Stenting and angioplasty for idiopathic intracranial hypertension: a case series with clinical, angiographic, ophthalmological, complication, and pressure reporting.

BACKGROUND: Previous studies have demonstrated that cerebral dural sinus stenosis (DSS) may be a potential patho-physiological cause of idiopathic intracranial hypertension (IIH). Endovascular therapy for DSS is emerging as a potential alternative to treat IIH. Here, we present the results of our case series. METHOD: We prospectively collected angiographic and manometric data on patients that underwent angioplasty/stenting for IIH. All patients had failed maximal medical therapy (MMT) and had confirmed sinus stenosis. Demographic, clinical and radiological presentation, and outcomes were collected retrospectively. RESULTS: A total of 18 patients underwent 25 procedures. Demographics revealed a mean age of 30 (range 15-59), 83% (15/18) were female, 72% (13/18) were white, and mean body mass index of 36 (range 23-59.2). All patients presented with classic IIH. Symptom improvement or resolution was reported in 94% (17/18) of patients. All patients had resolution and/or stabilization/improvement of their papilledema. Headaches related to increased pressure improved in 56% (10/18). Re-stenosis and retreatment occurred in 33% (6/18). No procedural related complications were reported. CONCLUSION: Dural sinus angioplasty and stenting is relatively safe, feasible, and clinically efficacious for patients with symptomatic sinus stenosis who have failed standard therapy. The long-term durability of patency and clinical improvement remains unknown.

The Penumbra system for mechanical thrombectomy in endovascular acute ischemic stroke therapy.

BACKGROUND: Efficacy of IV systemic thrombolysis is limited in patients with severe acute ischemic stroke and large-vessel occlusion. Mechanical thrombectomy has been the mainstay therapy in large-vessel occlusion. This review focuses on the Penumbra aspiration device. METHOD: Literature review. RESULTS: The Penumbra prospective studies were reviewed and results are presented. The pivotal single-arm prospective trial that led to its approval by the US Food and Drug Administration enrolled 125 patients within 8 hours of symptom onset and demonstrated an 82% recanalization rate, to Thrombolysis in Myocardial Ischemia (TIMI) scores of 2 and 3. The risk of symptomatic intracranial hemorrhage was 10%, and modified Rankin Scale (mRS) score of ≤ 2 was 25%. In the postmarketing registry, 157 vessels were treated, with 87% achieving TIMI 2 and 3 recanalization and 41% having an mRS score of ≤ 2. CONCLUSION: The Penumbra aspiration system is an effective tool to safely revascularize large-vessel occlusions in patients within 8 hours of onset of acute ischemic stroke who are either refractory to or excluded from IV thrombolytic therapy. Further prospective, randomized controlled trials will be needed to address whether this ability translates into neurologic improvement and better functional outcomes for our patients.

Initial experience with the coaxial dual-lumen ascent balloon catheter for wide-neck aneurysm coil embolization.

INTRODUCTION: Techniques for coil embolization of wide-neck cerebral aneurysms include the use of stents and temporary occlusion with compliant non-detachable balloons to safely allow dense packing of the aneurysm lumen with detachable coils. We describe the use of a new balloon device for assisting in wide-neck aneurysm coil treatment. METHODS: A single institution neuroendovascular database was accessed to identify cases in which the Ascent balloon (Codman Neurovascular, Raynham, MA, USA) was used for aneurysm coil embolization. Clinical, demographic, and angiographic data were obtained through chart review. RESULTS: Eleven cerebral aneurysm cases were treated using the Ascent balloon during the first 12-month period that the new device was available at our institution. Three of the patients presented with ruptured aneurysms. All aneurysms were large (maximum diameter 6 mm or greater), with an average maximum diameter of 9.4 mm, and an average neck diameter of 5.5 mm. Complete occlusion with coil embolization (Raymond class I) was achieved in all cases. The Ascent balloon was successfully positioned across the neck of the aneurysm in nine patients. CONCLUSION: This initial experience demonstrates the feasibility and immediate outcomes of the coaxial dual-lumen design Ascent balloon catheter used as an assistive device in coil embolization of wide-neck cerebral aneurysms. This device contributes to the growing number of assistive devices for the treatment of complex cerebral aneurysms.

Takotsubo cardiomyopathy associated with seizures.

BACKGROUND: Takotsubo syndrome is a reversible neuromyocardial failure that has been thought to be related to an acute catecholamine toxicity of the myocardium brought upon by a stressful event. The neurocritical care unit population is particularly vulnerable for this condition given the acute presentation of neurological emergencies, which most often can be catastrophic. We present a case series of this syndrome and a review of the literature. METHOD: Our recent experience with three cases that were prospectively identified with the diagnosis of Takotsubo syndrome is reported with clinical presentation, evaluation, and management approach. Review of the literature is presented in the discussion. RESULTS: We present three episodes of Takotsubo neuromyocardial syndrome in two patients that were admitted to our neurointensive care unit that presented with seizures and had typical clinical presentation, echocardiographic and cardiac catheterization findings. All the episodes were treated with vasoactive medications, ventilatory support, afterload and preload reduction, and treatment of the underlying condition. There was complete reversal of their symptoms and findings in each episode. CONCLUSIONS: Patients with critical neurological illnesses such as large ischemic or hemorrhagic stroke, status epilepticus, recurrent seizure activities as in our study may be at a higher risk for Takotsubo neuromyocardial syndrome.

Cerebral infarction associated with acute subarachnoid hemorrhage.

BACKGROUND: Cerebral infarction is a common complication of aneurysmal subarachnoid hemorrhage (SAH), but usually occurs several days after onset as a complication of vasospasm or aneurysm repair. The frequency, causes, and clinical impact of acute infarction associated with the primary hemorrhage are poorly understood. METHODS: We evaluated the presence of cerebral infarction on admission CT in 487 patients admitted within 3 days of SAH onset to our center between July 1996 and September 2002. Infarctions due to angiography or treatment complications were rigorously excluded. Outcome at 3 months was assessed with the modified Rankin Scale. RESULTS: A total of 17 patients (3%) had acute infarction on admission CT; eight had solitary and nine had multiple infarcts. Solitary infarcts usually appeared in the vascular territory distal to the ruptured aneurysm, whereas multiple infarcts tended to be territorial and symmetric. Global cerebral edema (P < 0.001), coma on presentation (P = 0.001), intraventricular hemorrhage (P = 0.002), elevated APACHE-II physiological subscores (P = 0.026) and loss of consciousness at onset (P = 0.029) were associated with early cerebral infarction. Mortality (P = 0.003) and death or moderate-to-severe disability (mRS 4-6, P = 0.01) occurred more frequently in the early cerebral infarction group. CONCLUSIONS: Early cerebral infarction on CT is a rare but devastating complication of acute SAH. The observed associations with coma, global cerebral edema, intraventricular hemorrhage, and loss of consciousness at onset suggest that intracranial circulatory arrest may play a role in the pathogenesis of this disorder.

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.

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.

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.

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.

Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage.

OBJECTIVE: To determine the effect that acute physiologic derangements have on outcome after subarachnoid hemorrhage (SAH) and to design a composite score summarizing these abnormalities. DESIGN: Prospective observational study. SETTING: Neuroscience intensive care unit in a tertiary care academic center. PATIENTS: Consecutive cohort of 413 patients with SAH admitted within 3 days of SAH onset with 3-month modified Rankin Scale scores. INTERVENTIONS: None. RESULTS: Among 20 physiologic variables assessed within 24 hrs of admission, four were independently associated with death or severe disability (modified Rankin Scale score, 4-6) at 3 months in a multivariate analysis: arterio-alveolar gradient of >125 mm Hg (odds ratio [OR], 4.5; 95% confidence interval [CI], 2.7-7.6), serum bicarbonate of <20 mmol/L (OR, 2.9; 95% CI, 1.6-5.6), serum glucose of >180 mg/dL (OR, 2.8; 95% CI, 1.6-4.8), and mean arterial pressure of <70 or >130 mm Hg (OR, 1.7; 95% CI, 1.0-2.9). Based on their proportional contribution to outcome, we constructed the SAH Physiologic Derangement Score (SAH-PDS; range, 0-8) by assigning the following weights for abnormal findings: arterio-alveolar gradient, 3 points; bicarbonate, 2 points; glucose, 2 points; and mean arterial pressure, 1 point. After controlling for known predictors of death or severe disability (age, admission neurologic status, loss of consciousness, aneurysm size, intraventricular hemorrhage, and rebleeding), the SAH Physiologic Derangement Score was independently associated with poor outcome (OR, 1.3 for each point increase; 95% CI, 1.1-1.6). By contrast, the systemic inflammatory response syndrome score and the Acute Physiology and Chronic Health Evaluation II physiologic subscore did not add predictive value to the model. CONCLUSION: Acute interventions specifically targeting hypoxemia, metabolic acidosis, hyperglycemia, and cardiovascular instability may improve the outcome of SAH patients. The SAH Physiologic Derangement Score may prove useful for rapidly quantifying the severity of important physiologic derangements in acute SAH.

Neurobehavioral differences in superselective Wada testing with amobarbital versus lidocaine.

Four patients with cerebral arteriovenous malformations (AVMs) underwent superselective Wada testing with intraarterial amobarbital and lidocaine before embolization. In all four patients, the use of lidocaine detected clinically significant neurologic deficits that amobarbital alone did not, likely because of the pharmacodynamic differences of the two agents. The use of lidocaine with amobarbital for superselective Wada testing in patients with cerebral AVMs may improve the sensitivity and predictive value of this test in the future.

Monitoring of cerebral vasodilatory capacity with transcranial Doppler carbon dioxide inhalation in patients with severe carotid artery disease.

BACKGROUND AND PURPOSE: Cerebral vasodilatory capacity (CVC) testing with transcranial Doppler has been shown to be useful in the assessment of stroke risk in patients with symptomatic and asymptomatic internal carotid artery (ICA) stenosis and occlusion, but whether hemodynamic status improves, deteriorates, or remains the same over time is uncertain. METHODS: Thirty-five patients with >or=80% carotid artery stenosis or complete occlusion underwent CVC testing at baseline and 6 months later. CVC was assessed by measuring the increase in ipsilateral middle cerebral artery mean flow velocity in response to 5% inhaled CO2. Continuous tracings of left and right middle cerebral artery flow velocity, heart rate, respiratory rate, and Pco2 were recorded and then analyzed offline. One-way analysis of variance was used to compare baseline CVC in symptomatic and asymptomatic patients with control subjects. A paired t test was used to compare CVC before and after revascularization. Also, chi2 analysis was used to compare rates of cerebrovascular events in patients with low compared with normal CVC over the 6-month period and in 14 patients whose ICAs were revascularized. RESULTS: Patients with high-grade stenosis or occlusion of the ICA who had ICA disease had an average CVC of 2.4+/-1.9%/mm Hg Pco2; control subjects averaged 4.2+/-1.1%/mm Hg Pco2. (P=0.01). In the revascularization group, CVC increased from an average of 1.4+/-1.7%/mm Hg Pco2 at baseline to an average of 2.8+/-1.0%/mm Hg Pco2 after revascularization, significantly different from the spontaneous change in the natural history group over 6 months (P=0.003). Over the 6-month follow-up period, in the natural history group and in the treatment group after revascularization, 4 ischemic events occurred, all in patients with abnormal CVCs; abnormal CVC was associated with ischemic events (Fisher's exact test, P=0.03). CONCLUSIONS: In a timeframe pertinent to clinical decision making and clinical trial outcomes, cerebral hemodynamic status may not be constant. A higher ischemic risk may be present in patients with severe carotid artery disease whose CVC is poor at baseline, becomes poor over 6 months, or fails to normalize after revascularization.