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Jun. 07, 2021
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This article includes discussion of neuroimaging in acute stroke, neuroimaging in stroke, acute stroke neuroimaging, acute stroke brain imaging, acute ischemic stroke imaging, imaging guided thrombolysis for acute ischemic stroke, and imaging guided thrombectomy for acute ischemic stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Rapid diagnosis of acute ischemic stroke has become exceedingly important given modern stroke therapies and is highly dependent on neuroimaging findings. Neuroimaging directly guides treatment of acute stroke patients by identifying appropriate candidates for acute therapies and informing the workup of stroke etiology. The authors provide an update on the use of neuroimaging in the diagnosis and management of the acute ischemic stroke patient.
• When performing neuroimaging evaluation of acute stroke and transient ischemic attack patients, there are several appropriate imaging strategies.
• Consistency of the imaging strategy within a given institution is critical to facilitate reliable technical execution, rapid evaluation, and accurate interpretation of results.
• The primary goal of acute imaging in ischemic stroke is to identify candidates for powerful and effective reperfusion therapies including intravenous thrombolysis and endovascular thrombectomy. The indications for these therapies have expanded thanks to high quality research.
• A second but fundamental goal of stroke imaging is to inform the diagnostic workup for stroke mechanism, treatment, and secondary prevention. Adequate expertise in vascular neurology with understanding of cerebrovascular anatomy and pathology and their manifestation on imaging should form the basis of this workup.
• Advancements in expediting stroke imaging workflow including artificial intelligence, the “direct to angiography” pathway, and prehospital imaging are under investigation now and have the capacity to advance the field of stroke intervention.
Brain parenchymal imaging. Advances in imaging of the brain parenchyma have contributed immensely to the diagnosis of ischemic stroke (22). In 1971, CT was invented by engineer Godfrey N Hounsfield and revolutionized brain parenchymal imaging. This is especially apparent when one considers that prior to its advent the primary ways to image brain parenchyma were with pneumoencephalography and catheter angiography. Magnetic resonance imaging was developed shortly after CT with Peter Lauterbur, who shared in the Nobel Prize in 2003, when Peter Mansfield demonstrated the first images produced by magnetic resonance in 1973 (21; 22). MRI now represents a means of obtaining far superior resolution of parenchymal anatomy than CT without the effects of ionizing radiation. Of significant importance to acute stroke imaging was the introduction of diffusion-weighted MRI to identify areas of acute ischemia in 1990 (29), as well as the development and refinement of perfusion imaging with CT or MR.
Brain vascular imaging. Advances in vascular imaging began with catheter angiography of the carotid arteries first performed in 1927 by Egas Moniz. Moniz and others considerably developed cerebral angiography in the 1930s. In the 1960s, the transfemoral approach essentially replaced direct puncture of the carotid and brachial arteries. The development and improvement of MR angiography in the 1980s and 90s along with the advent of helical CT angiography in 1991 represent major advances in vascular imaging, which now make rapid and noninvasive contrast-enhanced angiography possible. Despite these advances in MR angiography and CT angiography, catheter angiography remains the reference standard for vascular imaging today because of its combined superior temporal and spatial resolution.
Brain imaging in the endovascular reperfusion era. Two thousand and fourteen and 2015 saw the publication of multiple positive trials for endovascular mechanical thrombectomy in treating acute ischemic stroke due to large vessel occlusion. By proving the effectiveness of this powerful therapy, these trials revolutionized the field of acute ischemic stroke like the NINDS trial of IV-tPA before them. Furthermore, these trials underscore the importance of early vascular imaging with CTA or MRA to identify large vessel occlusion in patients suspected to have acute ischemic stroke. Advanced perfusion imaging in high volume centers with appropriate interpretation can be quite complementary to these forms of lumenography for multiple reasons. First, perfusion imaging can establish candidacy for endovascular therapy in the late time window or for wakeup strokes as was shown in both the DAWN and DEFUSE 3 trials (03; 31). These trials established the benefit of endovascular thrombectomy in the selected patient populations, those with strokes in the 6 to 24 and the 6- to 16-hour windows, respectively. Second, perfusion imaging proves very sensitive in identifying more distal occlusions that are amenable to effective and safe endovascular reperfusion (Haruyama et al 2019; 26). These distal occlusions are more conspicuous on perfusion imaging than on vascular imaging with MRA or CTA alone (07).
The future of large vessel occlusion imaging. Thrombectomy for acute large vessel stroke is 1 of the most effective therapies in all of medicine and is of course critically dependent on time. In the endovascular reperfusion era, it has become imperative to rapidly identify patients with acute stroke and large vessel occlusion. Multiple innovative strategies for expediting identification and treatment of large vessel occlusion are now available and under investigation. First of all, early identification of large vessel occlusion now represents a very promising potential application of artificial intelligence. Indeed, software now exists that uses artificial intelligence to identify large vessel occlusion from CTA, allowing for near real-time alert of an advanced stroke team. This technology has the capacity to dramatically impact the field of acute stroke and is the current subject of the ALERT multicenter clinical trial (clinicaltrials.gov). Second, in patients with physical exam signs of large vessel stroke, significant time savings have been demonstrated in taking these patients directly to the angiography suite for evaluation and possible thrombectomy (35). Third and finally, vascular imaging in the prehospital setting may also serve to hasten the identification of emergent large vessel occlusion in patients able to be evaluated with vascular or perfusion imaging in a mobile stroke unit (15).
Acute ischemic stroke affects approximately 700,000 persons each year and remains the leading cause of adult long-term disability. The first discernible sign of ischemia on MRI is restricted diffusion of water on diffusion-weighted imaging caused by cytotoxic edema (29). In acute ischemia, the increased water in the intracellular compartment is restricted in its diffusion because the intracellular environment is packed with nuclei and organelles unlike the extracellular environment. Diffusion-weighted MRI is highly sensitive to ischemia and easily interpreted.
Noncontrasted CT, on the other hand, is less sensitive for diagnosing acute ischemia because cytotoxic edema does not produce profound decreases in brain density. However, cytotoxic edema probably does underlie the subtle early changes seen on CT, including decreased density in gray matter best seen in gray and white junctions, such as cortical ribbons, thalami, and basal ganglia (38). The density of normal gray and white matter is very similar, at 35 Hounsfield units (HU) and 25 HU respectively. Therefore, to better visualize subtle differences in gray and white matter junctions, adjusting the center level to 30 HU and window width to 30 HU on CT reading software can be helpful. This is sometimes referred to as using narrow windows or stroke windows. A center level of around 30 HU will place the center of the gray scale between gray and white matter, and window width of around 30 HU will make the gray scale range from 15 HU (black) to 45 HU (white), thereby producing a grayscale window that is well-tuned for differences in the gray/white junction.
Vasogenic edema occurs after more prolonged ischemia and results in increased water in the brain from the intravascular space. On MRI, this is characterized by hyperintense signal on T2-weighted imaging, such as FLAIR and T2 hyperintense shine-through on ADC maps. Because water (0 HU) is less dense than brain parenchyma (25 to 30 HU), vasogenic edema is seen on CT as more conspicuous areas of hypodensity. Evidence of vasogenic edema on FLAIR imaging suggests some chronicity and can be used as a means of estimating time of ischemia onset. An MRI diffusion FLAIR mismatch can now establish thrombolysis candidates who have unknown time of stroke onset (40).
Brain perfusion imaging, which can be performed reliably on MRI or CT in acute stroke, is based on the equation stating that cerebral blood flow is equal to cerebral blood volume minus mean transit time (CBF = CBV – MTT). Each of these parameters change in predictable ways in response to ischemia and infarction. Years of empiric observation of these parameters on perfusion imaging has led to iterative refinement of the thresholds for ischemic penumbra and infarct core. Brain with a Tmax of longer than 6 seconds has now been relatively widely adopted as brain at risk in the setting of acute stroke. Work shows that several thresholds for relative CBV (0.30 to 0.34) and CBF (0.32 to 0.34) provide an accurate estimate of core infarct (28). Perfusion imaging to distinguish core infarct from salvageable brain is now a proven approach to establishing candidacy of both thrombectomy and thrombolysis in patients presenting in a late time window and wake up stroke patients (03; 31; 23).
The major indication for acute stroke neuroimaging workup is acute onset neurologic deficit as reported retrospectively or as seen on examination by an experienced clinician. Although some have used an NIH stroke scale cutoff, eg, NIHSS greater than 6 as a threshold for vascular imaging, this cutoff will still miss 13% of large vessel occlusions (39). As described below, the risks of intravenous contrast are much lower than previously thought and can be mitigated with modern techniques. Finally, as stated above in our key points, consistency of the imaging strategy within a given institution is critical to facilitate reliable technical execution, rapid evaluation, and accurate interpretation of results. Therefore, at our institutions acute stroke imaging including head and neck vessel angiography and perfusion imaging is standardly performed for all acute stroke patient evaluations.
Although acute imaging to identify candidates for reperfusion therapy is optimally performed within 6 hours from last known normal time, many patients can still greatly benefit from endovascular reperfusion when they present in a delayed manner, as has been shown in both the DAWN and DEFUSE 3 trials. More recently, the EXTEND and WAKE UP trials also show benefit from thrombolysis in many patients who present beyond the conventional thrombolysis window. Therefore, it is imperative that even patients presenting in a delayed manner still be evaluated with a rapid and complete acute stroke imaging protocol.
Impaired renal function has historically been a reason for caution in administering contrast agents given the risks of nephrogenic systemic fibrosis with gadolinium MR contrast and contrast-induced nephropathy with iodinated CT contrast. However, it should be noted that the risk of renal injury with iodinated contrast is far less than previously thought (25). Evidence suggests the risk of contrast-induced nephropathy with present-day low-osmolality intravenous iodinated contrast is only significant if eGFR is less than 30. Patients with GFR less than 30 and with signs and symptoms of large vessel occlusion on an expert’s clinical evaluation should still be seriously considered for vascular imaging with CTA, accepting some risk of contrast-induced nephropathy in exchange for identifying large vessel occlusion. This recommendation matches current guidelines (33). Alternatively, at centers where MRI can be conducted without delaying evaluation of the acute stroke patient, high resolution time of flight MRA can be used, as it does not require intravenous gadolinium contrast.
A second reason for caution with intravenous iodinated CT contrast is documentation of a contrast allergy. However, this should not represent an absolute contraindication to iodinated contrast in the evaluation of the acute ischemic stroke patient. Rather, we recommend establishing a pretreatment protocol per institutional guidelines in patients with documented iodine allergy who may have a large vessel occlusion causing acute stroke. For example, it is reasonable to use diphenhydramine and steroids prior to CTA or CTP in patients with documented allergies rather than forgoing the imaging evaluation. Again, MRA without contrast can be performed at institutions where it does not delay evaluation.
The primary goals of stroke neuroimaging are to discover factors that directly change the management of the acute stroke patient.
Candidates for thrombolytic therapy. The most widespread use of acute imaging when making the intravenous thrombolytic decision in acute stroke is whether or not hemorrhage is present, ie, any intracranial hemorrhage is a contraindication for thrombolytic therapy. As such, the only imaging necessary to complement expert clinical evaluation for alteplase administration is a negative head CT. Other imaging findings need not delay administration of thrombolytics in patients who are deemed good candidates on experienced clinical evaluation. However, imaging evaluation of the acute stroke patient should not stop at ruling out hemorrhage. There are other findings on acute stroke imaging with MRI or perfusion imaging that can aid the thrombolysis decision in challenging clinical scenarios. These findings are useful correlates to the acute clinical evaluation of a stroke patient when evaluated in real time in conjunction with the clinical picture of a potential stroke patient.
Endovascular candidates: vascular imaging. Approximately 20% of acute ischemic stroke patients will present with a large vessel occlusion. Among these patients, it is critical to diagnose persistent flow-limiting vascular lesion. In those presenting beyond 6 hours since last known well time, endovascular intervention is still beneficial for selected patients. Several methods for selecting endovascular candidates in the delayed time window can be used. These include perfusion imaging (11; 03; 31), the status of collateral vessels (13), or simply an ASPECTS score on CT (08).
Distal occlusions amenable to reperfusion therapy. Of 6 positive thrombectomy clinical trials in early presenting patients, 4 used advanced perfusion imaging to establish candidacy for thrombectomy. However, 2 did not employ perfusion studies and still demonstrated benefit of endovascular thrombectomy. Nevertheless, there are 3 principle reasons that the authors of this review still strongly recommend advanced perfusion imaging of the acute stroke patient even in the early time window. First, perfusion imaging is more sensitive than vascular imaging in isolation for the identification of distal occlusions, which are very conspicuous on perfusion imaging. Patients who undergo endovascular revascularization of these distal lesions can have significant benefit (07; Haruyama et al 2019; 26). Second, with the publication of the EXTEND trial, perfusion imaging is an important tool in identifying late presenting patients who can benefit from thrombolysis. Third, and possibly most importantly, reliable technical execution and interpretation of perfusion imaging requires regular performance of such imaging rather than its use only in “special cases”.
Extensive infarction. Identification of large, completed infarcts is important for multiple reasons. First, in a patient who is a candidate for intravenous tPA and endovascular therapy, large infarcts predict higher risk of reperfusion-associated hemorrhage. Although large infarcts benefit less from endovascular therapy, evidence suggests benefit of endovascular therapy in patients with infarcts as large as 100cc prior to intervention (11). Finally, large infarct volume predicts risk of malignant middle cerebral artery syndrome and should prompt early consideration of decompressive hemicraniectomy. Data on infarct size are, thus, helpful for making medical decisions, counseling patients and families regarding likely clinical outcomes, and involving neurosurgical colleagues early when appropriate.
Stroke etiology. An essential function of neuroimaging beyond guiding acute interventions is to provide data that would otherwise change our clinical management of the patient. Specifically, stroke imaging combined with appropriate clinical acumen informs the workup of stroke etiology and therefore secondary prevention.
A joint statement from the American Society of Neuroradiology, the American College of Radiology, and the Society of Neurointerventional Surgery has recommended an algorithmic approach for the imaging workup for patients with acute stroke or transient ischemic attack symptoms (44). If the patient is a candidate for intravenous tPA, the recommendation is to proceed to noncontrast CT. MR diffusion and GRE sequences may be obtained instead of noncontrast CT at centers where this does not cause a delay in treatment. If the patient is being considered for endovascular reperfusion therapy, any of 3 strategies are deemed equivalent. The first strategy is to perform noncontrast CT followed immediately by digital subtraction angiography for vascular assessment. The second strategy is to perform noncontrast CT and CT angiography for vascular assessment with or without CT perfusion imaging. The third strategy is to perform MRI and MRA with or without MR perfusion imaging at centers that offer MRI 24 hours per day without delaying treatment.
In acute stroke patients with anterior circulation stroke or transient ischemic attack who are not eligible for acute reperfusion therapy, the carotid arteries should be evaluated after the brain parenchyma has been imaged. This can be done with carotid Doppler ultrasonography, CT angiography, or MRA, which are considered equivalent strategies. Discrepancy across these imaging modalities can be settled by catheter angiography, the reference standard for vascular imaging of the carotid arteries.
Establishing absence or presence of intracranial hemorrhage: thrombolysis candidacy. Intracranial hemorrhage is considered an absolute contraindication for intravenous thrombolytics. On CT, intracranial hemorrhage (60 to 100 HU) is significantly contrasted against a background of brain with gray and white matter densities (25 to 35 HU) and, therefore, does not require aggressive windowing to identify. Detecting CT signs of early ischemia may require narrow stroke windows or use of CT angiography source images in patients with unclear presentation, but absence of these signs should not delay administration of intravenous thrombolytics when ischemic stroke is otherwise suspected. On MRI, the classic signature of hyperacute intraparenchymal hemorrhage is seen on GRE as a rim of hypointense deoxygenated blood surrounding an oxygenated isointense core. The GRE sequence is at least as sensitive as noncontrast CT for the purpose of identifying intraparenchymal hemorrhage (19). FLAIR imaging is at least as sensitive for identifying subarachnoid hemorrhage as CT because CSF mixed with blood in the subarachnoid space appears hyperintense on FLAIR (30).
If hemorrhage has been ruled out with a noncontrast CT or GRE, administration of tPA does not need to be delayed by additional imaging findings. However, some ancillary findings may complement clinical findings when making this decision in ambiguous or challenging clinical situations. A wedge-shaped perfusion defect in the correct area of clinical impairment on perfusion imaging or restricted diffusion on MRI can help to rule in ischemic stroke and prompt more definitive use of thrombolytics.
Endovascular thrombectomy candidacy. Randomized clinical trials from 2014 and 2015 have established AHA Level 1 Class A evidence demonstrating the clinical efficacy of endovascular treatment performed with second generation thrombectomy devices (08; 11; 13; 17; 36; 27), all of which show overwhelming clinical benefit from modern endovascular treatment in patients with large vessel occlusion. The primary function of neuroimaging in endovascular therapy is to select appropriate endovascular candidates who have persistent proximal flow-limiting vascular occlusive lesion. These studies support the notion that time to revascularization remains 1 of the most critical factors in any effort to achieve a good clinical outcome. We strongly recommend parallel evaluation for endovascular therapy while thrombolytic candidacy is being determined. CTA, a widely available modality, is a quick and reliable way of identifying large vessel occlusion in patients presenting with acute ischemic stroke. The risk of contrast-induced nephrotoxicity should not delay performance of a CTA to determine presence of large vessel occlusion if suspected clinically. Perfusion imaging also increases overall sensitivity for distal vessel occlusion, such as M2 or M3 occlusions, which are candidates for intravenous or intraarterial reperfusion therapy (07; 26).
A secondary role of acute neuroimaging in evaluation of endovascular candidates is to characterize penumbral tissue and collateral vessels. There is a particular benefit of reperfusion therapy in patients who have a significant volume of brain at risk on perfusion imaging prior to intervention (20). The goal of CTP/MR DWI-PWI based endovascular patient selection is to detect volume of infarct core and select patients with a mismatch of this core to salvageable “at-risk” tissue. Because mismatch ratios are highly variable and depend on patient specific physiology, perfusion imaging allows for selection of patients with delayed presentations and so-called “wake-up” strokes (18; 03; 31).
When MR or CT perfusion imaging is used, Tmax of greater than 6 seconds is a reasonable threshold for brain at risk (44). Some of the published clinical trials have used absolute minimum mismatch ratios and core infarct volume cut-offs as part of their inclusion criteria (11; 36). Optimal use of these criteria requires availability of real-time postprocessing of perfusion imaging data at the time of acquisition (02). In the absence of a standardized advanced workflow with perfusion imaging, a “clinical penumbra” may be the best surrogate marker to select patients for mechanical thrombectomy. This requires a clinical concern of large vessel occlusion by an experienced provider and an estimate of small core based on available imaging.
Imaging aimed at evaluating collateral vessels status in acute stroke may also aid in identifying patients for whom endovascular therapy will not likely benefit (01; 13; 32). However, we advise extreme caution against using perfusion imaging alone to exclude patients presenting early (inside 6 hours) from thrombectomy because a “ghost core” may be present that overestimates core infarct especially in young patients presenting early (24).
Extensive infarction. Large, completed infarcts may affect management decisions regarding intravenous tPA treatment, endovascular reperfusion, and consideration of early decompressive hemicraniectomy for malignant middle cerebral artery syndrome. Regarding the decision to give intravenous tPA, a post-hoc analysis in the seminal ECASS trial demonstrated that patients with completed infarcts of greater than one third of the middle cerebral artery distribution are at higher risk of hemorrhage when given intravenous tPA (14). Therefore, a completed infarct of greater than one third of the middle cerebral artery is considered a relative but not absolute contraindication of intravenous tPA administration. Large infarcts that present this increased risk are best measured by an ASPECTS score of less than 7 on noncontrast CT, lesions of greater than 70 to 100 ml of DWI positivity on MRI, and mean cerebral blood volume of less than 1.8 or Tmax delay of greater than 8 seconds for greater than 100 ml of brain tissue on perfusion imaging (04; 16; 09). Importantly, to achieve 100% specificity in identifying patients who will have poor outcome despite intravenous or intra-arterial reperfusion therapy, a threshold of 103 ml of DWI positivity was required (37). Moreover, data from the HERMES metanalysis showed benefit of revascularization therapy even if there was a core infarct of 100cc of brain on pretreatment perfusion imaging (11). Whether endovascular thrombectomy will prove beneficial in patients with large core infarcts, is the subject of the randomized clinical trial TESLA (clinicaltrials.gov), which is currently enrolling.
With respect to malignant middle cerebral artery syndrome, in a pooled analysis of the DECIMAL, DESTINY, and HAMLET trials, patients younger than 60 years of age with DWI lesions greater than 145 ml or CT evidence of greater than 50% of the middle cerebral artery territory had a clear survival benefit with decompressive hemicraniectomy compared to conservative management (41). These trials were conducted in the era prior to thrombectomy and therefore the complete degree to which thrombectomy and hemicraniectomy may interact has yet to be seen.
Stroke etiology. Ischemic stroke may be caused by cardioembolic sources, carotid artery stenoses, vertebrobasilar stenosis, arterial dissection, intracranial atherosclerotic disease, vasculitis, and small artery occlusive disease. All of these entities are managed differently; therefore, identifying the underlying mechanism in stroke is important. The infarct pattern on MRI or CT can be quite useful as a guide to informing the workup for these potential etiologies. For example, in infarcts that extend from cortex to subcortical structures, a cardioembolic source or large artery atherosclerosis is often found and, therefore, should be deeply investigated (43). Understanding of cerebrovascular anatomy and vascular distribution of ischemia should direct the appropriate workup and treatment strategy for secondary prevention of ischemic stroke.
Stenting or carotid endarterectomy are appropriate and powerful treatments for ipsilateral stroke in a vascular territory served by a stenotic cervical carotid artery (10). Maximal medical therapy is the appropriate first-line therapy for intracranial atherosclerotic disease (12), but other strategies such as intracranial stenting can be considered after failure of maximal medical therapy (05). With vertebral or basilar artery stenosis resulting in ischemic stroke, quantification of flow can aid in determining the ongoing stroke risk so treatment is proportional to this risk (06). Establishing small vessel stroke resulting from lipohyalinosis and thrombosis of perforator arteries is important to direct efforts toward treating risk factors for small vessel stroke, such as diabetes, hypertension, and smoking. Additionally, establishing small vessel stroke may help direct efforts away from identifying or treating other causes of embolism, such as atrial fibrillation or patent foramen ovale.
Extracranial carotid and vertebral dissections may account for 10% to 25% of strokes in patients from 16 to 45 years of age, and conventional angiography is the gold standard for its evaluation given its superb resolution (42). The classic finding of intimal flap or double lumen is seen rarely and dissecting pseudoaneurysm is seen more frequently (34). MR/MRA and CT/CTA are less invasive diagnostic measures that attempt to identify the same features of dissection. In addition, T1-weighted, fat-suppressed images may show hyperintense methemoglobin of an intramural hematoma in the false lumen of a dissection. In 1 study, CT/CTA and MR/MRI were comparable for detecting internal carotid artery dissection whereas CT/CTA was superior for vertebral dissections (42). The most appropriate study for evaluating dissection is likely to be that in which a given institution has the most experience.
An 84-year-old man with history of aortic stent graft and recent diagnosis of prostate cancer with a high functioning baseline was golfing every Friday morning prior to his presentation to the hospital. The patient was last seen to be at his normal state of high functioning by his wife the night prior to admission at 9:00 pm. On the day of admission, the patient woke up and fell when he attempted to get out of bed. He was noticed by his wife at that time to be unable to speak, and he was weak on the right side. He arrived at the hospital as a “wake up stroke,” and at the time of his evaluation it had been 11 hours since his last known normal time.
On evaluation of the patient by vascular neurology, he had an NIHSS of 16 with severe aphasia, dysarthria, weakness of the right upper more than the lower extremity, and leftward gaze preference. His pulse was 58, blood pressure was 141/58, and oxygen saturation was 99% on room air. He underwent emergent imaging evaluation including CT, CT perfusion, and CT angiogram of the head. His head CT showed ASPECTS score of 9.
CT perfusion showed preserved cerebral blood volume consistent with minimal if any completed infarct and 42 cc of brain volume with Tmax longer than 6 seconds, consistent with at-risk territory.
CTA confirmed left middle cerebral artery occlusion, and the patient was taken emergently to neuroangiography suite for endovascular thrombectomy.
Catheter angiography demonstrated occlusion of the M1 segment of the middle cerebral artery distal to the lenticulostriate arteries and the anterior temporal artery.
Thrombectomy was performed, and after 2 pulls there was TICI 3 restoration of cerebral blood flow. MRI conducted 4.5 hours after the procedure was negative for an infarction.
The patient’s neurologic examination also improved to an NIHSS of 5 immediately after the procedure with residual minor aphasia, dysarthria, and flattened nasolabial fold. The day following the procedure his NIHSS was 0, and he was discharged to home without requirement for rehab. With regard to secondary stroke prevention, he was discharged on dual antiplatelet therapy and statin therapy with a ziopatch to evaluate for occult AFib. Two weeks later, his ziopatch showed paroxysmal atrial fibrillation; he was switched to anticoagulation with apixaban. At the time of writing this review, he was back to golfing 18 holes every Friday.
Jason W Tarpley MD PhD
Dr. Tarpley of Pacific Neuroscience Institute Providence Southern California received consulting fees from Medtronic.See Profile
George P Teitelbaum MD
Dr. Teitelbaum of Pacific Neuroscience Institute Providence Southern California received consulting fees from Medtronic.See Profile
David S Liebeskind MD
Dr. Liebeskind of the University of California, Los Angeles, received consulting fees from Cerenovus, Genentech, Medtronic, and Stryker.See Profile
Steven R Levine MD
Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.See Profile
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