Stroke Notes

NNT and NNH with t-pa by time administered

2012-02-01T19:41:00.000-05:00

Lansberg et al. Stroke 2009 meta-analysis of 6 stroke trials of t-pa.

Time to treat      NNT            NNH   (NNT= number needed to treat or number needed to harm)

0-90 minutes       3.6               65
90-180 minutes   4.3                38
180-270 min       5.9                30
270-360 min       19.3              14

Debates on Intracranial artery disease (ICAD) at ISC 2012, and imaging

2012-02-01T19:17:00.001-05:00

Lessons from Sampris-- Wingspan stent trial was stopped due to more deaths in stent group. However, issues that were brought out include that sites had inexperienced interventionalists with an average enrollment of 2 per site, total enrollment fairly small, plus criteria for enrollment was not (necessarily) ideal since we don't know who best candidates are. One comment was that randomized trials if done too early (as here) retard innovation.

An important finding of Sammpris ties in with the theme of the year, which is that medical management has improved. 2 year mortality of ICD declined from 20 percent in earlier trials to about 12 % in Sammpris. The putative hero is aggressive 2011 medical management, with all it entails for tighter blood pressure control, tighter LDL-c reduction, attention to so called minor risk factors including metabolic syndrome, HDL, CRP and others.

One woman commented on her own "no metal " experience with angioplasty and made a case for a clinical trial with "no metal." The main risk of failure was not seen in her series of series. (Thanh Nguyen). Thereupon a discussion ensued about whether or not brain arteries are like coronary arteries where we already have learned so much. Brain arteries have no external lamina are smaller caliber and more prone to perforation.

Tom Brott opined that future trials of ICAD will need to compare procedures with new "best medical."

IMAGING

Debate again, is over what is best imaging protocol for stroke. Data was presented that CT-P does NOT improve 90 day modified Rankin scores over regular noncontrast CT as a stratifier. CT-P does add to time to catheter. Time to order is a major delay point. Whatever is used should be comfortable at facility.

Purpose of extra procedures (advanced MRI or CT) is to exclude futile procedures and cases likely to hemorrhage (do no harm) as well as tell anatomy of occlusion to guide procedure. D-P mismatch, as last year, is not key, core infarct size is much more important (can tell best on MRI diffusion studies or possibly CBV). Exceptions are malignant pattern (see DEFUSE trial) Evaluation of collateral flow is gaining prominence. One speaker commented that they still intervene on the ten percent that imaging says are futile.

Dissection and i-v alteplase treatment

2012-01-21T18:02:00.000-05:00

Quereshi et al. Arch Neurol 2011; 68: 1536-42

Authors reviewed database finding about 1 % of 48,000 stroke patients had an underlying dissection. Alteplase was less effective in this stroke type in lowering disability, but the rates of hemorrhage were similar to other stroke types, and the lower outcome was not due to alteplase therapy.

Cognitive and Neurologic Outcomes after CABG

2012-01-18T21:25:00.000-05:00

Selnes, Gottesman, ....McKhann. NEJM 2012; 366: 250-7 Review article

Bullet points STROKE
1. 1.6 % rate overall, but rate may increase 10x if radiographic/clinically silent CVA's included

2. Mechanism of micro/macroemboli with cross clamping needs to be modified to include hypotension and inflammatory response. Caplan et al , proposed the combination of hypotension and microemboli leads to more injury because microemboli aren't washed out as readily.

3. risk factors for neurologic morbidity: age, DM, HTN, history of stroke Others: PREOPERATIVE FACTORS (and odds ratio) : athero of ascending aorta (2.0), h/o of TIA/CVA (2.1); h/o of subcortical disease (4.1), carotid stenosis (5.3); PVD (2); DM (1.2 or 2.8);HTN (1.8 or 1.3); high pulse pressure (1.1);prior cardiac surgery (1.4); smoking history (1.6). OPERATIVE FACTORS: Hypotension (8.4); manipulation of aorta (1.8); bypass time > 2 hours (1.4). POSTOP FACTORS: AD (.8 to 2.6). (article gives references for each risk factor).

4. PREVENTION: Use of individualized factors, and use of preop or postop ASA which are both controversial. Use of eipaortic ultrasound to guide decision to cross clamp. Use of carotid screening preop. Avoiding combined carotid/coronary procedures. All of these ideas have limited data. Operative monitoring with TCD or near infraredspectroscopy has been used.

COGNITIVE DECLINE

Factors include:
1. preop cognitive abilities/disabilities
2,

Recovery after spinal cord infarcts; long term outcomes in 115 patients

2012-01-18T20:50:00.001-05:00

Neurolgy 2012;;78: 114-121 Robertson, Brown, Wijdicks, and Rabinstein. Mayo Clinic

Authors debunk myths of spinal cord infarcts. Retrospective study of patients show many improved over time. Among their findings

1. Gradual improvement was common after hospital dismissal. More than half walked aided or unaided eventually.

2. One third of those catheterised at dismissal did not require catheter long term

3. MRI's were frequently normal initially and even occassionally on followup MRI

4. ASIA A/B predicted a poor outcome, but not invariably. Other predictors of poor outcome included absent Babinski sign, sensory level, longitudinally extensive MRI, and lesions in highest thoracic level. NON RISK FACTORS included age, mechanism, gender were not predictive of a poor functonal outcome

5. There was a fairly high early mortality, around 26 % that was associated with HTN, DM, smoking, PVD, severity of impairment, and age (ie traditional risk factors mostly).

6. Pain especially back pain was a common initial finding and a common longterm problem of survivors.

Lacune subtypes and risk factors

2012-01-18T20:31:00.000-05:00

Authors divided lacunes into very small (<3 mm) and small (3-7 mm) and larger (8-20 mm). The hypothesized mechanism for very small lacunes and small lacunes was lipohyalinosis and larger lacunes was microatheroma.

Risk factors for small lacunes (lipohyalinosis) in 1548 patients analyzed included age, African American race, HTN, diabetes, ever smoking. HBA1C could be substituted for DM.

Very small lacunes had similar risk factors as small lacunes. Diabetes was key risk factor here.

8-20 mm lacunes (microatheroma) were associated with ever smoking, age, and LDL levels.

Conclusion is that diabetes leads to disorder of systemic microcirculation leading to very small lacunes. LDL and smoking lead to microatheroma

Opioids: Might depress cerebral perfusion pressure

2011-11-29T18:46:00.001-05:00

Sedation for critically ill adults with severe traumatic brain injury: A systematic review of randomized controlled trials; Roberts DJ, Hall RI, Kramer AH, Robertson HL, Gallagher CN, Zygun DA; Critical Care Medicine 39 (12),

OBJECTIVES: To summarize randomized controlled trials on the effects of sedative agents on neurologic outcome, mortality, intracranial pressure, cerebral perfusion pressure, and adverse drug events in critically ill adults with severe traumatic brain injury. DATA SOURCES: PubMed, MEDLINE, EMBASE, the Cochrane Database, Google Scholar, two clinical trials registries, personal files, and reference lists of included articles. STUDY SELECTION: Randomized controlled trials of propofol, ketamine, etomidate, and agents from the opioid, benzodiazepine, α-2 agonist, and antipsychotic drug classes for management of adult intensive care unit patients with severe traumatic brain injury. DATA EXTRACTION: In duplicate and independently, two investigators extracted data and evaluated methodologic quality and results. DATA SYNTHESIS: Among 1,892 citations, 13 randomized controlled trials enrolling 380 patients met inclusion criteria. Long-term sedation (≥24 hrs) was addressed in six studies, whereas a bolus dose, short infusion, or doubling of plasma drug concentration was investigated in remaining trials. Most trials did not describe baseline traumatic brain injury prognostic factors or important cointerventions. Eight trials possibly or definitely concealed allocation and six were blinded. Insufficient data exist regarding the effects of sedative agents on neurologic outcome or mortality. Although their effects are likely transient, bolus doses of opioids may increase intracranial pressure and decrease cerebral perfusion pressure. In one study, a long-term infusion of propofol vs. morphine was associated with a reduced requirement for intracranial pressure-lowering cointerventions and a lower intracranial pressure on the third day. Trials of propofol vs. midazolam and ketamine vs. sufentanil found no difference between agents in intracranial pressure and cerebral perfusion pressure. CONCLUSIONS: This systematic review found no convincing evidence that one sedative agent is more efficacious than another for improvement of patient-centered outcomes, intracranial pressure, or cerebral perfusion pressure in critically ill adults with severe traumatic brain injury. High bolus doses of opioids, however, have potentially deleterious effects on intracranial pressure and cerebral perfusion pressure. Adequately powered, high-quality, randomized controlled trials are urgently warranted.

Blogger note: take home message is in bold above. Until the definitive study is done, pay attention if, to nothing else, that one sentence.

Bevacizumab, metastasis, and brain hemorrhage, True, true and unrelated?

2011-11-29T18:35:00.001-05:00

Intracranial hemorrhage in patients treated with bevacizumab: Report of two cases; Nishimura T, Furihata M, Kubo H, Tani M, Agawa S, Setoyama R, Toyoda T; World Journal of Gastroenterology 17 (39), 4440-4 (Oct 2011)

Treatment with bevacizumab, an antiangiogenic agent, in patients with metastatic or unresectable colorectal cancer was approved less than 4 years ago in Japan. Bevacizumab improves the survival of patients with metastatic colorectal cancer; however, it may lead to complications such as bleeding, which are sometimes fatal. Bevacizumab should be administered only after careful consideration because the potential risks of therapy outweigh its benefits. Therefore, pharmaceutical companies do not recommend bevacizumab therapy for patients with brain metastases. While some reports support the cautious use of bevacizumab, others report that it is not always necessary to prohibit its use in patients with metastases to the central nervous system (CNS), including the brain. Thus, bevacizumab therapy in colorectal cancer patients with brain metastases is controversial, and it is unclear whether brain metastases are a risk factor for intracranial hemorrhage during anti-vascular endothelial growth factor (VEGF) therapy. We report a 64-year-old man and a 65-year-old man with recurrent colorectal cancer without brain metastases; these patients developed multifocal and solitary intracranial hemorrhage, respectively, after the administration of bevacizumab. Our findings suggest that intracranial hemorrhage can occur even if the patient does not have brain metastases prior to bevacizumab treatment and also suggest that brain metastases are not a risk factor for intracranial hemorrhage with bevacizumab treatment. These findings also question the necessity of excluding patients with brain metastases from clinical trials on anti-VEGF therapy.

Blogger note: Paper intrigues but any number of conclusions could be drawn out of it. Larger experience is required.

Stroke centers and survival

2011-11-29T18:25:00.001-05:00

Does primary stroke center certification change ED diagnosis, utilization, and disposition of patients with acute stroke?; Ballard DW, Reed ME, Huang J, Kramer BJ, Hsu J, Chettipally U; American Journal of Emergency Medicine (Nov 2011)

BACKGROUND AND PURPOSE: We examined the impact of primary stroke center (PSC) certification on emergency department (ED) use and outcomes within an integrated delivery system in which EDs underwent staggered certification. METHODS: A retrospective cohort study of 30 461 patients seen in 17 integrated delivery system EDs with a primary diagnosis of transient ischemic attack (TIA), intracranial hemorrhage, or ischemic stroke between 2005 and 2008 was conducted. We compared ED stroke patient visits across hospitals for (1) temporal trends and (2) pre- and post-PSC certification-using logistic and linear regression models to adjust for comorbidities, patient characteristics, and calendar time, to examine major outcomes (ED throughput time, hospital admission, radiographic imaging utilization and throughput, and mortality) across certification stages. RESULTS: There were 15 687 precertification ED visits and 11 040 postcertification visits. Primary stroke center certification was associated with significant changes in care processes associated with PSC certification process, including (1) ED throughput for patients with intracranial hemorrhage (55 minutes faster), (2) increased utilization of cranial magnetic resonance imaging for patients with ischemic stroke (odds ratio, 1.88; 95% confidence interval, 1.36-2.60), and (3) decrease in time to radiographic imaging for most modalities, including cranial computed tomography done within 6 hours of ED arrival (TIA: 12 minutes faster, ischemic stroke: 11 minutes faster), magnetic resonance imaging for patients with ischemic stroke (197 minutes faster), and carotid Doppler sonography for TIA patients (138 minutes faster). There were no significant changes in survival. CONCLUSIONS: Stroke center certification was associated with significant changes in ED admission and radiographic utilization patterns, without measurable improvements in survival.

Blogger note: Small select group of stroke patients, those given alteplase, may be less than 5 percent of the total and are the only ones who would be expected to do better in primary stroke centers. However, the target group is likely to be buried in the statistics of 15,000 patients reviewed. This type of stroke center evaluation might be better suited for evaluating specific populations receiving specific treatments.

Which antihypertensive? Beta blockers risky

2011-10-25T17:44:00.001-05:00

Webb et al. Lancet 2010 375:905-915

Idea BP variability is worse than absolute measurement of a high BP. Certain drugs such as Beta blockers are associated with high variability and therefore higher risk, whereas Calcium channel blockers have less variability in BP and are therefore better for stroke prevention. ACE inhibitors trend bad, ARBs slightly better.

lifestyle choices and stroke prevention risk

2011-10-25T17:40:00.001-05:00

Chiuve et al. Circulation 2008; 118:947-954

43,685 men Health professionals followup study

71,243 women Nurses health study

Five factors:

1. Not smoking

2. healthy diet

3. 30 minutes per day vigorous activity

4. Weight BMI< 25

5. one alcoholic drink per day for women, 1-2 for men

80 percent reduction in risk, dose dependent on how many followed.

Partly related to secondary effects of above on blood pressure. Amount of BP reduction per lifestyle aspect adopted

10 kg weight reduction= 5-20 mm HG

DASH eating plan 8-14 mm

dietary sodium restriction 5-8

physical activity 4-9 mm

moderate alcohol consumtpion 2-4 mm

Chobanian JAMA 2003; 289:2560

Every 10 mm reduction in BP leads to a 31 % stroke risk

Lawes et al. Stroke 2004; 35:776

Carrascal and Guerrero- Stroke and CABG part II

2011-06-12T14:54:00.000-05:00

from the Neurologist

Perioperative risk factors:
1. CPB use and factors that are uncontrollable including low flow
2. Type of procedure-- 3 fold risk in patients undergoing open chamber procedure.Combined procedures eg. CABG + valve causes baseline increase from 5 to 16 % or so
3. Duration-- number of emboli increase by 90.5 % for every hour
4. Postoperative complications including low CO (due to MI eg.) or postoperative AFIB which is common in first 4 days.

III Preventive Procedures--
Operatively
A. Minimize aortic manipulation -- one cross clamp not multiple, or even zero with pediculate anastomoses
B. Heart Port Clamp-- instead of external clamp, use a saline filled balloon and clamp internally avoiding manipulation
C. Identify aortic disease with epiaortic ultrasound; if needed use femoral or axillary catheterization and / or profound hypothermia.
D. Use side hole not end hole cannulas-- less displacement of particle
E. Use intraaortic filtration-- not shown to be beneficial YET
F.Dispersion aortic cannulas when friable valves are diagnosed
G. Carotid surgery according to above criteria
H. Prophylactic resection of atrial appendage in patients with preexisting AF who also need MVR

Reduce microemboli in CPB Circuit
A. heparin bound CPB circuit
B. Membrane rather than bubble oxygenator
C. CO2 sufflation into thoracic wound to decrease air bubbles
D. Filter in arterial line; leukocyte filter to decrease inflammatory response
E. Decrease CPB time
F. Decrease cardiotomy suction to prevent lipid microemboli and improve cognitive; us ultrasound to help
G. Early slow rewarming 0.2 degrees C per minute
H. Alphastat protocol for pH and CO2
I. Reduce perfusionists' interventions which are directly tied to cognitive decline
J. Avoid collecting/reinfusing mediastinal blood
K. Emblocker ultrasound transducer on aorta redirects debris to descending aorta, tried in animals so far

Prevention of ischemic injury
A. Keep MAP> 50
B. Avoid maneuvers that increase CVP (CPP = MAP-CVP)
C. Avoid cardiac luxation during off pump procedures which can lower CO
D. Pulsatile flow not shown to be superior to continuous flow
E. Substitute Aprinin for amicar or transxemic acid
F. Avoid profound hemodilution especially in octagenerarians

Metabolic
A. Avoid hyperglycemia
B. Keep HCT over 30

Neuroprotection
Summary
Many have been studied none have shown effective

Bypass and stroke Pt !

2011-06-12T14:29:00.000-05:00

also see blog post regarding Lou Caplan's opinion regarding the issue http://strokenotes.blogspot.com/search?q=cabg

Carrascal Y, Guerrerro AL. Neurological damage related to cardiac surgery; pathophysiology, diagnostic tools, and prevention strategies. Using actual knowledge for planning the future. The Neurologist 2010; 16:152-164.

Summary-- the population undergoing cardiac surgery is older and sicker. Prevention efforts should include improvements in surgical techniques and cerebral protection, pharmacotherapy, and adequate neuropsychologic assessments.

Bullet points: Intro
1. 1-6 % of patients have neurologic complications, but number is up to 15 % in high risk group and up to 50 % if you count cognitive dysfunction. Neurologic complications increase one year mortality tenfold in first year, and doubles ICU care time. 31 % of patients with neurologic damage return home, 75 % with "minor" cognitive damage, 85 % without neurologic damage.

I. Mechanism of damage in cardiopulmonary bypass: emboli (micro or macro), inflammatory response, metabolic response to hypoxemia or vasogenic or cytotoxic edema, and cerebral hypoperfusion

A. Emboli
1) Macro, > 200 um, related to manipulation of aorta, calcium, valvular debris. Causes focal deficits.
2) Micro, <200 um, due to a) air, related to opening chambers of heart, generation in CPB machine, and during patient rewarming b) lipids, especially due to cardiotomy suction especially with lipid reinfusion into CPB circuit c) cellular aggregate esp platelets d) Exogenous material from heart lung machine such as silicon. Microemboli go to border zone, to basal ganglia and white matter tracts. TCD detection of microemboli over 60 correlates with a 70 % risk of cognitive damage. TCD does not detect type of particle.
Intraoperative TEE detects air bubbles in chambers and diseased arteries that can be avoided for cross clamping. Aortic intimal thickening over 3 mm, especially with rounded, protruberant or ulcerated plaque is associated with a 4.5 x risk of neurologic sequelae. Post op stroke is 25 % with a mobile plaque, 8 % with a fixed plaque, and 1.8 % if there is no plaque.

B. Inflammatory response activation-- duet to CPB, leads to a coagulation cascade and damage to blood brain barrier.

C. Disorders in Neuronal Metabolism secondary to hypoxemia or vasogenic or cytotoxic edema-- related to hypothermia during procedure, which has good and bad points, although mild hypothermia seems to benefit. Severe may lead to brain edema.

D. Hypoperfusion--

II Detection
A..Biochemical markers of neuropsychological damage-- adenylate kinase (good), CK-BB (bad marker, totally nonspecific), neuronal specific enolase (good marker, raised levels over 35 ng/ml after 48 hours correlates with bad prognosis, S100 B is a white matter marker, good marker more than 24 hours out (early rise occurs during CPB and is not prognostic) Level of > .5 ug/mL at 48 hours have a 78 % mortality compared to 18 % with a level under .5. S100B < 1.1 24 hours after surgery has a 97 % specificity to exclude stroke.
B. Imaging- DWi and NIRS (near infrared spectroscopy) show clinically silent events in a MAJORITY of patients or at least 50 %. Fluroescein retinal angiography can detect clinically silent retinal events. and disappear 7 days postop
C. Neuropscyh-- Studies not clear. Risk factors (incremental) include DM, CRF, ascending aortic atherosclerosis, CVD, PVD, or previous severe neurologic disease.

III Major risk factors for complications
A. Age
B. Carotid disease (controversial)-- this author suggests there is a 10 % reduction of stroke risk if the artery is symptomatic and stenosis is > 50 %. For asymptomatic , procedure only if patient has life expectancy > 5 years, is 40-70, mortality of procedure < 3 %.
C. Prior stroke confers 13-15 % risk no matter when the prior stroke
D. PVD increases risk of perioperative stroke by 4.5 %, and affects 33 % of octagenarians.
E. Severe LV dysfunction and poor EF
F. Indirect risk factors : DM, RF, HTN, COPD
G. Baseline intellectual function
H. Genetic factors (apoE) unsettled
I Gender-- women do worse

see next post

Reconsidering MI as a contraindication for IV thrombolysis for stroke

2011-06-11T19:31:00.000-05:00

De Silva DA et al. Neurology 2011; 76:1838-1840.

General points

1. Some guidelines suggest 90 days not to use t-pa, but risk exists only in those with transmural MI (for cardiac rupture) and in those cases the wall is healed within 7 weeks, or at least healing, with fibrosis and scarring maximized by then, to mitigate risk in younger stroke patients without transmural rupture.

2. There are only 3 reports of 5 elderly women with tamponade after stroke thrombolysis.

3. In cardiac literature, wall rupture occurs in first 48 hours in those with transmural MI.

Atraumatic convexal subarachnoid hemorrhage

2011-06-11T18:35:00.000-05:00

Clinical presentations, imaging patterns and etiologies. Kumar S. et al. Neurology 2010; 74: 893-399

Authors include LR Caplan

Convexal SAH is about 8 percent of all SAH. Authors found 29 patients at Beth Israel, about two thirds were women. There was a dichotomy in presentation by age. The under 60's had a strong tendency to present with a severe headache, whereas that was rare in the over 60's, who presented with TIA-like presentations, migraine creeping numbness mimic (even repetitively) or lethargy. Angiography/MRA/CTA was almost always negative. The under 60's were most likely to have reversible cerebral vasoconstriction syndrome (formerly Call syndrome), whereas the over 60's were more likely to have amyloid angiopathy. The latter group tends to have recurrent disease, but this study does not have good followup. Headaches often were prolonged, associated with retching or vomiting, and described as "thunderclap" in younger patients. Surface eeg's were always negative for seizures among those presenting with repetitive sensory phenomena. They were more likely to have superficial siderosis on imaging.

The differential of the presentation includes, in addition to the two above causes, cortical vein occlusion, PRES, coagulopathy, cocaine, lupus vasculitis, cavernoma, brain aneurysm, ephedra, HELLP syndrome, post LP headache, and arterial dissection.

Activated prothrombin complex for dabigratan bleed? one opinion

2011-06-04T18:32:00.001-05:00

We recently had a 67-year-old man with atrial fibrillation who was
admitted from the EP lab after developing pericardial hemorrhage during
the procedure. He had been taking dabigatran and had received his last
dose seven hours prior to the procedure. He was undergoing an ablation
when a transseptal perforation occurred and hypotension ensued. He had
received 5000 units of heparin prior to the start of the procedure.
Pericardiocentesis was undertaken and 4500 cc of blood was withdrawn. He
was given two units of FFP & Protamine 100 mg with persistent bleeding.
He was then given FEIBA (activated prothrombin complex) 3159 units (26
units per kilogram over 15 minutes). One minute after initiating FEIBA
infusion slowing of the bleeding was observed. Bleeding stopped from
pericardiocentesis within minutes of administration of FEIBA. His PTT the
prior to the procedure was 53. ACT prior to administration of heparin was
233. The PTT decreased to 35 after protamine infusion but prior to the
FEIBA administration, and decreased further to 29 following FEIBA. ACT
decreased to 131 following FEIBA.

Our single experience would suggest that FEIBA was effective in reversing
the anticoagulant effect of dabigatran. I wonder if any others have had
an opportunity to use this treatment and what their experience has been?
Has anyone used other ways of reversing dabigatran and with what success?

normal thrombin time and dabagitan

2011-04-30T10:39:00.001-05:00

(reprinted not practice in our facility)

A normal thrombin time essentially rules out any anticoagulant effect due to Dabigatran. Thrombin time is a widely available and inexpensive test. For patients known or suspected to be on Dabigatran, our stroke team policy is to consider treatment with IV-t-PA only when thrombin time is normal.

CADASIL typical temporal lobe imaging involving temporal pole

2011-04-25T06:14:00.000-05:00

SAMMPRIS trial stopped

2011-04-11T12:36:00.001-05:00

CLINICAL ALERT

The National Institute of Neurological Disorders and Stroke (NINDS) has stopped enrollment in a clinical trial that is evaluating whether intracranial angioplasty combined with stenting adds benefit to aggressive medical therapy alone for preventing stroke in patients with symptomatic intracranial arterial stenosis. The Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis (SAMMPRIS) study is the first prospective randomized multicenter trial to compare aggressive medical management alone versus aggressive medical management plus angioplasty combined with stenting in patients with symptomatic high grade (70-99%) stenosis of a major intracranial artery (intracranial carotid, middle cerebral artery, intracranial vertebral artery, and basilar artery).

Full NINDS Alert (PDF)

billing code for administering alteplase by MS

2011-04-10T10:12:00.001-05:00

You can use the CPT code 37195 if you are personally at the bedside while
> the tPA is given by a physician.

Lambl's excrescences and fibrous strands

2011-04-04T12:33:00.001-05:00

The serpentine mitral valve and cerebral embolism

James Ker

Cardiovascular Ultrasound 2011, 9:7

Vilem Dusan Lambl, a Bohemian physician (1824-1895) were the first to describe the occurrence of small, filiform processes he observed on the aortic valve in 1856[5] . Today, these Lambl's excrescences are also referred to as valvular strands and have been observed on all native and prosthetic valves[5] . These strands may occur as single strands, in rows or even in clusters[5] . They can vary in length from 1 mm to 10 mm and are usually less than 1 mm in thickness[5] .

Valvular strands are composed of a fibroelastic, avascular core, covered by a layer of endothelial cells [5,6] .

The exact pathogenesis of formation of these structures are still unclear, however current opinion is that the initiating factor is that of an endocardial lesion in areas of trauma and/or high shear stress [5,6] . These denuded areas are then covered by fibrin with subsequent covering by an endothelial layer [5,6] . The prevalence of valvular strands has been estimated as 5.5% in a general population referred for transesophageal echocardiography and 40% in patients with stroke of unknown cause [1,2] .

The differential diagnosis for valvular strands includes the following[5] : a myxoma, thrombi, valvular vegetations, nonbacterial thrombotic (marantic) endocarditis, cardiac metastases, a fibroelastoma and other primary cardiac neoplasms.

Of all of the above, the most difficult distinction is that between a valvular strand and a fibroelastoma [5,7] . Histologically, these two entities are very similar with both containing a central core of elastic connective tissue, covered by endothelium. However, valvular strands are covered by a single layer of endothelial cells, but fibroelastomas contain regions of multiple layers of endothelial cells [5,7] .

Echocardiographically, fibroelastomas are more bulky, with stalks or pedestals sometimes present and multiple, fingerlike projections on their surface[5] . As fibroelastomas are usually found on the mechanically less strained parts of valves and endocardium they tend to be larger than valvular strands[5] . Valvular strands (Lambl's excrescences) are always found on the affected valve's line of closure and this limits their growth[5] .

Several published case reports have shown that valvular strands are associated with emboli to the coronary, pulmonary, spinal, retinal and cerebral circulation[1] .

Specifically regarding stroke, numerous reports have demonstrated an association with valvular strands, particularly in young patients [3,4,8,9] . The mechanism for embolic events is either that of thrombi forming on the strands which then embolize or it is possible that the valvular strand itself can embolize[2] . Direct visualization of thrombus on a valvular strand have indeed been described before[10] .

In conclusion, a case of a valvular strand, attached to the coapting edge of the mitral valve is presented, giving a serpentine appearance to the mitral valve. This valvular strand was the cause for a cerebral embolism which presented with a transient right sided hemiparesis. This is the only current case in the literature, where the combination of aspirin and clopidogrel is used for the prevention of further episodes of cerebral embolism. In the only randomized treatment study to date, no difference in relation to efficacy of warfarin compared to aspirin was found in patients with valvular strands and previous embolic episodes[2] . For this reason a combination of antiplatelet therapy was initiated as a therapeutic trial.

It is proposed that a randomized controlled study involving the combination of aspirin and clopidogrel is warranted in patients with valvular strands presenting with a first episode of cerebral embolism.

Wolf RC, Spiess J, Vasic N, Huber R: Valvular strands and ischemic stroke.
Eur Neurol 2007, 57:227-231.
Homma S, Di Tullio MR, Sciacca RR, Sacco RL, Mohr JP: Effect of aspirin and warfarin therapy in stroke patients with valvular strands.
Stroke 2004, 35:1436-1442.
Freedberg RS, Goodkin GM, Perez JL, Tunick PA, Kronzon I: Valve strands are strongly associated with systemic embolization: A transesophageal echocardiographic study.
J Am Coll Cardiol 1995, 26:1709-1712.
Roberts JK, Omarali I, Di Tullio MR, Sciacca RR, Sacco RL, Homma S: Valvular strands and cerebral ischemia. Effect of demographics and strand characteristics.
Stroke 1997, 28:2185-2188.
Jaffe W, Figueredo VM: An example of Lambl's excrescences by transesophageal echocardiogram: A commonly misinterpreted lesion.
Echocardiography 2007, 24:1086-1089.
Roldan CA, Shively BK, Crawford MH: Valve excrescences: Prevalence, evolution and risk for cardioembolism.
J Am Coll Cardiol 1997, 30:1308-1314.
Gowda RM, Khan IA, Nair CK: Cardiac papillary fibroelastoma: A comprehensive analysis of 725 cases.
Am Heart J 2003, 146:404-410.
Lee RJ, Bartzokis T, Yeoh TK, Grogin HR, Choi D, Schnittger I: Enhanced detection of intracardiac sources of cerebral emboli by transesophageal echocardiography.
Stroke 1991, 22:734-739.
Tice FD, Slivka AP, Walz ET, Orsinelli DA, Pearson AC: Mitral valve strands in patients with focal cerebral ischemia.
Stroke 1996, 27:1183-1186.
Nighoghossian N, Derex L, Loire R, Perinetti M, Honnorat J, Riche G, Barthelet M, Ninet J, Chazot G, Chassignolle J, Trouillas P: Giant Lambl excrescences.
Arch Neurol 1997, 54:41-44.

CLEAR trial link" t-pa plus integrilin

2011-03-26T09:23:00.001-05:00

http://www.ncbi.nlm.nih.gov/pubmed/18772447

Random notes on abstracts from ISC meeting radiology

2011-02-13T19:35:00.001-05:00

1. Hyperdense MCA sign can disappear, but rarely does if LONGER THAN ONE CM

2. High rCBV predicts good outcome irrespective of treatment suggesting collateral presence

3. Multiple (>4) left hemisphere DWI lesions is predictive of aortic arch stroke

4. The"brush sign" on 3 Tesla MRI may predict hemorrhagic conversion after stroke

ASPECTS score

2011-02-13T18:48:00.001-05:00

is asociated with prognosis

http://www.aspectsinstroke.com/

http://radiopaedia.org/articles/alberta-stroke-program-early-ct-score

neurodoc

LAPSS and other stroke related scales

2011-02-13T17:58:00.001-05:00

Los Angeles prehospital stroke screen : LAPSS

http://www.strokecenter.org/trials/scales/lapss.html

LAMS Los Angeles Motor Scale

http://stroke.ahajournals.org/cgi/content/full/39/8/2264#TBL1508127

other scales

http://www.strokecenter.org/trials/scales/

neurodoc

Notes on Grotta talk- "Extending reach of patient eligibility"

2011-02-10T01:54:00.000-05:00

presented at Genentech submeeting by Dr Grotta. A few of his ideas
1. We need to relax many of the criteria for i-v tpa so that 10-20 percent of patients get drug. What IS needed to give drug is: NIHHSS, time of onset, plain CT head, (no CTA till after infusion started), history of bleeding, seziures, surgery, stroke, meds, glucose, platelets and HCT. NO Foley, CXR (unless suspicion of dissection), ECHO or INR unless on warfarin or heparin
2. At his center, he has experience treating patients with wake-up strokes with success middling between placebo and standard 0-3 hour patients.
3. Grotta believes that just as trauma is tiered into level one and two, so should stroke, and patients with level one stroke should be sent to comprehensive, not primary stroke centers where they can get better care. The scale utilized could be one that differentiates likelihood of major vessel occlusion, the Los Angeles...... scale.
4. His research includes tpa followed y arbogatran

Notes of MRI talks at ISC 2011 by Michael Lev and by Greg Albers

2011-02-10T01:47:00.004-05:00

These two talks demonstrate patients for whom intervention is NOT likely to help.

* BASIS (reference here: http://www.ajnr.org/cgi/reprint/29/6/1111 )

Lev

1. Contrary to hypothesis, mismatch IS NOT discriminatory regarding clinical outcome after recanalization. Most all M1 occlusions with small admission DWI have mismatch, but not all respond to therapy. The independent outcome predictors, are, NIHSS <= 10 and BASIS* negative have good outcomes, NIHSS > 10 and BASIS + have poor outcomes and those with one or other are intermediate.

2. What you need to know, basically, is the amount of core infarct less than 70 cc. If so, recanalization can be of benefit. You can measure this best, through DWI although CT can be used (see notes below).

3. The other thing you need to know is that a corresponding perfusion deficit exists. These 2 criteria by MRI are specific but not sensitive for core.

4. Idea of time is brain uses clock that starts with imaging of a DWI lesion less than 70 cc, not onset of symptoms.

5. Yoo Aj et al. Stroke 2010. DWI and MTT volumes predicts outcome > mismatch. DWI > 72 ml and NIHSS > 20 are associated with a poor outcome. MTT < 47 mL and NIHSS < 8 have good outcome. Combining gives prognosis over 70 %, much better than NIHSS alone (43 %) or imaging alone (54 %).

6. Protocol is to do noncontrast head CT, then a CTA, then a DWI and only do CT perfusion if patient is not able to get a MRI. Also notes current focus on radiation.

7. Uses above characteristics to assess wake up strokes.

8. Good collaterals is highly specific for small DWI

9. THRESHOLDED CBF IS LESS VARIABLE THAN CBV AND IS MORE SENSITIVE FOR SALVAGEABLE BRAIN (CBV MORE SPECIFIC). CT CBF NOT CBV IS "NEXT BEST THING" IF DWI IS NOT AVAILABLE TO DETERMINE SIZE OF CORE. However there are issues with CT including luxury perfusion, standardization, post-processing and others.

ALBERS TALK

Discusses DEFUSE trial and adds that he criticizes Lev's talk because there is ANOTHER group of patients who do badly with recanalization and that is those with very large perfusion deficit even with a tiny DWI deficit who have a "malignant pattern" of infarct who will do much worse if treated. A discussion ensued and Wade Smith mentioned a case with a "so-called malignant pattern" who was observed deteriorating, was promptly treated, and got better, therefore felt clinical part was important. Again mismatch was overrated and not key.

Albers also spoke of converging evidence that > 5.5 or 6 seconds for contrast to reach brain was a threshold of very sick brain. He also mentioned a case where one branch was not recanalized, but the branch that was recanalized reperfused dead tissue.

Wade Smith talk

Many points not mentioned. Of interest he thinks IMS 3 is going to really open up intervention therapies.

Grotta talk "Extending reach of tpa eligibility"

2011-02-10T01:11:00.001-05:00

presented at Genentech submeeting by Dr Grotta. A few of his ideas

1. We need to relax many of the criteria for i-v tpa so that 10-20 percent of patients get drug. What IS needed to give drug is: NIHHSS, time of onset, plain CT head, (no CTA till after infusion started), history of bleeding, seziures, surgery, stroke, meds, glucose, platelets and HCT. NO Foley, CXR (unless suspicion of dissection), ECHO or INR unless on warfarin or heparin

2. At his center, he has experience treating patients with wake-up strokes with success middling between placebo and standard 0-3 hour patients.

3. Grotta believes that just as trauma is tiered into level one and two, so should stroke, and patients with level one stroke should be sent to comprehensive, not primary stroke centers where they can get better care. The scale utilized could be one that differentiates likelihood of major vessel occlusion, the Los Angeles...... scale.

4. His research includes tpa followed by arbogatran, and TCD and hypothermia.

neurodoc

another opinion, references on cilostazol

2011-02-07T14:52:00.001-05:00

A brief pubmed search about the topic showed a few studies and reviews on the subject. It appears that Cilostazol is non-inferior to aspirin per one study, and is effective in lowering cerebrovascular events with low rates of bleeding. I did not come across any studies that mention adverse events from using this drug. However, since it is not considered standard of care, it probably should only be used on an experimental basis with documentation as such- if it is used at all. Hope this helps.

Lancet Neurol. 2010 Oct;9(10):959-68. Epub 2010 Sep 15.

Cochrane Database Syst Rev. 2011 Jan 19;1:CD008076

J Stroke Cerebrovasc Dis. 2009 Nov-Dec;18(6):482-90.

cilostazol and stroke in Asians

2011-02-06T23:06:00.001-05:00

Cochrane Database Syst Rev. 2011 Jan 19;1:CD008076.

Cilostazol versus aspirin for secondary prevention of vascular events after stroke of arterial origin.

Kamal AK, Naqvi I, Husain MR, Khealani BA.

Stroke Service, Section of Neurology, Department of Medicine, Aga Khan University Hospital, Stadium Road, PO Box 3500, Karachi, Pakistan, 74800.

Abstract

BACKGROUND: Aspirin is widely used for secondary prevention after stroke. Cilostazol has shown promise as an alternative to aspirin in Asian people with stroke.

OBJECTIVES: To determine the relative effectiveness and safety of cilostazol compared directly with aspirin in the prevention of stroke and other serious vascular events in patients at high vascular risk for subsequent stroke, those with previous transient ischaemic attack (TIA) or ischaemic stroke of arterial origin.

SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched September 2010), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2009, Issue 4), MEDLINE (1950 to May 2010) and EMBASE (1980 to May 2010). In an effort to identify further published, ongoing and unpublished studies we searched journals, conference proceedings and ongoing trial registers, scanned reference lists from relevant studies and contacted trialists and Otsuka Pharmaceutical Co Ltd.

SELECTION CRITERIA: We selected all randomised controlled trials (RCTs) comparing cilostazol with aspirin where participants were treated for at least one month and followed systematically for development of vascular events.

DATA COLLECTION AND ANALYSIS: Data extracted from eligible studies included: (1) a composite outcome of vascular events (stroke, myocardial infarction or vascular death) during follow up (primary outcome); (2) separate outcomes of stroke (ischaemic or haemorrhagic, fatal or non-fatal), myocardial infarction (MI) (fatal or non-fatal), vascular death and death from all causes; and (3) main outcomes of safety including any intracranial, extracranial or gastrointestinal (GI) haemorrhage and other outcomes during treatment follow up (secondary outcomes). We computed an estimate of treatment effect and performed a test for heterogeneity between trials. We analysed data on an intention-to-treat basis and assessed bias for all included studies.

MAIN RESULTS: We included two RCTs with 3477 Asian participants. Compared with aspirin, cilostazol was associated with a significantly lower risk of composite outcome of vascular events (6.77% versus 9.39%, risk ratio (RR) 0.72, 95% confidence interval (CI) 0.57 to 0.91), and lower risk of haemorrhagic stroke (0.53% versus 2.01%, RR 0.26, 95% CI 0.13 to 0.55). In terms of outcome of safety compared with aspirin, cilostazol was significantly associated with minor adverse effects (8.22% versus 4.95%, RR 1.66, 95% CI 1.51 to 1.83).

AUTHORS' CONCLUSIONS: Cilostazol is more effective than aspirin in the prevention of vascular events secondary to stroke. Cilostazol has more minor adverse effects, although there is evidence of fewer bleeds.

PMID: 21249700 [PubMed - in process]

Pearls on Intracranial atherosclerosis

2010-12-30T17:01:00.000-05:00

Turan TN, Chimowitz MI. . 10 questions about intracranial atherosclerosis.The Neurologist. 16:6 400-405 1020.

1. MRA and TCD have high negative predictive values but low positive predictive values for detecting intracranial stenosis. (86-91. v. 36-59 % respectively). They are therefore adequate screening tests but need CTA for diagnosis or catheter angiography. CTA studies have limited statistical power therefore catheter studies are the "gold standard" to determine the degree of stenosis, but also confer risk. A single preliminary study showed CTA had a sensitivity and specificity to detect intracranial stenosis greater than 50 % of of 97.1 and 99.5 % respectively. In ACAS the risk of stroke with catheter angiography was 1.2 %. The SONIA study was the study that helped evaluate the above.

2. The risk of stroke with intracranial stenosis is the highest of any stroke subtype, with respect to symptomatic stenosis of greater than 50 %. The risk of ischemic stroke in any territory within two years was 20 % in aspirin arm and 17 % in the warfarin arm (WASID). Over 70 % of strokes occurred in the same territory. Thus the risk in the symptomatic artery was 15/13 % in aspirin and warfarin arms respectively. This is higher than the risk with atrial fibrillation or cardioembolic stroke.

3. The risk of stroke was proportional to the severity of stenosis (risk of stroke within the symptomatic artery occurred in 6/18 % of patients, respectively, with < 70 and >70 % stenosis.

4. Other risk factors for stroke in the territory included recent symptoms, female gender, and baseline NIHSS >1. Vertebrobasilar arterial disease was NOT a risk factor.

5. Asymptomatic stenosis was very low risk, with a one year risk of stroke of 0 % in one study and 3.5 % in WASID by MRA.

6. "Antithrombotic failures" ie patients already on antiplatelet drugs at time of their stroke, were not at higher risk for recurrent stroke than patients who were not on antiplatelet drugs at the time of their qualifying event.

7. Most important risk factors for recurrent stroke were dyslipidemia and hypertension (SBP> 140).

8. SSYLVIA (stenting of symptomatic atherosclerotic lesions in the vertebral or intracranial arteries) was a ph I study of a bare metal stent that showed technical success and a 10.9 % stroke rate in one year with all strokes within the same artery.

9. SSAMPRIS study is ongoing (Stenting and Aggressive Medical Management of for Prevention of Recurrent Stroke in Intracranial Stenosis) NIH sponsored study. In 764 patients it compares angioplasty and stenting plus aggressive medical management v. medical management alone in patients with 70-99 % stenosis. Patients must have a TIA or nondisabling stroke within 30 days in an appropriate artery to be eligible. The protocol includes ASPIRIN for duration, plavix for first 90 days, aggressive bp and lipid management.

10. See http://www.ssampris.org/ or http://www.sammpris.org/.

HINTS to diagnose stroke in acute vestibular syndrome: 3 step oculomotor exam

2010-12-18T07:53:00.000-05:00

Stroke. 2009 Nov;40(11):3504-10. Epub 2009 Sep 17.
HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging.
Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE.
Department of Neurology, The University of Illinois College of Medicine at Peoria and the Illinois Neurological Institute at OSF Saint Francis Medical Center, Peoria, Ill, USA.

Abstract
BACKGROUND AND PURPOSE: Acute vestibular syndrome (AVS) is often due to vestibular neuritis but can result from vertebrobasilar strokes. Misdiagnosis of posterior fossa infarcts in emergency care settings is frequent. Bedside oculomotor findings may reliably identify stroke in AVS, but prospective studies have been lacking.
METHODS: The authors conducted a prospective, cross-sectional study at an academic hospital. Consecutive patients with AVS (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with >or=1 stroke risk factor underwent structured examination, including horizontal head impulse test of vestibulo-ocular reflex function, observation of nystagmus in different gaze positions, and prism cross-cover test of ocular alignment. All underwent neuroimaging and admission (generally <72 hours after symptom onset). Strokes were diagnosed by MRI or CT. Peripheral lesions were diagnosed by normal MRI and clinical follow-up.
RESULTS: One hundred one high-risk patients with AVS included 25 peripheral and 76 central lesions (69 ischemic strokes, 4 hemorrhages, 3 other). The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was 100% sensitive and 96% specific for stroke. Skew was present in 17% and associated with brainstem lesions (4% peripheral, 4% pure cerebellar, 30% brainstem involvement; chi(2), P=0.003). Skew correctly predicted lateral pontine stroke in 2 of 3 cases in which an abnormal horizontal head impulse test erroneously suggested peripheral localization. Initial MRI diffusion-weighted imaging was falsely negative in 12% (all <48 hours after symptom onset).
CONCLUSIONS: Skew predicts brainstem involvement in AVS and can identify stroke when an abnormal horizontal head impulse test falsely suggests a peripheral lesion. A 3-step bedside oculomotor examination (HINTS: Head-Impulse-Nystagmus-Test-of-Skew) appears more sensitive for stroke than early MRI in AVS.

neurodoc

Patient foramen ovale

2010-12-15T21:30:00.000-05:00

Kent DM, Thaler DE. Is Patent foramen ovale a modifiable risk factor for stroke recurrence?Stroke 2010: 41 (supplement 1) S 26-S30.

Authors make statistical arguments about PFO management. Facts that form a basis:

1. PFO occurs in 25 % of autopsies.
2. PFO occurs in a higher rate in cryptogenic stroke, but in at least 33 % of strokes with PFO the PFO is incidental.
3. PFO in Cryptogenic Stroke Study (PICSS) shows near identical stroke recurrence risk in patients with cryptogenic stroke whether or not they have a PFO. Further, small PFO's had a higher recurrence rate than large ones. This simply indicates, however, that PICSS included patients who were eventually given a TEE , even if they had a different defined mechanism for their stroke. Other occult mechanisms such as occult afib or subthreshold aortic atherothrombotic disease may have a higher recurrence rate.
4. Consistently, studies show that patients with cryptogenic stroke and PFO have less conventional stroke risk factors than patients without PFO. Since recurrence risk of stroke is about equal in PFO + and - patients, PFO singlehandedly compensates for lack of other risk factors. Therefore, PFO IS a risk factor for stroke. Younger patients without DM or HTN are much more likely to have a PFO.
5. When a PFO is found in setting with an atrial septal aneurysm, the PFO is rarely incidental to the stroke.
6. "PFO propensity" is likelihood based on age or other factors that a CS patient has a PFO. A higher PFO propensity correlates with a lower chance of incidental PFO. A younger patient without other risk factors may have a very high PFO propensity and therefore probability of nonincidental PFO.
7. The margin of benefit in PFO closure is narrow. Even a low rate of procedure complications could nullify benefit. "Testing the procedure (closure) in a population in which many incidental PFOs occur may falsely suggest the procedure is of no benefit."

Blackbox contraindication intravenous nimodipine

2010-08-03T07:53:00.000-05:00

August 2, 2010 — As if a "black box" warning currently on the label were not enough to get anyone's attention, today the US Food and Drug Administration (FDA) again reminded clinicians that nimodipine (Nimotop; Bayer Pharmaceuticals) should be given only by mouth or through a feeding tube and never by intravenous (IV) administration, a method that could be fatal.

Nimodipine, available only as an oral capsule, is used in critical-care settings to treat neurologic complications from subarachnoid hemorrhage.

The FDA states that it continues to receive reports of IV administration of the drug, which sometimes has resulted in death or near-death events. Intravenous administration of nimodipine can cause cardiac arrest, dramatic drops in blood pressure, and other cardiovascular adverse events, according to the agency.

In 1996, Bayer added a bolded statement to the drug's label to warn against incorrect administration after 1 patient who received nimodipine the wrong way died. In 2006, the company added a boxed warning against giving nimodipine intravenously or by other parenteral routes.

Through its Adverse Event Reporting System (AERS) and other sources, including published literature, the FDA has identified 31 cases of nimodipine errors between 1989 and 2009, with 25 involving the prescription or administration of the drug intravenously. Four patients who received nimodipine intravenously died while another 5 came close. One patient suffered permanent harm, according to the agency.

Errors Sometimes Occur With Patients Who Cannot Swallow Capsule

Sometimes nimodipine is administered intravenously despite repeated warnings to the contrary when a patient is not able to swallow the capsule. Such patients are supposed to receive it through a nasogastric tube. The drug comes with instructions for making a hole in both ends of the capsule with a standard 18 gauge needle, removing the contents with a syringe, and emptying the syringe into the tube.

The agency noted that because a standard needle will not fit on an oral syringe, it must be attached to an intravenous syringe. "The use of intravenous syringes to deliver nimodipine increases the chance that the medication will be given intravenously instead of by mouth or nasogastric tube," the FDA stated.

Clinicians can minimize confusion in these circumstances by labeling the syringe with the words "Not for IV Use" and removing the needle, according to the agency. They then should empty the syringe contents into the nasogastric tube followed by 30 mL of normal saline.

More information about today's announcement is available on the FDA's Web site.

To report adverse events related to nimodipine capsules, contact MedWatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.

Mendelsohn maneuver for stroke

2010-07-16T05:41:00.003-05:00

The Mendelsohn maneuver is taught by having the patient place

their fingers lightly over the thyroid cartilage and then trying to

swallow. When the thyroid cartilage reaches the top part of its

elevation during the swallow the patient is supposed to try to keep it

in this position for a second or two. The crycopharyngeus upper

esophageal sphincter is stretched by this excursion and is mechanically

opened. There may also be some reflex inhibition of the sphincter, but

the benefit is probably mostly mechanical. Logeman's book on dysphagia

has a much better description.

Homocystinuria and stroke

2010-05-04T21:02:00.000-05:00

Testai FD, Gorelick PB. Hommocystinuria, organic acidurias and urea cycle disorder. Arch Neurol 2010; 67: 148-153.

Features of homocystinuria
Genetics (classical) Aut rec, chromosome 21, deficient cystathione synthase, 90 + mutations, elevated Homocystine and metabolite, methionine(or elevated homocysteine and normal methionine with MTHFR mutations or errors of B12 metabolism.

Clinical -- myopia, osteoporosis, mental retardation, decreased pigmentation of hair and skin, downwards ectopic lenses, dolichostenomelia, and if untreated, seizures, psychiatric disorders, thromboembolic events (PE, MI, stroke). Clinically there is an equal distribution of the milder B6 (pyridoxal phosphate) responsive form and more severe unresponsive form.

Thromboembolic events-- distribution-- 51 % peripheral vein (one fourth PE's), 32 % strokes, 11 % peripheral arterial, 4 % MI, 2 % other. 25 % stroke by age 15, half by age 30. Treatment of pyrodoxal phosphate responders delays first event.

Mechanism-- of thromboembolism is multi. Increased homocysteine causes premature atherosclerosis due to endovascular dysfunction due to deficient nitrous oxide and oxidative stress. Also, hypercoagulability due to increased thrombosis and platelet activation may affect stability of arterial wall and cause dissections, arterial thrombosis, and arteriopathy mimicking FMD.

Diagnosis-- Based on clinical and lab features. Brand reaction is screening test using urinary cyanide nitroprusside. Blood usually has elevated homocysteine and methionine and decreased cysteine. Urine excretion of homocysteine, homocystine (the oxidized form) and methionine occurs. Cystathionine B synthase cultures in fibroblasts, amniotic fluid and chorionic villi can be assessed.

Treatment-- judicious use of B6 (300-600 mg/day) to prevent PN. Folate, betaine and B12 cause conversion of homocysteine to methionine. A methionine free diet with cysteine supplementation is suggested. Vitamin C and antiplatelet agents are commonly used.

Aneurysm presentation-- random clinical pearls

2010-04-10T19:29:00.001-05:00

Diagnosis
1. Of patients with the worst headache of their life, ten percent have aneurysms
2. Sensitivity of LP to detect aneurysms decreases by seven percent per day
3. CT-A removes need for catheter angiography in those with more than 5 rbc's
4. SAH- aneurysmal peaks in April and September and nadirs in June and July
5. Population prevalence of aneurysm in 2 %
Treatment
6. **FENESTRATION OF LAMINA TERMINALIS IS EASY, DECREASES HYDROCEPHALUS INCIDENCE FROM 13 TO 2 PERCENT AND ALLOWS LUMBAR DRAINS
7.   EEG is a "pseudoexam " under anesthesia
8. St Julien NSURG 2008 cardiopulmonary bypass without a chest incision (endovascular)allows fine control of BP and avoids circulatory arrest, hypothermia improves outcomes ( outcome of St Julien) Grade 0 , 1 (1.5 %), 2 (6.2%), 3 (12.1%), 4 (17.4 %). CP bypass is good for giant aneurysms
9. Fisher scale stratifies the risk of vasospasm . Grade 1: no blood   Grade 2: vertical layer < 1mm
      Grade 3:    vertical layer > 1 mm, local clot     Grade 4: ICH/IVH but minimal or no SAH. GRADE  THREE IS MAXIMAL RISK> GRADE FOUR.  Risk of vasospasm is 23 %.   With modified Fisher scale, vasospasm is greatest with grade 4. About 20-30 % of vasospasms stroke.
10. Risk of rebleed is 4 % in first 24 hours, then 1-2 % per day for 4 weeks. Cumulative risk is 20 % at 2 weeks, 30 % at one month, 40 % at 6 months. Ventriculostomy which otherwise can be lifesaving also can precipitate a rebleed.
10. Risk of rebleed is

Hemorrhagic shock plus TBI no longer uniformly fatal

2010-04-10T08:47:00.000-05:00

Combination is less lethal than formerly provided that CPP is maintained. Treatment algorithm: stop bleeding (factor 7), restore volume (whole blood, crystalloid), saline, plasma, platelets, pressors (phenylephrine, vasopressin, norepinephrine, DA), prophylactic phenytoin, for 7 days, treat fevers with tylenol, aggressive nutrition, use hemicraniectomy for impending herniation is efficacious, use GCS to communicate.

Prehospital care: avoid hypoxia-- give oxygen, avoid hypotension, hypertonic saline is good; mannitol only if intravascular volume can be maintained, generally avoid hyperventilation unless herniating.

ICP monitor if GCS < 8 and abnormal CT scan. Want ICP< 20, intervention threshold around 25. ICP plateau or A waves are sine qua non of herniation. These are best seen with changing sweep speed on monitor to minutes. B waves last from 0.5 to 2 minutes and are associated with changing brain compliance not increased ICP. C waves are ICP waves associated with respiration.

Components of a "brain code" are 1) elevated HOB to 45 degrees 2) HV to pCO2 around 35 3) mannitol .5 grams/kg 4) saline bullet (see http://neurologyminutiae.blogspot.com/2010/04/saline-bullets-and-hypertonic-saline.html) 5) CSF drainage

from lecture by Dr Ling

Vasospasm after traumatic brain injury

2010-04-10T08:30:00.000-05:00

Unlike its better known couin that occurs after SAH, vasospasm after TBI follows a different time course of 10-21 days is often subclinical and is best treated with nicardipine and endovascular therapy. It can be monitored with TCD.

Source-- lecture Col. Geoffrey Ling , MD

Pearls on blood pressure, misc and hemorrhagic stroke care

2010-04-03T19:33:00.000-05:00

1. PET studies do not support the concept of an ischemic penumbra, hence blood pressure control should be used judiciously (Schellinger et al, Stroke 2003)

2. The occurrence of ICH is strongly related to prevailing blood pressure, however no definitive evidence exists that recurrent ICH in the acute setting relates to blood pressure or control thereof (Jauch et al. Stroke 2006)

3. Intracranial hypertension is associated with a worse outcome

4. Prior statin use is associated with decreased perihemorrhage edema and decreased 30 day mortality ; however this data is retrospective (Naval et al., 2 refs Neurocritical Care 2008)

5. The Stroke Council continues to advocate for 2-4 weeks of prophylactic antiepileptic therapy in patients with SICH and SAH

6. Hematoma size (Stoke 1997, Brott et al) and growth (Davis et al, Neurology 2006) are correlated with mortality

7. The "spot sign" or contrast extravasation in CTA may identify patients at high risk of hematoma expansion

8. ICH < 30 cc may benefit from intraclot alteplase

9. MIS minimal invasive surgery is also considered under investigation although certain types of ICH do not benefit

Carotid artery webbing

2010-03-28T10:52:00.000-05:00

case report at AAN 2010 also known as "atypical FMD" a 41 year old woman with headache for months, facial droop and aphasia cutely. MRI showed an M1 occlusion, and delayed time to peak in entire MCA. Catheter showed bilateral ICA webbing with stagnant flow. No standard of care is known.

MCA arrow sign in MCA aneursmal SAH

2010-03-28T09:46:00.000-05:00

In a review, arrow sign was present in 4 patients with SAH all Fisher 3. That is 16 % of total MCA aneurysms and was not seen in any other type of aneurysm.

below is an arrow sign for an MCA trifurcation aneurysm (from neurology.org)

Ptosis and astasia with thalamic infarcts: case report (s)

2010-03-28T09:27:00.001-05:00

Jain D. et al. Cerebral ptosis and astasia "Lateral pulsion" due to a left anterior thalamic lesion. Mechanisms are reviewed.AAN 2010:PO2:102

Alderazi Y. Thalamic infarction causing astasia-abasia, ataxia and asterixis. clinical and radiological features of two cases. PO2:108. Wide based gait past pointing and intention tremor on right, with left posterolateral thalamic infarct. Second case with left arm drift, left asterixis, inability to stand unassisted with right lateral thalamic acute stroke and old left cerebellar hemorrhage.

Sneddon's syndrome need for angiography

2010-03-28T09:08:00.000-05:00

Faris et al. Sneddon's syndrome without antiphospholipid antibodies: a report of 26 cases with cerebral angiography (Rabat). Neurology 2010 74:9:PO2:099.

Authors emphasize Sneddon's syndrome (stroke plus livedo racemosa) is NOT identical to APL syndrome. 26 patients were studied retrospectively with a combination of focal motor deficits and dementia. Imaging always showed infarcts with white matter involvement. Angio showed a distal arteriopathy in 18 cases with pial networks in cases. Two had hematomas. The authors suggested angiography to prevent the unwarranted and dangerous potential use of anticoagulation.

NSE after cardiac arrest during hypothermia predicts outcome

2010-03-26T16:32:00.000-05:00

AN 2010 Po1.048 JEF Fugate, Wijdicks et al. NSE was measured serially in comatose patients undergoing hypothermia. A cutoff was used of 33 ug/L. NSE was measured at day one and day three, with higher NSE suggesting poor prognosis (defined as one year mortality). 48 patients, 41 had first day NSE, 14 had third day NSE. For first day NSE, the number with high level is given with number of survivors at one year in parenthesis 19 (3) with a low NSE being 22 (11). Trend in NSE on day 3 was highly predictive (p<.015). The sensitivity for first day NSE was 59 % for one year mortality with improvement to 66 % if 3 day NSE is included.

Four score is predictor of outcome in coma after cardiac arrest

2010-03-25T13:03:00.000-05:00

Neurology AAN 2010 PO1.045 Wijdicks et al.

The Four Score differs from the GCS because it has 4 components-- eye, motor, brainstem and respiration (latter two are not included in GCS) . Prospectively looked at patients from 2006-2009 (n=131) and looked at outcome after one year. 91 died. 31 had four score less than 4 at day one and of these, zero survived. Of patients with GCS of 3, 4 (7 %) survived at one year. The Four Score had a specificity for absent survival at one year of 100 % versus 90 % for GCS of 3.

Description of the FOUR Score

The FOUR score has 4 components: eye responses, motor responses, brainstem reflexes, and respiration pattern. Each component has a maximal value of 4 (Figure 1). Assessing all components of this score usually takes only a few minutes.5 The eye response component of the FOUR score allows differentiation between a vegetative state (eyes open but do not track) and a locked-in syndrome (eyes open, blink, and track vertically on command). The motor assessment component of the FOUR score combines the withdrawal reflex and decorticate rigidity responses because these conditions are often difficult to distinguish clinically. The motor component includes a complex command (the patient is asked to produce a thumbs-up hand signal, a fist, and the peace sign) that determines whether patients are alert.7 Similarly, the motor component of the FOUR score can detect signs of severe cerebral dysfunction, such as myoclonic status epilepticus. Such dysfunction is often a poor prognostic sign for patients with suspected anoxic brain injury.8 The brainstem components of the FOUR score assess the pons, the mesencephalon, and the medulla oblongata in various combinations. The FOUR score also includes an assessment of Cheyne-Stokes respiration and irregular breathing; such signs can indicate bihemispheric or lower brainstem dysfunction of respiratory control. For patients who have undergone intubation, the FOUR score records the presence or absence of a respiratory drive.

FIGURE 1.

Description of Full Outline of UnResponsivenes (FOUR) score. Eye response: E4 = eyelids open or opened, tracking, or blinking to command; E3 = eyelids open but not tracking; E2 = eyelids closed but open to loud voice; E1 = eyelids closed but open to pain; E0 = eyelids remain closed with pain. Motor response: M4 = thumbs-up, fist, or peace sign; M3 = localizing to pain; M2 = flexion response to pain; M1 = extension response to pain; M0 = no response to pain or generalized myoclonus status. Brainstem reflexes: B4 = pupil and corneal reflexes present; B3 = one pupil wide and fixed; B2 = pupil or corneal reflexes absent; B1 = pupil and corneal reflexes absent; B0 = absent pupil, corneal, and cough reflex. Respiration pattern: R4 = not intubated, regular breathing pattern; R3 = not intubated, Cheyne-Stokes breathing pattern; R2 = not intubated, irregular breathing; R1 = breathes above ventilatory rate; R0 = breathes at ventilator rate or apnea.

The Broken Heart Syndrome

2010-03-21T17:31:00.001-05:00

llan Wittstein has published and given lectures and states there are clinical criteria, diagnostic criteria and treatment and prognosis information that can be readily identified. Synonyms include neurogenic stunned myocardium, acute coronary syndrome, stress myocarditis, and Takotsubo syndrome (named after the japanese pot used to capture octopus). The syndrome is a REVERSIBLE disorder with very abnormal EKG, U waves, ST elevations, Q waves, elevated troponins, normal coronaries on cath, and return of EF to normal within days to weeks. The pathology includes contraction band necrosis in myocardium, and is linked to hypersympathetic state. It is a huge problem involving 2 percent of patients undergoing cath and 5-7 % of women. Most patients are postmenopausal Caucasian women with risk factors who present with chest pain and shortness of breath. Many have mood disorders

Diagnostic criteria are divided into "helpful" and "required"
HELPFUL-
1. Acute trigger-- could be emotional (anxiety, joy, grief, fear, anger) or physical (procedure, respiratory drugs) even surprise party.
2. Characteristic EKG-- presenting EKG has steep ST elevation without reciprocal changes, T wave inversions everywhere, QT prolongation, that becomes milder within 2-4 days
3. Troponin elevation is mild-- less than 5, never more than 20

REQUIRED
1. Absent coronary thrombosis
2. Wall motion abnormalities extend beyond a single coronary artery territory ( 3 patterns: apical, basal, and midventricular)
3. Rapid recovery of systolic function within 2 weeks at most

Diagnostic tests that are helpful (but possibly hard/unlikely to obtain esp. acutely)
1. MRI heart unlike ECHO differentiates dead and stunned tissue. Dead cardiac tissue lights up with Gadolinium but stunned heart will not

Therapy:
1. supportive-- possibly not in ICU- arbs, ACEi's, diuretics. Anticoag if apex not moving to prevent clot kicking, avoid pressors (catechols are a problem)
2. Balloon pump better than pressors
3. HHH good for brain, bad for heart

Prognosis
1. recurrence 3-10 percent with 2 % mortality
2. Death is due to etiology not to cardiac dysfunction per se.

Pathophysiology
contraction band necrosis- direct myocyte injury related to calcium overload.

air embolism and air travel

2010-03-21T17:11:00.001-05:00

The Neurologist 2010 A 62 year old woman with cerebral artery air embolism during commercial air travel. 16: 136-137.

Notes

usual list of associations with air embolus-- surgery, scuba diving, induced abortion, angiography and pneumothorax, orogenital sex on a woman with cerebral air emboli (see Crit Care Med 1988).

A new one is air travel. In this case, pulmonary bullae due to emphysema occurred as the bullae expanded as the pressure in the cabin was reduced, leading to rupture of the bullae, pneumothorax and air embolism. Barotrauma was presumably the proximate cause.

Pearls on pediatric strokes

2010-03-21T15:01:00.000-05:00

hat tip to Lori Jordan MD JHU

1. Strokes in kids are as common as brain tumors, about 2-3/100,000
2. In children ICH = bland infarcts, different than adults (Fullerton, Neurology, 2003). ICH is often due to AVM's
3. Among bland infarcts, 25-35 % are cardioembolic, 25 % are dissections, other unusual causes include moya moya, sickle cell disease, HIV and varicella (not in order).
4. Subarachnoid hemorrhage in kids is usually aneurysmal
5. Kids at risk often have an inciting event such as trauma or surgery
6. Kids have a high risk of delay in diagnosis
7. Sicklers have 10 % stroke, but 20 % more of silent stroke; with SCA and CVA stat consult Hematology for transfusion
8. Many barriers to alteplase use exist, including diagnosis, , lack of evidence and mimics, and delays, but document why alteplase is not given
9. MERCI and multi MERCI are not studied in kids
10.AHA guidelines for pediatric stroke published Stroke 2008
11. Presentation in children is much more likely to include seizure (25 % v. 5 % in adults)
12 . Suggested eval: MRI, MRA H/N, hypercoagulability workup complete, TTE/bubble, HB electropheresis, HIV,
13 references
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, et al.
Management of stroke in infants and children: A scientific statement from a
special writing group of the american heart association stroke council and the
council on cardiovascular disease in the young. Stroke 2008;39:2644-91.
• Amlie-Lefond, C. et al. Use of alteplase in childhood arterial ischaemic stroke: a
multicentre, observational, cohort study. 2009: Lancet Neurol. 8, 530-536.
• Jordan LC, Johnston SC, Wu YW, Sidney SS, Fullerton HJ. The importance of
cerebral aneurysms in childhood hemorrhagic stroke: a population-based study.
Stroke 2009;40:400-405.
• Beslow LA, Licht DJ, Smith SE, Storm PB, Heuer GG, Zimmerman RA, Feiler
AM, Kasner SE, Ichord RN, Jordan LC. Predictors of outcome in childhood
intracerebral hemorrhage: a prospective consecutive cohort study. Stroke 2009;

CAA with vasculitis and edema responsive to steroids references

2010-03-17T21:59:00.000-05:00

inflammation related CAA as described in : Ann Neurol 2004; 55: 250-256; Brain 2005; 128: 500-515; Neurology 2007; 68 (17); 1411-1416.

ISC Abstract highlights 2010 San Antonio (pruned and edited)

2010-03-07T16:11:00.003-05:00

1. Restrepo et al. (UCLA) Stroke pretreatment screening for fast Mag trial, involved a 90 second screen with a neurologist, focused, 72 % of patients so diagnosed had acute ischemic stroke, 24 % ICH, rest other

2. Albright et al. (Penn) studied the potential for the use of air ambulances to increase availability of services and found The combination of pre-hospital regionalization & air ambulance transport of acute stroke
patients would reduce the 135.7 million Americans without 60 minute access to a PSC by
half, to 62.9 million.

3. Kleindorfer et al. (Cincinatti) stratified t-PA eligibility by age and found contrary to hypothesis, the eligibility for rt-PA significantly increased with increasing age.
Age-Based Eligibility for and Treatment with Rt-PA
Age of Pt       # Patients % Eligible for rt-PA % of Eligible Treated
18–44                   97                        4 (4.1%)              2 (50.0%)
45–54                 219                       15 (6.8%)             5 (33.3%)
55–64 320                       21 (6.6%)            12 (57.1%)
65–74                 392                       32 (8.2%)            20 (62.5%)
75–84                 502                       47 (9.4%)             23 (48.9%)
85     300                       29 (9.7%)             10 (34.5%)
Total                  1830       148 (8.1%)             72 (48.6%)

4. Riccio et al (Buenos Aires) Occult v. non -occult AF compared in TIA and AIS. Age, female gender and left atrial area (LAA) are traditional determinants of AF. Out of 194 patients, there were 36 with known AF and 24 with occult AF. Patients with occult AF were younger, showed a higher proportion of males, had
a smaller LAA, and had more severe strokes. Traditional determinants of AF were associated
with known AF.Diabetes was associated with occult AF.

5. Gupta et al. (multicenter) General anesthesia during stroke resulted in worse outcomes.

Infective endocarditis and stroke: pearls

2010-02-07T18:26:00.000-05:00

. The classic triad of infective endocarditis and stroke of fever, murmur and acute neurologic deficit is uncommon, occurring in less than half of patients, with murmur occurring in less than one third (due to decline of valvular disease as a cause) ; fever, embolism and high sed rate may also be seen in NBTE, arteritis with PAN, other rheumatologic disease, or atrial myxoma.

2. Organisms are more diverse than previously with Streptococcus representing only 60 percent, including resistant Group D Strep viridans (enterococcus faecalis) and Strep bovis (associated with GI neoplasia). Staph aureus is seen in up to 30 % especially those with i-v drug abuse, recent surgery, and no preexisting valve lesion. Patients with prosthetic valves may get S aureus and S epidermidis. Others, including immunocompromised may get HACEK bacteria and fungi ( hemophilus, actinobacillus, cardiobacterium, Eikinella, Kinzella). Among pretreated groups, culture negative disease has increased to 5.5 %.

3. Early onset (at presentation of first 48 hours) of neurologic symptoms is more common with Staph aureus than with streptococcal infections, that can occur late (54 v 19 %). Late embolism is especially common among patients with prosthetic valves (14/15 late strokes in one series had prosthetic valves). In native valve endocarditis, anticoagulation is of no benefit , certainly for at least 48 hours or until infection is controlled.

4. Cardiac vegetations initially larger than 10 mm are high risk, and are best seen with TEE rather than TTE. Embolic rate is much higher in presence of visible lesions, and vice versa, visible lesions are much more common among patients with detectable emboli. The 10 mm size may "open the debate" about the need for valve replacement.

5. The discovery of endocarditis without emboli does not dictate the cessation of otherwise needed anticoagulant therapy.

6. If cardiac surgery is needed, timing is dictated by common sense. One such protocol is to wait at least five days (until the edema of the stroke has settled) before considering operation, if possible.

7. Use heparin fairly early on (certainly within 48 hours) of stroke with prosthetic valves with endocarditis, especially if subclinical INR was found on presentation. Discontinue anticoagulation if possible in most cases of fungal endocarditis.

8. Intracranial hemorrhage (3-6 % of patients) occurs with aneurysm rupture, septic arteritis, conversion of a bland infarct, and late effects of immune deposition. Septic bacterial aneurysms may occur at distal branch points, but mycotic aneurysms, large ones, may occur proximally. However, one study suggested the vast majority of patients with aneurysms had abnormal CT scan. Present blood on CT or (if headache is present) pleocytosis on CSF examination weighs towards four vessel angiogram.

9. Serial angiography is indicated for mycotic aneurysms which may heal with antibiotics.

10. Special concern exists among patients with line induced sepsis and bland infarction that could result in late S Aureus superinfection of an initially bland infarct. Full infective endocarditis treatment regimen may be warranted in these patients and TEE may alternatively show evidence of vegetations.

Unknown angles
1. Role of MRA/ CTA
2. When surgery is required

Percentage of patients with stroke with prior TIA

2010-02-02T09:48:00.000-05:00

Hackam DG, Kapral MK, Wang JT et al. Most stroke patients do not get a warning: a population based cohort study. Neurology 73: 1074-1075, 2008.

cites data suggesting 17 % of CVA patients have prior TIA. Authors review 16, 409 charts. Timing of TIA is not addressed. 12.4 % had prior TIA, but 20% of those with large arter TIA's, much lower with hemorrhagic stroke (5%), somewhat higher with ischemic stroke (15 %). Risk factors to have prior TIA: older, DM, HTN, AF, CHF,angina, PAD. Patients without TIA were more likely to die in hospital, arrest, or not be discharged to home.

covered stents for carotids

2010-01-09T08:44:00.001-05:00

The use of covered stents for the endovascular treatment of extracranial internal carotid artery stenosis: a prospective study with a 5-year follow-up; Szólics A, Sztriha LK, Szikra P, Szólics M, Palkó A, Vörös E; European Radiology

OBJECTIVES: To evaluate the safety and feasibility of the use of covered stents for the treatment of extracranial carotid artery stenosis caused by highly embologenic plaques, and to study the long-term outcome of patients receiving such covered stents. METHODS: Between 2002 and 2007, 46 patients (63% symptomatic, 78.3% male, 67 +/- 8.6 years old) with internal carotid artery stenosis caused by embologenic plaques or restenosis were treated with self-expanding covered stents (Symbiot, Boston Scientific). Pre-dilatation or protecting devices were not used. Post-dilatation was applied in every patient. Each patient was followed long-term. The outcome measures were the occurrence of neurological events, and the development of in-stent restenosis, as detected by clinical examination and duplex ultrasound. RESULTS: The technical success rate of stenting was 100%. There were no neurological complications in the peri-procedural period. The mean follow-up period was 34.3 +/- 27.7 months (the rate of patients lost to follow-up was 15.2%) during which no stroke or stroke-related deaths occurred. Restenosis was detected in 3 patients (6.5%). CONCLUSION: Covered stents provide efficient peri- and post-procedural protection against neurological complications due to embolisation from high-risk plaques during carotid artery stenting. Restenosis of covered stents appears to be infrequent during long-term follow-up.

hemodialysis causes cerebral microbleeds in about one fourth

2010-01-09T08:41:00.001-05:00

Cerebral microbleeds in predialysis patients with chronic kidney disease; Shima H, Ishimura E, Naganuma T, Yamazaki T, Kobayashi I, Shidara K, Mori K, Takemoto Y, Shoji T, Inaba M, Okamura M, Nakatani T, Nishizawa Y; Nephrology Dialysis Transplantation (Dec 2009)

BACKGROUND: Gradient-echo T2-weighted magnetic resonance imaging (T2-weighted MRI) is highly sensitive for detecting cerebral microbleeds (CMBs). CMBs have been reported to be a risk factor for future cerebrovascular events and a marker of cerebral small vessel disease in the general population. Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease. The relationship between CKD and CMBs, which has not been clarified to date, is examined. METHODS: In this cross-sectional study, T2*-weighted MRI of brain was performed with a 1.5-T MRI system in 162 CKD patients (CKD stages 1-5, excluding CKD stage 5(D)) and 24 normal subjects. RESULTS: CMBs were found in 35 CKD patients (25.6%), but not in control subjects. CMBs were more prevalent in male patients, in those with higher blood pressure, advanced age and poor kidney function. There was a significant association between the prevalence of CMBs and the CKD stage, with higher prevalence of CMBs as the CKD stages advanced (P<0.01). Estimated glomerular filtration rate was a significant factor associated with the prevalence of CMBs, independent of age, gender and hypertension. There was no significant relationship between CMBs and the presence of diabetes mellitus and dyslipidemia. CONCLUSIONS: Decreased renal function is a significant risk factor for CMBs, independent of the presence of hypertension. Poor kidney function could be associated with future cerebrovascular events.

Viagra and stroke

2010-01-09T08:30:00.001-05:00

The effect of sildenafil citrate (Viagra) on cerebral blood flow in patients with cerebrovascular risk factors; Lorberboym M, Mena I, Wainstein J, Boaz M, Lampl Y; Acta Neurologica Scandinavica (Dec 2009)

Objectives - Sildenafil citrate is widely used for erectile dysfunction. The present study examined the short-term effects of sildenafil administration in individuals with cerebrovascular risk factors, including patients with a history of stroke. Materials and Methods - Twenty-five consecutive male patients with erectile dysfunction and vascular risk factors were included in the study. A perfusion brain SPECT study was performed at baseline and 1 h after the oral administration of sildenafil. Results - Associations between any of the risk factors and the perfusion scores were not detected, with the exception of stroke. Stroke patients showed significantly more areas with diminished perfusion after sildenafil administration compared to baseline. Conclusions - In patients with diabetes or hypertension, a dose of 50 mg sildenafil does not appear to produce detrimental effects on cerebral blood flow. However, patients with a history of stroke may be at increased risk of hemodynamic impairment after the use of sildenafil.

avoid plavix plus nexium/prevacid

2009-12-06T12:22:00.001-05:00

FDA: Avoid Coadministration of Clopidogrel and Omeprazole, Esomeprazole

SILVER SPRING, Md -- November 17, 2009 -- The US Food and Drug Administration (FDA) has new data showing that the proton pump inhibitor (PPI) omeprazole (Prilosec/Prilosec OTC) reduces the anti-blood clotting effect of clopidogrel (Plavix) by almost half when these 2 medicines are taken by the same patient. Patients at risk for heart attacks or strokes who use clopidogrel to prevent blood clots will not get the full effect of this medicine if they are also taking omeprazole; therefore, the FDA recommends that the coadministration of omeprazole and clopidogrel be avoided.

The new recommendations, updated from a January 2009 Early Communication, are based on study results from the manufacturers of clopidogrel. The studies confirm that coadministration of omeprazole with clopidogrel results in decreased levels of clopidogrel's active metabolite, reducing clopidogrel's anticlotting effect.

Omeprazole inhibits the drug-metabolising enzyme (CYP2C19), which is responsible for the conversion of clopidogrel into its active metabolite. The new studies compared the amount of clopidogrel's active metabolite in the blood and its effect on platelets in patients who took clopidogrel plus omeprazole versus those who took clopidogrel alone. A reduction in active metabolite levels of about 45% was found in those who received clopidogrel with omeprazole compared with those taking clopidogrel alone. The effect of clopidogrel on platelets was reduced by as much as 47% in patients receiving clopidogrel and omeprazole together. These reductions were seen whether the drugs were given at the same time or 12 hours apart.

Since the level of inhibition among other PPIs varies, it is unknown to what amount other PPIs may interfere with clopidogrel. However, esomeprazole (Nexium), a PPI that is a component of omeprazole, inhibits CYP2C19 and should also be avoided in combination with clopidogrel.

Other stomach acid-reducing drugs, such as ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid), or antacids, are not expected to interfere with the anticlotting activity of clopidogrel because they do not inhibit CYP2C19 activity. However, cimetidine (Tagamet/Tagamet HB) does inhibit CYP2C19 activity and should not be used.

In addition to cimetidine, other drugs that are potent inhibitors of the CYP2C19 enzyme would be expected to have a similar effect and should be avoided in combination with clopidogrel. These include fluconazole (Diflucan), ketoconazole (Nizoral), voriconazole (VFEND), etravirine (Intelence), felbamate (Felbatol), fluoxetine (Prozac, Sarafem, Symbyax), fluvoxamine (Luvox), and ticlopidine (Ticlid).

Sanofi-aventis and Bristol-Myers Squibb, the makers of Plavix (clopidogrel), are updating this drug's label with the details of the studies and are conducting follow-up studies to further explore drug interactions with clopidogrel.

Until further information is available, FDA recommends the following:
• The concomitant use of omeprazole and clopidogrel should be avoided because of the effect on clopidogrel's active metabolite levels and anticlotting activity. Patients at risk for heart attacks or strokes, who are given clopidogrel to prevent blood clots, may not get the full protective anticlotting effect if they also take prescription omeprazole or the OTC form.
• Separating the dose of clopidogrel and omeprazole in time will not reduce this drug interaction.
• Other drugs that should be avoided in combination with clopidogrel because they may have a similar interaction include esomeprazole, cimetidine, fluconazole, ketoconazole, voriconazole, etravirine, felbamate, fluoxetine, fluvoxamine, and ticlopidine.
• At this time the FDA does not have sufficient information about drug interactions between clopidogrel and PPIs other than omeprazole and esomeprazole to make specific recommendations about their coadministration. Healthcare professionals and patients should consider all treatment options carefully before beginning therapy.
• There is no evidence that other drugs that reduce stomach acid, such as most H2 blockers ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid), except cimetidine (Tagamet and Tagamet HB - a CYP2C19 inhibitor), or antacids interfere with the anticlotting activity of clopidogrel. Ranitidine and famotidine are available by prescription and OTC to relieve and prevent heartburn and antacids are available OTC to relieve heartburn.
• Talk with your patients about the OTC medicines they take. Be aware that patients may be taking nonprescription forms of omeprazole and cimetidine.

The FDA will continue to investigate other drug interactions with clopidogrel. The FDA plans on presenting this issue at the next meeting of the FDA's Drug Safety Oversight Board in November. The Agency will communicate any further recommendations or conclusions once additional information is available.

Effectiveness of Clopidogrel May Be Reduced by Common Heartburn Drugs: Presented at SCAI

Certain PPIs Increase Risk of Heart Attacks for Patients on Clopidogrel

SOURCE: US Food and Drug Administration

erythropoietin and vasospasm after SAH- synergistic with statins

2009-12-02T06:00:00.001-05:00

J Neurosurg

Interaction of neurovascular protection of erythropoietin with age, sepsis, and statin therapy following aneurysmal subarachnoid hemorrhage; Tseng MY, Hutchinson PJ, Kirkpatrick PJ; Journal of Neurosurgery (Nov 2009)

Object In a previous randomized controlled trial, the authors demonstrated that acute erythropoietin (EPO) therapy reduced severe vasospasm and delayed ischemic deficits (DIDs) following aneurysmal subarachnoid hemorrhage. In this study, the authors aimed to investigate the potential interaction of neurovascular protection by EPO with age, sepsis, and concurrent statin therapy. Methods The clinical events of 80 adults older than 18 years and with<72 hours of aneurysmal subarachnoid hemorrhage, who were randomized to receive 30,000 U of intravenous EPO-beta or placebo every 48 hours for a total of 3 doses, were analyzed by stratification according to age (< or≥ 60 years), sepsis, or concomitant statin therapy. End points in the trial included cerebral vasospasm and impaired autoregulation on transcranial Doppler ultrasonography, DIDs, and unfavorable outcome at discharge and at 6 months measured with the modified Rankin Scale and Glasgow Outcome Scale. Analyses were performed using the t-test and/or ANOVA for repeated measurements. Results Younger patients (<60 years old) or those without sepsis obtained benefits from EPO by a reduction in vasospasm, impaired autoregulation, and unfavorable outcome at discharge. Compared with nonseptic patients taking EPO, those with sepsis taking EPO had a lower absolute reticulocyte count (nonsepsis vs sepsis, 143.5 vs. 105.8 x 10(9)/L on Day 6; p = 0.01), suggesting sepsis impaired both hematopoiesis and neurovascular protection by EPO. In the EPO group, none of the statin users suffered DIDs (p = 0.078), implying statins may potentiate neuroprotection by EPO. Conclusions Erythropoietin-related neurovascular protection appears to be attenuated by old age and sepsis and enhanced by statins, an important finding for designing Phase III trials.

Platelets transfusions does not help mortality in mild TBI in ASA/Plavix takers

2009-12-02T05:55:00.001-05:00

Am Surg Does platelet administration affect mortality in elderly head-injured patients taking antiplatelet medications?; Monson B, Butler KL, Fortuna GR, Saxe JM, Dolan JP, Markert RJ, McCarthy MC, Downey DM; American Surgeon 75 (11), 1100-3 (Nov 2009)

A significant portion of patients sustaining traumatic brain injury (TBI) take antiplatelet medications (aspirin or clopidogrel), which have been associated with increased morbidity and mortality. In an attempt to alleviate the risk of increased bleeding, platelet transfusion has become standard practice in some institutions. This study was designed to determine if platelet transfusion reduces mortality in patients with TBI on antiplatelet medications. Databases from two Level I trauma centers were reviewed. Patients with TBI 50 years of age or older with documented preinjury use of clopidogrel or aspirin were included in our cohort. Patients who received platelet transfusions were compared with those who did not to assess outcome differences between them. Demographics and other patient characteristics abstracted included Injury Severity Score, Glasgow Coma Scale, hospital length of stay, and warfarin use. Three hundred twenty-eight patients comprised the study group. Of these patients, 166 received platelet transfusion and 162 patients did not. Patients who received platelets had a mortality rate of 17.5 per cent (29 of 166), whereas those who did not receive platelets had a mortality rate of 16.7 per cent (27 of 162) (P = 0.85). Transfusion of platelets in patients with TBI using antiplatelet therapy did not reduce mortality.

Neuropsych and carotid stenosis

2009-11-28T12:43:00.001-05:00

M. Silvestrini, MD, I. Paolino, MD, F. Vernieri, MD, C. Pedone, MD, R. Baruffaldi, MD, B. Gobbi, MD, C. Cagnetti, MD, L. Provinciali, MD and M. Bartolini, MD . Cerebral hemodynamics and cognitive performance in patients with asymptomatic carotid stenosis. NEUROLOGY 2009;72:1062-1068

Objective: The aim of this study was to investigate whetherthe presence of severe internal carotid artery stenosis maybe associated with different cognitive performance in relationto the side of the stenosis and its hemodynamic consequences.

Methods: Eighty-three patients with asymptomatic severe unilateralinternal carotid stenosis were included. A neuropsychologicalinvestigation including Verbal Fluency using phonemic and categoryaccess, Coloured Progressive Matrices, and Complex Figure TestCopy was performed. Each patient underwent an assessment ofcerebrovascular reactivity (CVR) to hypercapnia with transcranialDoppler ultrasonography using the breath-holding index (BHI).Thirty healthy subjects comparable for demographic characteristicsand vascular risk profile served as controls. Subjects withcarotid stenosis were classified into two groups: preservedCVR (BHI 0.69), 48 patients (25 with left and 23 with rightstenosis); and impaired CVR (BHI <0.69), 35 patients (19with left and 16 with right stenosis).

Results: Subjects with left stenosis and reduced CVR had significantlylower performances at phonemic verbal fluency with respect tocontrols and the other groups of stenosis. In subjects withright stenosis and reduced CVR, scores obtained in ColouredProgressive Matrices and in Complex Figure Test Copy were significantlylower with respect to the other groups.

Conclusions: These results suggest that an alteration of cerebrovascularreactivity may be responsible for reduction in some cognitiveabilities involving the function of the hemisphere ipsilateralto carotid stenosis. Such findings may be of interest for providinga more comprehensive indication to surgical treatment in subgroupsof subjects with asymptomatic carotid stenosis.

safety of CT perfusions per FDA

2009-10-21T09:46:00.001-05:00

For more information, please see FDA's Safety Investigation of CT Brain Perfusion Scans: Initial Notification at:

http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm185898.htm <http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm185898.htm>

d-dimer predicts cardioembolic stroke

2009-10-05T19:03:00.001-05:00

D-dimer assay may differentiate subtypes of ischemic stroke; study of 126 patients hospitalized with acute ischemic stroke;
stroke subtypes were cardioembolic in 34 (27%),
atherothrombotic in 34 (27%),
lacunar in 31 (25%),
unknown in 27 (21%);

mean D-dimer levels on day 1 were 2.96 mcg/mL with cardioembolic stroke, 1.34 mcg/mL with atherothrombotic stroke and 0.67 mcg/mL with lacunar stroke; similar results at days 6 and 12; D-dimer > 2 mcg/mL had 59% sensitivity and 93% specificity for predicting cardioembolic stroke, D-dimer < 0.54 mcg/mL had 61% sensitivity and 96% specificity for predicting lacunar stroke

(Arch Intern Med 2002 Dec 9/23;162(22):2589)

Biomarkers for stroke

2009-10-04T19:09:00.002-05:00

Foerch C, Montaner J, Furie KL,Ning MM, Lo EH. Searching for oracles: blood biomarkers for acute stroke . Invited Article. Neurology 2009; 73: 393-399.

Article discusses batteries of biomarkers used together to diagnose acute stroke or intracranial hemorrhage. They note that CT excludes hemorrhage, but does not include stroke, so a panel of markers may play a useful role.

To diagnose acute ischemic stroke, authors suggest a need for higher sensitivity than specificity to avoide missing treatable strokes.

NMDA antibodies are typically high early in stroke (first 3 hours) but may be false positive in patients with atherosclerosis or old strokes. New research focuses on fragments of NMDA rather than antibodies.

Reynolds et al. (Clin Chemisty2003) tested 50 markers and found a panel of four or five significantly predicted ischemic stroke. They were S100b, B type neurotropic growth factor, VWF, MMP-9, and monocyte chemotactic protein 1.They had a combined sens/spec of 91/97 for IS within 12 hours of stroke onset. The same group in a 2d study found S100b, MMP-9. vascular adhesion molecule, and VWF to have a combined sens/spec of 90/90. (Lynch JR Stroke 2004). Laskowitz found a panel of BNP, CRP, d-dimer, MMP-9, and S100b has a sens/spec of 81/70. Laskowitz et al. published a prospective multicenter trial (Stroke 2009) of 1100 patients using d-dimer, BNP, MMP-9, and S100b within 24 hours of stroke onset and found a s/s of 86/37.

For intracranial hemorrhage, markers include GFAP, which is also high in gliomas. In another analysis, RAGE and S100b best differentiated group from controls. ApoC1 and especially ApoC3 differentiate ICH from controls.

Montaner et al (Circulation 2003) found that MMP-9 was a powerful predictor of hemorrhagic risk in patients given alteplase. MMP-9 is also a predictor of HT in non lysed patients. Fibronectin has a similar pattern.

S100B which tends to correlate with infarct size, was also a predictor of malignant edema in one study (Foerch et al., Stroke 2004).

Bypass, strokes and Lou Caplan's call for action

2009-09-23T19:28:00.003-05:00

Caplan LR. Translating what is known about neurological complications of coronary artery bypass graft complications into action. Arch Neurol 2009; 66: 1062-1064.

Dr Caplan editorializes about stroke and CABG and distills knowledge into 3 pages and a number of points that can be bulleted.

1. Complications from bypass are increasing as bypass patients are sicker. In 1994, the rate of stroke and delirium after bypass were 2.9 and 7.7 % respectively, at Johns Hopkins Hospital. In 2004, the respective rates were 4.5 and 13.8 %.

2. There is virtually no relationship between carotid disease, especially asymptomatic, and cardiac risk during bypass. In the large series, 95 % had strokes not in the territory of a diseased carotid artery. Of the four patients who did have strokes in the diseased carotid territory, the carotid was occluded in 3 of 4 so the mechanism was not hemodynamic but embolic.

3, Aortic atheromatosis is the most important cause of stroke after bypass, with cardiac factors second. The use of aortic filters, the use of off pump bypass or avoidance of cross clamping and identifying patients in advance results in improved outcomes. Identifying susceptible patients can be done with TEE, chest x ray, chest CT, or intraoperative epiaortic ultrasound before clamping. Most patients have not had this done.

4. ECHO to look at ventricular contractile function and thrombi is often not done but should be done.

5. Identification of a cardiologist and in some cases, neurologist in house to see patient preop would be helpful.

6. Risk of stroke is highest in those with previous TIA or stroke.

hypercoagulation profile based on scenario-Oregon

2009-09-03T08:03:00.001-05:00

NEUROLOGY VENOUS THROMBOSIS PANEL:
- Protein C Activity
- Protein S Activity
- Antithrombin Activity
- Activated Protein C Resistance
- Prothrombin G20210A PCR
- Lupus Anticoagulant
- Anticardiolipin IgG and IgM
- Homocysteine

NEUROLOGY ARTERIAL THROMBOSIS PANEL
- Lupus Anticoagulant
- Anticardiolipin IgG and IgM
- Homocysteine
- Lipoprotein (a)

NEUROLOGY ARTERIAL THROMBOSIS PANEL, WOMEN>40
- Lupus Anticoagulant
- Anticardiolipin IgG and IgM
- Homocysteine
- Lipoprotein (a)
- Activated Protein C Resistance
- Prothrombin G20210A PCR

Hypercoagulable workup (incl effects warfarin on tests)

2009-09-02T10:27:00.001-05:00

hat tip David Gordon, MD Professor/Chairman Neurology at OKL

Hypercoagulable Profile
􀂃 Protein C
􀂃 Protein S free and total
􀂃 Antithrombin III
􀂃 Fibrinogen
􀂃 Factor VII
􀂃 Factor VIII
􀂃 Activated protein C resistance (APCR)
􀂃 Factor V Leiden mutation
􀂃 Prothrombin G20210A mutation
􀂃 Anticardiolipin antibodies
􀂃 Anti-beta-2-glycoprotein I antibodies
􀂃 Antiphosphatidylserine antibodies
􀂃 Lupus anticoagulant
􀂃 Lipoprotein (a)
􀂃 C-reactive protein
􀂃 Methyltetrahydrofolate reductase C677T and A1298C
􀂃 Sickle prep (if African heritage)
Affect of Coumadin on Hypercoagulable Profile
􀂃 Protein C (may be decreased with warfarin)
􀂃 Protein S free and total (may be decreased with warfarin)
􀂃 Antithrombin III (not affected by warfarin)
􀂃 Fibrinogen (not affected by warfarin)
􀂃 Factor VII (may be affected by warfarin)
􀂃 Factor VIII (not affected by warfarin)
􀂃 Activated protein C resistance (must alter methods to compensate for warfarin)
􀂃 Factor V Leiden mutation (not affected by warfarin)
􀂃 Prothrombin 20210 mutation (not affected by warfarin)
􀂃 Anticardiolipin antibodies (not affected by warfarin)
􀂃 Anti-beta-2-glycoprotein I antibodies (not affected by warfarin)
􀂃 Antiphosphatidylserine antibodies (not affected by warfarin)
􀂃 Lupus anticoagulant (screening tests not affected by warfarin, but “mixing studies” to
confirm are affected by warfarin)
􀂃 Lipoprotein (a) (not affected by warfarin)
􀂃 C-reactive protein (not affected by warfarin)
􀂃 Methyltetrahydrofolate reductase C677T and A1298C (not affected by warfarin)
􀂃 Sickle prep (if African heritage) (not affected by warfarin

North American moya moya is different

2009-06-06T15:49:00.002-05:00

Hallemeier et al. Stroke 2006. Authors looked at 34 adults with the condition. 22 had bilateral and 12 unilateral moya moyal vessels. North Americans present more often with ischemic stroke whereas Asians present with hemorrhage more often. 0/12 unilateral patients subsequently developed contralateral symptoms. Symptomatic patients had high levels of recurrence both homolaterally and contralaterally, and asymptomatic patients had a low risk of ischemic events. Surgical treatment revascularization led to less recurrence, with a fairly high perioperative morbidity and mortality ( as high as 17 % for the latter). N American moya moya may be a different entity than the Japanese kind.

Statins prevent vasospasm after subarachnoid hemorrhage

2009-06-06T15:40:00.002-05:00

McGirt Mj et al. J Neurosurg 2006; 105: 671-674. (Duke) 115 patients were retrospectively reviewed with multivariate regression analysis. Statin therapy started on admission with SAH resulted in a elevenfold decrease in vasospasm. ACA/ICA aneurysm also was associated with vasospasm. Tseng MY al (Stroke 2005; J Neurosurg 2007) also published 2 articles on the subject . The mechanism is thought to be cholesterol independent, perhaps related to nitrous oxide.

Number to harm with iv tpa

2009-06-06T12:54:00.002-05:00

Saver JL Hemorrhage after thrombolytic therapy for stroke. The clinically relevant number needed to harm Stroke 2007; 38: 2279-2283

Author reviews original NINDS data on hemorrhages, n=20/312 patients treated, and noted that they tended to be older, have mass effect on CT, have higher serum glucose, and more severe strokes. The number needed to harm, ie an additional dead or disabled outcome (MRS>= 3) attributable to SICH is 707, based on the expected outcome of these 20 patients.

NNH for dead disabled outcome MRS (.=4) 126, for fatal outcome 36.5, and for worsening of any degree between 30 and 40.

Basic conclusion is that most patients with SICH are destined for bad outcomes from the get go.

IV alteplase plus mutlimerci is safe

2009-06-06T12:44:00.003-05:00

Smith WS et al. Safety of mechanical thromobectomy and iv tpa in acute ischemic stroke. Results of the Multi Mechanical Embolus in Cerebral Ischemia (Merci) trial part I. AJNR 2006; 27: 1177- 1182.

Study enrolled patients who either did not receive iv tpa or received it and did not recanalize. It was an international prospective single arm trial up to 88 hours post stroke. 111 patients received the procedure with mean NIHSS of 19 +/= 6.3 30/111 received tpa prior. 60/111 recanalized with retriever alone, 77/111 with adjunctive therapy. 9 % has SICH. 5 % had procedural complications.

Clinical outcomes not given

Blogger note: Like many radiology studies, this one has important limitations. The study does show that Multi Merci is safe and efficacious using recanalization, but fails to look at clinical outcome of the patient. PROACT 2 is the single study showing clinical benefit of interventional therapy for stroke, namely intrarterial lysis.

Warfarin in elderly -- Birmingham study

2009-06-06T12:28:00.002-05:00

Mant J et al. for BAFTA investigators. Warfarin v. aspirin in an elderly community population with atrial fibrillation (the Birmingham Atrial Fibrillation Treatment of the Aged Study, BAFTA): a randomized clinical trial

patients: 973 patients 75+ age, mean 81, SD 4 from primary care were randomized to aspirin 75 mg or warfarin with INR target of 2-3, and followed a mean 2.7 years. The endpoint was fatal or disabling stroke, ICH, an arterial embolism.

results: in warfarin group there were 24 events, with 2 ICH and remainder ischemic strokes, in aspirin group there were 48 events. Yearly risk reduction was 3.8 percent in aspirin group, 1.8 percent in warfarin group, risk reduction 2 %, p=0.003. Risk of hemorrhagic events increased 0.2 % in warfarin group, 1.4 to 1.6 percent.

Warfarin is treatment of choice.

Aspirin v. anticoagulation in carotid dissection

2009-06-05T15:18:00.002-05:00

Georgiadis D, Arnold M, et al. Neurology 2009; 72:1810-1815

A study of 298 patients with spontaneous Carotid artery dissection

Main points

ischemia is relatively rare after dissection in 3 months ischemic stroke occurred in 0.3 %, TIA 3.4 %, retinal ischemia 1 % with no significant difference between groups. Ischemic events were commoner in those with ischemic events at onset. It is important to separate these two groups. Anticoagulation had a predictable 2 % complication rate. There was 97 % followup with exam or structured telephone interview. In literature review , 2 recent meta analyses showed no difference. (see Cochrane database Syst Rev 2003, and Lyrer et al, Stroke 2004). This was not a RCT, and warfarin was prescribed up to 1997 and aspirin thereafter. The number of patients was too small to evaluate treatment differences. The primary finding was the low rate of strokes after sicd.

criteria for alteplase in community setting

2009-05-19T10:19:00.000-05:00

from a highly placed stroke neurologist:
IA therapy has already been endorsed as reasonable in selected patients
by AHA/ASA, ACC - virtually all comprehensive stroke centers are doing
it. FDA approval is years away and is not required per se. IA case
selection variables have been quasi standardized: NIHSS > 10; major
vessel occlusion (M1/M2 MCA and basilar artery are favored sites for
intervention; carotid T and ICA occlusion somewhat more controversial
but doable); < 6 hours from stroke onset (some argue intervention should
be completed < 8 hours from stroke onset based on PROACT 2 . MERCI
retriever for clot removal is give
n as 8 hours); no standard thrombolytic exclusions. Many would add MR
or CT mismatch imaging as another selection factor especially as
you.approach 6 to 8 hours or in patients > 80 years of age with NIHSS >
20 (no standard criteria yet but 20% mismatch is probably too low; if
you had >50% mismatch and DW volume < 100 cc that would be favorable).
So until and unless you want to randomize into a (nonexistent) clinical
trial you.could simply not do IA (using the specious (in my view)
â€œunprovenâ€ argument) or you could have access to an experienced
comprehensive stroke center and do â€œdrip and ship.â€ You could
possibly develop IA at a certified primary stroke center if resources
(angio suite; interventionalist 24/7 etc) were available. Otherwise I do
not advocate IA stroke therapy at community hospitals.

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ALL ASA guidelines re stroke in one website

2009-04-18T08:31:00.000-05:00

http://www.americanheart.org/presenter.jhtml?identifier=3004586

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Stroke Outcome by NIHSS and type

2009-04-18T08:11:00.001-05:00

rates of recanalization after iv tpa BA 10 % M1 25 %, M2-5 50-60 %,

Outcome based on NIHSS
3-6 90 % excellent regardless
16-22 40 % excellent
lacunar-- 30 % greater chance of improved outcome
NIH > 23, high rate hemorrhage

a radiology link site

2009-04-18T08:10:00.001-05:00

http://www.radswiki.net/main/index.php?title=Category:Neuro&until=Nose

Critical management SAH

2009-04-14T21:54:00.001-05:00

Pearls very quick hits new stuff last 20 y
Nimodipine is still used to prevent vasospasm, so is asa and tirilizad
fludrocortison is used to prevent /treat cerebral salt wasting
nonconvulsive seizures occur in about 18%

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CADASIL notes

2009-04-14T21:35:00.000-05:00

Major criteria-- headaches, migraine, mood disorder, stroke, tia
Other neurologic --epilepsy, scord infarcts, ICH, episodic increased ICP
path-- osmiophilic granular deposits on vascular basal lamina
increased oxygen extraction rate
notch 3 protein beneficial
thalamic predominance
cerebral microbleeds
CSF may have mild increase protein, otherwise normal
prenanatal testing available with CVS or amnio
chr 19, 50 + mutations
cysteine residue mutation

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Stroke pearls valvular disease

2009-04-14T21:27:00.000-05:00

infective endocarditis== high stroke risk, 20 % usu in first 48 hours, dramatically reduced c ABX, late stroke risk lower 5 %

mechanical valves-- stroke risk highest MV on anticoag rate 3-4 %, AV is 1.2 %, ASA + warfarin is superior

Mycotic aneurysms-- distal branch point serial reimaging, clip if no response to ABX

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decompressive craniectomy

2009-04-14T21:22:00.001-05:00

Cerebral hemorrhage pearls
peaks after age 50
women more than men
anterior more than posterior
aneurysm anterior, AVM posterior
Rupture risk: higher with BA, budding tip,
Size and risk: < 10 mm, 0.05 % per year; 10 mm 1 %/yr; > 25 mm 6 % per year

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U MASS protocol for patient selection for stroke

2009-04-14T20:55:00.001-05:00

0-3 hours

*CT, CTA , CT perfusion
*BA, ICA, M-1 occlusion OR ineligible for iv-- consider IA alteplase
*Others i-v alteplase

3-6 hours

CT, CTA, CT perfusion
(alt.) MRI, MRA, MR D/P
Mismatch and occlusion-- proceed with intrarterial

No patient eligible for alteplase intravenously is denied.

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VerifyNow Platelet function assay system (Accumetrix)

2009-04-01T16:11:00.001-05:00

Distilled:
Plavix PF (for Plavix and Ticlid) ICD-9 code V58.63
Aspirin PF (For aspirin) ICD-9 Code V58.66
separate tests for integrilin and reopro (not interested)

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FDA recommendation re clopidogrel and PPI's

2009-03-23T08:16:00.001-05:00

http://www.fda.gov/Cder/drug/early_comm/clopidogrel_bisulfate.htm

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Neuroflo device in acute ischemic stroke AAN abstract

2009-03-09T12:01:00.000-05:00

[P02.087] A Novel Treatment in the Management of Acute Ischemic Stroke

Mohamed M. Ibrahim, Maher Saqqur, Arabesque Parker, Monica Saini, Dulka Manawadu, Ken Butcher, Derek Emery, Ashfaq Shuaib, Edmonton, AB, Canada

OBJECTIVE: Role of Transcranial Doppler (TCD) monitoring in acute stroke patients treated with NeuroFlo device . BACKGROUND: The NeuroFlo device has been implemented as an experimental tool for potential interventional treatment in non- IV rt-PA responder patients with acute ischemic stroke. The presumed mechanism of action is enhancement of blood flow diversion to cerebral collaterals to minimise infarct volume and improve clinical outcomes. DESIGN/METHODS: Patients presenting to our ER with acute ischemic stroke, who did not show significant improvement after thrombolysis were screened; after an informed consent, they were enrolled in the Feasibility and Safety of NeuroFlo in Stroke Patients Receiving rt-PA. An intra-aortic balloon was inflated after completion of the rtPA infusion, resulting in the partial occlusion of abdominal Aorta for 45 minutes. TCD was performed at baseline, at the end of IV rt-PA treatment, before and during balloon inflation. RESULTS: We enrolled 9 cases, 4 patients did not had TCD study, of the remaining 5 patients 3 patients had MCA occlusion and 2 Terminal ICA occlusion. Three patients had good long term outcome Modified Rankin Scale (MRS) at 90 days were 1, zero and Zero respectively. There TCD during balloon inflation revealed: 1- Enhancing flow at the occlusion site (mean flow velocity increased from 18 to 24, 8 to 22 and 14 to 46 cm/sec) 2- Two patients had anterior cross filing developed through anterior communicating artery (ACom). 3- Enhancing flow through contralateral MCA (MFV 108 to 177 cm/sec) and ips ACA flow (MFV 22 to 81 cm/sec) in one patient. Two patients had poor outcome (MRS at 90 days 3) both had no enhancing flow during balloon inflation. CONCLUSIONS/RELEVANCE: NeuroFlo device might provide a new treatment for acute stroke patients beyond the 3 hours window by enhancing the flow at the occlusion site and opening up collateral flow.
Category - Cerebrovascular Disease - Acute Stroke Therapy

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negative effect of alteplase on stroke patients with CHF AAN abstract

2009-03-09T11:59:00.000-05:00

[P02.083] Clinical Outcomes of Patients with Congestive Heart Failure Who Receive Thrombolytic Therapy for Acute Ischemic Stroke

Kachikwu Illoh, Miriam Morales, Tamara Humphrey, Alexander Katcheves, Nneka Ifejika, Francisco Fuentes, Mc Lean, VA, Houston, TX

OBJECTIVE: To determine whether thrombolytic therapy improved outcome among patients with CHF presenting with AIS. BACKGROUND: Patients with severe congestive heart failure (CHF) often have impaired cerebral perfusion. They have poor clinical outcomes on presenting with acute ischemic stroke (AIS). In these patients, it is likely that prompt thrombolysis would stem further decline in an already compromised cerebral perfusion state. Whether thrombolytic therapy improves the outcome in these patients is unclear. DESIGN/METHODS: In a cohort study with retrospective review of records from a prospectively collected database, we included AIS patients who were consecutively admitted to the stroke service of a large tertiary care center. Poor clinical outcome was defined as a modified Rankin score (mRS) of greater than 3. We examined the characteristics of AIS patients with history of CHF by their thrombolytic therapy status and compared their clinical outcomes with non-CHF patients. RESULTS: A total of 2,180 AIS patients with a mean age of 65 (SD, 15) years and 53% females were enrolled. Of the entire cohort, 26% (576/2180) received intravenous thrombolytic therapy, and 9% (196/2180) had history of CHF. The in-hospital mortality overall was 6% (129/2081); among CHF patients mortality was 8%. Of the 196 CHF patients, 66 (34%) got thrombolytic therapy. Yet, the CHF patients who received thrombolytic therapy did not achieve better mortality outcome compared to those not receiving the treatment (9% versus 8%, P = 0.786). Likewise, there was no difference in functional outcome between CHF patients who got thrombolytic therapy and CHF patients without the treatment (mRS >3; 49% versus 50%; P = 1.000). CONCLUSIONS/RELEVANCE: In patients with history of CHF who presented with AIS, thrombolytic therapy was not associated with an improvement in their clinical outcome. This finding needs further exploration in larger studies as more aggressive management of CHF may be required to augment thro mbolytic therapy.
Category - Cerebrovascular Disease - Acute Stroke Therapy

Tuesday, April 28, 2009 11:30 AM

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alteplase and malignancy at AAN

2009-03-09T11:58:00.000-05:00

[P02.082] Outcomes of Patients with Malignancy Treated with Thrombolytics

Ramy El Khoury, Miriam M. Morales, Oleg Chernyshev, Anitha Abraham, M. Rick Sline, Indrani Acosta, Vivek Misra, Andrew Barreto, Sean Savitz, Kachikwu Illoh, James Grotta, Nicole R. Gonzales, Bellaire, TX, Mc Lean, VA, Houston, TX

OBJECTIVE: Treating patients with a history of cancer for ischemic strokes with thrombolytics may not alter patient's outcome. BACKGROUND: Very limited literature discusses the outcome of patients with malignancy treated with thrombolytics for ischemic stroke. The purpose of our research is to describe our experience in treating patients who have malignancy with thrombolysis. DESIGN/METHODS: We conducted a retrospective case-control study comparing the outcomes of patients receiving thrombolysis with a history of or active cancer (cancer positive, CP) compared with a control group (cancer negative, CN) matched for age and baseline NIHSS. Primary outcome measure was symptomatic intracerebral hemorrhage (sICH). Secondary outcome measures included good outcome (discharge modified Rankin Scale (mRS) <3), and good discharge disposition (discharge home or in-patient rehabilitation). RESULTS: From 2003-2008, 679 patients were treated with thrombolytics (IV, IV/IA, or IA only). Of these, 60 patients were CP with a mean age 73 (SD, 13) years and 120 CN patients were matched for age and baseline NIHSS. Baseline median NIHSS was 12 in both groups with similar ranges (p=0.835). There were no significant differences among baseline characteristics between the two groups. The most common malignancies were prostate 27% and breast 22%. There was no significant difference among 24 hour post-tPA NIHSS, good outcomes, length of stay, sICH, or good disposition. CONCLUSIONS/RELEVANCE: Our data demonstrates that patients with malignancy (or a history of) who receive thrombolysis have outcomes similar to CN patients and do not appear to be at increased risk of sICH. It also suggests that the presence or history of malignancy should not preclude thrombolysis if the patient is otherwise a thrombolytic candidate.
Category - Cerebrovascular Disease - Acute Stroke Therapy

Tuesday, April 28, 2009 11:30 AM

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AAN venous anomaly and malignant MCA infarction

2009-03-09T11:57:00.000-05:00

[P02.080] Ipsilateral Cerebral Venous Outflow Obstruction Is Associated with Life-Threatening Brain Edema of Middle Cerebral Artery Infarction

Wengui Yu, Joanna Rives, Babu Welch, Jonathan White, Duke Samson, Dallas, TX

OBJECTIVE: The aim of this study was to investigate the role of cerebral venous anomaly in the development of life-threatening brain edema after middle cerebral artery (MCA) infarction. BACKGROUND: Approximately 35% of the patients with complete MCA infarction develop life-threatening brain edema and herniation. Although infarct size was the major determinant, its predictive value was only moderate. DESIGN/METHODS: This is a retrospective study of consecutive patients with complete MCA infarction who were admitted to our Neurointensive Care Unit from January 2007 to October 2008. Patient demographics and clinical features were reviewed. Brain edema on serial CT or MRI scans and cerebral venous anatomy on CTA or digital subtraction angiography were evaluated. Functional outcome at discharge was estimated using modified Rankin scales. RESULTS: A total of 14 patients were identified to have complete MCA infarction and cerebral venography. Four patients (25.6%) were found to have ipsilateral cerebral venous anomaly, including transverse sinus atresia (1), hypoplasia (2), and previous surgical ligation of internal jugular vein (1). All of them had fatal brain edema. The severity and timing of maximal edema were correlated with the degree of cerebral venous outflow obstruction. They all refused surgery and died from transtentorial herniation. The remaining 10 patients had symmetric or ipsilateral dominant cerebral venous drainage. Only one of them developed life-threatening edema possibly due to poor collateral circulation and bilateral carotid stenosis. He underwent decompressive surgery and recovered with moderate left hemiparesis. Patient age, sex, co-morbidity, carotid artery occlusion, or infarct size was not independently associated with life-threatening edema. CONCLUSIONS/RELEVANCE: Our preliminary results suggest that ipsilateral cerebral venous outflow obstruction is independently associated with life-threatening brain edema after MCA infarction and may be an indication for early decompressive craniectomy.
Category - Cerebrovascular Disease - Acute Stroke Therapy

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HHT and stroke

2009-03-08T15:23:00.004-05:00

Felix S et al., Neurology 2008; 71: 2012-2013.

Hereditary hemorrhagic telangiectasia (HHT) is a rare aut dom disease caused by one of 2 mutations, designated HHT1 and HHT2. The mutations are in the ENG and ALK1 genes. Diagnosis required 3 of the following 4: spontaneous epistaxis, cutaneous telangiectasias. av malformations of the interior organs and positive family history. Complications are anemia, portal hypertension, hypoxemia, brain abscess and stroke.

Authors of a case report demonstrate occurrence of a stroke after embolization of the pulmonary artery venous malformation. Authors note the need to check platelet function prior to using antiplatelet drugs in patients with HHT for prevention before endovascular procedures.

AHA abstract of note: Relationship of BNP level to cardiac thromus in patients with CVA and AF

2009-03-08T10:32:00.000-05:00

Presentation Number: ASA P12

Publishing Title: Brain Natriuretic Polypeptide is a Marker Associated with Cardiac Thrombus in Stroke Patients

with Atrial Fibrillation

Author Block:

Yoko Okada, Ehime hospital, Toon, Japan; Kensaku Shibazaki, Kazumi Kimura, Noriko Matsumoto, Yasuyuki

Iguchi, Kawasaki Medical Sch, Kurashiki, Japan

Abstract Body:

Background and purpose

Brain natriuretic peptide (BNP) is used as a biological marker of heart diseases. 8-10% of acute stroke patients

with atrial fibrillation (AF) have cardiac thrombus (CTh), which is considered as a high risk of stroke recurrence.

We investigated whether high BNP levels could be a biological marker of CTh in acute stroke patients with AF.

=0 A

Methods

Between November 2006 and June 2008, acute ischemic stroke patients with AF within 7 days of stroke onset

who underwent transesophageal echocardiography (TEE) were enrolled. We measured BNP using rapidly assay

(SHIONOSPOT® BNP) on TEE examination. Patients were divided into two groups according to the absence and

presence of CTh (Negative and Positive groups). We compared clinical characteristics including age, gender,

previous ischemic stroke, vascular risk factors, National Institutes of Health Stroke Scale (NIHSS) score on

admission, and BNP level between the two groups. Moreover, the factors associated with CTh were investigated

by multivariate logistic regression model.

Results

67 patients (male 40; mean age, 76.5±11.1 years) were enrolled. 17 (25.4%) patients had CTh. Hypertension

(88.2% vs. 58.0%, p= 0.037) was higher in the Positive group than in the Negative group. There were no

significant differences between the Positive group and Negative group in age (76.5±9.5 vs. 76.4±11.7, p=0.730),

female (58.8% vs. 34.0%, p=0.072), previous ischemic stroke (23.5% vs. 30.0%, p=0.760), diabetes mellitus

(35.3% vs. 20.0%, p=0.201), hyperlipidemia (17.6% vs. 14.0%, p=0.706), smoking (41.2% vs. 52.0%, p=0.441),

and NIHSS score on admission (9.8±8.3 vs. 7.0±7.8, p=0.237). The mean±SD BNP level was significantly higher

in the Positive group than in the Negative group (307.3±270.6 vs. 146.5±119.0 pg/ml, p=0.024). The optimal cutoff

level, sensitivity, and specificity of BNP levels to distinguish the Positive group from the Negative group were

145.0 pg/ml, 70.6% and 64.0%, respectively. Multivariate logistic regression analysis demonstrated that plasma

BNP level of >145.0 pg/ml (odds ratio, 4.61; 95%CI, 1.29 to 16.51, p=0.019) was independent factor associated

with CTh.

Conclusions

BNP is a marker associated with CTh in stroke patients with AF.

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risk factors for arterial dissection

2009-03-07T09:16:00.001-05:00

tobacco use,
HTN, OCPs, migraines , MTHFR genotype, alpha 1 antitripsin deficiency,
hyperhomocysteinemia, ADPKD, Ehlers-Danlos (vascular type), TRAUMA

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More on statins and stroke

2009-03-05T14:36:00.002-05:00

Coull BM, Johnston SC Statins: not just for the faint of heart. (editorial) Neurology 2009; 72: 684-685.

Nice discussion of statins and stroke.
"Ironclad" evidence of reduction of cvd and cva in patients treated with HMGCOA.

Chaturverdi et al. compared 2000+ patients over 65 with those under 65 in posthoc analysis of SPARCL data. They found rr of stroke in elderly group was reduced by 10 %, and in the younger group by 26 %; only the second was statistically significant. However, with reduced sample sizes the two groups were not different (go figure, ask a math guy).

For atorvastatin, there was a 1.5 % reduction in second stroke at 5 years, giving a NNT of 327 for STROKE in elderly. However, for all heart disease and stroke the reduction was 4.1 % with a NNT of 120 per year, which was highly significant and probably cost effective. No one knows if simvastatin is better but it is cheaper. Authors urge use of a HIGH DOSE statin.

Inflammatory bowel disease

2009-03-02T21:14:00.001-05:00

Strokes occur in one percent
Elevated fibrinogen, decreased protein S or increased clotting factors usually are implicated.Other causes include increased homocysteine due to B12 deficiency, or optic neuropathy, or vasculitis.

Cogan's syndrome

2009-03-02T21:09:00.003-05:00

is caused by a vasculitis similar to PAN, causing bilateral deafness (often simultaneous), uveitis and blindness secondary to retinal ischemia. Fever, chills, weight loss, thrombocytopenia, and abnormal CSF also occur. Treatment is with immunosuppressive drugs.

Pearls: Infectious stroke

2009-03-02T20:58:00.002-05:00

1. For most infections, CSF exam is the tipoff
2. In syphilitic meningovascular disease, a branch of the MCA or aorta may be involved
3. HIV itself, coexisting syphilis or NBTE , fungal or zoster infections occur in HIV infected patients.
4. Zoster stroke in MCA distribution occurs several weeks after cutaneous zoster infection. Steroids are critical, and antiplatelet drugs also are used.
5. Cysticercosis has stroke in about ten percent, usually lacunes, CSF may be helpful, and treatment is with albendazole, praziquental, and steroids or occassionally surgery.
6. Mucormycosis has typical and dramatic presentation, but it can include cavernous sinus thrombosis with ICA occlusion and stroke. Signs of include bilateral exopthalmos, proptosis, chemosis, ocular impairments and visual loss.
7. Cat scratch disease due to bartonella can cause an arteritis and stroke

Moya moya disease pearls

2009-03-02T20:52:00.004-05:00

Review article NEJM 2009; 360:1226-1237

1. There are many disease associations esp SCD, NF1, irradiation, and Down's syndrome, and less commonly cardiac anomaly, renal artery stenosis, giant cervicofacial hemangioma and hyperthyroidism.
2. It occurs throughout the world but especially in northeast Asia, 10x frequency as in N America
3. In Japan the responsible gene is 17q25
4. The disease is more fulminant in children ; can be triggered by exertion, crying, hyperventilation, dehydration, or anaesthesia, presumably related to decreased CO2 tension in a compensated and fragile system.
5. Ischemic stroke is more common in children and adults, but hemorrhagic stroke occurs much more frequently in adults than in children
6. Headache, often refractory, occurs in two thirds, and may resolve within a year of revascularization surgery
7. Choreiform movement disorders in children occassionally resolve with revascularization surgery
8. Morning glory disc is associated and should prompt a consideration of the diagnosis
http://images.google.com/imgres?imgurl=http://www.nature.com/eye/journal/v21/n10/images/6702851f7.jpg&imgrefurl=http://www.nature.com/eye/journal/v21/n10/fig_tab/6702851f7.html&usg=__ycWmZRS6FxhD_gWU8YhCPzJQ1v8=&h=306&w=390&sz=112&hl=en&start=2&sig2=ybxbCPAci2WQ5GHSHYrFqQ&tbnid=oCbcKU1tcEBAIM:&tbnh=97&tbnw=123&prev=/images%3Fq%3Dmorning%2Bglory%2Bdisc%26gbv%3D2%26hl%3Den&ei=OGPJSY_1M5usMvW3wdYD
9. Pathology is smooth muscle proliferation and caspace dependent apoptosis. Some walls are stressed with microaneurysms which can explain hemorrhage.
10. EC IC bypass may be indicated in some . This is because the disease is inexorably progressive without surgical treatment and standard medical treatment does not work. Metaanalysis studies suggest treatment can halt progression.
11. Suzuki.Takaku developed a grading system for arterial changes
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=119568&Ausgabe=235294&ProduktNr=224273&filename=119568.pdf
10. Cessation of smoking and birth control pills is indicated
11. "Ivy sign" radiographically may be seen in 70 % and resolve with bypass, consists of leptomeningeal enhancement with pial engorgement going into cortex. This is seen on FLAIR and post contrast images and resembles ivy creeping up on stone.

PXE pseudocanthicum elasticum

2009-03-02T20:50:00.002-05:00

laxity of the skin, redundant skin, and ocular fundus abnormalities. Associations include MVP, cardiac abnormalities. Complications include stroke, intracranial hemorrhage, seizures and dementia.

Buerger disease

2009-03-02T20:47:00.003-05:00

Signs and symptoms include
1. Digital ischemia leading to ulceration
2. Claudication of the upper and lower limbs
3. Superficial thrombophlebitis

History-- heavy tobacco use, three fourths are young or middle aged men

Rarely strokes occur

Treatment is smoking cessation, possibly antiplatelets

Pearls on fibromuscular dysplasia

2009-03-02T19:15:00.005-05:00

1. Predominance of women
2. Associations: young adults, Ollier's disease, saccular aneurysms
3. String of beads, long tapered segment, and false aneurysm may be found radiographically
4. Usual location is 1.5 cm above bifurcation although other sites may be implicated
5. Complications include dissection or vasospasm due to angiography
6. Half may develop TIA or stroke
7. Other signs include asymptomatic bruit, pulsatile tinnitus
8. Overall prognosis is relatively benign with less recurrent strokes than with atheromatous disease
9.HTN

Causes of dilated or other cardiomyopathy

2009-03-02T19:07:00.002-05:00

1. Ischemic heart disease
2. Post partum
3. Chronic alcohol use
4. Viral illness
5. Mitochondrial disease (Melas, Merrf)
6. Myotonic, limb girdle and scapuloperoneal dystrophy
7. Primary oxalosis leads to calcification and heart embolus

Atrial myxoma

2009-03-02T19:01:00.002-05:00

Presentation is obstructive, constitutional syndromes and stroke. Obstruction presents with sudden decreased cardiac output, even death with obstruction of mitral orifice. The usual sign is a murmur with a change in posture. Constitutional signs include low grade fever, arthralgias, skin eruptions and fleeting neurological signs. Elevated sed rate and abnormal serum proteins may lead to a misdiagnosis of lupus. One third will have neurological symptoms, including stroke, that can be the presenting sign of the illness. EKG shows nonspecific signs. Tumor embolus can act as a nidus for intracranial aneurysm formation. Rarely, a fibroelastic or malignant tumor of the heart can cause a stroke. Surgical resection is indicated. Anticoagulation does not work.