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New onset or exacerbation of preexisting neurologic symptoms during pregnancy often necessitates brain or spinal cord imaging. Magnetic resonance techniques are preferred imaging modalities during pregnancy and the postpartum period. Ionizing radiation with computed tomography and intravenous contrast material with magnetic resonance or computed tomography should be avoided during pregnancy. New onset of headaches in the last trimester or in the postpartum period may indicate cerebrovascular disease or a mass lesion, for which brain imaging is necessary. The continuum of cerebrovascular complications of pregnancy and enlarging lesions may produce neurologic symptoms later in pregnancy and after delivery, necessitating imaging.

Pregnant women may have exacerbation of preexisting neurologic disorders or new-onset neurologic symptoms for which brain or spinal cord imaging is appropriate. Primary headaches in early pregnancy can be diagnosed and treated without imaging. Headaches later in pregnancy or in the peripartum period may need to be evaluated by brain and/or vascular imaging. Cerebrovascular complications have distinctive imaging but overlapping presentations. Mass lesions can enlarge, producing neurologic symptoms, late in pregnancy. Imaging may be necessary to diagnose neurologic disorders in pregnancy and the peripartum period. MRI is preferred during pregnancy; imaging involving ionizing radiation and/or contrast should be avoided.

INTRODUCTION Acute disseminated encephalomyelitis (ADEM) is a rare demyelinating disease of the central nervous system (CNS) that classically occurs in children and adolescents. It characteristically presents with acute inflammation, resulting in demyelination, often following an infectious disease. ADEM has been described in adult patients, but the incidence in the adult and especially elderly population is low. CASES We describe five older adults (age 57 to 85) who presented with acute neurological symptoms. Three patients presented with an infectious illness preceding the event, 4 patients were encephalopathic, and oligoclonal bands (OCBs) were negative in all tested cases. The clinical scenario and imaging studies suggested alternative diagnoses, such as metastasis, primary CNS tumor, or stroke. Two patients had contrast enhancing lesions, two other patients had lesions with restricted diffusion on diffusion-weighted imaging. Neuropathologic diagnostic from biopsy or autopsy was eventually conclusive, showing perivascular zones of myelin loss with relative axonal sparing in all five cases. CONCLUSION Each of these patients was found to have pathological findings of acute demyelination on tissue diagnosis, suggesting ADEM or ADEM-like disease. The initial presentation and imaging was pointing toward other diagnoses. Broad differential diagnosis is important, especially for older patients, and pathological proof might be warranted for a conclusive diagnosis.

Nonneurologists who treat patients with headaches should be able recognize common headache types and to initiate therapy for tension-type headaches and migraines. Patients with complicated headache scenarios should be referred to a neurologist for consultation.

Pregnant women are most likely to have primary headaches, such as migraine and tension-type headaches, which can be diagnosed and treated without brain imaging. Primary headaches may even start de novo during pregnancy, especially in the first few months. However, when the headache occurs late in pregnancy or in the peripartum period, secondary causes of headaches need to be considered and evaluated by brain and/or vascular imaging, generally using magnetic resonance techniques. There is considerable overlap between the cerebrovascular complications of pregnancy, including preeclampsia/eclampsia, posterior reversible encephalopathy syndrome (PRES), reversible cerebral vasoconstriction syndrome (RCVS), and both hemorrhagic and ischemic strokes; although, their imaging may be distinctive. Imaging is necessary to distinguish between arterial and venous pathology causing headache in the peripartum patient, as there can be similar presenting symptoms. Mass lesions, both neoplastic and inflammatory, can enlarge and produce headaches and neurological symptoms late in pregnancy.

Acute disseminated encephalomyelitis (ADEM) is a rare demyelinating disease of the central nervous system (CNS) that classically occurs in children and adolescents. It characteristically presents with acute inflammation, resulting in demyelination, often following an infectious disease. ADEM has been described in adult patients, but the incidence in the adult and especially elderly population is low.We describe five older adults (age 57 to 85) who presented with acute neurological symptoms. Three patients presented with an infectious illness preceding the event, 4 patients were encephalopathic, and oligoclonal bands (OCBs) were negative in all tested cases. The clinical scenario and imaging studies suggested alternative diagnoses, such as metastasis, primary CNS tumor, or stroke. Two patients had contrast enhancing lesions, two other patients had lesions with restricted diffusion on diffusion-weighted imaging. Neuropathologic diagnostic from biopsy or autopsy was eventually conclusive, showing perivascular zones of myelin loss with relative axonal sparing in all five cases.Each of these patients was found to have pathological findings of acute demyelination on tissue diagnosis, suggesting ADEM or ADEM-like disease. The initial presentation and imaging was pointing toward other diagnoses. Broad differential diagnosis is important, especially for older patients, and pathological proof might be warranted for a conclusive diagnosis.

Dabigatran is effective in decreasing the risk of ischaemic stroke in patients with atrial fibrillation. However, like all anticoagulants, it is associated with a risk of bleeding. In cases of trauma or emergency surgery, emergency reversal of dabigatran-induced anticoagulation may be required. A specific reversal agent for dabigatran, idarucizumab, has been approved by the US Food and Drug Administration. Alternative reversal agents are available, such as prothrombin complex concentrates (PCCs) and activated PCCs (aPCCs). In this review we evaluate the role of PCCs and aPCCs in the reversal of dabigatran anticoagulation and consider which tests are appropriate for monitoring coagulation in this setting. Pre-clinical studies, small clinical studies and case reports indicate that PCCs and aPCCs may be able to reverse dabigatran-induced anticoagulation in a dose-dependent manner. However, dosing based on coagulation parameters can be difficult because available assays may not provide adequate sensitivity and specificity for measuring anticoagulation induced by dabigatran or the countering effects of PCCs/aPCCs. In addition, PCCs or aPCCs can potentially provoke thromboembolic complications. Despite these limitations and the fact that PCCs and aPCCs are not yet licensed for dabigatran reversal, their use appears to be warranted in patients with life-threatening haemorrhage if idarucizumab is not available.

Stroke, a major cause of morbidity and mortality in the general population, varies in incidence in men and women of different age groups: more boys than girls have strokes; the incidence of stroke is greater in men in their 60s and 70s; and stroke is more common in women after age 80 years. These differences are attributed to hormonal (sex-related) changes and variable risk factors in women, as well as lifestyle and environmental (gender-related) co-morbid conditions. A woman, who is more likely to have a stroke in her lifetime than a myocardial infarction, has a different response to primary and secondary prevention as compared with a man. Although response to thrombolysis is similar, older age and more severe strokes in women lead to poorer outcomes in female stroke survivors.

Early stroke management, and early initiation of secondary stroke prevention, may improve outcomes in patients with acute ischemic stroke. However

The risk for recurrent stroke following a stroke or transient ischemic attack (TIA) is high. Prevention of a secondary event is a priority, as the associated morbidity and mortality are great. Antiplatelet agents have been shown to reduce this risk, but the choice of treatment modality depends on a number of factors, including the underlying cause of the stroke and the patient's comorbidities. For example, a cardioembolic stroke is best treated with anticoagulants, whereas one of noncardioembolic origin requires antiplatelet therapy. A number of challenging patient scenarios are explored in this article, and appropriate medical management is discussed, with the goal of examining the most recent trial data and information in the context of an actual case. Eight sample cases are presented: stroke prevention in a patient with recent stent placement, low ejection fraction, intracranial stenosis, carotid stenosis, atherosclerosis of the aortic arch, symptomatic coronary artery disease, antiplatelet failure, and stroke prevention in a patient already on warfarin. Journal of Hospital Medicine 2008;3(4 Suppl):S20–S28. © 2008 Society of Hospital Medicine.

A systems approach to stroke care is a multidisciplinary team strategy with the goal of reducing stroke risk. This strategy may start with community-based primary prevention education. For individuals who experience stroke, the inpatient component of a stroke system is designed to integrate evidence-based acute treatment and secondary prevention strategies. A key component to stroke systems care is the use of standardized, evidence-based treatment protocols. During the acute (or subacute) phase of care, the team must be prepared to prevent stroke progression, prevent complications of stroke, manage comorbidities, and reduce the risk of secondary stroke. Hospitalists may take a leadership role both in establishing stroke systems protocols at their institutions and in providing inpatient care for stroke patients. The objective of this article is to review the components of inpatient stroke systems, with a focus on care of patients with noncardioembolic ischemic stroke. Methods to minimize common barriers to establishing stroke systems programs are also presented. Journal of Hospital Medicine 2008;3(4 Suppl):S29–S35. © 2008 Society of Hospital Medicine.

Transient ischemic attack (TIA) carries a substantial short-term risk for stroke, which is a leading cause of disability and death in the United States. Despite the existing evidence-based guidelines for secondary prevention of stroke, variability in the assessment, diagnostic testing, and treatment of patients with TIA in actual clinical practice remains. Identification of stroke etiology via radiological examination is of paramount importance for the appropriate treatment of patients after TIA or stroke. Management of ischemic stroke or TIA includes lifestyle modifications, reduction of modifiable risk factors (eg, hypertension, diabetes, and elevated cholesterol), and appropriate therapeutic treatments. Antiplatelet therapy is the cornerstone of secondary prevention of stroke; guidelines for its use for noncardioembolic cases have been developed from a solid evidence base. Additional therapeutic approaches include HMG-CoA reductase inhibitors (statins), antihypertensives, and anticoagulants. The results of ongoing large trials will further clarify the role of specific antiplatelet agents for the secondary prevention of stroke in patients with noncardioembolic ischemic stroke

Stroke is a prevalent and often devastating condition that is likely to affect a growing proportion of the United States population in the coming decades. Individuals who have experienced a stroke or transient ischemic attack are at elevated risk for recurrent events, which are frequently more severe. Therefore, secondary prevention has become the focus of much clinical research and widespread initiatives to deliver evidence-based care. Hospitalists are in a unique position to contribute substantially to these efforts. The 4 articles in this supplement are a call to action for hospital-based physicians. They are based on the conclusions of a panel of hospitalists, neurohospitalists, vascular neurologists, and neurointensivists who met for a roundtable discussion in March 2007. This, the first of the 4 articles, discusses the opportunity for hospitalists to take a leadership role in creating stroke systems of care that integrate secondary stroke prevention with inpatient treatment of acute stroke. The articles that follow will summarize the consensus of roundtable participants on stroke care best practices and their implementation. Journal of Hospital Medicine 2008;3(4 Suppl):S1–S5. © 2008 Society of Hospital Medicine.

Despite recent advances in the acute treatment of stroke, prevention and risk factor modification remain the mainstays of management for patients with ischemic stroke and transient ischemic attack. The majority of noncardioembolic ischemic strokes are atherothrombotic, presumed to be associated with the activation and aggregation of platelets. Antiplatelet medications have been shown to be effective in the secondary prevention of stroke of presumed arterial origin, both as monotherapy and in combination. Among combination of antiplatelet agents, aspirin plus extended-release dipyridamole has demonstrated statistically significant additive benefit over monotherapy with each agent. Clopidogrel plus aspirin does not prevent recurrent ischemic stroke over each component individually, and the combination increases the risk of hemorrhagic side effects. This article reviews the most recent studies on antiplatelet medications, including the combination of aspirin and clopidogrel or extended-release dipyridamole, and discusses some of the controversies that still exist with the use of antiplatelet agents.

Although meningovascular syphilis may result in cerebral ischemia, the effect of syphilis screening on the management of patients with ischemic stroke is unclear. This is due to the variability in syphilis incidence and prevalence, as well as the diverse manifestations that vary with stage of infection. We prospectively screened patients with cerebrovascular disease (CVD) for syphilis and analyzed seropositivity rates as well as assessed the impact of screening on patient management. There were relatively high rates of seropositivity in both CVD (12.5%, n = 104) and control (9.9%, n = 211) populations without a significant difference between groups. Overall, syphilis screening had little impact on the management of the patients with CVD. No cerebral event was attributed to meningovascular syphilis, and there was no identifiable group in which syphilis screening was more likely to result in treatment for meningovascular syphilis, although there were significantly (p < 0.001) higher rates of seropositivity in black patients than whites. The relatively high incidence of seropositivity in both groups is representative of local syphilis prevalence and suggests that screening is warranted in patients with neurological disease, but not necessarily as part of the evaluation for cerebral ischemia.

The introduction of the triptans (5-hydroxytryptophan [5-HT] (1B/1D) agonists) in the past decade has brought migraine-specific pain relief to those suffering from migraine. These drugs activate the serotonin receptors 5-HT(1B) and 5-HT(1D) on cerebral vessels. Concerns about their safety, particularly in patients with vascular risk factors, have been raised because triptans also activate the 5-HT(1B) receptors on coronary arteries. Although triptans are contraindicated in patients with cardiac or cerebrovascular disease, they are safer than many other medications used to treat patients with migraine, including the nonspecific serotonin-agonist ergot preparations.

Headaches are a universal experience and one of the most common causes for physician consultation. The physician must determine whether a neuroimaging study is warranted to aid in the diagnosis of primary or secondary headaches. Guidelines on neuroimaging of headache patients have been developed based on review of the literature; however, their applicability must be adapted to specific clinical situations. In general, neuroimaging is most likely to be useful if the history is not typical of a primary headache type (e.g., tension type, migraine, cluster headaches) or the neurological examination is abnormal. Neuroimaging has been crucial in the investigation of the pathogenesis of migraine and cluster headaches. Secondary headaches, which may be diagnosed by neuroimaging studies, include subarachnoid hemorrhage, cerebral venous thrombosis, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, aqueductal stenosis, and arterial dissection.

Disorders associated with prominent headaches, such as migraine with aura and cerebral arterial and venous diseases, increase the risk of ischemic and hemorrhagic stroke. Central nervous system vasculitis, posterior reversible encephalopathy syndrome, reversible cerebral vasoconstriction syndrome, and cerebral venous thrombosis are all disorders associated with severe or persistent headache in which the risk for ischemic and hemorrhagic stroke is increased. Hemorrhagic strokes, more frequently than ischemic strokes, present with distinct headaches, usually accompanied by focal neurological symptoms. Pregnancy, and especially the postpartum period, is a time of overlap between new-onset headache and stroke risk.

Serum levels of lipoprotein(a), Lp(a), have been shown to be associated with increased risk of atherosclerosis (AS) and AS-related diseases such as myocardial and ischemic cerebral infarcts (ICI). Lp(a) has been detected in the vascular wall of the aorta and coronary vessels, and we documented the presence of apo(a) in cerebral vessels of the Circle of Willis, associated with AS changes. In this study we further investigated and characterized the biochemical nature of Lp(a) detected in both large and small cerebral parenchymal vessels. Autopsy specimens of cerebral vessels of 51 patients were examined by immunohistochemistry with monoclonal antibodies against apo(a), apoB, and plasminogen. Lp(a) was detected in cerebral capillaries and arterioles. All of the 8 patients with ICI expressed Lp(a) in parenchymal vessels, generally (6/8) in both capillaries and arterioles. Of 43 patients without ICI only 25 had Lp(a) detected. Among the patients without ICI, there was a slightly increased incidence of parenchymal Lp(a) in those patients who had severe hypoxic brain damage (12/20) compared to those patients without severe hypoxic damage (9/23). Thus, the presence of Lp(a) in small cerebral parenchymal vessels may reflect the role of Lp(a) in ICI.

Practice PearlThis trial demonstrated the efficacy of combination therapy with dosages of aspirin (30–325 mg/day) plus dipyridamole (200 mg twice daily) in the prevention of vascular events after a noncardioembolic, mild-to-moderate ischemic stroke or transient ischemic attack, and showed a clear benefit of the aspirin/dipyridamole combination regimen over an aspirin-alone (30–325 mg/day) regimen.

Background Patients who have had an endarterectomy for symptomatic high-grade internal carotid artery (ICA) stenosis (70 to 99) still have a 9 risk of having an ischemic stroke in the same surgical region 2 years later. Significant cardiac or aortic sources of embolization (CASOE) may coexist with high-grade stenosis and occlusion of the ICA. Methods : A retrospective-inpatient chart review of patients with a diseased ICA (high-grade stenosis or occlusion) that was confirmed by carotid duplex ultrasonography was performed. These charts contained the clinical reason for carotid ultrasonography, recent echocardiography, and when available, brain neuroimaging scans. Echocardiography was reviewed for the presence of a CASOE. Neuroimaging was reviewed for all types of infarctions. Brain neuroimaging was considered predictive of finding a CASOE by echocardiography when infarctions were present in vascular territories other than that supplied by the diseased ICA. Results : There were 46 patients that met the criteria of the study. From all the CASOEs present, aortic arch plaque greater than 4 mm (48) and left ventricular ejection fraction of less than 30 (44) were the sources most frequently found. Twenty-nine patients had ischemic hemispheric symptoms ipsilateral to the diseased ICA. A CASOE was present in 18 (62) of 29 patients who had ischemic hemispheric symptoms ipsilateral to the diseased ICA. Neuroimaging predicted that there would be a CASOE present by echocardiography ( P Conclusion : A CASOE may coexist with high-grade stenosis and occlusion of the ICA. A complete evaluation for both CASOEs and carotid embolism is necessary to determine the cause of the stroke symptoms.

There is evidence to suggest that elevated plasma levels of lipoprotein (a) [Lp(a)] represent a risk factor for the development of atherosclerotic vascular disease, but the mechanism by which this lipoprotein localizes to involved vessels is only partially understood. In view of studies suggesting a link between inflammation and atherosclerosis and our previous finding that leukocyte defensin modulates the interaction of plasminogen and tissue-type plasminogen activator with cultured human endothelial cells, we examined the effect of this peptide on the binding of Lp(a) to cultured vascular endothelium and vascular smooth muscle cells. Defensin increased the binding of Lp(a) to endothelial cells approximately fourfold and to smooth muscle cells approximately sixfold. Defensin caused a comparable increase in the amount of Lp(a) internalized by each cell type, but Lp(a) internalized as a consequence of defensin being present was not degraded, resulting in a marked increase in the total amount of cell-associated lipoprotein. Abundant defensin was found in endothelium and in intimal smooth muscle cells of atherosclerotic human cerebral arteries, regions also invested with Lp(a). These studies suggest that defensin released from activated or senescent neutrophils may contribute to the localization and persistence of Lp(a) in human vessels and thereby predispose to the development of atherosclerosis.

Guidelines have been established for the management of acute ischemic stroke; however, specific recommendations for endovascular revascularization therapy are lacking. Burgeoning investigation of endovascular revascularization therapies for acute ischemic stroke, rapid device development, and a diverse training background of the providers performing the procedures underscore the need for practice recommendations. This review provides a concise summary of the Society of Vascular and Interventional Neurology endovascular acute ischemic stroke roundtable meeting. This document was developed to review current clinical efficacy of pharmacologic and mechanical revascularization therapy, selection criteria, periprocedure management, and endovascular time metrics and to highlight current practice patterns. It therefore provides an outline for the future development of multisociety guidelines and recommendations to improve patient selection, procedural management, and organizational strategies for revascularization therapies in acute ischemic stroke.

Endplate acetylcholinesterase (AChE) consists of globular catalytic subunits attached to the basal lamina by a collagen-like tail. Different genes encode the catalytic subunit and the tail portion of the enzyme. Endplate AChE deficiency was reported previously in a single case (Engel et al., 1977, patient 1). We describe here our observations in four additional patients (patients 2-5). Three cases were sporadic; patients 2 and 3 were sisters. All had generalized weakness increased by exertion but ophthalmoparesis was not a constant feature. All had mild slowing of the pupillary light reflex; other dysautonomic features were absent. None benefited from anticholinesterase therapy. All patients had a decremental electromyogram response; in four of the five patients, single nerve stimuli evoked a repetitive response. Miniature endplate potential amplitude was reduced in patient 5 only. Endplate amplitudes and currents were prolonged but the open-time of the acetylcholine receptor ion channel was normal. In patients 1-4 the quantal content of the endplate potential was reduced due to a reduced number of readily releasable quanta. Quantitative electron microscopy revealed abnormally small nerve terminals, abnormal encasement of the presynaptic membrane by Schwann cells and degeneration of junctional folds and of organelles in the junctional sarcoplasm. Acetylcholinesterase was absent from all endplates of all patients by cytochemical and immunocytochemical criteria. Density gradient ultracentrifugation of muscle extracts from patients 1, 3, 4 and 5 revealed an absence of the collagen-tailed form of the enzyme in patients 1, 3 and 4 but not in patient 5. The kinetic properties of the residual AChE in muscle were normal. Erythrocyte AChE activity and Km values, determined in three patients, were also normal. Studies of the catalytic subunit gene of AChE in patients 2 and 3 revealed no abnormality in those exons that encode the domain to which the tail subunit binds. In patients 1-4 the molecular defect is likely to reside in the gene encoding the tail subunit of AChE, or in a protein necessary to assemble the catalytic and tail subunits. In patient 5, the absence of AChE from the endplate may be due to a faulty tail subunit, a defect in the basal lamina site that binds the tail subunit or failure of transport of the assembled asymmetric enzyme from the cell interior to the basal lamina. The cause of the weakness in these patients is not fully understood but possible mechanisms are discussed.

Background Stroke is a major cause of morbidity and mortality in the general population and especially in older women. Review summary The incidence of stroke differs between men and women of a range of ages, with a higher lifetime risk for women than men. Pregnancy and the postpartum period are times of increased risk of stroke. Use of exogenous estrogen, especially in vulnerable populations, increases stroke risk. Women and men have different responses to primary and secondary stroke prevention. Women may not be offered acute ischemic stroke treatment as frequently as men; and female stroke survivors have worse outcomes. Conclusions Gender-related differences in stroke are attributed to the hormonal changes that women experience through their lifetime, diverse risk factors for stroke in men and women, and specific lifestyles, and comorbid conditions. Neurologists need to be aware of aspects of stroke that are particularly relevant to women.

The patient presenting with a cerebral infarction must undergo a thorough investigation for causes of infarction, which include atherosclerotic thromboembolic disease, cardiac disease, arterial wall abnormalities, and hematologic disorders. The investigation should include neurologic as well as cardiac and neuroradiologic evaluation. Treatment of acute hypertension should be cautious. New treatment modalities that show promise in maximizing return of function are being used. Efforts must be directed toward the prevention of recurrent infarction.

We studied the relation of serum glucose level measured in the first 12 hours of symptoms to the clinical findings, results of computed tomography (CT), and patterns of cerebral metabolism in 39 patients who had acute ischemic cerebral infarction. Structural damage was assessed by CT. Metabolic disruption was assessed using 18F-fluorodeoxyglucose and positron emission tomography (PET). Median initial serum glucose concentration was 155 mg/dl (6.7 mM). Clinical recovery was significantly poorer in patients with initial serum glucose levels higher than the median (p less than 0.05, chi square). PET tended to show normal results or minor abnormalities in patients with initial glucose levels less than the median, as opposed to lobar or multilobe abnormalities in patients with levels that were higher than the median (p less than 0.05, Kendall's Tau b). The severity of hypometabolism in the ischemic region, expressed as the percent asymmetry of local cerebral glucose metabolism between homologous brain regions, was greater in patients with initial glycemia concentrations higher than the median (p less than 0.001, t test). Relationships of serum glucose level with metabolic derangement and structural damage, but not outcome, held true in patients without a history of diabetes mellitus.

Survivors of ischemic stroke are at significant risk for recurrent stroke. Appropriate therapy for stroke prevention is needed given the significant morbidity and mortality associated with stroke, the high financial costs, and the neurologic disability associated with treatment failure. A treatment strategy based on assessed risk represents an appropriate use of medical resources and results in improved outcomes. This approach requires evaluation of major risk factors, the most serious of which is a history of ischemic stroke or transient ischemic attack. The annual risk for recurrent stroke is 6% during the first 5 years after an initial stroke. Non-modifiable risk factors include age, race, ethnicity, gender, family history, and geography. The most important modifiable risk factor is hypertension. Diabetes mellitus, hyperlipidemia, left ventricular hypertrophy, atrial fibrillation, and lifestyle factors such as smoking, alcohol abuse, and obesity contribute to stroke risk. Antihypertensive, lipid-lowering, and antiplatelet therapies have been successful in reducing the incidence of secondary stroke. Clinical trials validate the benefits of statin therapy in reducing the risk for secondary stroke. Studies of antiplatelet agents, including aspirin, clopidogrel, and aspirin combined with extended-release dipyridamole, have evaluated the risk reduction in recurrent stroke and have been concerned particularly with the risk for hemorrhage. Therapy for stroke prevention based on risk stratification can identify patients who are appropriate targets for aggressive intervention.

Background and Purpose —The sensitivity of the brain to brief periods of profound ischemia or prolonged periods of modest ischemia mandates an aggressive approach to acute stroke care. Past studies have shown that many stroke patients do not receive acute care in an urgent and timely fashion. The formation of acute stroke teams (AST) is one approach that can be used to accelerate the delivery of acute stroke care. Methods —We conducted a survey of major stroke program directors and neurovascular experts throughout the United States. The survey focused on issues related to the presence of AST, their staffing, operational features, and utilization at the surveyed programs and hospitals. Results —Surveys were returned from 45 of 60 centers. Ninety-one percent of the respondents indicated that they currently had an AST, with 66% formed between 1995 and 1997. Staffing of ASTs consisted of attending physicians (95%), nurses or study coordinators (73%), fellows (49%), and residents (46%). In almost all cases (98%), the AST was led by a neurologist or neurosurgeon, and 98% of the ASTs operated on a 24-hours-per-day, 7-days-per-week basis. The most common call frequency was 2 to 3 times per week (41%), followed by >5 calls per week (29%). In 59% of the cases, the teams cost ≤$5000 per year to operate. The vast majority (78%) of ASTs responded within 10 minutes of receiving a call. Conclusions —The formation of ASTs is quite common at the surveyed programs. Although staffing patterns vary, most teams are led by neurologists or neurosurgeons. The utilization of ASTs varies by facility, but they appear to be useful, with only a modest incremental financial cost. The use of ASTs may assist in providing more rapid medical care to stroke patients and increase the use of some acute therapies. Extension of the AST concept to nonacademic hospitals appears feasible.

Patients experiencing stroke or transient ischemic attack (TIA) are at high risk for recurrent (secondary) strokes, which comprise 29% of all strokes in the United States. Current recommendations for prevention of secondary stroke from the American College of Chest Physicians (ACCP) call for the broad use of platelet antiaggregation (antiplatelet) agents for patients with a history of noncardioembolic stroke or TIA. Five agents—aspirin, ticlopidine, clopidogrel, extended-release dipyridamole (ER-DP), and triflusal—have demonstrated efficacy in large-scale clinical studies in the prevention of recurrent vascular events and/or stroke in patients with a history of stroke. The results of the following studies are reviewed and compared: the Swedish Aspirin Low-Dose Trial (SALT), the United Kingdom Transient Ischaemic Attack (UK-TIA) Aspirin Trial, Dutch Transient Ischemic Attack (Dutch TIA) study (aspirin), the Canadian American Ticlopidine Study (CATS), the Ticlopidine Aspirin Stroke Study (TASS), the African American Antiplatelet Stroke Prevention Study (AAASPS) (ticlopidine), the Clopidogrel versus Aspirin in Patients at Risk of Recurrent Ischemic Events (CAPRIE) trial, the Management of Atherothrombosis With Clopidogrel in High-Risk Patients study (MATCH) (clopidogrel), the second European Stroke Prevention Study (ESPS2) (aspirin plus ER-DP), and the Triflusal versus Aspirin in Cerebral Infarction Prevention (TACIP) study. In comparative monotherapy studies of patients with previous stroke, ticlopidine demonstrates statistically significant improved efficacy over aspirin, and clopidogrel demonstrates nonsignificant slight improvement over aspirin for the prevention of ischemic cardiac and cerebrovascular events; however, the adverse event profile of ticlopidine (including rash, diarrhea, and neutropenia) will probably limit its long-term use. Among combination approaches, only aspirin plus ERDP has demonstrated statistically significant, clinically meaningful additive benefit over monotherapy with each agent. Clopidogrel plus aspirin did not significantly improve preventive efficacy and increased the risk of serious side effects, including life-threatening bleeding episodes. The 15,500-patient PRoFESS (the Prevention Regimen for Effectively Avoiding Second Strokes) study, with results expected in 2008, will directly compare aspirin plus ER-DP with clopidogrel monotherapy for the prevention of recurrent stroke and should provide statistically robust estimates of comparative efficacy for the development of improved recommendations.

Atherosclerosis is associated with arterial deposition of low density lipoprotein (LDL) and lipoprotein(a), Lp(a). Both lipoproteins have been detected in atherosclerotic vessels; however, while LDL has been shown to be only blood-derived, it is not clear whether Lp(a) is also produced within the vessel wall. In the present investigation we studied gene expression of apo(a) and apoB in human blood vessels. Aorta, carotid arteries and liver specimens from 29 adult and pediatric autopsy cases were studied by RT–PCR and Southern blot analysis with primers and probes specific for apo(a), apoB and GAPDH (a control housekeeping gene). The mRNA of apo(a), but not apoB, was found within the vessel wall in both adult atherosclerotic arterial vessels and in pediatric non atherosclerotic vessels. Neither apo(a) nor apoB mRNA was detected in femoral veins. To verify the nature of the detected transcripts, we cloned the 162 base pair (bp) RT–PCR product derived from the arterial wall total RNA. Nucleotide sequencing revealed 100% homology with the apo(a) gene. Thus, while LDL in atherosclerotic arteries is exclusively blood-derived, the accumulation of Lp(a) within the artery may be due in part to in situ production of apo(a) within the vessel wall.

This article highlights information from the 2000 National Conference for Nurse Practitioners symposium held in Washington, D.C., on November 9, 2000. It was sponsored by The Nursing Institute of Springhouse Corporation and funded by an unrestricted educational grant from Merck & Co., Inc. The firsttopic, "Overview of Migraine: Compelling Effects on Patients and Society," was presented for Dedie Downey Russell, CNP, ANP/GNP, MS. The second topic, "Understanding Pathophysiology: Evolving from Traditional to Current Therapeutic Options," was presented by Dara G. Jamieson, MD. Maureen Moriarty-Sheehan, MS, CRNP, who also served as chairperson, presented the third topic, "Developing a Management Plan for Optimal Patient Benefit."

Eight patients were evaluated with 18F-fluorodeoxyglucose positron emission tomography between 3 and 30 days after isolated stroke involving the middle cerebral artery territory that caused homonymous hemianopia. Diffuse hypometabolism was present throughout the damaged cerebral hemisphere, even in cortical areas not obviously ischemic by clinical examination or neuro-imaging. Glucose metabolism in primary and association visual cortex of the damaged hemisphere was decreased by more than 47% (p less than 0.01). Metabolism in the undamaged hemisphere was less profoundly affected, but significant decrements were found in calcarine (40%; p less than 0.01) and lateral occipital cortex (35%; p less than 0.05).

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.

We used 18F-2-fluoro-2-deoxyglucose and positron emission tomography to evaluate the effect of visual deprivation on brain glucose metabolism. In experiment 1, we compared local cerebral metabolic rates for glucose in seven normal volunteers studied with eyes closed to 11 age- and sex-matched normal volunteers studied with eyes open. Whole brain metabolism was similar in the two groups, and region/whole brain analysis of metabolic data showed that metabolism in the calcarine posterior cortex was decreased by 14% (P less than .05) with eye closure. Glucose metabolism in other regions was not different between the two groups. In experiment 2, we compared glucose metabolism in six patients with severe bilateral optic neuropathies to 12 age- and sex-matched normal controls. Whole brain glucose metabolism was unchanged in the optic neuropathy group compared to controls. However, statistically significant reductions in glucose metabolism in the optic neuropathy group were found in anterior calcarine cortex (17%), posterior calcarine cortex (27%), peristriate cortex (27%), and lateral occipital cortex (15%). The metabolic effects of damage to the pregeniculate visual system went well beyond those of simple eye closure.

The authors examined eight patients with dementia of the Alzheimer's type (DAT), five with prominent visual symptoms early in the illness (VS) and three with no visual symptoms (NVS). Results of neuro-ophthalmologic examinations on VS patients showed relatively consistent abnormalities in figure copying, color vision tested by isochromatic plates, and stereopsis. Cerebral glucose metabolism determined by 18F-fluoro-2-deoxyglucose positron emission tomography (PET) was unchanged in primary visual cortex of VS and NVS patients compared with 12 normal volunteers of similar age and sex. Glucose metabolism in VS patients was decreased by 45 and 34% in left and right visual association cortex (P less than 0.01 and P less than 0.05, respectively) and 34 and 37% in left and right inferior parietal cortex (P less than 0.05) compared with controls; NVS patients had no significant metabolic alteration in these areas. Symptoms, physical examination, and metabolic imaging imply that these patients are a heterogenous but distinct clinical subgroup of DAT often with mild dementia who have visual symptoms due primarily to visual agnosia.

Positron emission tomography (PET) is a technique of transverse tomographic imaging in which detection of two photons emitted from the annihilation of a positron and an electron is used to reconstruct the distribution of a positron emitting isotope within an object. PET provides the capacity to quantitatively measure the local tissue distribution of a variety of radionuclides that are attached to compounds that distribute according to function. Although this technique has been used to measure multiple functions and receptors within the brain, one of the most widespread uses is the measurement of local cerebral glucose metabolism based on the deoxyglucose method. In this article, the application of PET to clinical disorders such as dementia, brain tumors, psychiatric disease, epilepsy, movement disorders, and stroke as well as to normal states such as aging are examined.

We describe a patient with meningitis caused by lymphocytic choriomeningitis virus. Oligoclonal IgG bands were found in the patient's cerebrospinal fluid during acute and convalescent stages of the illness, and results of liver function tests were abnormal. Acute attacks of lymphocytic choriomeningitis virus infection in humans can be added to the list of diseases associated with cerebrospinal fluid oligoclonal IgG.

The extracranial carotid systems of 105 patients with retinal ischemia were examined using B-mode ultrasonography with integrated pulsed Doppler. Sixty-four patients had amaurosis fugax (AF), 17 central retinal artery occlusions (CRAO), and 21 branch retinal artery occlusions (BRAO). The prevalence of carotid stenosis (greater than or equal to 60%) ipsilateral to the symptomatic eye was low (16%). Eighty-six percent of AF patients had either no plaque causing less than a 60% stenosis. A significant proportion of subjects with normal duplex scans had alternative explanations for their retinal ischemia (eg, migraine, cardiac embolus). Patients with Hollenhorst plaques were more likely to have stenotic or ulcerated plaque (p = 0.04). The degree of carotid stenosis correlated significantly with the number of vascular risk factors identified in individual patients (p = 0.02). The presence of risk factors was more common in CRAO and BRAO patients compared with the AF group. Combined ultrasound-Doppler investigations of the carotid bifurcation are valuable noninvasive tools for the screening of patients with retinal ischemia.

Two cases of vertebral haemangiomas are reported which presented as spinal cord syndromes during pregnancy. Eleven additional cases of epidural haemangiomas in the literature which became symptomatic during pregnancy are reviewed. In 11 out of 13 cases symptoms presented during the third trimester of pregnancy and in all but two cases the epidural lesions were in the upper six thoracic vertebrae. These features can be explained by the effect of the gravid uterus on the relatively sparse vascular supply of the upper thoracic spinal cord.