We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Typical neuroimaging presentation of preeclampsia/eclampsia are posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS).Eclampsia carries a high risk for stroke, both hemorrhagic and ischemic. Besides eclampsia, pregnancy-specific causes of ischemic stroke are peripartum cardiomyopathy, postpartum benign angiopathy, amniotic fluid embolization and choriocarcinoma.The incidence of cerebral venous thrombosisis the highest during postpartum and is increased in older women, cesarean delivery, or epidural anesthesia, in the presence of infection, obesity or thrombophilia. Risk factors for hemorrhagic stroke during pregnancy and postpartum are older age, pregestational and gestational hypertension, preeclampsia/eclampsia, coagulopathies, and smoking
Stroke is an episode of sudden neurological dysfunction caused by focal ischemia of the central nervous system leading to cell death. Transient ischemic attack (TIA) is a transient episode of neurological dysfunction, without acute infarction. Stroke is a leading cause of long-term disability and the fifth leading cause of death in the United States. Advancing age remains a leading nonmodifiable risk factor for stroke. Targeting modifiable risk factors is critical to preventing recurrent strokes. This includes screening for diabetes, initiating statin therapy, and identifying and treating atrial fibrillation and hypertension. Aspirin remains the preferred antiplatelet drug for secondary prevention of ischemic stroke (in the absence of an indication for anticoagulation); however, patients with minor stroke or TIA should be treated for at least 21–30 days with both aspirin and clopidogrel. The management of acute ischemic stroke centers around thrombolytic treatment and mechanical thrombectomy, to maximize cerebral perfusion to the ischemic brain tissue. This must be balanced against the risks for hemorrhagic complications. Common poststroke complications include venous thromboembolic disease, dysphagia, and depression. All members of the health-care team and physicians should communicate openly and frequently with patients, their families, and/or their caregivers to ensure that their goals of care are met.
To determine the association between delay in transfer to a central stroke unit from peripheral institutions and outcomes.
Methods:
We conducted a retrospective cohort study of all patients with acute stroke, admitted to a comprehensive stroke center (CSC) from three emergency departments (EDs), between 2016 and 2018. The primary outcomes were length of stay, functional status at 3 months, discharge destination, and time to stroke investigations.
Results:
One thousand four hundred thirty-five patients were included, with a mean age of 72.9 years, and 92.4% ischemic stroke; 663 (46.2%) patients were female. Each additional day of delay was associated with 2.0 days of increase in length of stay (95% confidence interval [CI] 0.8–3.2, p = 0.001), 11.5 h of delay to vascular imaging (95% CI 9.6–13.4, p < 0.0001), 24.2 h of delay to Holter monitoring (95% CI 7.9–40.6, p = 0.004), and reduced odds of nondisabled functional status at 3 months (odds ratio 0.98, 95% CI 0.96–1.00, p = 0.01). Factors affecting delay included stroke onset within 6 h of ED arrival (605.9 min decrease in delay, 95% CI 407.9–803.9, p < 0.0001), delay to brain imaging (59.4 min increase in delay for each additional hour, 95% CI 48.0–71.4, p < 0.0001), admission from an alternative service (3918.7 min increase in delay, 95% CI 3621.2–4079.9, p < 0.0001), and transfer from a primary stroke center (PSC; 740.2 min increase in delay, 95% CI 456.2–1019.9, p < 0.0001).
Conclusion:
Delay to stroke unit admission in a system involving transfer from PSCs to a CSC was associated with longer hospital stay and poorer functional outcomes.
Large-sized clinical trials have failed to show an overall benefit of surgery over medical treatment in managing spontaneous intracerebral hemorrhages (ICH); less invasive techniques have shown to decrease brain injury caused by surgical manipulation in the standard open approach improving the clinical outcomes of patients. Thereby, we propose a low-cost 3D-printed endoport for a less invasive ICH evacuation. In this study, the authors compare the clinical outcomes of early surgical evacuation using a 3D-printed endoport vs. a standard open surgery (OS).
Methods:
A retrospective analysis was conducted comparing patients who underwent early evacuation of a deep hypertensive ICH through an endoport vs. OS at a single center from August 2017 to March 2019. Demographic, clinical, and radiologic data were reviewed. The primary outcomes were the 90-day post-stroke functional outcome and mortality.
Results:
A total of 36 patients were included. The two cohorts (18 endoport; 18 OS) showed no statistically significant differences in demographic, clinical, and radiologic characteristics, including median admission hemorrhage volume, Glasgow Coma Scale, and ICH scores. At 90-day post-stroke, 44% of patients in the endoport group and 17% in the OS group had a favorable functional outcome (mRS 0–3) (p = 0.039); moreover, the endoport group showed lower mortality (33% vs. 72%, p = 0.019).
Conclusions:
This study suggests that an endoport-assisted ICH evacuation may have better functional outcomes and lower mortality than OS. The proposed device could provide a safe, low-cost alternative for ICH’s surgical treatment. More rigorous research is hence needed to assess the potential benefits of this technique.
Brainstem stroke due to an embolus to the basilar artery, is one of the most common causes of initially unexplained coma. This chapter explains why and how patients become comatose after an ischemic or hemorrhagic stroke. Acute coma from a stroke may be due to an embolus to the basilar artery destroying the ascending reticular formation in the dorsal pons and mesencephalon. The approach to a patient with coma and abnormal consciousness requires three steps. First, determine whether the patient is truly comatose and exclude confounders or misleading signs. Second, with a focused neurological examination, it is possible to localize the lesion using information on brainstem reflexes and motor responses to noxious stimuli. Third, breathing patterns, blood pressure, pulse, and temperature characteristics may also indicate a certain cause. Coma is expected in catastrophic and often fatal ganglionic cerebral or pontine hemorrhages.
Stroke has long been recognized as one of the most common causes of epileptic seizures, particularly in older people. This chapter provides an overview of the various epidemiological studies on poststroke seizures (PSS) and poststroke epilepsy (PSE), and attempts to give an understanding of their pathogenesis, outcome, and management. The most consistent risk factors for PSS at stroke onset are size and cortical involvement. Abnormal electroencephalography's (EEGs) have been noted in up to 38% of patients with lacunar infarction, and lateralizing EEG abnormalities in over 80% of patients with early seizures in lacunar strokes also supports the concept of associated cortical infarction. Large, anterior circulation, ischemic strokes carry the highest risk of seizures. Patients who develop PSE usually require pharmacological treatment. Seizures following stroke occur in less than 10% of patients in the first few weeks after stroke.
Cerebral microbleeds (CMBs) reflect an underlying angiopathy currently thought to result mainly from hypertension or from the deposition of beta-amyloid in small and micro vessel walls. This chapter describes the prevalence of, and risk factors for, CMBs and methodological issues related to their study. CMBs can be present in up to 80% of a clinical hemorrhagic stroke sample. Most studies with a reasonable distribution of subject age and sample size show CMB prevalence increases with age. There is robust evidence that high blood pressure, measured in different ways, is a risk factor for CMB. Most genetic diseases with increased susceptibility to CMBs are rare. The only candidate susceptibility gene identified as risk modifying is APOE. Research on risk factors for CMBs will bring into better focus issues related to comorbidity with other vascular and neurodegenerative lesions and location and number of lesions.
This chapter provides an overview of the prevalence and associations, temporal evolution and prognostic significance of cerebral microbleeds (CMBs) in patients with cerebrovascular diseases. The spatial distribution of microbleeds, as markers of small vessel microhemorrhagic or microaneurysmal lesions, may be of particular interest in attempts to understand the causes of macroscopic intracerebral hemorrhage (ICH) in life. Cerebral amyloid angiopathy is an important cause of primary ICH, particularly of lobar location. Chronic hypertension has been repeatedly identified as a strong influence on the frequency and extent of CMBs, in patients with established stroke as well as in healthy subjects without stroke. Hypertension is an important risk factor for CMBs. As CMBs reflect the bleeding tendency of the brain through fragile microvascular walls, interest has increased in utilizing CMBs in risk stratification of hemorrhagic complications for patients with antithrombotic treatment.
This chapter explores the management issues surrounding a hemorrhagic stroke of the cerebellum, one of the most common sites for intracerebral hemorrhage, and one where proper management can have a profound impact on outcome. It presents a case study of a 75-year-old female with a history of hypertension and end-stage renal disease requiring dialysis. Examination consistently revealed appropriate, symmetric limb movements and limited cranial nerve exams. Computed tomography scans showed satisfactory decompression of the posterior fossa and absence of hydrocephalus. Intracerebral hemorrhage is most commonly associated with chronic hypertension, amyloid angiopathy, anticoagulation, trauma or underlying pathology such as tumor or vascular malformation. As ventricular obstruction may occur when the patient is positioned, prepared or opened, allowing access for an emergency external ventricular drainage device is desirable in preparing and draping the patient.
Cysticercosis is caused by infection with the larval stage ofTaenia solium, the pork tapeworm. A brief description of the many changes that cysticerci induce in the central nervous system (CNS) is necessary to understand the pathogenesis of neurocysticercosis (NCC) related stroke. Lacunar infarctions occur as the result of inflammatory occlusion of small penetrating branches of the middle cerebral artery (MCA). Another cerebrovascular complication of NCC is hemorrhagic stroke. Stroke is common among patients with subarachnoid NCC, but it is seldom observed in other forms of the disease. CT and MRI show the infarction as well as the characteristic findings of subarachnoid NCC, including abnormal enhancement of leptomeninges, hydrocephalus, and cystic lesions located at the sylvian fissure or basal cisterns. Introduction of cysticidal drugs (albendazole and praziquantel) have greatly improved the prognosis of NCC by destroying intracranial cysts and improving the neurological manifestations in most patients with parenchymal NCC.
Arteriovenous malformations (AVMs) are complex vascular lesions that typically present with hemorrhage or seizures. Computed tomography (CT) scan, magnetic resonance imaging (MRI), and conventional cerebral angiography are the standard essential diagnostic tools utilized in planning the treatment of an AVM. Brain AVMs are complex cerebrovascular lesions capable of protean symptomatology. They are an infrequent, but serious cause of stroke that often occurs in young people. Most commonly, they result in hemorrhagic stroke by bleeding into the parenchyma of the brain. Much less commonly, they result in subarachnoid hemorrhage. Ischemic stroke is distinctly uncommon with cerebral AVMs but occurs occasionally due to retrograde thrombosis of feeding arteries frequently associated with complete or partial thrombosis of the AVM. The three treatment modalities available to patients with cerebral AVMs, embolization, radiosurgery, and surgical excision, should be carefully considered in each patient and should not be thought of as being interchangeable.
The underlying pathological mechanism of thrombotic thrombocytopenic purpura (TTP) is the presence of microvascular thrombi that partially occlude the vascular lumins with overlying proliferative endothelial cells. Coombs-negative hemolytic anemia and severe thrombocytopenia owing to platelet clumping in the microcirculation are the most outstanding laboratory abnormalities. Classically, TTP has been recognized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, neurological symptoms, fever, and renal involvement, though only 20 to 40 percentage of patients will manifest the classic pentad. TTP remains a life-threatening disease the mortality rate of which may be as high as 90 percentage when untreated. Diagnosis is mainly based on hematological findings and a broad variety of neurological abnormalities, including ischemic or, less often, hemorrhagic stroke. Plasma exchange (PE) is currently the mainstay of treatment; however, rapid advances in the understanding of TTP pathophysiology may offer more specific and effective therapies in the near future.
Rupture of an aneurysm is associated with a very high degree of morbidity and mortality. Stroke-like apoplectic clinical syndromes occur with aneurysmal intra cerebral hemorrhage and correspond to the affected area. Lateralized focal neurologic deficits are most common with intra parenchymal hemorrhages due to middle cerebral aneurysms. Intracranial aneurysms are not a rare cause of both hemorrhagic and ischemic stroke. Although the initial and most serious manifestation of an intracranial aneurysm, subarachnoid hemorrhage (SAH), does not typically result in focal neurologic deficits, several complications of ruptured or unruptured aneurysms can lead to focal neurologic deficits, which may develop suddenly in a stroke-like fashion. This is most often seen as a result of intracerebral hemorrhage from the initial rupture of the aneurysm. Cerebral vasospasm after SAH is another common cause of stroke-like, focal deficits. Thromboembolism from the dislodgement of an intra-aneurysmal clot is a less frequent cause of ischemic stroke.
Stroke refers to any damage to the brain or spinal cord caused by a vascular abnormality. This chapter shows how specific diagnostic information available from non-invasive investigations can be applied to the management of individual patients. The complexity of managing stroke patients is increasing. Early stroke classifications relied on clinical information. Terms such as 'transient ischemic attack (TIA)', 'minor stroke', 'reversible ischemic neurologic deficit (RIND)', 'stroke in progress' and 'completed stroke' were used to distinguish stroke subtypes. The initial diagnostic step should be to determine if the event is due to stroke or a non-vascular stroke mimic. The next level of stroke diagnosis is primarily to distinguish hemorrhagic from ischemic stroke. A detailed diagnosis of stroke etiology is required to plan management strategies for secondary stroke prevention. Stroke severity is an important diagnostic consideration in determining stroke prognosis, which in turn influences management decisions.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.