Random notes on abstracts from ISC meeting radiology

 

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

 

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

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"

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

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"

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

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

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]