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Stephan A Mayer

Publications and source records attributed to Stephan A Mayer.

At least 37 records · Page 2Linked to original sources

Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage.

BACKGROUND: Cardiac troponin I (cTI) release occurs frequently after subarachnoid hemorrhage (SAH) and has been associated with a neurogenic form of myocardial injury. The prognostic significance and clinical impact of these elevations remain poorly defined. METHODS AND RESULTS: We studied 253 SAH patients who underwent serial cTI measurements for clinical or ECG signs of potential cardiac injury. These patients were drawn from an inception cohort of 441 subjects enrolled in the Columbia University SAH Outcomes Project between November 1998 and August 2002. Peak cTI levels were divided into quartiles or classified as undetectable. Adverse in-hospital events were prospectively recorded, and outcome at 3 months was assessed with the modified Rankin Scale. Admission predictors of cTI elevation included poor clinical grade, intraventricular hemorrhage, loss of consciousness at ictus, global cerebral edema, and a composite score of physiological derangement (all P< or =0.01). Peak cTI level was associated with an increased risk of echocardiographic left ventricular dysfunction (odds ratio [OR], 1.3 per quintile; 95% CI, 1.0 to 1.7; P=0.03), pulmonary edema (OR, 2.1 per quintile; 95% CI, 1.6 to 2.7; P<0.001), hypotension requiring pressors (OR, 1.9 per quintile; 95% CI, 1.5 to 2.3; P<0.001), and delayed cerebral ischemia from vasospasm (OR, 1.3 per quintile; 95% CI, 1.07 to 1.7; P=0.01). Peak cTI levels were predictive of death or severe disability at discharge after controlling for age, clinical grade, and aneurysm size (adjusted OR, 1.4 per quintile; 95% CI, 1.1 to 1.9; P=0.02), but this association was no longer significant at 3 months. CONCLUSIONS: cTI elevation after SAH is associated with an increased risk of cardiopulmonary complications, delayed cerebral ischemia, and death or poor functional outcome at discharge.

Adult↗

Recombinant activated factor VII for acute intracerebral hemorrhage.

BACKGROUND: Intracerebral hemorrhage is the least treatable form of stroke and is associated with high mortality. Among patients who undergo computed tomography (CT) within three hours after the onset of intracerebral hemorrhage, one third have an increase in the volume of the hematoma related to subsequent bleeding. We sought to determine whether recombinant activated factor VII (rFVIIa) can reduce hematoma growth after intracerebral hemorrhage. METHODS: We randomly assigned 399 patients with intracerebral hemorrhage diagnosed by CT within three hours after onset to receive placebo (96 patients) or 40 microg of rFVIIa per kilogram of body weight (108 patients), 80 microg per kilogram (92 patients), or 160 microg per kilogram (103 patients) within one hour after the baseline scan. The primary outcome measure was the percent change in the volume of the intracerebral hemorrhage at 24 hours. Clinical outcomes were assessed at 90 days. RESULTS: Hematoma volume increased more in the placebo group than in the rFVIIa groups. The mean increase was 29 percent in the placebo group, as compared with 16 percent, 14 percent, and 11 percent in the groups given 40 microg, 80 microg, and 160 microg of rFVIIa per kilogram, respectively (P=0.01 for the comparison of the three rFVIIa groups with the placebo group). Growth in the volume of intracerebral hemorrhage was reduced by 3.3 ml, 4.5 ml, and 5.8 ml in the three treatment groups, as compared with that in the placebo group (P=0.01). Sixty-nine percent of placebo-treated patients died or were severely disabled (as defined by a modified Rankin Scale score of 4 to 6), as compared with 55 percent, 49 percent, and 54 percent of the patients who were given 40, 80, and 160 microg of rFVIIa, respectively (P=0.004 for the comparison of the three rFVIIa groups with the placebo group). Mortality at 90 days was 29 percent for patients who received placebo, as compared with 18 percent in the three rFVIIa groups combined (P=0.02). Serious thromboembolic adverse events, mainly myocardial or cerebral infarction, occurred in 7 percent of rFVIIa-treated patients, as compared with 2 percent of those given placebo (P=0.12). CONCLUSIONS: Treatment with rFVIIa within four hours after the onset of intracerebral hemorrhage limits the growth of the hematoma, reduces mortality, and improves functional outcomes at 90 days, despite a small increase in the frequency of thromboembolic adverse events.

Adult↗

Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Phenytoin (PHT) is routinely used for seizure prophylaxis after subarachnoid hemorrhage (SAH), but may adversely affect neurologic and cognitive recovery. METHODS: We studied 527 SAH patients and calculated a "PHT burden" for each by multiplying the average serum level of PHT by the time in days between the first and last measurements, up to a maximum of 14 days from ictus. Functional outcome at 14 days and 3 months was measured with the modified Rankin scale, with poor functional outcome defined as dependence or worse (modified Rankin Scale > or =4). We assessed cognitive outcomes at 14 days and 3 months with the telephone interview for cognitive status. RESULTS: PHT burden was associated with poor functional outcome at 14 days (OR, 1.5 per quartile; 95% CI, 1.3 to 1.8; P<0.001), although not at 3 months (P=0.09); the effect remained (OR, 1.6 per quartile; 95% CI, 1.2 to 2.1; P<0.001) after correction for admission Glasgow Coma Scale, fever, stroke, age, National Institutes of Health Stroke Scale > or =10, hydrocephalus, clinical vasospasm, and aneurysm rebleeding. Seizure in hospital (OR, 4.1; 95% CI, 1.5 to 11.1; P=0.002) was associated with functional disability in a univariate model only. Higher quartiles of PHT burden were associated with worse telephone interview for cognitive status scores at hospital discharge (P<0.001) and at 3 months (P=0.003). CONCLUSIONS: Among patients treated with PHT, burden of exposure to PHT predicts poor neurologic and cognitive outcome after SAH.

Cognition Disorders↗

Predictors and impact of aneurysm rebleeding after subarachnoid hemorrhage.

BACKGROUND: Aneurysm rebleeding has historically been an important cause of mortality after subarachnoid hemorrhage (SAH). OBJECTIVE: To describe the frequency and impact of rebleeding in the modern era of aneurysm care, which emphasizes early surgical or endovascular treatment. DESIGN: Inception cohort. SETTING: Tertiary care medical center. PATIENTS: A total of 574 patients enrolled in the Columbia University SAH Outcomes Project between August 1996 and June 2002. Early aneurysm repair was performed whenever feasible. MAIN OUTCOME MEASURES: Rebleeding was defined by prespecified clinical and radiographic criteria, excluding prehospital, intraprocedural, and postrepair events. Functional outcome was assessed at 3 months with the modified Rankin Scale. Multiple logistic regression was used to identify predictors of rebleeding, poor functional outcome, and mortality. RESULTS: Rebleeding occurred in 40 (6.9%) of the 574 patients; most cases (73%) occurred within 3 days of ictus. Hunt-Hess grade on admission (odds ratio [OR], 1.92 per grade; 95% confidence interval [CI], 1.33-2.75; P<.001) and maximal aneurysm diameter (OR, 1.07/mm; 95% CI, 1.01-1.13; P = .005) were independent predictors of rebleeding. After controlling for Hunt-Hess grade and aneurysm size, rebleeding was associated with a markedly reduced chance of survival with functional independence (modified Rankin Scale score, </=4; OR, 0.08; 95% CI, 0.02-0.34) at 3 months. CONCLUSIONS: Despite an aggressive management strategy, rebleeding still occurred in 6.9% of patients and was associated with a dismal outcome. Poor Hunt-Hess grade and larger aneurysm size are related to rebleeding. Pharmacologic therapy to reduce the risk of rebleeding before aneurysm repair, particularly in patients with poor grade neurologic status and large aneurysms, deserves renewed attention.

Aged↗

Paroxysmal apnea and vasomotor instability following medullary infarction.

BACKGROUND: Central hypoventilation and paroxysmal hypertension are uncommon complications of medullary infarction. To our knowledge, the combination of these autonomic complications of medullary stroke has not previously been reported. OBJECTIVE: To describe a patient who experienced life-threatening paroxysmal attacks of central apnea and vasomotor instability 3 months after medullary infarction, a combination of symptoms that is unusual. PATIENT, METHODS, AND RESULTS: Following a right lateral medullary infarction, an otherwise stable 70-year-old woman developed recurrent episodes of apnea (PCO2), > 100 mm Hg), blood pressure instability (systolic blood pressure, > 200 to < 100 mm Hg), and mental status changes (from agitation to coma) within hours of removal from mechanical ventilation. These attacks occurred repeatedly after removal from mechanical ventilation and were prevented by diaphragm pacing with a phrenic nerve pacemaker and nocturnal mechanical ventilation via a tracheostomy. CONCLUSIONS: A syndrome of life-threatening central hypoventilation and vasomotor instability can occur after medullary infarction. Placement of a phrenic nerve pacemaker can prevent these complications, without the functional limitations imposed by continuous mechanical ventilation.

Aged↗

Treatment of massive cerebral infarction.

Stroke is the third leading cause of death in the United States, with a person dying every 3 minutes of a stroke. Massive ischemic stroke accounts for 10% to 20% of ischemic strokes, has traditionally been associated with a high mortality and morbidity, and requires a unique management strategy. Recent advances in management, fueled by an increased understanding of the pathophysiology, may help decrease mortality and improve outcomes. Rapid access to reperfusion therapies remains the most critical element of stroke care and the cornerstone of therapy. This article focuses on newer therapies, including osmotic therapy, hypothermia, maintained normothermia, strict glycemic control, induced hypertension, and hemicraniectomy, all of which show promise for reducing mortality and improving functional outcome. These interventions have become integrated into neurologic intensive care units around the world. They are complicated, require a high level of expertise, and carry a significant learning curve. In order for these new management techniques to be effective, an expedited, aggressive, meticulous, and potentially prolonged medical management approach is needed. To accomplish this there is a growing need for focused specialists in the areas of neurointensive care and stroke.

Blood Pressure↗

Intensive care unit management of interventional neuroradiology patients.

The management of interventional neurologic patients in the intensive care unit is based on their underlying disease for the most part. Patients with ischemic stroke are largely managed like patients with ischemic stroke who have not undergone interventional procedures, and the same is true for those with an aneurysmal subarachnoid hemorrhage or intracerebral hemorrhage secondary to an arteriovenous malformation, for example.Having said this, there are some special considerations that require special mention when it comes to managing patients after catheter-based procedures.

Brain Ischemia↗

Treatment of intracerebral haemorrhage.

Apart from management in a specialised stroke or neurological intensive care unit, until very recently no specific therapies improved outcome after intracerebral haemorrhage (ICH). In a recent phase II trial, recombinant activated factor VII (eptacog alfa) reduced haematoma expansion, mortality, and disability when given within 4 h of ICH onset; a phase III trial (the FAST trial) is now in progress. Ventilatory support, blood-pressure reduction, intracranial-pressure monitoring, osmotherapy, fever control, seizure prophylaxis, and nutritional supplementation are the cornerstones of supportive care in intensive care units. Ventricular drainage should be considered in all stuporous or comatose patients with intraventricular haemorrhage and acute hydrocephalus. Given the lack of benefit seen in a the recent STICH trial, emergency surgical evacuation within 72 h of onset should be reserved for patients with large (>3 cm) cerebellar haemorrhages, or those with large lobar haemorrhages, substantial mass effect, and rapidly deteriorating condition.

Brain↗

Continuous EEG monitoring in patients with subarachnoid hemorrhage.

Patients with subarachnoid hemorrhage (SAH) are at risk for seizures and delayed cerebral ischemia, both of which can be detected with continuous EEG monitoring (cEEG). Ischemia can be detected with EEG at a reversible stage. CEEG may be most useful in patients with poor grade SAH, as the neurological exam is of limited utility in these stuporous or comatose patients. Seizures have been detected in 19% of SAH patients undergoing cEEG, with the vast majority (95%) of these seizures being nonconvulsive and without any detectable clinical correlate. Applying quantitative analysis to the cEEG (relative alpha variability, post-stimulation alpha/delta ratio) allows reliable detection of ischemia from vasospasm, with EEG changes often preceding changes in the clinical exam and other non-continuous monitoring techniques by up to two days. In patients at risk for developing vasospasm, cEEG monitoring, preferably with quantitative EEG analysis, should be started as early as possible and carried out for up to 14 days after the SAH. CEEG findings may lead to therapeutic (e.g., antiepileptic medication, hypertensive therapy, angioplasty) or additional diagnostic interventions such as angiography, CT or MRI.

Electroencephalography↗

Multimodal brain monitoring in the neurological intensive care unit: where does continuous EEG fit in?

Continuous EEG (cEEG) is a vital component of patient monitoring in the neurologic intensive care unit, allowing the intensivist to diagnose nonconvulsive seizure activity. Though still in its infancy, Fourier-transformed cEEG data are also increasingly being used in ICUs to monitor global cerebral activity and cortical function. In conjunction with other components of multimodality neurologic monitoring, including intracranial pressure, cerebral blood flow, brain tissue oxygen tension monitoring, transcranial Doppler, and microdialysis monitoring, cEEG provides unique data regarding the electrical activity of the brain. The main challenge for clinicians and researchers will be to understand how these different aspects of multimodality monitoring relate to each other, and how physiologic variables such as blood pressure, osmolality, and temperature can be manipulated to optimize cerebral function and tissue survival in the setting of acute injury.

Brain↗

Dobutamine versus milrinone after subarachnoid hemorrhage.

OBJECTIVE: Neurogenic stunned myocardium is a well-recognized complication of subarachnoid hemorrhage. Dobutamine and milrinone are both used for neurogenic stunned myocardium, but there are few data comparing them after subarachnoid hemorrhage. METHODS: We compared the physiological dose response of dobutamine and milrinone in patients with subarachnoid hemorrhage requiring a pulmonary artery catheter. We located 11 patients who received either inotrope. Physiological data were fitted to a mixed model accounting for drug, dose, and between-patient variation. RESULTS: There were 11 patients who had 152 pulmonary artery catheter measurements. Two received both inotropes (but not within 4 h of each other), 2 only milrinone, and 7 only dobutamine. The groups had similar clinical and physiological characteristics. After adjustment for vasopressin, milrinone was significantly more potent in increasing cardiac output (P <0.0001) and stroke volume (P=0.03), while decreasing vascular resistance (P <0.0001) and systolic blood pressure (P=0.008), than dobutamine. CONCLUSION: These data suggest that milrinone and dobutamine should be used in different clinical situations. Milrinone may be more effective in patients with severely depressed systolic function but who have at least normal vascular resistance and blood pressure and in whom raising cardiac output is the primary goal. Dobutamine may be superior when vascular resistance or blood pressure is low.

Adrenergic beta-Agonists↗

Decompressive hemicraniectomy for poor-grade aneurysmal subarachnoid hemorrhage patients with associated intracerebral hemorrhage: clinical outcome and quality of life assessment.

OBJECTIVE: Decompressive hemicraniectomy has been proposed as a potential treatment strategy in patients with poor-grade aneurysmal subarachnoid hemorrhage presenting with focal intracerebral hemorrhage causing significant mass effect. Although hemicraniectomy improves overall survival rates, the long-term quality of life (QoL) for survivors in this patient population has not been reported. METHODS: Using adjudicated outcome assessments, we compare long-term clinical outcomes and QoL between a group of patients with poor-grade aneurysmal subarachnoid hemorrhage receiving decompressive hemicraniectomy (n=12) and a control group of similar patients managed more conservatively (n=10). RESULTS: Patients receiving decompressive hemicraniectomy experienced a statistically insignificant decrease in short-term mortality compared with controls (25 versus 42%); however, long-term QoL in hemicraniectomy survivors was generally poor. Furthermore, hemicraniectomy patients did not experience an increase in mean quality-adjusted life years over control patients (2.31 versus 2.22 yr). CONCLUSION: Decompressive hemicraniectomy prolongs short-term survival in patients with poor-grade aneurysmal subarachnoid hemorrhage with associated intracerebral hemorrhage; however, this trend is not statistically significant, and the overall QoL experienced by survivors is poor. Decompressive hemicraniectomy may be indicated if performed early in a select subset of patients. On the basis of our preliminary data, large prospective studies to investigate this issue further may not be warranted.

Adult↗

Effect of prior statin use on functional outcome and delayed vasospasm after acute aneurysmal subarachnoid hemorrhage: a matched controlled cohort study.

OBJECTIVE: Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), which exhibit beneficial cerebrovascular effects by modulating inflammation and nitric oxide production, have not been evaluated in acute aneurysmal subarachnoid hemorrhage (SAH) patients. The effect of prior statin use on 14-day functional outcome and on prevention of vasospasm-induced delayed cerebral ischemia (DCI) or stroke during hospitalization was analyzed. METHODS: We conducted a 1:2 matched (age, admission Hunt and Hess grade, vascular disease/risk history) cohort study of 20 SAH patients on statins and 40 SAH controls. The primary outcome was functional outcome at 14 days (Modified Lawton Physical Self-Maintenance Scale and Barthel Index scale scores). Secondary outcomes were 14-day mortality, Modified Rankin Scale score, DCI, DCI supported by angiography/transcranial Doppler [TCD], cerebral infarctions of any type, and TCD highest mean velocity elevation. RESULTS: Statin users demonstrated a significant protective effect on 14-day Barthel Index scale and Modified Lawton Physical Self-Maintenance Scale scores (77 +/- 10 versus 39 +/- 8, P = 0.003; 12 +/- 7 versus 19 +/- 9, P = 0.03, respectively). Moreover, statin users demonstrated a significantly lower incidence of DCI and DCI supported by angiography/TCD (10% versus 43%, P = 0.02; 5% versus 35%, P = 0.01, respectively), cerebral infarctions of any type (25% versus 63%, P = 0.01), and baseline-to-final TCD highest mean velocity change of 50 cm/s or greater (18% versus 51%, P = 0.03). CONCLUSION: SAH statin users demonstrated significant improvement in 14-day functional outcome, a significantly lower incidence of DCI and cerebral infarctions of any type, as well as prevention of TCD highest mean velocity elevation. However, we did not find a significant statin impact on mortality or global outcome (Modified Rankin Scale) in this small sample. This study provides clinical evidence for the potential therapeutic benefit of statins after acute SAH.

Adult↗

Hyperosmolar agents in neurosurgical practice: the evolving role of hypertonic saline.

Medical management of cerebral edema and elevated intracranial pressure (ICP) is a critical component of perioperative care in neurosurgical practice. Traumatic brain injury, arterial infarction, venous hypertension/infarction, intracerebral hemorrhage, subarachnoid hemorrhage, tumor progression, and postoperative edema can all generate clinical situations in which ICP management is a critical determinant of patient outcomes. Although osmotic agents are among the most fundamental tools to control ICP, prospective data to establish clear guidelines on their use are lacking. Hypertonic saline is emerging as an alternative to mannitol. Early data suggest that indications for each agent may ultimately depend on ICP etiology.

Brain Diseases↗

Herniation secondary to critical postcraniotomy cerebrospinal fluid hypovolemia.

OBJECTIVE: Cerebrospinal fluid hypovolemia resulting in postural headaches is a well-known clinical entity, but severe forms of cerebrospinal fluid hypovolemia with altered mental status and signs of transtentorial herniation ("brain sag") have rarely been reported. This article describes the clinical features of brain sag after craniotomy in an attempt to increase recognition of this syndrome. METHODS: Between April 2001 and January 2003, 220 consecutive patients with subarachnoid hemorrhage were prospectively enrolled in the Columbia Subarachnoid Hemorrhage Outcomes Project; 137 underwent craniotomy for aneurysm clipping. Among these patients, the diagnosis of brain sag was made when all three of the following criteria were present: clinical signs of transtentorial herniation, head computed tomographic scans revealing effacement of the basal cisterns with an oblong brainstem, and improvement of symptoms after placement of the patient in the Trendelenburg position (-15 to -30 degrees). For each patient, the symptoms, clinical course, and subsequent response to treatment were characterized. In addition, brainstem dimensions were measured on computed tomographic scans taken before, during, and after resolution of brain sag. A "sag ratio" was generated for these time points by dividing the maximum anteroposterior distance by the maximum bipeduncular distance. RESULTS: Eleven (8.0%) of 137 aneurysmal subarachnoid hemorrhage patients treated by craniotomy and an intraoperative spinal drain met the criteria for brain sag. Signs of transtentorial herniation developed most commonly between 2 and 4 days postoperatively. Pupillary asymmetry was noted in 10 (91.0%) of 11 patients, whereas the other patient demonstrated extensor posturing. The Trendelenburg position reversed the symptoms in all patients. The mean sag ratios before, during, and after resolution of brain sag were 0.91 +/- 0.03 (mean +/- standard error), 1.18 +/- 0.03, and 0.91 +/- 0.03, respectively. This represented a 30.9% elongation of the brainstem during sag (P < 0.001) and a 23.6% change back to baseline after resolution of the syndrome (P < 0.002). There was no significant difference between the presag and postsag ratios. CONCLUSION: Severe cerebrospinal fluid hypovolemia after craniotomy may produce a dramatic herniation syndrome that is completely reversed by the Trendelenburg position. Brain sag should be included in the differential diagnosis for acute postoperative clinical deterioration in this patient population.

Adult↗

Normal pressure "herniation".

INTRODUCTION: Hydrocephalus with normal intracranial pressure has rarely been reported to result in herniation. METHODS: Case report. RESULTS: A 52-year-old man became acutely comatose with extensor posturing and ventriculomegaly 17 days after experiencing a primary ventricular hemorrhage. An external ventricular drain revealed normal intracranial pressure. After 24 hours without improvement with the drain set at a level of 5 mm H2O, negative-pressure siphoning (50 mL of cerebrospinal fluid [CSF] removed) reduced ventricular size and led to dramatic clinical recovery. CONCLUSION: Normal pressure hydrocephalus can result in delayed brainstem herniation after ventricular hemorrhage. CSF siphoning in these patients can reverse the syndrome.

Acute Disease↗