Acute Cortical Infarction Research Articles

Imaging features for the identification of atrial fibrillation in cryptogenic stroke patients

BackgroundWhether specific imaging aspects can be used to identify cryptogenic stroke (CS) patients with high risk of underlying atrial fibrillation (AF) remains unclear. The purpose of this study was to evaluate brain-imaging features in CS patients and their utility as AF predictors.MethodsThe Nordic Atrial Fibrillation and Stroke study was a prospective observational study of CS and transient ischemic attack patients undergoing 12-month cardiac-rhythm monitoring, biomarker and clinical assessments. In this imaging sub-study, brain magnetic resonance imaging and computed tomography scans from 106 patients were assessed for acute and chronic ischemic lesions in relation to AF occurrence and included in a score to predict AF. Receiver operating characteristics (ROC) curve was used to evaluate the discriminative ability of the score and for its dichotomization for predictive model.ResultsAge, periventricular white-matter hyperintensities (PVWMH), acute lesion size, and vessel occlusion were significantly associated with AF. Acute and chronic cortical infarcts as well as chronic cerebellar infarcts were numerically more frequent in the AF group than the non-AF group. A score consisting of six features (0–6 points) was proposed (age ≥ 65 years, chronic cortical or cerebellar lesions, acute cortical lesions, PVWMH ≥ 2 in Fazekas scale, vessel occlusion, and acute lesion size ≥ 10 mm). Area under ROC curve was 0.735 and a score of ≥ 3 points was a predictor of AF.ConclusionsThe suggested score was shown to identify CS patients with an increased risk of underlying AF.

Acute Onset Rhythmic Tremor in Acute Frontal Cortical Infarction: A Case Report (P5-5.023)

Acute Onset Rhythmic Tremor in Acute Frontal Cortical Infarction: A Case Report (P5-5.023)

Abstract 103: Acute Onset Rhythmic Tremor In Acute Frontal Cortical Infarction: A Case Report

Introduction Acute ischemic stroke varies in presentation, and it is crucial to quickly identify patients presenting with stroke for timely intervention. Secondary movement disorders occurring after a delayed period following ischemic stroke have been well‐documented, though rare. Holmes tremor specifically has been described as a delayed result of ischemic infarction involving subcortical structures such as mollaret triangle, thalamus, and basal ganglia. However, it is novel for frontal cortical infarcts to present with acute‐onset contralateral limb tremor, especially as an isolated symptom. Our case suggests a “secondary insult” involving the frontal cortex can disinhibit the motor pathway that leads to tremor in preexisting midbrain and thalamic lesions. We present a 67‐year‐old male with acute onset, constant, rhythmic tremor in the setting of acute ischemic frontal cortical infarction. Methods n/a, case report Results A 67‐year‐old male with medical history of pineal gland cyst status‐post shunt placement and hypertension who presented for evaluation of acute onset right upper extremity rhythmic tremor that started 24 hours prior. He did not have any associated weakness, numbness, vision changes, nausea, or vomiting. He had never had this tremor before. Neurologic examination was significant for a 4.0 Hz rhythmic resting tremor that was present throughout exam and was non‐distractible. This tremor remained consistent even with kinetic movements and postures. Electroencephalogram (EEG) was performed STAT during this tremor and was not based in seizure. Non‐contrast head computerized tomography (CT) was negative for any acute hemorrhage or intracranial pathology. CT angiogram head and neck showed left internal carotid artery (ICA) long segment tapered occlusion from the proximal cervical ICA to the distal petrous segment, likely dissection of undetermined chronicity. Magnetic resonance imaging (MRI) Brain with and without contrast was significant for acute punctate foci involving the precentral cortex of the left frontal lobe consistent with acute ischemic infarction. Encephalomalacia was also present involving the bilateral posterior thalami and left midbrain chronic ischemic infarctions. This suggests the tremor was caused by disinhibition of the motor pathway from the ischemic insult to the frontal cortex, as he had pre‐existing asymptomatic ischemic insult to the typical structures known to cause this tremor. He was outside of the Tenecteplase window and was given a load of Aspirin followed by aspirin 81 mg daily. He was trialed on propranolol for treatment of symptomatic tremor however this was discontinued before discharge as it was ineffective and patient preferred to hold off on other treatments. He is now awaiting outpatient Neurology follow up. Conclusion This case suggests that acute onset Holmes tremor can be the sole presenting sign in acute ischemic frontal cortical infarction. The pre‐existing asymptomatic infarctions in the midbrain and thalamus also support that a “second hit” located in the frontal cortex can disinhibit the motor pathway between the cortex and rubral tract. This is important as Holmes tremor is more commonly known to be from a mechanism of damage to the red nucleus or thalamic structures in a delayed manner, typically at least two weeks after stroke. This knowledge will help identify rare strokes in a timely manner.

Abstract 093: Carotid Stump Syndrome: an Insidious Source of Recurrent Ischemic Strokes

Introduction Carotid stump syndrome (CSS) is a paradoxical phenomenon that occurs when there are repeated ischemic events in the carotid vascular territory despite demonstrated occlusion of the ipsilateral internal carotid artery (ICA). It is thought to be caused by turbulent blood flow in the patent stump of the occluded ICA creating microemboli which reach the brain through anastomotic channels and retrograde flow. We present a case of recurrent infarctions in setting of known ipsilateral ICA occlusion, who was diagnosed with carotid stump syndrome. Methods A male veteran in his 60s with a medical history of DVTs on apixaban, PVD, and ischemic stroke with residual right‐sided weakness, presented with worsening right‐sided weakness and difficulty with ambulation. Two months prior to the presentation he was diagnosed with acute infarcts in left frontal, parietal, and temporal lobes due to thromboembolism from left ICA occlusion. On presentation his neurological exam revealed right‐sided hemiparesis. MRI brain showed multiple acute and chronic cortical and subcortical infarcts in the left frontotemporoparietal lobes and lack of flow void in the left distal ICA. To further evaluate the dynamics of blood flow patient underwent a cerebral angiogram which confirmed the diagnosis of complete occlusion of left ICA and demonstrated reconstitution of the intracranial ICA through retrograde filling via the ophthalmic artery and anastomotic branches with the internal maxillary artery (IMax). For secondary prevention he was started on statin and aspirin while his home Apixaban was continued. Surgical and endovascular treatment approaches were discussed but the patient declined any intervention. In his four months follow up clinic visit he had no further concerns of recurrent strokes or new symptoms. Results Carotid stump syndrome is a rare cause of cerebral and retinal ischemia; however, it must be considered in patients with recurrent ischemic strokes and chronic ipsilateral ICA occlusion. Due to the patent proximal, or perhaps in some cases distal, carotid stump, there’s turbulent flow and hence the thrombus formation can occur. Hemodynamic and embolic factors attribute towards the microembolization from the proximal carotid stump through the external carotid artery (ECA), into the facial artery and IMax and their distal branches which anastomose with the ophthalmic artery, causing the emboli to end up in the major branches of the carotid terminus. If a distal stump is symptomatic, then the microemboli can readily end up in the distal ICA branches. In addition to medical management with DAPT or anticoagulation and high intensity statin, our literature review supports endovascular or surgical interventions due to reportedly good outcomes. Interventional approaches may include ECA‐ICA stenting with a covered stent or stent‐assisted coil embolization of the proximal stump. Surgical procedures include an endarterectomy on the ipsilateral ECA or contralateral ICA to increase collateral circulation. ECA‐ICA bypass is another option. Conclusion Carotid stump syndrome is a rare and underrecognized cause of recurrent ischemic strokes, though it is a potentially treatable entity. The therapeutic goals include medical management along with endovascular or surgical treatment whenever possible.

298 An atypical presentation of Creutzfeldt-Jakob Disease as a stroke mimic—experience from an Irish tertiary centre

Abstract Background Sporadic Creutzfeldt-Jakob Disease (sCJD) is a rare neurodegenerative prion disease that presents with symptoms of rapid neuropsychiatric decline including dementia, behavioural abnormalities and loss of higher cortical function. Patients commonly present with rapidly-progressive neuromotor symptoms such as ataxia and myoclonus. Very few cases of CJD have been reported in which the patient initially presents with stroke symptoms such as hemiparesis as their primary presenting symptom. We present a case of a 56 year old male who initially presented to the stroke unit with waxing and waning left sided weakness and a non-corresponding ipsilateral left-sided acute parietal infarct on diffusion-weighted MRI. Over four weeks, his condition progressively worsened with declining cognitive function, motor dysfunction, sphincter dysfunction and eventual death. Methods Methods used to confirm the suspected diagnosis included: (1) Periodic sharp wave complexes are the most classical EEG finding for CJD and are seen in two third of the patients diagnosed with sporadic CJD, (2) The presence of the 14–3-3 protein in CSF has been found to be a sensitive and specific marker for sporadic CJD, (3) Neuroimaging plays a vital role in the diagnosis of CJD including serial MRIs and EEG sufficient to exclude other differential diagnoses. Results MRI brain revealed an acute cortical infarct within left parietal lobe measuring 3 mm.A n EEG demonstrated periodic sharp wave complexes occurring maximally in the left centro-temporal region. EEG finding was suggestive of a diagnosis of a prion disease. CJD Surveillance Unit confirmed the cerebrospinal fluid analysis was positive for RT-QuIC indicating sporadic CJD. Conclusion In cases of patients presenting with clinical signs and symptoms of a stroke with subsequent ipsilateral neurological findings on MRI, CJD should be included as a differential diagnosis. Additionally, a lumbar puncture, not routinely recommended in stroke patients, should be performed early to aid in early detection of CJD in order to confirm diagnosis and optimise the ceiling of care.

S3593 Eosinophilic Gastritis in Idiopathic Hypereosinophilic Syndrome: A Case Report

Introduction: Idiopathic hypereosinophilic syndrome (IHES) is a group of myeloproliferative disorders causing multi-organ dysfunction with unknown etiology. We report a case of IHES in a patient presenting with gastric wall thickening, multiple organ damage including acute coronary syndrome, encephalopathy, and multiple cortical infarcts. Case Description/Methods: A 47-year-old male patient with past medical history significant for type 2 diabetes mellitus and hypertension presented with nausea, vomiting, abdominal pain, and food intolerance for 7 days. He also complained of intermittent, substernal chest pain for 1-2 days at presentation. His labs were significant for elevated troponin of serum creatinine of 2.85mg/dL and significant leukocytosis (32.80 10^3/cmm). Absolute eosinophilic count was elevated at 14.70 10^3/cmm. Echocardiogram showed hypokinetic mid inferior and inferolateral walls. CT chest/abdomen angiogram was done for concerns of dissection. It showed diffuse gastric wall thickening with upper abdominal retroperitoneal lymphadenopathy and extensive retroperitoneal fat stranding. He was started on antiplatelet agent and heparin drip. Ischemic workup was deferred as troponin plateaued and patient had new-onset altered mental status. MRI brain showed numerous punctate cortical and subcortical foci of restricted diffusion consistent with acute watershed distribution infarcts. In view of possible need for dual anti-platelet therapy and the high concern for gastric malignancy on CT that required tissue biopsy, gastroenterology was consulted for esophagogastroduodenoscopy (EGD). It did not show any gastric mass but diffuse gastritis. Biopsy showed mild chronic gastritis and a focal area showing increased eosinophilic infiltration with eosinophilic cryptitis (Figure). An extensive workup for eosinophilia including infectious etiology returned negative. No secondary causes of hypereosinophilia were identified. Patient was started on 1mg/kg of prednisone with normalization of eosinophils to 0 within 24 hours. Steroids were tapered and patient improved clinically with resolution of altered mental status, abdominal pain, and chest pain. Follow-up EGD has been scheduled to re-evaluate eosinophilic deposits. Discussion: The stomach biopsy showing eosinophilia was the key to diagnosis. Resolution of peripheral eosinophilia with steroids confirms the diagnosis in the absence of a secondary cause. A repeat EGD with biopsy is scheduled to look for histopathological resolution.Figure 1.: Gastric mucosa with increased eosinophilic infiltration within the lamina propria and focal glandular involvement with eosinophils.

Wallerian degeneration in experimental focal cortical ischemia

Wallerian degeneration (WaD), commonly secondary to cerebral infarction, is the descending damage of fiber tracts with their accompanying myelin sheaths. However, whether this sequential injury can occur in non-ischemic corpus callosum (CC) and striatum in focal cortical ischemic model has not been fully demonstrated. The present study aimed to elucidate detailed histopathologic changes in CC and striatum after acute focal cortical infarction induced by permanent distal middle cerebral artery occlusion (dMCAO) in Sprague–Dawley rat. We found that myelin integrity, myelin-related proteins, MBP and MAG, and NF200-marked neurofilaments were all compromised in non-ischemic white matter regions, bilateral CC and ipsilateral striatum, along with cortical ischemia (all P < 0.05). Electron microscopy showed wide gaps between myelin sheath layers or between axon and myelin, with an abnormal folding of myelin sheath, and enlarged fluid-filled areas. APP accumulations were noted at 24 h post-dMCAO in those non-ischemic regions, and the deposition prolonged until 14 days after cortical ischemia (all P < 0.05). Moreover, in these areas, microglia and astrocytes were robustly and persistently activated in different patterns. No substantial changes were observed in contralateral striatum. In conclusion, our results suggest that WaD may be involved in non-ischemic CC and striatum after focal cortical infarction, accompanied by APP aggregation and neuroglia initiation forming the glial scar.

Is isolated hand weakness associated with subtypes of stroke?

Isolated hand weakness is an uncommon condition in stroke patients. It is frequently confused with peripheral nerve system (PNS) pathologies; misdiagnosis may delay identification of the etiology and treatment of stroke. Herein, we aimed to underline the necessity of keeping the diagnosis of stroke in mind in case of patients with isolated hand weakness and to assess the etiology of stroke. A total of eight patients (four females and four males), who are presented with isolated hand weakness and had acute cortical infarction documented via cranial MRI, were enrolled in the study. Demographic characteristics, physical and radiological findings of the patients, as well as the lateralization and etiology of infarction were evaluated. The mean age of the patients was 61.8 ± 12 years. Isolated hand weakness was in the dominant hand in four patients. According to the etiology and clinical signs, the stroke was cardioembolic in three patients and they had predominant radial-side (thumb and index) finger weakness. Large vessel atherosclerosis was present in three patients; two patients with predominant ulnar-side (little and ring) finger weakness and one patient with uniform finger weakness; there were two patients with stroke of undetermined etiology and they had uniform finger weakness. Keeping stroke in mind together with PNS pathologies in case of isolated hand weakness is critical for early diagnosis and treatment of the patients. In addition, cardioembolic focus should be considered in case of predominant radial-side finger weakness, whereas particular attention should be paid to carotid artery diseases in case of predominant ulnar-side finger weakness.

Clinical and radiological risk factors for poststroke epilepsy in childhood

BackgroundThere are few studies evaluating risk factors for poststroke epilepsy (PSE) after an arterial ischemic stroke (AIS) in childhood. This study aimed to evaluate clinical and radiological predictors for PSE in a cohort of children with a first-ever AIS. MethodsA retrospective analysis of a single-center prospective consecutive cohort of children beyond neonatal age with a first-ever AIS admitted at the Pontifical Catholic University of Chile's Clinical Hospital between 2003 and 2013. All participants had a brain magnetic resonance imaging at the time of diagnosis. All children underwent follow-up for at least three years with an annual clinical evaluation. We used the current epilepsy definition of the International League Against Epilepsy. Studied variables include demographics, clinical manifestations at onset, stroke risk factors, and radiological characteristics of AIS. Cox proportional hazards regression analysis was used to evaluate PSE risk adjusted for clinical and radiological variables. ResultsAmong 98 children who met the study criteria, 41 (41.8%) with PSE. Following multivariate analysis, it was determined that the predictors of PSE include young age at AIS (hazard ratio [HR] = 0.91; confidence interval [CI] = 0.84–0.99), the occurrence of acute symptomatic seizures (HR = 3.29; CI = 1.35–8.01), cortical infarction (HR = 5.01; CI = 2.00–12.6), and multifocal infarction (HR = 3.27; CI = 1.01–10.8). ConclusionSeizures, young age, cortical lesions, and multiple infarction at the time of stroke are independent risk factors for PSE in children following a first-ever AIS.

Characterization of Patients with Embolic Strokes of Undetermined Source in the NAVIGATE ESUS Randomized Trial

The New Approach Rivaroxaban Inhibition of Factor Xa in a Global Trial vs. ASA to Prevent Embolism in Embolic Stroke of Undetermined Source (NAVIGATE-ESUS) trial is a randomized phase-III trial comparing rivaroxaban versus aspirin in patients with recent ESUS. We aimed to describe the baseline characteristics of this large ESUS cohort to explore relationships among key subgroups. We enrolled 7213 patients at 459 sites in 31 countries. Prespecified subgroups for primary safety and efficacy analyses included age, sex, race, global region, stroke or transient ischemic attack prior to qualifying event, time to randomization, hypertension, and diabetes mellitus. Mean age was 66.9 ± 9.8 years; 24% were under 60 years. Older patients had more hypertension, coronary disease, and cancer. Strokes in older subjects were more frequently cortical and accompanied by radiographic evidence of prior infarction. Women comprised 38% of participants and were older than men. Patients from East Asia were oldest whereas those from Latin America were youngest. Patients in the Americas more frequently were on aspirin prior to the qualifying stroke. Acute cortical infarction was more common in the United States, Canada, and Western Europe, whereas prior radiographic infarctions were most common in East Asia. Approximately forty-five percent of subjects were enrolled within 30 days of the qualifying stroke, with earliest enrollments in Asia and Eastern Europe. NAVIGATE-ESUS is the largest randomized trial comparing antithrombotic strategies for secondary stroke prevention in patients with ESUS. The study population encompasses a broad array of patients across multiple continents and these subgroups provide ample opportunities for future research.

RISK FACTOR PROFILES PREDICTING DELAYED VASCULAR COGNITIVE IMPAIRMENT IN YOUNG AND OLD ISCHEMIC STROKE SURVIVORS

Vascular cognitive impairment (VCI) can affect both young (<60 years old at onset) and old ischemic stroke survivors. Elucidating the specific risk profiles for delayed VCI in young and old patients will be useful in risk stratification and intervention with pharmacological and non-pharmacological measures. 854 ischemic stroke survivors from Singapore and Hong Kong with no pre-stroke decline were studied. Risk factor and MRI data from time of stroke was collected. Subjects were reviewed at 6 months post-stroke for cognitive assessment. A subcohort of 637 subjects was additionally reviewed 18 months post-stroke. Prevalence of VCI at both time-points was compared between old and young subjects. Stepwise logistic regression models predicting VCI and 6 months and 18 months for old and young subjects were used to describe specific risk profiles. 206 subjects (24.12%) were <60 years old at time of stroke. Overall prevalence of VCI was 44.6% at 6 months, and 49.3% at 18 months. Older subjects had less education and more risk factors, such as hypertension, prior stroke, atrial fibrillation, cortical atrophy, white matter hyperintensities, and chronic lacunes. VCI at 6 months was 18.9% for young subjects and 52.8% for old subjects.[Table 1] Increase of VCI between 6 months and 18 months was greater among the older stroke subjects (51.2% to 56.8%) as seen in the follow-up subcohort.[Figure 1] Education and chronic lacunes were significant predictors of VCI at both time-points for young subjects. Age, education, diabetes mellitus, and chronic lacunes were significant predictors for VCI for older subjects, with acute cortical large infarcts being an additional risk factor only at 6 months.[Table 2]. Older stroke survivors have a greater prevalence of VCI and continue to have higher increase in prevalence from months 6 to months 18 compared to younger patients. Low education and burden of chronic lacunes are common risk factors for VCI at all age and chronicity levels. Acute infarct characteristics are salient only for VCI in older subjects at months 6, but not for VCI at month 18. Chronic risk factors, not acute, are more predictive of long-term cognitive status in ischemic stroke survivors. Prevalence of VCI in young and old stroke survivors at 6 months and 18 months post-stroke in the follow-up subcohort

The cause of the stroke: a diagnostic uncertainty

A 39-year-old man with a history of sickle cell disease (SCD) presented with left leg weakness. He had a normal CT head and CT angiogram, but MRI head showed multiple...

Isolated Unilateral Hand Weakness Due to Cortical Cerebral Ischemia

Isolated hand weakness is a relatively common clinical presentation. The differential diagnoses include peripheral and central neurological lesions. This is a report of sudden onset, pure hand weakness, without any other neurological signs or symptoms in the setting of a prolonged hospital stay for bilateral diabetic foot ulceration. A cerebral magnetic resonance image identified an “inverted omega sign” along the right precentral gyrus and paracentral lobule, consistent with an area of acute cortical infarction. Patients with acute pure hand weakness, and risk factors for cerebral vascular disease, should be carefully evaluated for a cortical lesion in addition to the routine peripheral neurologic workup.

Thumb Tremor in Acute Cortical Infarct.

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Cognitive Impairment after Mild Stroke: Development and Validation of the SIGNAL2 Risk Score.

Post stroke cognitive impairment (PSCI), an important complication of strokes, has numerous risk factors. A scale adequately classifying risk of cognitive impairment 3-6 months after mild stroke will be useful for clinicians. To develop a risk score based on clinical and neuroimaging variables that will be useful in identifying mild ischemic stroke patients at high risk for PSCI. The risk score development cohort comprised of a retrospective dataset of 209 mild stroke patients with MRI confirmed infarcts, without pre-stroke cognitive impairment, and evaluated within 6 months post-stroke for PSCI. Logistic regression identified factors predictive of PSCI and a risk score was developed based on regression coefficients. The risk score was checked for stability using 10-fold cross-validation and validated in an independent prospective cohort of 185 ischemic mild stroke patients. Within 6 months post-stroke, 37.32% developed PSCI in the retrospective dataset. A 15-point risk score based on age, education, acute cortical infarcts, white matter hyperintensity, chronic lacunes, global cortical atrophy, and intracranial large vessel stenosis was highly predictive of PSCI with an AUC of 0.829. 10.11% with low scores, 52.69% with moderate scores, and 74.07% with high scores developed PSCI. In the prospective validation cohort, the model had an AUC of 0.776, and exhibited similar accuracy and stability statistics at both 6 and 12 months. The seven item risk score adequately identified mild stroke patients who are at an increased risk of developing PSCI.

Tongue Tremor in Acute Cortical Infarct.

Tongue Tremor in Acute Cortical Infarct.

Carotid Stump as a Cause of Recurrent Embolism-Endovascular Treatment in a Case of Congenital Carotid Stump Syndrome.

Dear Sir: Cryptogenic stroke, a stroke for which there is no specific attributable cause after a comprehensive evaluation for the most common causes, accounts for about one-fourth of stroke patients. Most cryptogenic strokes are thromboembolic and occur more frequently in younger patients. There have been efforts to detect paradoxical embolism in patients with cryptogenic embolic stroke because chronic anticoagulation can effectively prevent recurrent stroke in these patients. However, other causes may also cause cryptogenic embolic stroke, and the various causes of cryptogenic strokes have been increasingly recognized recently [1]. Herein, we present a case of recurrent strokes possibly associated with a carotid stump related to congenital non-bifurcating common carotid artery (CCA) and its successful treatment using stenting. A 39-year-old man was admitted to our hospital due to recurrent ischemic strokes. He had no risk factors for stroke except for smoking. He had a history of recurrent stroke despite the use of antithrombotics. Three years ago, he had a cortical infarction in the left anterior cerebral artery area with symptoms of transient right-sided weakness and was treated with cilostazol owing to an aspirin allergy (Figure 1). One year ago, he was admitted for transient right-sided weakness and motor aphasia that lasted 5 minutes. Magnetic resonance imaging (MRI) revealed an acute cortical infarction in the left middle cerebral artery (MCA) area (Figure 1). He was treated with warfarin temporarily, and was subsequently treated with clopidogrel. Figure 1. A total of three recurrent left hemispheric strokes occurred in 3 years. (A) Diffusion-weighted imaging findings of recurrent left middle or anterior cerebral artery area cortical infarcts. The patient first had a left anterior cerebral artery cortical ... While taking clopidogrel, the patient experienced a third ischemic stroke. He presented with sensory change in the right hand. The neurologic exam result was normal, except for numbness in his right hand area. Diffusion-weighted imaging revealed an acute cortical infarction in the left MCA area and a chronic infarction in the left MCA and the anterior cerebral artery areas (Figure 1). Magnetic resonance angiography showed congenital agenesis of the left internal carotid artery (ICA) and an ICA stump. The left carotid area was supplied by a connection between the distal ICA and the external carotid artery (ECA) (Figure 1B). There was no stenotic lesion in the intracranial vessels and in the distal left common carotid artery of ECA origin. Carotid CT angiography did not show any atherosclerotic plaque in the carotid stump area. A selective left CCA injection revealed a bulbous carotid stump and turbulent flow within the ICA stump (Figure 2A). Comprehensive diagnostic work ups, including laboratory tests for coagulopathy, echocardiography with the bubble test to detect paradoxical embolism, 24-hour Holter monitoring, and coronary CT angiography for aortic pathology yielded negative results. Laboratory test for clopidogrel resistance was negative. Figure 2. Conventional angiographic findings. (A) Cerebral angiography revealed turbulent flow in the left carotid stump. (B) Stenting and stent-assisted coiling were performed across the origin of the left internal carotid artery. (C) No residual stump on postprocedure ... The decision was made to insert a stent and coil to block the stump because the patient suffered a recurrent left hemispheric stroke despite receiving antithrombotics, and only an ICA stump could be a possible source of the embolism. Stent insertion and stent-assisted coiling were successfully performed without complications (Figure 2B and ​andC).C). A closed cell-type self-expanding stent (Wall stent, Boston Scientific, Ireland) was used. The patient was discharged with triflusal and clopidogrel treatment, and remained asymptomatic at 5 months of follow-up. Carotid stump syndrome remains a rare entity, but it is a treatable cause of recurrent retinal and hemispheric symptoms after ICA occlusion. Rarely, after complete occlusion of the ICA, a short patent portion of the proximal ICA can be shown by angiography as well as by other imaging modalities, and is referred to as the “carotid stump.” In this case, congenital non-bifurcating CCA with an anomalous ECA-ICA connection, rather than acquired ICA occlusion could be the cause of the carotid stump [2]. Both surgical exclusion of the carotid stump with endarterectomy of the ECA, and carotid stenting of the distal common and external carotid arteries to exclude the ICA stump, can be used. Lakshminarayan and colleagues reported the results of a small case series that used endovascular treatment suggesting that long-term outcomes are equivalent to those achieved by surgery [3]. Our and other cases suggest that in the case of recurrent retinal or hemispheric symptoms with an ipsilateral carotid stump but no other demonstrable cause, carotid stenting with/without coiling should be considered to normalize the regional hemodynamics associated with the carotid stump.

A Rare Clinical Presentation Due to Small Cortical Infarction: Isolated Wrist Drop

Isolated wrist drop due to stroke is infrequently observed, and often misdiagnosed as peripheral neuropathy. It is important to make the differential diagnosis correctly because drop hand that results from peripheral pathology requires a completely different treatment strategy than central pathology. In addition, small infarcts are important to identify in order to optimise secondary prophylaxis. In this report, we describe an 83-year-old man, with isolated drop hand due to acute small cortical infarction in the left precentral gyrus and present this situation in light of the literature.

Palatal tremor as a manifestation of epilepsia partialis continua caused by acute precentral gyral infarction

We describe a patient with palatal tremor (PT) as a manifestation of focal seizure caused by acute cortical infarction. Brain MRI showed acute infarction in the left precentral gyrus without evidence of brainstem lesions or hypertrophy of the inferior olivary nucleus. We discuss the differences between our patient and previous reports of symptomatic PT and the mechanisms involved in the development of PT associated with cortical lesions.

Can Transient Drop in Blood Pressure in High-Risk Hypertensive Patients Cause Small Cerebral Infarcts?

Background. Multiple, simultaneous, acute cerebral infarcts in different arterial territories are usually secondary to embolic occlusion of multiple cerebral arteries. We observed, however, that no cardiac or aortic source could be found in many of these patients. We therefore undertook this study to attempt to identify other factors that may be important in the causation of these infarcts. Materials and Methods. We performed a five-year retrospective review of all patients with multiple, near simultaneous, acute cerebral infarcts detected on diffusion-weighted MRI scans. Results. We identified 78 patients with acute infarcts, in different cerebral arterial territories. We found a cardiac embolic source in 15 (19 percent) patients. Forty-one patients (53%) had no obvious cause for their infarcts after detailed cardiovascular and hematological evaluation. In 16 of these patients (20% of all 78 patients), all with a history of chronic hypertension who had multiple, acute, small (&lt;2 cms), deep subcortical or superficial cortical infarcts (and most, 93%, with extensive evidence of chronic small vessel disease on MRI FLAIR images), blood pressure was low or normal on initial presentation (mean arterial pressure, MAP: 85 ± 11.4 mm Hg). Analysis of the last prestroke blood pressure, within the previous 1 to 11 days available in 13 of 16 patients, revealed much higher BP (MAP: 113.6 ± 11.3 mm Hg), indicating a mean drop of 25.1 percent (range 11 to 44 percent). Two weeks after the stroke, blood pressure had risen again to greater than 160/100 mm Hg (MAP: 128.2 ± 14.3). Conclusion. Our study suggests that transient drop in blood pressure in high-risk hypertensive patients with severe, small vessel disease may sometimes result in small, cerebral infarcts. More research is needed to further clarify and confirm this possibility.