American Heart Association

Monthly Archives: February 2015

Physical Activity: A potential target for post stroke fatigue?

Michelle Christina Johansen, MD

Duncan F, Lewis SJ, Greig CA, Dennis MS, Sharpe M, MacLullich AMJ, and Mead GE. Exploratory Longitudinal Cohort Study of Associations of Fatigue After Stroke. Stroke. 2015

“I’m tired already.” “I just can’t do what I used to.” “All I want to do is sleep.” 


Fatigue is a familiar complaint in any clinical practice. Both experience and literature confirms the invisible symptom of post-stroke fatigue but there is no current treatment. The problem in studying this phenomenon is that fatigue can be a difficult variable to quantify and there are many potential confounders. An individual with an ACA stroke may be abulic, a widow forced to relocate to a nursing home may be depressed or a gentleman with a brainstem stroke might develop sleep apnea leading to poor sleep quality. When considering a patient’s reduced physical activity, is this a contributor to post stroke fatigue or simply a consequence? 



Duncan et al study associations between fatigue and physical activity in stroke in hopes of better establishing a causal relationship. The study had three main aims: 1) Investigate if fatigue was significantly associated with measured physical activity at one, six and 12 months post stroke 2) Examine relationships between physical activity and patient characteristics at baseline and reported fatigue 3) Determine if physical activity was a predictor of later fatigue independent of other variables. The team measured levels of physical activity using an accelerometer and step count. 157 patients who had a stroke of any kind in the preceding month were enrolled. Unfortunately, only 136 attended any of the assessments with 58 returning for the final 12 month study visit.

The investigators looked for the presence of many conditions that have been previously noted in the literature to be associated with post-stroke fatigue. Stroke subtype and patient characteristics were extracted from the medical record. At time of enrollment, an NIHSS, mini-mental status exam as well as a physical activity scale for the elderly questionnaire was performed. At the one, six and 12 month assessments, the patients reported level of fatigue by filling out the Fatigue Assessment Scale (FAS) and also had a structured interview probing for clinically significant fatigue. Activity level was assessed using step count with an accelerometer worn at all times on the thigh unaffected by stroke. Additional assessment tools included anxiety and depression questionnaires, a quality of Life assessment (EuroQoL), Epworth Sleepiness Scale probing for sleep disorders and finally blood pressure.

Accelerometer (ActivPaL) data was available for 64%, 66% and 58% respectively of the total enrolled at each of the three assessments. The authors report that a positive fatigue case definition (structured interview mentioned above) was associated with lower daily step counts. At all three time point, more fatigue was associated with lower step count, higher depression, anxiety scores and sleepiness as well as a poorer quality of life. Lower daily step count and greater anxiety at one month independently predicted more fatigue at six and 12 months. The authors conclude that lower step counts at one month independently predicted fatigue for up to 12 months and therefore physical activity might serve as a potential target for intervention to prevent post-stroke fatigue.

How do we interpret these results? It is important to note that the study was powered to enroll 170 patients at baseline and have 120 at 12 month follow up. They had a high dropout and as per above only had 58 participants at 12 months. Another important consideration is that the NIHSS was more severe in the population without activity data limiting the generalizability of their results. The investigators should be applauded for using multiple scales to assess for any variables such as anxiety, depression, sleepiness, gender, stroke characteristics and pre-stroke fatigue that has been shown in the literature to have a relationship to post-stroke fatigue. The numbers once again limit application as they only had 18 patients at the 12 month time point where the case definition of fatigue was fulfilled. They were unable to perform logistic regression due to power so our ability to draw relationships is limited. While the concept that increasing physical activity may drive away fatigue is laudable for the clear cardiovascular and therapy benefits, more data is needed prior to stating that reduced activity leads to post stroke fatigue.

By |February 27th, 2015|clinical|Comments Off on Physical Activity: A potential target for post stroke fatigue?
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Knocking Down Barriers: Relevance of BBB Disruption after Endovascular Treatment of Ischemic Stroke

Vikas Pandey, MD

Renú A, Amaro S, Laredo C, San Román L, Llull L, Lopez A, et al. Relevance of Blood–Brain Barrier Disruption After Endovascular Treatment ofIschemic Stroke: Dual-Energy Computed Tomographic Study. Stroke. 2015

With the emergence of interventional stroke trials showing some long-term benefit in those undergoing intervention versus simply IV tPA alone, new questions are now arising as a result of these interventional therapies. One of these questions comes with the often ordered follow up CT scan that is done after such intervention showing hyperdense areas that can resemble hemorrhage, however can also reasonably be contrast that has leaked into the parenchyma due to a disrupted blood-brain barrier (BBB), a common after-effect of the interventional procedures. Many times there is very little to rely on to make a diagnosis of contrast staining (CS) or brain hemorrhage (BH) aside from the clinician’s best guess on the initial scan and the pattern of resorption on follow up scans thereafter. The authors hypothesized that using Dual energy CT (DE-CT) would allow for a more accurate differentiation of CS vs BH and that the presence of either of these entities may be a prognostic factor to clinical outcome.



DE-CT is a technique based on identifying different attenuation effects of brain tissue, iodine and blood at different irradiation energy levels. The authors decided to use this technique as it has been shown in previous studies to be able to differentiate between CS and BH, and the presence of either of these after endovascular therapy may suggest different grades of BBB disruption. To evaluate if this had any prognostic significance, the group prospectively collected 132 patients with proximal artery occlusions without a malignant profile, treated at a single Comprehensive Stroke Center in Spain, and who underwent endovascular therapy aiming for a TICI grade of 2b or 3 at the end of the procedure. The patients then underwent DE-CT which showed (see attached figure) using plain CT, virtual non-contrast and iodine overlay modes whether the patient had CS, BH or both (categorized as BH). The numbers in each category were 53 patients (40%) with no highly attenuated areas, 32 patients (24%) with CS alone, and 47 patients (36%) with BH. The clinical outcomes after 90 days showed that 67 patients (51%) had poor outcome and these were linked to higher stroke severity, higher glucose and systolic blood pressure levels at baseline, absence of recanalization and longer length of endovascular procedures. The rate of poor outcome was increased in CS (OR 5.32, 95% CI 2.05 – 13.77) and BH (OR 5.94, 95% CI 2.5 – 14.12) compared to the patients with no high attenuation areas. Even in the 109 patients (83%) with complete recanalization, 46% of those had poor outcome. The increased rate of poor outcome in CS and BH patients persisted even when taking into account only those patients that had complete recanalization.

The authors showed a link between the presence of CS or BH (signifying BBB disruption) and poor clinical outcome and showed that using DE-CT was able to more reliably distinguish between CS and BH. They also found a very clinically relevant link that the subset of patients with CS alone, had an increased risk of delayed hemorrhagic transformation of the stroke. Their research has put added emphasis on work that is being done to protect the BBB during reperfusion therapies as this can lead to better patient outcomes. They also have further strengthened the potential role of DE-CT in every day clinical practice for both ascertainment of diagnosis as well as a predictor of prognosis.

@DrVikasNeuro

By |February 26th, 2015|diagnosis and imaging|1 Comment
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Effects of weather and air pollution on stroke incidence in Seoul, Korea

Seasonal variation of stroke across large regions with varying climates has been reported, though results have been mixed in prior studies. In this manuscript, Han et al evaluated the trends in ischemic and hemorrhagic stroke incidence across month and season in the Seongdong district of Seoul, Korea. This was undertaken to evaluate if variation is related to meteorological and air pollution parameters.

This district is located in an urban section of Seoul, has 4 distinct seasons, and has a single tertiary-care hospital that evaluates nearly all local stroke patients. Its approximately quarter million population remained stable over the 10 year study period. The average temperature, diurnal temperature range, average humidity, as well as particulate matter (PM10) and nitrogen dioxide (NO2) pollutant levels were obtained from meteorological and air quality agencies.



3,001 patients were in this study (2,202 ischemic stroke and 799 intraparenchymal hemorrhage); the average age was ~65 years. Monthly incidence (of all stroke) was highest in September (17.7/100,000) and lowest in October (14/100,000). The highest incidence for ischemic stroke (IS) was September (especially for men (OR 1.391) and individuals age >60 years (OR 1.268)) and highest incidence for hemorrhage (ICH) was in January. The seasonal IS rate in the summer (OR 1.183) and autumn (OR 1.127) was higher than that in the winter. There was no seasonal variation in history of traditional vascular risk factors. An association of mean temperature with IS risk was demonstrated, with a 0.6% higher risk of IS for every 1℃ increase in monthly temperature (RR 1.006, p=0.003). In the older age group, average temperature was associated with IS incidence (RR 1.007, p=0.007) and negatively correlated with ICH (RR 0.985, p=0.004). No association was demonstrated with humidity. Interestingly, PM10 levels were negatively correlated with IS (RR 0.97, p=0.009) and the association was more significant in men (RR 0.943, p=0.002). However, PM10 (RR 1.106, p=0.002) and NO2 (RR 1.262, p=0.001) levels were positively correlated with ICH incidence in older individuals.

Notable limitations of the study include being single-center (serving a small geographic region) and that a limited number of air pollution and meteorological variables was assessed. Nevertheless, the results are interesting. Future work will have to evaluate the biological mechanisms leading to such variation in stroke incidence and further elucidate the impact of environmental pollutants.

By |February 25th, 2015|epidemiology and genetics|Comments Off on Effects of weather and air pollution on stroke incidence in Seoul, Korea
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Experimental CT Perfusion parameter a good surrogate for angiographic collaterals in large artery acute ischemic stroke

Mark N. Rubin, MD

Chen H, Wu B, Liu N, Wintermark M, Su Z, Li Y, et al. Using Standard First-Pass Perfusion Computed Tomographic Data to EvaluateCollateral Flow in Acute Ischemic Stroke. Stroke. 2015


Collaterals are so hot right now, especially after they played a prominent role in some of the most important and strikingly positive treatmenttrials the stroke community has seen in decades. Better collaterals as measured by catheter angiography (reference diagnostic), CTA, CTP and arterial spin labeling have been associated with less severe stroke, better results with acute stroke treatment (tPA and/or endovascular reperfusion), more favorable multiparametric imaging (e.g., smaller core infarct and larger “penumbra”) and smaller final infarct volume. Particularly in light of the aforementioned trials, collateral flow score (CFS) is being looked at as an important diagnostic variable in triaging acute stroke patients to the angiography as well as a therapeutic target itself.

These investigators provide us with a timely description of a CTP parameter that, in brief, correlates well with direct subtraction angiography (DSA)-graded collaterals and, in their small retrospective cohort, good outcome. The design of this study was relatively simple in that they included patients with acute ischemic stroke with demonstrated M1 MCA occlusions who underwent noncontrast CT, CTA and catheter angiography for endovascular reperfusion. Collaterals were measured with CTA (maximum intensity projection, or MIP) and DSA using previously published criteria and correlated to a parameter derived from standard clinical CTP that the investigators call volume transfer constant (Ktrans). Inter- and intra-rater reliability was measured amongst these various modalities, and collateral grade was compared to clinical parameters such as 90 day outcome. Again, in brief, Ktrans had excellent agreement with the reference standard DSA (k >0.8) and higher scores of any method was correlated with better outcome.

Although Ktrans is not at this time a mainstream clinical variable, these data are timely and important as those of us who care for acute stroke patients want to find some way to identify patients who might best benefit from endovascular reperfusion therapies in light of the sterling treatment trial results presented just days ago. What will be our best (e.g., most sensitive, fastest, most widely available and cheapest in descending order of importance) means of estimating collateral flow around a large artery occlusion? CT ASPECTS, CTA, CTP (+/- Ktrans), or MRA? We may end up with more than one answer to this important question, and it is good that we have options to study.

By |February 24th, 2015|diagnosis and imaging|Comments Off on Experimental CT Perfusion parameter a good surrogate for angiographic collaterals in large artery acute ischemic stroke
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What results in neurological deterioration after spontaneous intracerebral hemorrhage?

Prachi Mehndiratta, MD

Lord AS, Gilmore E, Choi HA, and Mayer SA, on behalf of VISTA-ICH Collaboration. Time Course and Predictors of Neurological Deterioration After Intracerebral Hemorrhage. Stroke. 2015


Spontaneous Intracerebral Hemorrhage (sICH) can be serious and life threatening based on hemorrhage and clinical characteristics. If you remember the Hemphill ICH score, you can predict 30 day mortality from ICH based on a combination of clinical and imaging characteristics. We also know from prior studies that hematomas often snowball and increase in size in the first 24 hours and our best chance of good recovery lies in halting hematoma growth. The authors of this study aim to identify the predictors of neurological deterioration after a sICH. They enrolled patients into a retrospective cohort from the VISTA database and attempted to identify clinical and radiological features associated with a pre-defined neurological deterioration at various points in time. These patients were enrolled in the placebo arms of prospective, randomized trials of acute treatment for ICH and baseline as well as follow up CT scans, rigorous physical exam data and a 3 month mRS score. 



Neurological deterioration (ND) was defined as hyper-acute ( <1 hour), acute (1-24 hours), sub-acute (1-3 days) and delayed (3-15 days). Univariate and multivariate analyses were performed to identify demographic, clinical and radiographic factors that were associated with deterioration in each subgroup. Chi-square, Fisher’s exact test, Mann-Whitney-U test and logistic regression were used for analysis. A total of 376 patients were included in the cohort and ND occurred in 176 patients, 170 at discrete pre specified time points and in 6 patients gradually over multiple time periods. The predictors of ND were intuitive – patients with hyperacute and acute ND had lower GCS, higher NIHSS, larger hematoma volumes and presence of IVH. Patients with subacute ND were similar to those with acute ND but in addition had higher rates of fever and increased IVH blood volumes. Multivariate analysis revealed that delayed ND was associated with older age, higher troponin levels and infection in the 3-15 day period.

The study was well done and well-intended but does it really affect my practice? I don’t think so. I know that patients with certain ICH clinical and radiographic characteristics can get worse and as a stroke physician I need to make sure their hemorrhage volume does not increase, provide them the best supportive neurocritical care and make sure they don’t get infected in order to improve their chances for survival from an illness that already carries a very high morbidity and mortality.

By |February 23rd, 2015|prognosis|1 Comment
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Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: INTERACT2 results

Rajbeer Singh Sangha, MD

Chan E, Anderson CS, Wang X, Arima H, Saxena A, Moullaali TJ, et al. Significance of Intraventricular Hemorrhage in Acute Intracerebral Hemorrhage:Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial Results. Stroke. 2015

Brain hemorrhage can be devastating and lead to the highest morbidity and mortality of any stroke subtype. About 33% to 45% of spontaneous ICHs and 25% of aneurysmal SAHs extend into the ventricles. Patients with IVH are twice as likely to have poor outcomes (a modified Rankin scale [mRS] score of 4–6 at hospital discharge) and nearly three times more likely to die than their cohorts without IVH.1 The authors of this study analyzed risk associations of IVH and outcomes among participants of the main phase Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2) study. 



The INTERACT2 study was an international, multicenter, open, blinded endpoint, randomized controlled trial. The study enrolled 2839 patients with CT-confirmed spontaneous ICH within 6 hours of onset and elevated systolic BP (SBP, 150-220 mmHg) were randomly assigned to receive intensive (target SBP <180 mmHg). Patient characteristics that pointed towards a greater probability of IVH included older age and with greater neurological impairment, having a previous history of ischemic stroke, and having larger hematomas at presentation that were located in the deep hemisphere. Death or major disability occurred in 66% with IVH versus 49% in ICH-alone patients (adjusted odds ratio 1.68, 95% confidence interval 1.38-2.06; p<0.01).

Associations of IVH volume and clinical outcomes were strong, showing thresholds of approximately 5 and 10mL for significantly increased odds of death, and or major disability. This threshold should be recognized by clinicians and may prompt more aggressive therapy or intervention going further in the future. This analysis may be further confirmed by the results of the ongoing CLEAR III trial which hopefully gives us a positive result.

Reference:
1. Hallevi H, Albright KC, Aronowski J, et al. Intraventricular hemorrhage: anatomic relationships and clinical implications. Neurology. 2008;70(11):848–852

By |February 20th, 2015|treatment|Comments Off on Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: INTERACT2 results
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Subclinical infarction post cardiac surgery: What’s the damage?


The disability that results from acute infarction is easier to recognize and treat when the patient presents with clear physical sequela of stroke. The impact of subclinical infarction is an understudied area and thus the treating physician lacks clear guidance. Neurologists are all too familiar with ordering head imaging and discovering evidence of prior ischemic insult with the patient denying history of an acute event. What is the physician to do with this information? As our population ages, one can expect that this will become a more common occurrence. More procedures, such as cardiac surgery are also being performed in the latter years. This provides an excellent backdrop upon which to investigate the sequela of accumulating new subclinical infarcts post procedure in those with pre-existing cerebrovascular disease. 


Patel et al. used rapidly evolving technology, the 3T MRI, to assess for new lesions following cardiac surgery, quantified against levels of pre-existing cerebrovascular disease, and also compared neuropsychological testing conducted at identical time intervals. Patients undergoing either a CABG and/or valve surgery at the University of Leicester were eligible for inclusion. Only those who had contraindication to MRI or were not native English speakers were excluded. 3mm 3T MRI images were obtained at intervals 1-2 weeks prior to surgery as well as 6-8 weeks postoperatively. Neuropsychological evaluation with standard battery assessments occurred at the same time intervals. Acute or chronic ischemic change was determined by comparing the DWI and FLAIR sequences by a blinded neuroradiologist. Chronic ischemic change was characterized using a computer program which looked at location and volume of the lesions. Patient cognitive improvement or decline was indicated by a change in the Z score which incorporated the mean and standard deviation from a healthy population.

77 of the 103 patients enrolled successfully completed pre/post-operative MRI and cognitive assessments. FLAIR signal change was found in 49 patients pre procedure. New FLAIR lesions were identified in 24 patients (9 with >1) post procedure with the majority occurring in the MCA territory. There were no baseline characteristics that differed between those with new lesions after cardiac surgery and those without. 22/24 with new lesions had evidence of prior FLAIR signal change. Volume comparison suggested that the accumulation of lesions following surgery is relatively minor (0.004%) in comparison with pre-existing burden (0.1%) due to chronic cerebrovascular disease. Of the 35 patients who showed a decline >1SD in neuropsychological testing following surgery, the majority (24) had NO NEW postoperative lesions. The incidence of cognitive decline (46%) was therefore irrespective of presence, number or size of new lesions. 5 patients notably had acute perioperative stroke but only one patient showed decline in cognition following the procedure.

What conclusions is the practicing neurologist to draw? The good news is that lesions accumulated post cardiac procedure found on imaging appears to have no impact on a patient’s cognition. However, the authors show that patients with pre-existing lesions were ten times more likely to experience new lesions post-operatively. While we may not fully understand the impact of these subclinical lesions, it does confirm what we know to be true. There must be something about the patient population with silent ischemic disease that predisposes them to further insult making prevention all the more important.

By |February 18th, 2015|health care, outcomes, policy|Comments Off on Subclinical infarction post cardiac surgery: What’s the damage?
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No relation of lipid lowering agents to hematoma growth

Rajbeer Singh Sangha, MD

Priglinger M, Arima H, Anderson C, and Krause M. No Relationship of Lipid-Lowering Agents to Hematoma Growth: Pooled Analysisof the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trials Studies. Stroke. 2015

Controversy persists over whether statins increase the risk of intracerebral hemorrhage (ICH). A recent systematic overview of randomized trials found no association of statins and the risk of ICH, but less evidence exists for populations with high rates of ICH. Statins do not appear to increase risks of poor functional outcomes in ICH, but no study has examined their association with hematoma growth which may be promoted by ancillary mechanisms. Previous studies have was shown that statins increase fibrinolytic and/or decrease pro-thrombotic mechanisms in vitro. In aortic endothelial cells, statins increase mRNA and enzymatic activity of tissue type plasminogen activator (tPA) (Essig et al., 1998), and decrease mRNA and activity of plasminogen activator inhibitor-type1 (PAI-1) (Bourcier and Libby, 2000). These mechanisms suggest that statins may lead to inhibition of platelet aggregation and thrombogenesis and thereby postulated to affect hematoma growth. The authors of this study examined associations of lipid lowering therapy, hematoma growth and clinical outcomes in participants of the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trials (INTERACT).


The authors analyzed the data from the INTERACT trials (1 and 2) which were international, multicenter, open, blinded endpoint, randomized controlled trials with a common protocol that collectively compromised 3243 patients with spontaneous ICH (<6 hours of onset) and elevated systolic blood pressure (SBP 150-220mmHg) randomly allocated to receive intensive or guideline-based BP management. Out of 3184 participants included in the analyses, 204 (6.5%) were on lipid lowering therapy at the time of ICH. 90 day clinical outcomes were not significantly different after adjustment for confounding variables including region and age. In the CT substudy, analysis of 24 hour hematoma growth was greater in 124 patients (9%) with, compared to those without, prior lipid lowering therapy. However, this association was not significant between the two groups (9.2ml vs 6.8ml, p<0.13), after adjustment for prior antithrombotic therapy. This study found no difference in clinical outcomes, initial ICH volume, or 24 hour hematoma volume growth between patients with and without lipid lowering therapy at the time of acute ICH.

After multiple studies, analyses and debates, the evidence seems to be pointing towards the safe utilization of statins during acute ICH. While many of these studies are underpowered to determine a significant effect of statins, the safety profile continues to be established in favor of statin use. It seems that until no large multicenter center does not analyze the effect statins have on ICH we won’t have a conclusive answer and the “controversy” will continue to rage on. Of course, there is the very real possibility that statin use will be limited in the next five years as lipid lowering agents will most likely be comprised of a new class of drugs.

References:
1. Bourcier T, Libby P. HMG-CoA reductase inhibitors reduces plasminogen activator inhibitor-1 expression by human vascular smooth muscle and endothelial cells. Arterioscler Thromb Vasc Biol 2000;20:556–562
2. Essig M, Nguyen G, Prie D, Escoubet B, Sraer J-D, Friedlander G. 3-hydroxy-3-methylglutarylCoenzyme A reductase inhiitors increase fibrinolytic activity in rat aortic endothelial cells. Circ Res 1998;83:683–690.

By |February 17th, 2015|prognosis|Comments Off on No relation of lipid lowering agents to hematoma growth
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Endovascular Reperfusion Treatment Trials Presented at the ISC 2015

International Stroke Conference (ISC)
February 11-13, 2015

February 13, 2015
Attendees of the 2015 International Stroke Conference were treated to the overwhelmingly positive results of ESCAPE, EXTEND IA and SWIFT PRIME this morning, building on the excitement generated by MR CLEAN for mechanical thrombectomy of proximal intracranial occlusions causing acute cerebral ischemia. Today will likely mark a dramatic shift in the perception of mechanical thrombectomy for proximal anterior circulation occlusions in previously well patients with adequate neuroimaging-selection, a critical mass of multidisciplinary stroke expertise and lighting-fast acute stroke workflow. One of the lead investigators of ESCAPE closed his remarks with the claim that intervention in the studied context is the new standard of care for acute stroke patients. For sure, these trials will not only serve as a foundation for efficacy of endovascular reperfusion therapies in carefully selected patients but also as a blueprint for running the acute evaluation and management aspects of a comprehensive stroke center as a tight ship.


At the expense of being overly negative concerning admittedly exciting data, “the studied context” has a lot of qualifiers.

How many of our patients are pre-morbid mRS 0-1, onset to treatment 110 minutes? Is that your average patient? Do you routinely get acute non-invasive angiography let alone score collaterals in your acute stroke patients? Can you mobilize your endovascular team within 1h of counseling/trial enrollment? Do you have software that provides you with a discrete visual and numerical representation of the penumbra? Do you only see anterior circulation strokes? What of the many, many patients that do not fall within the careful clinical and neuroimaging selection criteria of these trials?

To be sure, these encouraging data presented today are important for stroke patients and those who care for them. Even outside of the demonstrated efficacy, the dramatic results and surrounding pomp will shift the acute stroke treatment ethos in an appropriately aggressive direction; it’s good to win every once and again. However, we cannot lose site of the fact that these glowing results were in a highly-selected group of patients, nor can it be forgotten that the vast majority of these patients received full-stroke-dose alteplase prior to intervention. Broadly espousing “intervention is better than tPA” for acute ischemic stroke is a leap of faith, and “real world” treatment trials are still in need of development and recruitment; these data should not be considered definitive for the broad phenotypic spectrum of acute ischemic stroke nor should they hinder recruitment into future treatment trials.

– Mark N. Rubin, MD

By |February 13th, 2015|Conference|1 Comment
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Imaging may help fill knowledge lacunae in lacunar strokes!

Chirantan Banerjee, MD


Jeong HG, Kim BJ, Yang MH, Han MK, and Bae HJ. Neuroimaging Markers for Early Neurologic Deterioration in Single Small Subcortical Infarction. Stroke. 2015

Perforator infarcts account for a quarter of all strokes and portend a favorable prognosis. Except, there are 20-30% cases where the deficits worsen over the ensuing hours to days, and lead to significant disability. The underlying pathophysiology of these processes has still not been clearly elucidated. The distinction between microatheroma causing proximal branch atheromatous disease v/s degenerative lipohyalinosis distally was beautifully elucidated by Dr.Caplan in 1989. But these two disparate processes are still not widely recognized. There have been several studies over the years trying to identify markers of progression in small subcortical strokes, and diabetes, pure motor stroke, hypertriglyceridemia and parent artery atherosclerosis have been identified. 


Jeong et al. hypothesized that atherosclerotic process would produce a greater contribution to early neurologic deterioration (END) compared with small vessel pathologies in small subcortical strokes(<20mm). They performed analysis on a prospectively collected large stroke registry of 4961 patients at Seoul National University Bundang Hospital between July 2007 and July 2013 to investigate associations between concomitant neuroimaging markers and END. 2 authors blinded to clinical data assessed MRIs for degree of white matter hyper intensity, cortical micro bleeds, old lacunar infarcts and parent artery stenosis (patients with stenosis >50% were excluded). Of the 587 eligible patients with small subcortical strokes, END occurred in 13.5% cases, mostly from stroke progression(enlargement of infarct size), at about 40 hours from onset causing an NIHSS increment of 2.3 points. Appropriate binary logistic regression models revealed that relevant artery stenosis and branch atheromatous lesions were significantly associated with occurrence of END in the cohort. These findings corroborate and reinforce Caplan’s description of lacunas actually being comprised of 2 different pathophysiologies, with atheromatous ones having potential for progression. This may potentially underlie the benefit of dual anti platelet therapy in these patients noted in the CHANCE trial. As we await results from POINT trial, neuroimaging is helping us understand pathophysiology of lacunar strokes better.

By |February 12th, 2015|diagnosis and imaging|Comments Off on Imaging may help fill knowledge lacunae in lacunar strokes!
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