29.3 +/- 36.4%; P = .0018). CONCLUSIONS: The results of our study suggest that the major complications of carotid endarterectomy may be due to hemodynamic factors. Stump pressure alone is not a reliable indicator of hemodynamic changes that predict cerebral ischemia. Particulate microembolism may cause more subtle changes in cerebral parenchyma, but further studies are needed to clarify this point.     

Transcranial Doppler and cortical microcirculation at increased intracranial pressure and during the Cushing response: an experimental study on rabbits

The effect of increased intracranial pressure on the flow velocity of the basilar artery was measured with transcranial ultrasonic Doppler in New Zealand White rabbits under alpha-chloralose anesthesia and artificial respiration. Laser Doppler flowmetry served to study changes of the cortical microcirculation. The results confirm a high inverse correlation of the diastolic flow velocity, the pulsatility index, and the resistance index with the cerebral perfusion pressure (CPP). During acute intracranial hypertension, however, these parameters do not show a good correlation with the local cortical blood flow. The absence of a correlation was evident over a wide CPP range down to values of 35 mm Hg. Only at CPP values below this critical threshold is the microcirculation impaired. The threshold is reached at pulsatility index values of more than 2.0 and at resistance index values of more than 0.8. Therefore, transcranial Doppler indices permit the detection of critical reductions of microcirculatory blood flow. The Cushing reaction occurred with a constant time lag of 5.5 +/- 0.7 seconds after the loss of CPP. The Cushing reaction did not establish systolic blood flow, which remained below the functional threshold, as concluded from the temporary loss of somatosensory evoked potentials.     

Specificity and sensitivity of distinctive chest radiographic and/or 67Ga images in the noninvasive diagnosis of sarcoidosis

1. Experimental chronic cerebral vasospasm induced by subarachnoid haemorrhage (SAH) in rabbits was studied in order to evaluate the efficacy of repeated i.v. infusion of Iloprost (ILO). 2. The mean diameter of the basilar artery of intact animals was calculated as 737.5 +/- 52.8 microns while this value was reduced to 237.5 +/- 22.96 microns after SAH. 3. In the ILO treated group the mean diameter of the basilar artery was significantly increased and found to be 593.75 +/- 64.0 microns. 4. No change was observed in intracranial pressure (ICP) except a slight decrease in mean arterial pressure when relatively higher doses of ILO were used. 5. These results were taken as evidence of the high therapeutic value and low side effects of ILO in the treatment of persisting cerebral vasospasm due to SAH.     

Experimental subarachnoid hemorrhage in rats: effect of intravenous alpha-alpha diaspirin crosslinked hemoglobin on hypoperfusion and neuronal death

BACKGROUND: Hemodilution with diaspirin crosslinked hemoglobin (DCLHb) ameliorates occlusive cerebral ischemia. However, subarachnoid hemoglobin has been implicated as a cause of cerebral hypoperfusion. The effect of intravenous DCLHb on cerebral perfusion and neuronal death after experimental subarachnoid hemorrhage was evaluated. METHODS: Rats (n = 48) were anesthetized with isoflurane and subarachnoid hemorrhage was induced by injecting 0.3 ml of autologous blood into the cistema magna. Each animal received one of the following regimens: Control, no hematocrit manipulation; DCLHb, hematocrit concentration decreased to 30% with DCLHb; or Alb, hematocrit concentration decreased to 30% with human serum albumin. The experiments had two parts, A and B. In part A, after 20 min, cerebral blood flow (CBF) was assessed with 14C-iodoantipyrine autoradiography. In part B, after 96 h, in separate animals, the number of dead neurons was determined in predetermined coronal sections by hematoxylin and eosin staining. RESULTS: Cerebral blood flow was greater for the DCLHb group than for the control group; and CBF was greater for the Alb group than the other two groups (P < 0.05). In one section, CBF was 45.5 +/- 10.9 ml x 100 g(-1) x min(-1) (mean +/- SD) for the control group, 95.3 +/- 16.6 ml x 100 g(-1) x min(-1) for the DCLHb group, and 138.1 +/- 18.7 ml x 100 g(-1) x min(-1) for the Alb group. The number of dead neurons was less in the Alb group (611 +/- 84) than in the control group (1,097 +/- 211), and was less in the DCLHb group (305 +/- 38) than in the other two groups (P < 0.05). CONCLUSIONS: These data support a hypothesis that hemodilution decreases hypoperfusion and neuronal death after subarachnoid hemorrhage. The data do not support the notion that intravascular molecular hemoglobin has an adverse effect on brain injury after subarachnoid hemorrhage.