Internal Watershed Infarction Research Articles

Risk factors, clinical presentation and 1-year outcome of ischemic stroke caused by small artery disease

BackgroundThe prevalence of ischemic stroke (IS) caused by small-artery disease (SAD) is increasing recently. The present study aimed to report the risk factors, clinical presentations and outcome in patients presented with IS due to SAD with follow up for one year. The present study included 100 patients with IS due to SAD diagnosed on the basis of clinical and radiological findings. All patients were submitted to careful history taking, thorough clinical examination and standard laboratory work-up. Assessment of neurological functions was achieved using the National Institute of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS). Cognitive functions were evaluated using Trail making test, Stroop color word test, Arithmetic test, Vocabulary test, Wechsler adult intelligence scale IV digit span forward assessment and backward assessment. Magnetic resonance imaging (MRI) was done using a standard 1.5 Tesla unit. According to radiological findings, patients were classified into three groups: GI (n = 40) with IS due to SAD, GII (n = 30) with IS due to SAD plus internal watershed infarcts and GIII (n = 30) with IS due to SAD plus large artery infarctions (n = 30).ResultsComparison between the three groups regarding the reported risk factors identified significantly lower frequency of hyperlipidemia in GI patients as compared to GII and GIII patients (35.0% versus 60.0% and 66.7% respectively, p = 0.018). Clinically, it was shown that GI patients had significantly higher frequency of dizziness, dysphasia and tinnitus in comparison to the other two groups. It was also shown that those patients had significantly lower mean cortical thickness at the end of follow up (3.12 ± 0.9 versus 2.22 ± 0.8, p = 0.031). Finally, MRI brain volumetric study showed significantly decreased total cerebral cortical volume (TCCV) (589,456 ± 1689 versus 559,152 ± 1459) and total cerebral white matter volume (TCWMV) (521,546 ± 1785 versus 501,306 ± 1259) at the end of follow up.ConclusionsIschemic stroke caused by small artery disease is related to poor outcome with deterioration of cognitive functions.

Straight Sinus Thrombosis with Bilateral Internal Watershed Infarcts Mimicking Large Vessel Arterial Disease.

Straight Sinus Thrombosis with Bilateral Internal Watershed Infarcts Mimicking Large Vessel Arterial Disease.

Compressed Sensing Algorithm-Based Magnetic Resonance Imaging Guided for Prognosis of Early Neurological Deterioration after Intravenous Thrombolysis in Ischemic Stroke Patients

This work was aimed to study the risk factors and prognostic treatment for acute ischemic stroke (AIS) patients with early neurological deterioration (END) after intravenous thrombolytic therapy via compressed sensing algorithm-based magnetic resonance imaging (CS-MRI). 231 patients who were diagnosed with AIS were selected, and the final involved number of patients was 182. Patients with AIS were treated with intravenous thrombolysis with alteplase within 4.5 hours of onset. After treatment, patients with early neurological deterioration were defined as the deteriorating group and those without early neurological impairment were defined as the nondeteriorating group. In univariate analysis, hypertension, white blood cell count, and National Institutes of Health Stroke Scale (NIHSS) score were correlated with the occurrence of END. Under the CS-MRI theory, the two groups of patients were evaluated for middle cerebral artery basal ganglia infarction and internal watershed infarction. After univariate analysis, the P < 0.1 variables were taken as the independent variable, and the binary logistic regression model was adopted for multivariate regression analysis. It was disclosed that NIHSS score was not correlated with the occurrence of early neurological function deterioration, while homocysteine was. Hypertension, white blood cell count, homocysteine, and NIHSS score were risk factors for END. The image analysis revealed that the incidence of deteriorating basal ganglia infarction group was lower relative to the nondeteriorating group, and the incidence of watershed infarction was higher in the deteriorating group versus the nondeteriorating group. The image analysis suggested that predicting the occurrence of END through risk factors can actively provide endovascular treatment for patients with AIS.

Cortical and Internal Watershed Infarcts Might Be Key Signs for Predicting Neurological Deterioration in Patients with Internal Carotid Artery Occlusion with Mild Symptoms

Background: Treatment for acute ischemic stroke due to large vessel occlusion (LVO) with mild symptoms is under discussion. Although most patients have good outcomes, some patients deteriorate and have unfavorable results. Imaging findings that predict the prognosis of LVO with mild symptoms are needed to identify patients who require treatment. In this study, we focused on watershed infarctions (WSIs), because this clinical phenomenon quite sensitively reflects changes in cerebral blood flow. The purpose of this study was to assess positive rates of WSI on MRI findings in patients with internal carotid artery (ICA) occlusion, and compare WSI-positive rates between patients divided according to their clinical course. Methods: We retrospectively collected data of 1,531 patients who presented with acute ischemic stroke between June 2006 and July 2019. Among them, we chose symptomatic ICA occlusion patients with a past history of atrial fibrillation who were treated conservatively. We divided these patients into two groups, those with maintenance or improvement in their NIHSS score after hospitalization, and those whose NIHSS score worsened. We compared WSI-positive rates between these two groups. Results: Thirty-seven of the 1,531 patients were included in this study. Of them, total NIHSS score was maintained or improved in 8 patients (group A), 3 of whom (37.5%) had internal watershed infarctions (IWIs). In group B, consisting of patients whose NIHSS score worsened by >2 at 7 days from symptom onset, 24 (82.8%) had IWIs. Group A thus had statistically lower IWI positivity rates than group B (p = 0.02). Three patients (37.5%) in group A had cortical watershed infarctions (CWIs), while 27 patients in group B (93.1%) had CWIs. Group A thus had a significantly lower CWI positivity rate than group B (p = 0.002). Conclusion: In patients with mildly symptomatic ICA occlusion, CWIs and IWIs might be key signs for predicting neurological deterioration after hospitalization.

Clinical significance of common-stem lenticulostriate arteries in patients with internal watershed infarction.

A common-stem origin of lenticulostriate arteries (CS-LSAs) is an anatomical variation that supplies a moderate to large section of the basal ganglia. We hypothesized that CS-LSAs with a patent orifice are located at distal positions of the acute-occluded middle cerebral artery (MCA) and that the blood flow of CS-LSAs is supplied by pail arterial anastomoses and results in hypoperfusion of CS-LSAs, similar to a deep watershed (DWS) infarction. Our study evaluated the possibility of CS-LSAs in patients with DWS infarction and MCA occlusion and also assessed the safety of endovascular therapy (ET) in these patients. A cohort of consecutive patients with DWS infarction and MCA occlusion and in whom full recanalization via ET was achieved were identified. Patients were divided into two groups based on the presence of CS-LSAs observed during ET. In addition, radiological and clinical data were retrospectively analyzed. Thirty-three patients were included, and CS-LSAs were observed in 48.5% (16/33) of patients. The possibility (72.2%, 13/18) of CS-LSAs was high in patients with DWS infarction companied with basal ganglia infarction. A good clinical outcome was similar in patients with CS-LSAs and basal ganglia infarction and in patients without CS-LSAs and basal ganglia infarction (69.2% vs. 81.8%, P = 0.649). The possibility of CS-LSAs was 48.5% in patients with DWS infarction and MCA occlusion, and the revascularization procedure was safe and feasible in these patients despite the moderate-to-large basal ganglia infarction.

Microemboli versus hypoperfusion as an etiology of acute ischemic stroke in Egyptian patients with watershed zone infarction

BackgroundBrain perfusion is most likely to be impaired in border zone regions, and clearance of emboli will be most impaired in these regions of least blood flow. Severe occlusive disease of the internal carotid artery causes both embolization and decreased perfusion as well as some cardiac diseases that cause microembolization.ObjectivesTo differentiate between hypoperfusion and microemboli as etiology of acute ischemic stroke in watershed zone.Subject and methodsFifty patients of acute ischemic stroke in watershed zones were recruited within 7 days from stroke onset. Methods used were transcranial Doppler (TCD) monitoring for the intracranial vessels to detect microembolic signals and magnetic resonance imaging (MRI) perfusion image to detect hypoperfusion signs.ResultsWe detect embolic causes of watershed infarction (WSI) by using TCD with 61.1% sensitivity and 84.4% specificity and hypoperfusion causes of WSI by using MRI perfusion studies with 94.9% sensitivity and 54.5% specificity.ConclusionWe detected the etiology of WSI, either embolic by using TCD or hypoperfusion by using MRI perfusion. The embolic causes of WSI usually cause external or mixed WSI, and hypoperfusion causes of WSI cause internal WSI.

Arterial spin-labeling magnetic resonance imagings in the cortical and internal watershed infarctions in patients with ipsilateral internal carotid artery stenosis/occlusion

Objective: To investigate the pathophysiological mechanism for the cortical and internal watershed (WS) infarction in patients with a symptomatic internal carotid artery (ICA) stenosis/occlusion, we assessed the cerebral hemodynamic state using arterial spin-labeling (ASL) perfusion MRI with image acquisition at two post-labeling delay (PLD) times

Clinical features and the degree of cerebrovascular stenosis in different types and subtypes of cerebral watershed infarction

BackgroundWhether there are differences in pathogenesis among different types and subtypes of cerebral watershed infarction (WSI) is controversial since they have been combined into a single group in most previous studies.MethodsWe prospectively identified 340 supratentorial WSI patients at Beijing Chao-Yang Hospital, Capital Medical University, China and classified them based on diffusion-weighted imaging(DWI) templates. Baseline characteristics, clinical courses and neuroradiological features were compared among patients with different types and subtypes of WSI.ResultsWe identified 92 patients with cortical watershed infarction (CWI), 112 with internal watershed infarction (IWI) and 136 with mixed-type infarction. Compared with CWI patients, more IWI patients had critical stenosis of internal carotid artery (ICA) (P < 0.001). For the CWI group, patients with anterior watershed infarction (AWI) were more prone to critical ICA stenosis than those with posterior watershed infarction (PWI) (P = 0.011). For the IWI group, critical ICA stenosis was more prevalent in patients with partial IWI (P-IWI) than in those with confluent IWI (C-IWI) (P = 0.026). IWI patients were more frequently found to have clinical deterioration during the first 7 days of hospitalization and a poor prognosis at the 90th day than in CWI patients (P = 0.003 and P = 0.014, respectively).ConclusionsIWI, especially the P-IWI subtype, is associated with hemodynamic impairment (HDI), whereas CWI has a weaker correlation with ICA steno-occlusion. Furthermore, IWI patients are more prone to poor prognosis.

Patterns of Acute Ischemic Strokes After Carotid Endarterectomy and Therapeutic Implications.

Acute ischemic strokes following surgical treatment of carotid stenosis lead to substantial disability and mortality, and vascular mechanisms underlying their development are not fully elucidated. The goal of this study was to analyze the topographic patterns of acute ischemic stroke following carotid endarterectomy (CEA) on diffusion-weighted and perfusion-weighted magnetic resonance imaging (MRI). Data were retrospectively collected from consecutive patients who underwent CEA and developed postoperative acute ischemic stroke. Based on the MRI data sets, the lesion patterns of acute stoke were characterized. Morphology of the circle of Willis, the 3-D time-of-flight (3D-TOF) of the cerebral arteries, and status of the carotid circulation were also analyzed in order to determine the vascular mechanisms involved in stroke development. Between January 2008 and May 2015, 821 patients were treated surgically for a symptomatic or asymptomatic carotid stenosis at the University Hospital of Nice. Nineteen (2.3%) patients had an acute ischemic stroke after surgery. Among them, 11 (57.9%) patients had a territorial infarction and 8 (42.1%) patients had an internal watershed infarction, cortical watershed infarction, or mixed border zone infarction. According to imaging data sets, embolic mechanism of stroke was reported for 12 (63.2%) patients, hemodynamic mechanism for 2 (10.5%) patients, and mixed mechanism for 5 (26.3%) patients. An asymmetry on 3D-TOF was observed in 60% and 50% of patients with hemodynamic and mixed stroke and in 25% of patients with embolic stroke. The latter 2 patients with embolic stroke underwent successful mechanical thrombectomy using stent-retriever devices. In this cohort, embolic mechanism leading to postoperative stroke was more frequently observed than hemodynamic mechanism. Immediate characterization of the cerebral lesion by postoperative brain MRI is of utmost importance because it may rapidly identify patients eligible for treatments such as mechanical thrombectomy.

The Pathophysiology of Watershed Infarction: A Three-Dimensional Time-of-Flight Magnetic Resonance Angiography Study

Most of the time, watershed infarcts (WIs) involve steno-occlusive carotid disease. The pathophysiological mechanism could be predicted by their pattern: internal WIs (IWIs) are thought to be due to hemodynamic impairment in contrast to cortical WIs (CWIs), which are more likely to be caused by microembolic phenomena. We used a 3D time-of-flight (TOF) magnetic resonance angiography (MRA) study to assess this hypothesis. In 45 consecutive patients with a recent WI and ipsilateral cervical carotid stenosis, clinical and radiological data were obtained retrospectively. 3D TOF MRA were analyzed both qualitatively and quantitatively (internal carotid and anterior, middle and posterior cerebral arteries). Then, 2 groups were determined depending on their radiological patterns: WIs with (IWI+) or without (IWI-) an internal watershed. Thirty-two of the 45 patients (71%) had IWIs that were or were not associated with CWIs (IWI+), while 13 patients (29%) had only CWIs (IWI-). There was no significant relationship between the radiological pattern and the demographic data, the cardiovascular risk factors, or the degree of stenosis. However, IWI+ patients more frequently had motor weakness (P = .03) than CWI patients. An ipsilateral reduced middle cerebral artery intensity on 3D TOF MRA in both qualitative and quantitative analyses was significantly associated with IWI+. Instead within IWI-, no significantly reduced signal intensity was found. These findings originally support the view that IWIs are mainly caused by a hemodynamic impairment related to carotid stenosis, whereas CWIs are mostly due to a microembolic mechanism. 3D TOF MRA, which gives pertinent information on pathophysiology on IWIs, can help in decision making.

Etiologic Subtypes of Watershed Infarcts

Two types of watershed infarcts (WI) are recognized. Internal WI are usually attributed to either severe stenosis in large arteries or acute hypotensive events, whereas external WI are thought to be caused by embolism. The aim of this study was to determine the etiologic background and prognosis of external and internal WI in our patients. We reviewed the medical records and diffusion-weighted images of the patients who were admitted to our stroke unit with acute ischemic stroke between January 2012 and November 2014. The demographics, clinical features, radiologic investigations, and other etiologic tests of the patients with internal or external WI were recorded. We determined etiologic stroke subtypes according to the automated Causative Classification System. Fifty-three patients with WI were detected in our registry. Twenty-two (41.5%) of them were women. The mean age was 69 ± 12.8 (33-98) years. Twenty-one (39.6%) patients had external WI: 7 (33.3%) of them had large-artery atherosclerosis (LAA), 8 (38.1%) patients had cardioembolism, 3 (14.3%) patients had stroke due to other causes (vasculitis; n = 3), and etiologic subtype was undetermined in 3 patients (14.3%). Thirty-two (60.4%) patients had internal WI: 21 (65.6.%) of them had LAA, 5 (15.6%) patients had cardioembolism, 3 (9.4%) patients had stroke due to other causes (aneurysm; n = 1, hypercoagulability due to chronic myeloid leukemia; n = 1, vasculitis; n = 1), and etiologic subtype of 3 (9.4%) patients remained cryptogenic. LAA was significantly associated with internal WI (P = .024). Hypertension was more common in patients with internal WI (P = .035). In this series, cardioembolism was the most common etiologic subtype in the patients with external WI, whereas internal WI were significantly associated with LAA. Uncommon causes should also be investigated in cryptogenic patients.

基于穿支动脉-神经组织单元论分水岭脑梗死分型及脑白质疏松的形成

At present, there is still controversy in the etiology and pathogenesis of cerebral watershed infarction (CWI). The classification of watershed infarction is also confusing. Great changes have taken place in the knowledge of CWI with the development of the medical and imaging technology. Based on the concept of the perforating artery-neural tissue units, the innovative speculation on the relation among leukoaraiosis (LA) (belong to white matter lesions), CWI and the mechanism of the perforating artery infarction formation was proposed in this paper. Based on the combination possibility of different perforating artery-neural tissue units, the CWI was classified as lateral watershed infarction (anterior cortical and posterior cortical watershed infarction), internal watershed infarction (anterior and interior type, posterior and interior type and interior type) and deep watershed infarction (deep anterior type, deep posterior type and the various subtypes). This paper suggests that LA might be caused by chronic watershed cerebral ischemia change, and perforating artery infarction and CWI are the same strain. This inference may help us to understand the relation among the mechanisms of the perforating artery infarction, CWI and LA.

Abstract W MP67: Etiology-Specific Clinical and Imaging Features in Ischemic Stroke

Background: Identification of clinical and imaging characteristics of ischemic stroke that can predict the underlying etiology is critical for accurate stroke subtyping. We sought to investigate the relationship between stroke characteristics and stroke etiology in 7,591 patients in the NINDS Stroke Genetics Network Study. Methods: We determined the probability of having a major etiology in the presence of certain stroke characteristics that were previously linked to specific stroke mechanisms. We excluded patients with multiple competing major etiologies. All patients had brain imaging, intra- and extra-cranial vascular imaging, and complete cardiac assessment. We defined major etiologies according to the Causative Classification of Stroke System Criteria without reference to the stroke characteristics under study. Results: History of 1 ipsilateral ischemic events within the last month, the presence of internal watershed infarcts or multiple, ipsilateral, unilateral, and temporally separate infarcts were associated with large artery atherosclerosis (Table). Multiple acute infarcts in different cerebral circulations were more common in patients with major cardiac source of embolism as well as in those with uncommon/cryptogenic causes. Stereotypic lacunar TIAs within the last week and lacunar syndrome were associated with lacunar infarction Discussion: Clinical and imaging stroke characteristics appear to predict stroke etiologies. This information may find utility in developing algorithms for a guided stroke evaluation as well as help identify the most likely causative etiology in the presence of multiple competing etiologies.

Watershed infarcts in a multiple microembolic model of monkey

It has long been debated whether watershed infarcts are caused by hemodynamic or embolic mechanisms. In the present study, we investigated microembolic roles in the pathogenesis of watershed infarcts by examining MRI in a macaque monkey model of multiple microinfarcts. 50μm microbeads were injected into each internal carotid artery twice with a month interval. Monkeys (n=4) injected with 2250–2800 microbeads per unilateral side showed both cortical and internal watershed infarcts in the acute phase and atrophic changes with microbleeds in the chronic phase. These results suggest embolic pathogenesis can contribute to the genesis of both cortical and internal watershed infarcts in primates.

Clinical and neuroradiological features of internal watershed infarction and the occlusive diseases of carotid artery system

Background: To describe the clinical and neuroradiological features of internal watershed (IWS) infarction and to analyze the relationship between IWS infarction and occlusive diseases of carotid artery system.Methods: We identified 27 IWS infarction patients with diffusion-weighted magnetic resonance imaging by commonly used templates within 10 days after the onset. Patients with potential cardiac sources of embolism were excluded. Occlusive diseases of carotid arteries were assessed by magnetic resonance angiography or digital subtraction angiography. Baseline characteristics, clinical course, prognosis, neuroradiological features and symptomatic arteries were analyzed.Results: Two patterns were identified: 14 patients had confluent IWS (C-IWS) infarction, and 13 patients had partial IWS (P-IWS) infarction. Twelve patients in C-IWS group and 10 patients in P-IWS group had severe stenosis (>70%) or occlusion in either the internal carotid artery (ICA) or middle cerebral artery (MCA). Occlusive diseases of ICA and non-lacunar syndrome were more prevalent in C-IWS group, while occlusive diseases of MCA and lacunar syndrome were more prevalent in P-IWS group. Concomitant small cortical lesions ipsilateral to IWS infarcts were more common in C-IWS group than in P-IWS group, and were significantly associated with ICA diseases. Clinical deterioration during the first seven days after admission and poor outcome assessed by the Modified Rankin Score 3 months after stroke were more prevalent in C-IWS group than in P-IWS group.Conclusions: There is a relatively definite relationship between IWS infarction and occlusive diseases of carotid arteries. The distribution of symptomatic arteries (ICA or MCA) in C-IWS group is significantly different from that in P-IWS group. Both hypoperfusion and microembolism are probable mechanisms. There may be some differences in their roles in pathogenesis of C-IWS and P-IWS infarction. Microembolism may contribute C-IWS infarction in addition to hypoperfusion, which is the major pathogenesis of P-IWS infarction.

Cerebral misery perfusion diagnosed using hypercapnic blood-oxygenation-level-dependent contrast functional magnetic resonance imaging: a case report

IntroductionCerebral misery perfusion represents a failure of cerebral autoregulation. It is an important differential diagnosis in post-stroke patients presenting with collapses in the presence of haemodynamically significant cerebrovascular stenosis. This is particularly the case when cortical or internal watershed infarcts are present. When this condition occurs, further investigation should be done immediately.Case presentationA 50-year-old Caucasian man presented with a stroke secondary to complete occlusion of his left internal carotid artery. He went on to suffer recurrent seizures. Neuroimaging demonstrated numerous new watershed-territory cerebral infarcts. No source of arterial thromboembolism was demonstrable. Hypercapnic blood-oxygenation-level-dependent-contrast functional magnetic resonance imaging was used to measure his cerebrovascular reserve capacity. The findings were suggestive of cerebral misery perfusion.ConclusionsBlood-oxygenation-level-dependent-contrast functional magnetic resonance imaging allows the inference of cerebral misery perfusion. This procedure is cheaper and more readily available than positron emission tomography imaging, which is the current gold standard diagnostic test. The most evaluated treatment for cerebral misery perfusion is extracranial-intracranial bypass. Although previous trials of this have been unfavourable, the results of new studies involving extracranial-intracranial bypass in high-risk patients identified during cerebral perfusion imaging are awaited.Cerebral misery perfusion is an important and under-recognized condition in which emerging imaging and treatment modalities present the possibility of practical and evidence-based management in the near future. Physicians should thus be aware of this disorder and of recent developments in diagnostic tests that allow its detection.

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

In carotid disease, infarcts can occur in the cortical as well as internal watershed (WS), or both. Better understanding the pathophysiology of WS infarcts would guide treatment. Two distinct hypotheses, namely low-flow and micro-embolism, are equally supported by neuropathological and physiological studies. Here we review the evidence regarding the mechanisms for WS stroke in carotid disease and whether they differ between cortical and internal WS infarcts. After a brief account of the anatomy of the WS and the cerebrovascular physiology in circumstances of low perfusion pressure, the literature concerning the mechanisms of WS infarction in carotid disease is reviewed and discussed with emphasis on imaging and ultrasound studies of the cerebral hemodynamics. The evidence strongly favors a hemodynamic mechanism for internal WS infarction, especially regarding the so-called rosary-like pattern in the centrum semiovale. However, the relationships between cortical WS infarction and hemodynamic compromise appear more complicated. Thus, although severe hemodynamic compromise appears to underlie combined cortical and internal WS infarction, artery-to-artery embolism may play an important role in isolated cortical WS infarcts. Based on the high prevalence of microembolic signals documented by ultrasound in symptomatic carotid disease, a recent hypothesis postulates that embolism and hypoperfusion play a synergetic role, according to which small embolic material prone to lodge in distal field arterioles would be more likely to result in cortical micro-infarcts when chronic hypoperfusion prevails. Future studies combining imaging of brain perfusion, diffusion-weighted imaging, and ultrasound detection of microembolic signals should help resolve these issues.

White Matter Medullary Infarcts: Acute Subcortical Infarction in the Centrum ovale

Acute infarction confined to the territory of the white matter medullary arteries is a poorly characterised acute stroke subtype. 22 patients with infarction confined to this vascular territory on CT and/or MRI were identified from a series of 1,800 consecutive admissions to our stroke unit (1.2%) between August 1993 and March 1997. 19 patients had small infarcts (<1.5 cm maximum diameter) and 3 large infarcts (>1.5 cm). Small infarcts were associated with a history of smoking (69%), hypertension (58%), and hyperlipidaemia (37%), and less frequently with atrial fibrillation (21%). Significant (>50%) ipsilateral carotid stenosis (16%) was a less frequent finding in this group. Patients most commonly presented with weakness and/or sensory disturbance affecting mainly the upper limbs, but dysarthria, dysphasia, and ataxia were also seen. Large infarcts were infrequent in our series, but did not differ significantly from small infarcts with respect to clinical presentation or risk factor profiles (p > 0.05 for all comparisons). The majority of symptomatic patients with white matter medullary infarcts are associated with small (<1.5 cm diameter) lesions and a risk factor profile consistent with small vessel disease. More data are required to elucidate the mechanism of larger (>1.5 cm) infarcts. Because of the potential overlap between white matter medullary infarcts and internal watershed infarcts, suggested criteria for each are presented.

American Heart Association Prevention Conference. IV. Prevention and Rehabilitation of Stroke. Etiology of stroke.

The diagnosis of arterial stroke differentiates ischemia from hemorrhage. The former may be due to arterial occlusion or stenosis, the latter to leakage or rupture of an artery. Computed tomography (CT) and magnetic resonance imaging (MRI) have shown that this basic differentiation cannot be reliably made from the history and clinical examination alone. Of the clinical stroke syndromes, only Wallenberg’s syndrome has not been reported to be due to hemorrhage. When CT or MRI is not available for diagnosis, spinal tap is reliably positive only when the aneurysm or arteriovenous malformation has ruptured into the subarachnoid space; the results are often normal when a small hemorrhage occurs in the parenchyma. For some therapies, notably neuroprotective agents, the potential benefits for ischemia do not seem to be offset by potential harm in the case of hemorrhage. However, because fibrinolytics, antithrombotic agents, or surgery are treatment options, diagnostic certainty is essential to avoid harming the patient. Most—but not all—strokes have a sudden or rapidly evolving onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually presumed due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype (embolism, thrombosis, decreased perfusion or “lacunar” infarction, leakage, or rupture) evades the best clinical skills. The classification of stroke mechanism depends on the presence of risk factors for stroke (preexisting condition or circumstance epidemiologically related to stroke) and etiologies (disease directly causing the mechanism) that implicate the cause of stroke in a given patient. However, more than one risk factor and etiology are frequently present in the same patient and may be related …

Clinical features, pathogenesis, and computed tomographic characteristics of internal watershed infarction.

Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction. Eighteen consecutive stroke patients with evidence of internal watershed infarction on computed tomography (CT) were studied. Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P < .001), cardiac disease (P < .01), and diabetes mellitus (P < .01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole. Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.