Bihemispheric Infarcts Research Articles

IN GRAVE DANGER: A CASE OF GRAVES THYROTOXICOSIS WITH MOYAMOYA SYNDROME

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Graves’ thyrotoxicosis has been associated with Moyamoya syndrome, a condition characterized by diffuse steno-occlusive disease of the cerebral vasculature. Ischemic strokes have been reported in this sub-population often presenting with focal neurological deficits. However, global encephalopathy could be the presenting symptom of this rare association. CASE PRESENTATION: A 43-year-old female with Graves’ disease was admitted with confusion, fevers, and tachycardia. She was diagnosed with sepsis due to urinary tract infection and her biochemical tests were suggestive of severe hyperthyroid state. Initial treatment included steroids, propranolol, and antithyroid agents along with antibiotics. However, on day 2 of admission, she developed right hemiparesis. Computed Tomography Angiograms (CTA) from both days showed evolving multifocal infarcts in bilateral cerebral hemispheres and worsening stenotic disease of anterior cerebral vessels (Figure 1). CT perfusion studies demonstrated markedly prolonged cerebral perfusion bilaterally, a pattern consistent with Moyamoya disease (Figure 2). Due to concern of acute ischemic infarction, the patient was started on vasopressor support to improve neuro-perfusion. Following discontinuation of vasopressors, the patient had further deterioration of neurological status. Magnetic Resonance Imaging (MRI) of the brain depicted evolving watershed infarcts bilaterally (Figure 3). Due to worsening sepsis with labile hemodynamics, plasmapheresis was deferred. Due to persistent comatose state, she was transitioned to comfort care. DISCUSSION: Hemiparesis was often the presenting symptom of this rare association. However, confusion was noted in our patient, not an uncommon finding in thyrotoxicosis. While the mechanism behind this association is unclear, one hypothesis suggests cross-reactivity between Thyroid-Stimulating Hormone (TSH) antibodies and cerebral arteries leading to immune-mediated arteritis. Another hypothesis suggests a demand-supply mismatch in stenosed cerebral vasculature caused by the hypermetabolic state in thyrotoxicosis. The role of accentuating cerebral perfusion with vasopressor support in these patients has not been discussed in literature. Cases of thyrotoxicosis with Moyamoya syndrome report improvement with hormonal control of thyrotoxicosis followed by cerebral revascularization. Malik et al reported improved neurological outcomes in patients managed with early plasmapheresis and aspirin. CONCLUSIONS: The association between Graves’ disease and Moyamoya syndrome is rare and can present as a spectrum of encephalopathy from confusion to coma. When present, it leads to multiple strokes with poor neurological outcomes. Early diagnosis with high index of suspicion is key, as management includes treating thyroid storm and cerebral revascularization. Further studies are required to stratify at-risk populations. Reference #1: Moyamoya Syndrome Associated With Graves' Disease: A Case Report and Review of the Literature. Shaneela M, Andrew N R. J Stroke Cerebrovasc Dis. 2011 Nov;20(6):528-36. Reference #2: Multiple Intracranial Arterial Stenoses Around the Circle of Willis in Association With Graves' Disease: Report of Two Cases. Kazuhiro N, Kiyoyuki Y. Neurosurgery. 2003 Nov;53(5):1210-4; discussion 1214-5. Reference #3: Rapidly Progressive Fatal Bihemispheric Infarction Secondary to Moyamoya Syndrome in Association with Graves Thyrotoxicosis. S.W. Hsu, J.C. Chaloupka and D. Fattal. American Journal of Neuroradiology March 2006, 27 (3) 643-647. DISCLOSURES: No relevant relationships by Ayesha Azmeen, source=Web Response No relevant relationships by Naga Vaishnavi Gadela, source=Web Response No relevant relationships by Viraj Modi, source=Web Response

Isolated Upper Limb Weakness From Ischemic Stroke: Mechanisms and Outcome

ObjectiveTo characterize isolated upper extremity (UE) weakness from stroke. MethodsIn our Get with the Guidelines-Stroke dataset (n = 7643), 87 patients (1.14%) had isolated UE weakness and underwent thorough stroke evaluation with diffusion-weighted magnetic resonance imaging and good-quality arterial imaging. We analyzed clinical-imaging features, etiology, management, and outcome. Since isolated UE weakness is typically associated with contralateral hand-knob area infarcts, patients were classified into Group-A (motor strip infarct) or Group-B (non-motor strip infarct). ResultsThe mean age was 68 years; 66% were male, 72% had hypertension, 22% diabetes, 53% hyperlipidemia, and 16% were smokers. In Group-A (n = 71), 18 patients had single and 53 had multiple infarcts involving the contralateral motor strip. In Group-B (n = 16), 6 patients had contralateral subcortical white matter infarcts, 9 had bihemispheric infarcts and 1 had a brainstem infarct. Compared to Group-B, patients in Group-A more often had carotid artery stenosis or irregular plaque (84.5% versus 50%, P = .006) and large-artery atherosclerosis mechanism (46% versus 19%, P = .05), and less often cardioembolic mechanism (13% versus 44%, P = .008). Among 36 patients with large-artery mechanism, 27 had less than 70% stenosis including 19 with plaque ulceration/thrombus. Recurrent strokes occurred in 10 patients (11.5%), including 5 with mild-moderate carotid stenosis and plaque ulceration/thrombosis, over 1515 days follow-up. ConclusionStroke mechanism in acute isolated UE weakness is variable. Contralateral motor-strip infarcts are associated with carotid stenosis, often with plaque ulceration (“vulnerable carotid plaque”), and infarcts in other locations with cardioembolism. Recurrent stroke risk is high especially with mild-moderate carotid artery stenosis and plaque ulceration/thrombus.

Unilateral traumatic hemorrhage of the basal ganglion and bihemisferic cerebral infarction

Abstract Among the various injuries caused by the cerebral tramatic lesion are traumatic brain contusions. Hemorrhagic contusions of the basal ganglia are unusual. Different injuries such as cranial fractures, epidural hemorrhage, subdural hematoma, subarachnoid hemorrhage among others may be associated with brain contusions. In some cases traumatic brain injury arises. We present a case of a patient with unilateral cerebral contusion associated with bihemispheric cerebral infarction.

Abstract W MP33: Baseline Clinical and Infarct Characteristics as Predictors of Poor Outcomes in Patients Not Thrombolysed Due to Mild or Resolving Symptoms ("Too Good To Treat")

Introduction: A common reason for non-treatment of time eligible patients with IV tPA is mild symptoms in patients that are “too good to treat (TGTT)”. Several studies have reported poor outcomes in this group. We sought to identify patient and imaging characteristics associated with poor outcomes in this group. Methods: Using our institutional GWTG database, we analyzed 2,745 consecutive stroke admissions (01/2009 - 07/2013). Univariate and multivariable analysis were carried out to determine factors associated with the poor outcome of not being discharged home. Results: Of the total 2,745 patients, 306 (11.1%) presented within the window for IV tPA but did not receive the treatment due to symptoms too mild or rapidly improving. Of these, imaging characteristics were available in 238 patients. Among TGTT stroke patients, 62.6% were discharged home, 26.9% to IRF, 8.4% to SNF and 2.1% death/hospice. Patients with poor outcome were older, more often Hispanic, with more vascular risk factors, and higher NIHSS. Infarcts in both hemispheres, and in posterior+/- anterior circulation were more common with poor outcome. On multivariable analysis, increasing age, Hispanic ethnicity, higher NIHSS and bihemispheric stroke were associated with poor outcome, with a trend toward small vessel stroke subtype. Conclusion: A substantial percentage of patients deemed “too good” for IV tPA are still unable to be discharged home. Factors such as advanced age, higher NIHSS, bi-hemispheric infarction should be considered in tPA decision-making in potential TGTT patients. Large, multi-center prospective studies are needed to better identify potential biomarkers of poor outcomes in this group.

Teaching Neuro Images : Treatment-resistant rapidly progressive amyloid β–related angiitis

A 76-year-old woman presented with 1 month of progressive aphasia, headache, and subsequent right hemiparesis. Initial brain MRI showed a punctate infarct (figure 1, A and C). Susceptibility-weighted imaging was unremarkable. A repeat study 16 days later demonstrated bihemispheric infarcts with multifocal attenuation of intracranial vessels on magnetic resonance angiography (figure 1, B and D). CSF showed a lymphocytic pleocytosis (101 leukocytes/µL) and elevated protein (480 mg/dL). Brain biopsy showed granulomatous angiitis with amyloid deposition and fibrinoid necrosis surrounded by inflammatory cells (figure 2). She rapidly deteriorated on immunosuppression with high-dose IV steroids and has not improved despite a combination of oral steroids and monthly cyclophosphamide.

Recovery of Swallowing after Dysphagic Stroke: An Analysis of Prognostic Factors

Dysphagia is a major complication of stroke, but factors influencing its recovery are incompletely understood. The goal of this study was to identify important prognostic variables affecting swallowing recovery after acute ischemic stroke. We retrospectively reviewed our patient database to identify acute ischemic stroke patients who developed dysphagia after stroke but were free of other confounding conditions affecting swallowing. Of the 1774 patients screened, 323 met the study criteria. We assessed the effect of age, sex, baseline National Institutes of Health Stroke Scale (NIHSS) score, level of consciousness (LOC), facial weakness, dysarthria, neglect, bihemispheric infarcts, right hemispheric infarcts, brainstem infarcts, intubation, aspiration, acute stroke therapies, occurrence of symptomatic hemorrhagic transformation, seizures, pneumonia, and length of hospitalization (LOH) on persistence of dysphagia at hospital discharge in a logistic regression analysis. The mean age and NIHSS scores (mean±standard deviation) were 75.9±13.6 years and 13.5±6.9, respectively; 58.5% were women. In a multivariate analysis, aspiration detected on a clinical swallowing evaluation (odds ratio [OR] 21.83; 95% confidence interval [CI] 8.16-58.42; P<.0001), aspiration on videofluoroscopic swallowing study (OR 10.50; 95% CI 3.35-32.96; P<.0001), bihemispheric infarcts (OR 3.72; 95% CI 1.33-10.43; P=.0123), dysarthria (OR 3.4; 95% CI 1.57-7.35; P=.0019), intubation (OR 2.86; 95% CI 1.10-7.39; P=.0301), NIHSS score ≥12 (OR 2.51; 95% CI 1.19-5.23; P=.0157) were significant predictors of persistent dysphagia. The area under the curve and Somer's Dxy statistics of the model were 0.8918 and 0.78, respectively, indicating good calibration and discriminative power. Prognostic factors affectingswallowing recovery identified in this study can help advance dysphagia research methodologies and the clinical care of stroke patients.

Transient acute tetraparesis revealing bihemispheric cerebral infarcts

A 74-year-old woman with a history of diabetes mellitus developed acute tetraparesis. The symptoms totally resolved in 15 min. Neurological examination performed 2 days after the symptoms onset was normal. Brain magnetic resonance imaging (MRI), performed 3 days after onset, showed on diffusion-weighted imaging bihemispheric cerebral infarcts (Fig. 1). Electrocardiogram, chest X-ray and laboratory studies were normal. Carotid ultrasonography, transthoracic and transoesophageal echocardiography were normal. The patient was discharged 10 days after admission on antiplatelet and antihypertensive agents, with a favourable outcome. This patient suffered from acute and transient tetraparesis revealing bihemispheric cerebral infarctions. The present case is of interest for two reasons. First, although tetraparesis may initially suggest spinal cord lesion, bilateral cerebral involvement should always be considered, particularly in the case of acute symptoms onset. Second, this case underlines the fact that all acute clinical symptoms, even for neurological events that are less than 1 h, should be investigated ideally with MRI.

Multiple subcortical acute ischemic lesions reflect small vessel disease rather than cardiogenic embolism

Multiple acute ischemic lesions in different hemispheres or vascular territories are mainly considered to be of proximal embolic origin. However, despite careful diagnostic work-up, the etiological classification often stays undetermined. We propose that multiple acute ischemic lesions can sometimes be a phenomenon observed in small vessel disease (SVD). From a prospectively collected database of more than 7,000 stroke patients, 173 patients with acute bihemispheric infarction were identified. We analyzed those subjects with multiple small (< 15 mm Ø) subcortical acute ischemic lesions on diffusion-weighted MRI (DWI) and concomitant severe small vessel disease (Fazekas grades II-III) without a proximal embolic source as evaluated by cardiological investigations. Twenty patients (mean age 66 ± 12 years, 12 men) with a mean number of 2.95 ± 1.24 acute lesions on DWI (range of 2-7 lesions per patient) were identified (n = 5 Fazekas II°, n = 15 Fazekas III°). Most of the lesions were located in typical areas of lacunar infarction. The mean NIHSS score on admission was 2.95 ± 2.0 (range 0-8). Multiple acute ischemic lesions in different vascular territories might not always be of proximal cardiovascular embolic origin. Simultaneous small subcortical ischemic lesions may reflect remote ischemia due to small vessel disease reflecting simultaneous hemorheological dysfunction.

Cerebral vasospasm after subarachnoid hemorrhage from severe arteriovenous malformation

Dear Editor,We read with great interest the article entitled“Outcomeof severe arteriovenous malformation-related intracranialhemorrhage: the importance of cisternal subarachnoidhemorrhage and early seizures.” by Rahme et al. [4]Theauthors reviewed the records of 16 consecutive patientswho presented with severe arteriovenous malformation(AVM)-related intracranial hemorrhage. They reportedthat three patients, who had subarachnoid hemorrhage(SAH), died from extensive bihemispheric infarction andrefractory intracranial pressure. Statistical analysisrevealed that SAH and early seizures were significantlyassociated with death. We completely agree with theauthors’ findings and wish to provide further comment.Cerebral vasospasm after SAH from AVM has beenreported to occur in 8-31% of patients [1, 3]. We believethat cerebral vasospasms might be one of the attributablefactors for cerebral infarctions in the three patients whodied in the authors’ series. We consider that physiciansneed to be particularly aware of cerebral vasospasm inpatients with massive SAH from AVM, and that thethreshold of digital subtraction angiography, computedtomography angiography, or magnetic resonance angiographyshouldbeloweredforearlydetectionofcerebralvasospasminpatients with SAH from AVM. Additionally, nimodipine,nicardipine, intra-arterial papaverine, or angioplasty may beefficient for preventing or treating cerebral vasospasm afterSAH from AVM [2, 3, 5]. However, treatment of cerebralvasospasm may augment blood flow to an untreated AVMand promote early rebleeding, especially in cases withuntreated intranidal aneurysms [2, 3, 5]. Early AVM resectioncan prevent rebleeding and also enable treatment of cerebralvasospasm. We consider that early AVM resection andawareness of cerebral vasospasm are required in patientswith massive SAH from AVM.

Outcome of severe arteriovenous malformation-related intracranial hemorrhage: the importance of cisternal subarachnoid hemorrhage and early seizures

Although arteriovenous malformations (AVM)-related intracranial hemorrhage (ICH) is infrequently devastating, there is a subgroup of patients that present comatose requiring immediate surgical treatment. We sought to determine the outcome and prognostic factors in those patients with severe AVM-ICH. Between 2003 and 2009, medical records of 16 consecutive patients presented with severe AVM-ICH were retrospectively reviewed. Outcome was determined using 30-day survival and Glasgow outcome scale and modified Rankin scale scores at last follow-up. There were seven males and nine females with a mean age of 32 years (range 6-66). All had Glasgow coma score 8 or less and most exhibited motor posturing and/or dilated pupils. Fifteen patients had intraprenchymal, ten had intraventricular, and four had subarachnoid hemorrhage (SAH). Twelve patients underwent hematoma evacuation with concomitant decompressive craniectomy in 11 and external ventricular drainage (EVD) in six. EVD was the only treatment offered to four patients. AVM excision was not routinely attempted in the acute phase. Three patients died from extensive bihemispheric infarction and refractory intracranial pressure. All 13 survivors improved neurologically and 12 had an acceptable functional outcome (modified Rankin scale ≤ 4) after a mean follow-up of 10 months (range 1-49). Among all clinical, radiological, and operative variables, only cisternal SAH (P = 0.007) and early seizures (P = 0.018) were significantly associated with death. Despite their poor initial clinical condition, most survivors of severe AVM-ICH achieve an acceptable functional outcome. Therefore, patients with severe AVM-ICH, particularly those without aneurysmal-like SAH, should be managed aggressively given their remarkable potential for neurological recovery.

Predictors of Percutaneous Endoscopic Gastrostomy Tube Placement in Patients With Severe Dysphagia From an Acute-Subacute Hemispheric Infarction

This study investigated the influence of age, National Institutes of Health Stroke Scale (NIHSS) score, time from stroke onset, infarct location and volume in predicting placement of a percutaneous endoscopic gastrostomy (PEG) tube in patients with severe dysphagia from an acute-subacute hemispheric infarction. We performed a retrospective analysis of a hospital-based patient cohort to analyze the effect of the aforementioned variables on the decision of whether or not to place a PEG tube. Consecutive patients were identified using International Classification of Diseases, Ninth Revision (ICD-9) codes for acute ischemic stroke, Current Procedural Terminology (CPT)-4 codes for a formal swallowing evaluation by a speech pathologist, and procedure codes for PEG placement over a 5-year period from existing medical records at our institution. Only patients with severe dysphagia were enrolled. A total of 77 patients met inclusion criteria; 20 of them underwent PEG placement. The relationship between age (dichotomized; < and ≥75 years), time from stroke onset (days), NIHSS score, acute infarct lesion volume (dichotomized; < and ≥100 cc), and infarct location (ie, insula, anterior insula, periventricular white matter, inferior frontal gyrus, motor cortex, or bilateral hemispheres) with PEG tube placement were analyzed using logistic regression analysis. In univariate analysis, NIHSS score (P = .005), lesion volume (P = .022), and presence of bihemispheric infarction (P = .005) were found to be the main predictors of interest. After multivariate adjustment, only NIHSS score (odds ratio [OR], 1.15; 90% confidence interval [CI], 1.02-1.29; P = .04) and presence of bihemispheric infarcts (OR, 4.67; 90% CI, 1.58-13.75; P = .018) remained significant. Our data indicates that baseline NIHSS score and the presence of bihemispheric infarcts predict PEG placement during hospitalization from an acute-subacute hemispheric infarction in patients with severe dysphagia. These results require further validation in future studies.

Acute ischemic stroke: Relationship of brain lesion location & functional outcome

Purpose. To establish, using brain spiral computerised tomography (SCT) and modified Barthel index (MBI), whether the location of cerebral infarction could be correlated with functional outcome in acute ischemic stroke patients who undergo early intensive rehabilitation.Methods. Observational cohort, assessor blinded and correlational prospective 12-weeks study that included 111 acute ischemic stroke patients, admitted consecutively to an early intensive inpatient rehabilitation programme (5 days a week, 3–5 h a day) during 2003. Confirmation of diagnosis and stratification was done by brain SCT. Brain lesion locations were correlated to motor performance and functional outcome, on admission and discharge, using MBI.Results. Statistical analysis demonstrated a significant correlation between motor performance, functional outcome and brain lesion locations. The groups with deep, combined deep and large superficial, small superficial and large superficial infarcts showed the most consistent improvement in that order of frequency. Normal brain SCT group did not reach statistical significance (p = 0.051) while the bi-hemispheric infarcts group did not show any change. The inter and intra group differences were highly significant (p < 0.05).Conclusions. Immediate non-contrasted brain SCT may act as an independent predictor of final functional outcome in acute ischemic stroke. It may provide clinicians with an opportunity to offer realistic expectations to stroke patients and their relatives.

Cluster Breathing Associated With Bihemispheric Infarction and Sparing of the Brainstem

To report cluster breathing pattern associated with a nonbrainstem lesion. Case report. Neurointensive care unit, St Mary's Hospital, Rochester, Minn. A patient with subarachnoid hemorrhage developed severe, diffuse, distal bilateral middle cerebral artery vasospasm with resultant cortical laminar necrosis and transient cluster breathing. Intervention Magnetic resonance imaging revealed bihemispheric lesions but no brainstem lesion. Cluster breathing may occur with nonbrainstem lesions.

Stroke in the Medical Intensive-Care Unit

To analyze the occurrence and outcome of new-onset stroke in critically ill patients admitted to a medical intensive-care unit. We reviewed the medical records of patients admitted to the medical intensive-care units of two hospitals between 1985 and 1995. In addition, computed tomographic scans or scan reports were assessed. We identified 19 patients with a critical medical illness and a new-onset stroke. Of this study group, ischemic stroke developed in 10 patients, 8 of whom were found to have bihemispheric infarction. A single territory infarct (the middle cerebral artery territory) was noted in two patients. The presumed mechanisms for ischemic stroke were disseminated intravascular coagulation (N = 6), cholesterol embolization (N = 1), discontinuation of warfarin therapy before an invasive procedure (N = 1), septic emboli (N = 1), and cardioversion (N = 1). In nine patients, an intracranial hemorrhage developed. Seven patients had a single lobar hematoma, whereas multiple intracerebral hematomas were found in two patients. Disseminated intravascular coagulation and rupture of a mycotic aneurysm in proven infective endocarditis were the most common mechanisms for hemorrhagic stroke. In all patients with an ischemic stroke, sudden hemiparesis rapidly progressed to coma. In patients with an intracranial hematoma and sudden onset of coma, unilateral fixed pupil was the most common initial manifestation. Of the 19 patients, 17 died and 2 remained severely disabled. Coma is a common initial manifestation of stroke in patients with a critical medical illness, and disseminated intravascular coagulation has a major etiologic role. New-onset stroke in the setting of critical medical illness generally is a complication in a terminally ill patient.