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J A Ulatowski

Publications and source records attributed to J A Ulatowski.

At least 19 recordsLinked to original sources
PubMed2003

A pilot randomized trial of induced blood pressure elevation: effects on function and focal perfusion in acute and subacute stroke.

BACKGROUND: Small, unrandomized studies have indicated that pharmacologically induced blood pressure elevation may improve function in ischemic stroke, presumably by improving blood flow to ischemic, but noninfarcted tissue (which may be indicated by diffusion-perfusion mismatch on MRI). We conducted a pilot, randomized trial to evaluate effects of pharmacologically induced blood pressure elevation on function and perfusion in acute stroke. METHODS: Consecutive series of patients with large diffusion-perfusion mismatch were randomly assigned to induced blood pressure elevation ('treated' patients, n = 9) or conventional management ('untreated' patients, n = 6). RESULTS: There were no significant differences between groups at baseline. NIH Stroke Scale (NIHSS) scores were lower (better) in treated versus untreated patients at day 3 (mean 5.6 vs. 12.3; p = 0.01) and week 6-8 (mean 2.8 vs. 9.7; p < 0.04). Treated (but not untreated) patients showed significant improvement from day 1 to day 3 in NIHSS score (from mean 10.2 to 5.6; p < 0.002), cognitive score (from mean 58.7 to 27.9% errors; p < 0.002), and volume of hypoperfused tissue (mean 132 to 58 ml; p < 0.02). High Pearson correlations between the mean arterial pressure (MAP) and accuracy on daily cognitive tests indicated that functional changes were due to changes in MAP. CONCLUSION: Results warrant a full-scale, double-blind clinical trial to evaluate the efficacy and risk of induced blood pressure elevation in selective patients with acute/subacute stroke.

Adult↗
PubMed2001

Reperfusion of specific brain regions by raising blood pressure restores selective language functions in subacute stroke.

We report a series of six single subject studies examining the effects of pharmacological blood pressure elevation on regional brain perfusion and language function. Previous reports indicate that hypoperfusion of specific brain regions, as delineated by magnetic resonance perfusion weighted imaging (PWI), is associated with disruption of selective lexical functions. On this basis, we hypothesized that reperfusion of the same regions, in the absence of infarct in that region, would restore the associated lexical function. We present five patients with impaired lexical-semantics associated with poor perfusion, but not infarction, of Brodmann's area 22 (BA 22), and one patient with impaired lexical-semantics and a superimposed deficit in retrieving the phonological representations of words, associated with poor perfusion Brodmann's area 37 (BA 37) as well as BA 22. Each patient was treated with induced blood pressure elevation to increase perfusion of the ischemic and dysfunctional tissue. Daily testing of naming and comprehension, with stimulus sets matched for frequency, familiarity, and length, showed improved lexical-semantics in the patients who showed reperfusion of BA 22 and improved oral naming (but not lexical-semantics) in the patient who showed reperfusion of BA 37. These cases illustrate that loss of function with hypoperfusion of a circumscribed area of the brain, and recovery of the same function with improved perfusion of that brain region, can reveal brain/language relationships prior to reorganization after brain injury.

Acute Disease↗
PubMed2001

Two-compartment exchange model for perfusion quantification using arterial spin tagging.

The original well-mixed tissue model for the arterial spin tagging techniques is extended to a two-compartment model of restricted water exchange between microvascular (blood) and extravascular (tissue) space in the parenchyma. The microvascular compartment consists of arterioles, capillaries, and venules, with the blood/tissue water exchange taking place in the capillaries. It is shown that, in the case of limited water exchange, the individual FAIR (Flow-sensitive Alternating Inversion Recovery) signal intensities of the two compartments are comparable in magnitude, but are not overlapped in time. It is shown that when the limited water exchange is assumed to be fast, flows quantified from the signal-intensity difference are underestimated, an effect that becomes more significant for larger flows and higher magnetic field strengths. Experimental results on cat brain at 4.7 T comparing flow data from the FAIR signal-intensity difference with those from microspheres over a cerebral blood flow range from 15 to 150 mL 100 g(-1) min(-1) confirm these theoretic predictions. FAIR flow values with correction for restricted exchange, however, correlate well with the radioactive microsphere flow values. The limitations of the approach in terms of choice of the intercompartmental exchange rates are discussed.

Animals↗
PubMed2001

Cerebral vasculitis: diagnosis and follow-up with transcranial Doppler ultrasonography.

The authors report a patient with postpartum intracerebral hemorrhage associated with cerebral vasculitis. Cerebral circulation was assessed with transcranial Doppler (TCD) ultrasonography, magnetic resonance angiography, and conventional cerebral angiography. Initial TCD studies demonstrated bilateral patchy increased cerebral blood flow velocity (CBFV) in the anterior circulation with complete normalization during remission. This case report provides evidence that cerebral vasculitis leads to relevant CBFV changes and that the TCD technique may assist in diagnosis and follow-up of these patients.

Adult↗
PubMed2001

Diagnostic impact of early transcranial Doppler ultrasonography on the TOAST classification subtype in acute cerebral ischemia.

OBJECTIVE: The impact of early transcranial Doppler ultrasonography (TCD) upon stroke subtype diagnosis is unknown and may affect therapeutic strategies. In this study, the diagnostic usefulness of TCD in stroke subtype diagnosis according to the criteria of the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) study was investigated in patients with acute cerebral ischemia. METHODS: TCD examination within 24 h of symptom onset was performed in 50 consecutive patients with acute cerebral ischemia. Of these 54% were female. Sixty percent of patients were black, 36% white, and 4% Asian. Initial TOAST stroke subtype diagnosis (ITSSD) was based upon clinical presentation and initial brain imaging studies. Modified TOAST stroke subtype diagnosis was determined subsequently after additional review of the TCD examination. Final TOAST stroke subtype diagnosis was determined at hospital discharge, incorporating all diagnostic studies. Using final TOAST stroke subtype diagnosis as the 'gold standard' ITSSD and modified TOAST stroke subtype diagnosis were compared in order to determine additional benefit from the information obtained by TCD. Data were collected retrospectively by a single investigator. RESULTS: ITSSD classified 23 of 50 (46%) patients correctly. After TCD, 30 of 50 (60%) patients were classified correctly, for an absolute benefit of 14% and a relative benefit of 30% (p = 0.018). Most benefit from TCD was observed in the TOAST stroke subtype category large-artery atherosclerosis, in particular in patients with intracranial vascular disease. In this category, ITSSD had a sensitivity of 27% which increased to 64% after TCD (p = 0.002). CONCLUSION: TCD within 24 h of symptom onset improves the accuracy of early stroke subtype diagnosis in patients with acute cerebral ischemia due to large-artery atherosclerosis. This may have clinical implications for early therapeutic interventions.

Acute Disease↗
PubMed2001

Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Current transcranial Doppler criteria for vasospasm after aneurysmal subarachnoid hemorrhage are not age specific. We analyzed the effect of age on cerebral blood flow velocity changes after subarachnoid hemorrhage and constructed an age-adjusted predictive model of cerebral blood flow velocity in subarachnoid hemorrhage patients. METHODS: We identified patients with aneurysmal subarachnoid hemorrhage admitted between 1991 and 1999 with a prospective transcranial Doppler database. Eighty-one patients, with complete medical records and transcranial Doppler examinations of the vessels of interest, were included. Patients were subdivided into 2 groups by age: younger, <68 years of age (n=47) and older, >/=68 years of age (n=34). Maximum mean flow velocity and incidence of symptomatic vasospasm were reported. Linear and nonlinear regression analyses were performed. RESULTS: Middle cerebral artery and internal carotid artery mean flow velocity were lower in older patients (median 76 versus 114 cm/s and 76 versus 126 cm/s, respectively; P<0.003). Incidence of symptomatic vasospasm was lower in older patients (44% versus 66%; P=0.05). Older patients developed symptomatic vasospasm at lower middle cerebral artery (median 57 versus 103 cm/s; P=0.04) and internal carotid artery (median 54 versus 81 cm/s, P=0.02) mean flow velocity. Relationship between middle cerebral artery and internal carotid artery mean flow velocity and age was quadratic (ANOVA, P<0.0001). CONCLUSIONS: Older patients have a lower incidence of symptomatic vasospasm, and such vasospasm develops at lower cerebral blood flow velocity than younger patients. A quadratic relationship was found between age and cerebral blood flow velocity. This model could be used to create an age-adjusted nomogram that might improve diagnostic capabilities of transcranial Doppler.

Adult↗
PubMed2000

Early predictors of outcome in patients receiving hypervolemic and hypertensive therapy for symptomatic vasospasm after subarachnoid hemorrhage.

OBJECTIVE: Symptomatic vasospasm after subarachnoid hemorrhage (SAH) is associated with a high incidence of permanent disability and death. For early identification of patients who are at risk for poor outcome, we determined the predictors of outcome in patients with symptomatic vasospasm after SAH. DESIGN: We retrospectively determined the prognostic value of clinical characteristics and computed tomographic scan both at admission and at the time of initiation of hypervolemic and hypertensive therapy. SETTINGS: Neurosciences critical care unit at a University hospital. PATIENTS: A total of 70 consecutive patients who developed symptomatic vasospasm after SAH. INTERVENTION: Treatment with oral nimodipine, hypervolemic therapy, and hypertensive therapy. Angioplasty and intra-arterial papaverine were used in patients with vasospasm resistant to standard treatment. MEASUREMENTS AND MAIN RESULTS: Poor outcome, defined as Glasgow Outcome Scale Score of 3-5 at 2 months or discharge, was observed in 32 (46%) patients. In the logistic regression analysis, a Glasgow Coma Scale (GCS) score of < or =11 (odds ratio, 11.0; 95% confidence interval, 3.6-39.3) and hydrocephalus (odds ratio, 4.3; 95% confidence interval, 1.2-18.2) at the time of initiation of hypervolemic and hypertensive therapy were significantly associated with poor outcome. Poor outcome was observed in 91% of the patients who had both a GCS score of < or =11 and hydrocephalus compared with 15% of patients with a GCS score of >11 and no hydrocephalus at the time of initiation of hypervolemic and hypertensive therapy. A GCS score of < or =11 was also independently associated with length of intensive care unit stay (F ratio = 18.0; p = .0011) and hospital stay (F ratio = 9.2; p = .0034) after initiation of hypervolemic and hypertensive therapy. CONCLUSIONS: The results of this study suggest that outcome in patients with symptomatic vasospasm can be effectively predicted by routinely available information, including GCS score at the time of initiation of hypervolemic and hypertensive therapy. This information can be used for selection and stratification of patients in future treatment studies of patients with symptomatic vasospasm.

Analysis of Variance↗
PubMed2000

Early identification of patients at risk for symptomatic vasospasm after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: To develop a scheme for early identification of individuals at risk for symptomatic vasospasm after subarachnoid hemorrhage (SAH). DESIGN: Analysis of prospectively collected data from the placebo-treated group in a multicenter clinical trial. SETTINGS: Fifty-four neurosurgical centers in North America. MEASUREMENTS AND MAIN RESULTS: We identified independent predictors of symptomatic vasospasm using stepwise logistic regression analysis from demographic, clinical, laboratory, and neuroimaging characteristics of the participants. We developed a scoring system (symptomatic vasospasm risk index) based on a combination of these predictors. Out of 283 patients in the analysis (all treated with oral nimodipine), 93 (33%) developed symptomatic vasospasm within 14 days after SAH. There were four independent predictors of symptomatic vasospasm: thickness of subarachnoid clot on computed tomographic scan (odds ratio [OR], 4.1; 95% confidence interval [CI], 1.8-10.0); early rise in middle cerebral artery mean flow velocity (MCA-MFV), defined as a value > or =110 cm/sec recorded on or before post-SAH day 5 (OR, 1.9; 95% CI, 1.1-3.3), Glasgow Coma Scale score <14 (OR, 1.8; 95% CI, 1.1-3.1); and rupture of anterior cerebral or internal carotid artery aneurysm (OR, 1.9; 95% CI, 1.0-3.4). The probability of identifying patients who would develop symptomatic vasospasm (percentage of area under receiver operating characteristics curve +/- SEM) was higher with symptomatic vasospasm risk index (68%+/-8%) compared with thickness of clot (62%+/-8%; p = .08) or MCA-MFV (45%+/-7%, p < .05) criteria alone. CONCLUSIONS: Patients at high risk for symptomatic vasospasm can be identified early in the course of SAH using a risk index. A risk index based on a combination of variables may represent a predictive paradigm superior to conventionally used criteria based on clot thickness or MCA-MFV criteria.

Adult↗
PubMed2000

Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions.

OBJECTIVE: To determine the short- and long-term outcomes after successful reversal of transtentorial herniation by medical treatment. Although it has been recognized that aggressive medical management can reverse transtentorial herniation, it is believed that overall outcome in such patients is poor. DESIGN: Prospective cohort study. SETTING: Neurocritical care unit of a university hospital. PATIENTS: A total of 28 consecutive patients who underwent an episode of transtentorial herniation (defined as decrease in level of consciousness accompanied by pupillary dilation) secondary to a supratentorial mass lesion followed by successful reversal. INTERVENTION: Herniation was reversed by using a combination of hyperventilation, mannitol and hypertonic saline. MEASUREMENTS AND MAIN RESULTS: The following outcomes were analyzed: risk of second herniation, radiologic evidence of structural damage or vascular compromise related to herniation on post-herniation computed tomographic scan, in-hospital mortality, and long-term functional outcome using Rankin score and Barthel index. A total of 32 episodes of transtentorial herniations were reversed in 28 patients during a 14-month period. The most common precipitating cause were edema (n = 23) or new/expanding intracerebral hematoma (n = 5). After first reversal of transtentorial herniation in 28 patients, a second herniation episode was observed in 16 patients after a mean interval of 88.2 hrs (range, 23-432 hrs); four were successfully reversed. On follow-up computed tomographic scan, hypodense lesion in midbrain (n = 6), temporal lobe contusion (n = 2), posterior cerebral artery (n = 3), and middle cerebral artery (n = 1) infarction were visualized in a minority of patients. The in-hospital mortality was 60% (n = 15) with brain death being the cause of death in 13 patients; care was withdrawn in eight patients. Second episode of herniation (p = .002) and midbrain involvement during herniation (p = .02) were associated with in-hospital mortality. During a mean follow-up period of 11.4+/-4.2 months, two patients died of cerebral neoplasm and human immunodeficiency virus-related sepsis, respectively. Of the 11 survivors, 7 were functionally independent (Rankin score <3 and Barthel index >60). CONCLUSIONS: Although mortality after transtentorial herniation is high, we found a prominent potential for meaningful recovery with aggressive medical reversal of transtentorial herniation. Our study implies that timely medical intervention for reversing transtentorial herniation can result in preservation of neurologic function.

Adult↗
PubMed2000

Treatment of intraventricular hemorrhage with urokinase : effects on 30-Day survival.

BACKGROUND AND PURPOSE: Intraventricular hemorrhage (IVH) remains associated with high morbidity and mortality. Therapy with external ventricular drainage alone has not modified outcome in these patients. METHODS: Twelve pilot IVH patients who required external ventricular drainage were prospectively treated with intraventricular urokinase followed by the randomized, double-blinded allocation of 8 patients to either treatment or placebo. Observed 30-day mortality was compared with predicted 30-day mortality obtained by use of a previously validated method. RESULTS: Twenty patients were enrolled; admission Glasgow Coma Scale score in 11 patients was </=8; 10 patients had pulse pressure <85 mm Hg. Mean+/-SD ICH volume in 16 patients was 6.21+/-7.53 cm(3) (range 0 to 23.88 cm(3)), and mean+/-SD intraventricular hematoma volume was 44.26+/-31.65 cm(3) (range 1.31 to 100.36 cm(3)). Four patients (20%) died within 30 days. Predicted mortality for these 20 patients was 68.42% (range 3% to 100%). Probability of observing </=4 deaths among 20 patients under a 68.42% expected mortality is 0.000012. CONCLUSIONS: Intraventricular urokinase may significantly improve 30-day survival in IVH patients. On the basis of current evidence, a double-blinded, placebo-controlled, multicenter study that uses thrombolysis to treat IVH has received funding and began January 1, 2000.

Adult↗
PubMed1999

In vivo determination of absolute cerebral blood volume using hemoglobin as a natural contrast agent: an MRI study using altered arterial carbon dioxide tension.

The ability of the magnetic resonance imaging transverse relaxation time, R2 = 1/T2, to quantify cerebral blood volume (CBV) without the need for an exogenous contrast agent was studied in cats (n = 7) under pentobarbital anesthesia. This approach is possible because R2 is directly affected by changes in CBF, CBV, CMRO2, and hematocrit (Hct), a phenomena better known as the blood-oxygenation-level-dependent (BOLD) effect. Changes in CBF and CBV were accomplished by altering the carbon dioxide pressure, PaCO2, over a range from 20 to 140 mm Hg. For each PaCO2 value, R2 in gray and white matter were determined using MRI, and the whole-brain oxygen extraction ratio was obtained from arteriovenous differences (sagittal sinus catheter). Assuming a constant CMRO2, the microvascular CBV was obtained from an exact fit to the BOLD theory for the spin-echo effect. The resulting CBV values at normal PaCO2 and normalized to a common total hemoglobin concentration of 6.88 mmol/L were 42+/-18 microL/g (n = 7) and 29+/-19 microL/g (n = 5) for gray and white matter, respectively, in good agreement with the range of literature values published using independent methodologies. The present study confirms the validity of the spin-echo BOLD theory and, in addition, shows that blood volume can be quantified from the magnetic resonance imaging spin relaxation rate R2 using a regulated carbon dioxide experiment.

Animals↗
PubMed1999

Administration of hypertonic (3%) sodium chloride/acetate in hyponatremic patients with symptomatic vasospasm following subarachnoid hemorrhage.

A retrospective study was carried out to evaluate the effect of hypertonic (3%) saline chloride/acetate on various hemodynamic parameters in mildly hyponatremic patients with symptomatic vasospasm following aneurysmal subarachnoid hemorrhage (SAH). We identified 29 hyponatremic (serum sodium < 135 mEq/L) patients who received hypertonic (3%) sodium chloride/acetate as a continuous infusion. Administration of hypertonic (3%) sodium chloride/acetate resulted in higher central venous pressures and positive fluid balance, with a concomitant increase in serum sodium and chloride concentrations without metabolic acidosis. There were no changes in mean cerebral blood flow velocities after infusion of hypertonic (3%) sodium chloride/acetate. We found no reports of congestive heart failure, pulmonary edema, metabolic acidosis, coagulopathy, intracranial hemorrhages, or central pontine myelinolysis in any of these patients. We conclude that hypertonic (3%) sodium chloride/acetate can be administered to patients with mild hyponatremia in the setting of symptomatic vasospasm following SAH without untoward effects. Sample size and limitations of a retrospective analysis preclude conclusions about safety and efficacy of hypertonic (3%) sodium chloride/acetate administration in this patient population. However, our results support justification for a prospective, randomized, double-blind trial of hypertonic (3%) sodium chloride/acetate versus normal saline in patients with symptomatic vasospasm following SAH.

Acetates↗
PubMed1999

Plasma exchange versus intravenous immunoglobulin treatment in myasthenic crisis.

We performed a retrospective multicenter chart review to compare the efficacy and tolerance of plasma exchange (PE) and intravenous immunoglobulin (i.v.Ig) in treatment of 54 episodes of myasthenic crisis. After adjustment for other variables, PE (compared with i.v.Ig) was associated with a superior ventilatory status at 2 weeks (partial F = 6.2, p = 0.02) and 1 month functional outcome (partial F = 4.5, p = 0.04). However, the complication rate was higher with PE compared with i.v.Ig (13 versus 5 episodes, p = 0.07).

Adult↗
PubMed1998

Quantitative assessment of blood flow, blood volume and blood oxygenation effects in functional magnetic resonance imaging.

The ability to measure the effects of local alterations in blood flow, blood volume and oxygenation by nuclear magnetic resonance has stimulated a surge of activity in functional MRI of many organs, particularly in its application to cognitive neuroscience. However, the exact description of these effects in terms of the interrelations between the MRI signal changes and the basic physiological parameters has remained an elusive goal. We here present this fundamental theory for spin-echo signal changes in perfused tissue and validate it in vivo in the cat brain by using the physiological alteration of hypoxic hypoxia. These experiments show that high-resolution absolute blood volume images can be obtained by using hemoglobin as a natural intravascular contrast agent. The theory also correctly predicts the magnitude of spin-echo MRI signal intensity changes on brain activation and thereby provides a sound physiological basis for these types of studies.

Animals↗
PubMed1998

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.

Adult↗
PubMed1998

Treatment of refractory intracranial hypertension with 23.4% saline.

OBJECTIVE: To evaluate the effect of intravenous bolus administration of 23.4% saline (8008 mOsm/L) on refractory intracranial hypertension (RIH) in patients with diverse intracranial diseases. DESIGN: Retrospective chart review. SETTING: A neurosciences intensive care unit in a university hospital. PATIENTS: We present eight patients and a total of 20 episodes of increased intracranial pressure (ICP) resistant to standard modes of therapy. Five patients had subarachnoid hemorrhage, one patient had traumatic brain injury, one had a brain tumor, and another had spontaneous basal ganglia hemorrhage. Seven patients had intraventricular catheters, and one had a subarachnoid pressure screw placed. We monitored continuously mean ICP, serum sodium concentrations, mean arterial pressure, cerebral perfusion pressure (CPP), central venous pressure, and urine output before and after the administration of hypertonic saline (HS). Post mortem examination of the brain was performed in two patients. INTERVENTION: Intravenous bolus administration of 30 mL of 23.4% saline. MEASUREMENTS AND MAIN RESULTS: There was a significant (p < .05) decrease in ICP from a median of 41.5 mm Hg before HS to 17 mm Hg at 1 hr, 16 mm Hg at 2 hrs, and 14 mm Hg at 3 hrs after HS administration. In 80% of cases, ICP decreased by >50% of the pretreatment value over a duration of 21.2+/-10.3 mins. ICP decreased to <20 mm Hg in 65% of all cases and the mean time for it to again exceed 20 mm Hg was 6.3+/-4.9 hrs. There was a significant improvement in CPP, from 64.7+/-19 (SD) mm Hg before HS to 85.6+/-18 mm Hg (1 hr) and 83+/-18 mm Hg (3 hrs) after HS. There were no significant differences in the other variables measured. The post mortem examinations showed no white matter changes or subdural collections. CONCLUSIONS: This preliminary case series suggests that the intravenous bolus administration of 23.4% saline reduces ICP and augments CPP in patients with resistant increased ICP. This reduction can be maintained for several hours while other therapeutic measures are being considered. The patient population most likely to respond to this therapy needs to be further defined. Although more research is needed, this treatment is promising as a new modality for RIH because of its ICP-lowering effect without intravascular volume depletion.

Adult↗
PubMed1998

Noninvasive detection of cerebral hypoperfusion and reversible ischemia from reductions in the magnetic resonance imaging relaxation time, T2.

The hypothesis was tested that hypoperfused brain regions, such as the ischemic penumbra, are detectable by reductions in absolute transverse relaxation time constant (T2) using magnetic resonance imaging (MRI). To accomplish this, temporal evolution of T2 was measured in several models of hypoperfusion and focal cerebral ischemia in the rat at 9.4 T. Occurrence of acute ischemia was determined through the absolute diffusion constant D(av) = 1/3 TraceD, while perfusion was assessed by dynamic contrast imaging. Three types of regions at risk of infarction could be distinguished: (1) areas with reduced T2 (4% to 15%, all figures relative to contralateral hemisphere) and normal D(av), corresponding to hypoperfusion without ischemia; (2) areas with both reduced T2 (4% to 12%) and D(av) (22% to 49%), corresponding to early hypoperfusion with ischemia; (3) areas with increased T2 (2% to 9%) and reduced D(av) (28% to 45%), corresponding to irreversible ischemia. In the first two groups, perfusion-deficient regions detected by bolus tracking were similar to those with initially reduced T2. In the third group, bolus tracking showed barely detectable arrival of the tracer in the region where D(av) was reduced. We conclude that T2 reduction in acute ischemia can unambiguously identify regions at risk and potentially discriminate between reversible and irreversible hypoperfusion and ischemia.

Animals↗