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Collaterals: an important determinant of prolonged ischemic penumbra versus rapid cerebral infarction?

Marsh EB, Leigh R, Radvany M, Gailloud P, Llinas RH - Front Neurol (2014)

Bottom Line: Studies have demonstrated that treating patients early leads to improved long-term outcomes.MR imaging currently allows quantification of the ischemic penumbra in order to better identify individuals most likely to benefit from intervention, irrespective of "time last seen normal." Its increasing use in clinical practice has demonstrated individual differences in rate of infarction.We report two cases that highlight the individual variability of infarction rate, and discuss potential underlying mechanisms that may influence treatment decisions and outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, The Johns Hopkins University School of Medicine , Baltimore, MD , USA ; Department of Neurology, Johns Hopkins Bayview Medical Center , Baltimore, MD , USA.

ABSTRACT
Intravenous tissue plasminogen activator is the mainstay for the treatment of acute ischemic stroke in patients presenting within 4.5 h of symptom onset. Studies have demonstrated that treating patients early leads to improved long-term outcomes. MR imaging currently allows quantification of the ischemic penumbra in order to better identify individuals most likely to benefit from intervention, irrespective of "time last seen normal." Its increasing use in clinical practice has demonstrated individual differences in rate of infarction. One explanation for this variability is a difference in collateral blood flow. We report two cases that highlight the individual variability of infarction rate, and discuss potential underlying mechanisms that may influence treatment decisions and outcomes.

No MeSH data available.


Related in: MedlinePlus

(A) Cerebral angiogram of Case 1 showing robust collateral flow through the pial vessels in the late arterial phase (black arrow). (B) Cerebral angiogram of Case 2 showing a lack of collateral flow through the pial vessels in the late arterial phase (black arrow).
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Figure 2: (A) Cerebral angiogram of Case 1 showing robust collateral flow through the pial vessels in the late arterial phase (black arrow). (B) Cerebral angiogram of Case 2 showing a lack of collateral flow through the pial vessels in the late arterial phase (black arrow).

Mentions: WS is a 70-year-old man with a history of hypertension, hyperlipidemia, and diabetes, who presented with aphasia and a right hemiparesis. He was last seen normal by his wife at 9 p.m. the evening prior to admission. When she came to bed at 2 a.m. she noted that he could not move his right side or communicate, and called EMS. He arrived in the Emergency Department at 2:34 a.m. His blood pressure was 121/60 mmHg. Serum glucose was 126. He was noted to be in atrial fibrillation. His troponin was elevated at 7.12 with mild ST segment changes. His NIH stroke scale was 12, with points given for disorientation, gaze preference, dysarthria, aphasia, and hemiparesis. He was outside of the window for treatment with IV tPA. Work-up was initiated. He vomited during CT angiogram, requiring intubation for airway protection. Coffee ground emesis was also noted. Cerebral perfusion was maximized with fluids and positioning and he was admitted to the Neurocritical Care Unit for further monitoring. Permissive hypertension was allowed as per our institution’s policy regarding treatment of acute stroke; however, his systolic blood pressures remained around 120 mmHg. He did not exhibit evidence of perfusion dependence on examination so hypertensive therapy was not pursued. Due to medical instability, an MRI of the brain was not performed until the following morning. Neuroimaging revealed a large perfusion deficit encompassing much of the left middle cerebral artery (MCA) territory, matching his clinical deficits, with no clear diffusion abnormality (Figures 1A,B). He remained symptomatic, and the decision was made to proceed with intra-arterial intervention given the lack of infarcted tissue. Over 16 h after being last seen normal, successful recanalization was achieved using the penumbra clot retrieval device. Angiography demonstrated robust collateral flow through the pial vessels (Figure 2A). Follow-up MR imaging showed only a small area of diffusion restriction. His aphasia and hemiparesis markedly improved after recanalization, and 4 days later he walked out of the hospital with no rehabilitation needs.


Collaterals: an important determinant of prolonged ischemic penumbra versus rapid cerebral infarction?

Marsh EB, Leigh R, Radvany M, Gailloud P, Llinas RH - Front Neurol (2014)

(A) Cerebral angiogram of Case 1 showing robust collateral flow through the pial vessels in the late arterial phase (black arrow). (B) Cerebral angiogram of Case 2 showing a lack of collateral flow through the pial vessels in the late arterial phase (black arrow).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4196524&req=5

Figure 2: (A) Cerebral angiogram of Case 1 showing robust collateral flow through the pial vessels in the late arterial phase (black arrow). (B) Cerebral angiogram of Case 2 showing a lack of collateral flow through the pial vessels in the late arterial phase (black arrow).
Mentions: WS is a 70-year-old man with a history of hypertension, hyperlipidemia, and diabetes, who presented with aphasia and a right hemiparesis. He was last seen normal by his wife at 9 p.m. the evening prior to admission. When she came to bed at 2 a.m. she noted that he could not move his right side or communicate, and called EMS. He arrived in the Emergency Department at 2:34 a.m. His blood pressure was 121/60 mmHg. Serum glucose was 126. He was noted to be in atrial fibrillation. His troponin was elevated at 7.12 with mild ST segment changes. His NIH stroke scale was 12, with points given for disorientation, gaze preference, dysarthria, aphasia, and hemiparesis. He was outside of the window for treatment with IV tPA. Work-up was initiated. He vomited during CT angiogram, requiring intubation for airway protection. Coffee ground emesis was also noted. Cerebral perfusion was maximized with fluids and positioning and he was admitted to the Neurocritical Care Unit for further monitoring. Permissive hypertension was allowed as per our institution’s policy regarding treatment of acute stroke; however, his systolic blood pressures remained around 120 mmHg. He did not exhibit evidence of perfusion dependence on examination so hypertensive therapy was not pursued. Due to medical instability, an MRI of the brain was not performed until the following morning. Neuroimaging revealed a large perfusion deficit encompassing much of the left middle cerebral artery (MCA) territory, matching his clinical deficits, with no clear diffusion abnormality (Figures 1A,B). He remained symptomatic, and the decision was made to proceed with intra-arterial intervention given the lack of infarcted tissue. Over 16 h after being last seen normal, successful recanalization was achieved using the penumbra clot retrieval device. Angiography demonstrated robust collateral flow through the pial vessels (Figure 2A). Follow-up MR imaging showed only a small area of diffusion restriction. His aphasia and hemiparesis markedly improved after recanalization, and 4 days later he walked out of the hospital with no rehabilitation needs.

Bottom Line: Studies have demonstrated that treating patients early leads to improved long-term outcomes.MR imaging currently allows quantification of the ischemic penumbra in order to better identify individuals most likely to benefit from intervention, irrespective of "time last seen normal." Its increasing use in clinical practice has demonstrated individual differences in rate of infarction.We report two cases that highlight the individual variability of infarction rate, and discuss potential underlying mechanisms that may influence treatment decisions and outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, The Johns Hopkins University School of Medicine , Baltimore, MD , USA ; Department of Neurology, Johns Hopkins Bayview Medical Center , Baltimore, MD , USA.

ABSTRACT
Intravenous tissue plasminogen activator is the mainstay for the treatment of acute ischemic stroke in patients presenting within 4.5 h of symptom onset. Studies have demonstrated that treating patients early leads to improved long-term outcomes. MR imaging currently allows quantification of the ischemic penumbra in order to better identify individuals most likely to benefit from intervention, irrespective of "time last seen normal." Its increasing use in clinical practice has demonstrated individual differences in rate of infarction. One explanation for this variability is a difference in collateral blood flow. We report two cases that highlight the individual variability of infarction rate, and discuss potential underlying mechanisms that may influence treatment decisions and outcomes.

No MeSH data available.


Related in: MedlinePlus