Stroke‐related epilepsy

Stroke is the cause of about 10% of all epilepsy and 55% of newly diagnosed seizures among the elderly. Although recent advances in acute stroke therapy have improved longevity, there has been a consequent rise in the prevalence of stroke‐related epilepsy (STRE). Many clinical studies make a distinction between early (within 7 days of onset of stroke) and late (beyond 7 days of onset of stroke) seizures based on presumed pathophysiological differences. Although early seizures are thought to be the consequence of local metabolic disturbances without altered neuronal networks, late seizures are thought to occur when the brain has acquired a predisposition for seizures. Overall, STRE has a good prognosis, being well controlled by antiepileptic drugs. However, up to 25% of cases become drug resistant. STRE can also result in increased morbidity, longer hospitalization, greater disability at discharge and greater resource utilization. Additional controlled trials are needed to explore the primary and secondary prevention of STRE as well as to provide high‐quality evidence on efficacy and tolerability of antiepileptic drugs to guide treatment of STRE. Robust pre‐clinical and clinical prediction models of STRE are also needed to develop treatments to prevent the transformation of infarcted tissue into an epileptic focus.     

Computed tomographic changes of the brain and clinical outcome of patients with seizures and epilepsy after an ischaemic hemispheric stroke.

It is not well established whether seizures and epilepsy after an ischaemic stroke increase the disability of patients. Seventy-two patients with delayed seizures after a hemispheric infarct (37 with a single seizure and 35 with epilepsy) were included in the study. The modified Rankin scale was used to compare disability of the patients at 1 month after stroke and at 2 weeks after single or the last seizure, in case of epilepsy. The size of the X-ray hypoattenuation zone was compared on computed tomographic (CT) scans, performed in the weeks after the stroke and 1 week after single or repeated seizures. Lesion size was determined by superimposing the CT slices on digital cerebral vascular maps, on which the contours of the infarct area were delineated. The extent of the infarcts was expressed as the percentage fraction of the total surface area of the cerebral hemisphere. Groups with a single seizure and with epilepsy were mutually compared. Infarcts predominated in the parieto-temporal cortical regions. In the overall group the median Rankin score worsened significantly after seizures. The average size of the X-ray hypoattenuation zone was also significantly increased on the CT scans after the seizures, compared with those after stroke, without clear evidence of recent infarction. Mutual comparison of patients with a single seizure episode and of those with epilepsy showed only a trend of more severe disability and of increase in lesion size in the post-stroke epilepsy group. Delayed seizures and epilepsy after ischaemic stroke are accompanied by an increase in lesion size on CT and by worsening of the disability of the patients. This study does not allow to determine whether this is due to stroke recurrence or due to additional damage as a result of the seizures themselves.     

Prospects of modeling poststroke epileptogenesis

This Review describes the current status of poststroke epilepsy (PSE) with an emphasis on poststroke epileptogenesis modeling for testing new therapeutic agents. Stroke is a leading cause of epilepsy in an aging population. Late‐onset “epileptic” seizures have been reported in up to 30% cases after stroke. Nevertheless, the overall prevalence of PSE is 2–4%. Rodent models of stroke have contributed to our understanding of the relationship between seizures and the underlying ischemic damage to neurons. To understand whether acutely generated stroke events lead to a chronic phenotype more closely resembling PSE with recurrent seizures, a limited variety of approaches emerged in early 2000s. These limited methods of causing an occlusion in mice and rats show different infarct size and neurological deficits. The most often employed procedure for inducing focal ischemia is the middle cerebral artery occlusion. This mimics the pathophysiology seen in humans in terms of extent of damage to cortex and striatum. Photothrombosis and endothelin‐1 models can similarly evoke episodes of ischemic stroke. These models are well suited to studying mechanisms and biomarkers of epileptogenesis or optimizing novel drug discoveries. However, modeling of PSE is tedious, is highly variable, and lacks validity; therefore, it is not widely implemented in epilepsy research. Moreover, the relevance of ischemic models to specific forms of human stroke remains unclear. Stroke modeling in young male rodents lacks clinical relevance to elderly populations and especially to women, likely as a result of sex differences. Nevertheless, because of the neuronal damage and epileptogenic insult that these models trigger, they are helpful tools in studying acquired epilepsy and prophylactic drug therapy. © 2016 Wiley Periodicals, Inc.     

Seizures in childhood ischemic stroke in Taiwan

In this retrospective study, we collected clinical and radiographic data on children (age range, 1 month to 18 years) with symptoms and radiographic confirmation of seizure after ischemic stroke for the period of January 1996 to July 2006. Thirty-nine out of 94 children with ischemic stroke had poststroke seizures. Thirty-three out of 39 children with poststroke seizures had new onset seizures but only data of 28 were available. Infection was the most common etiology in the early poststroke seizure group (52.4%) but not in the late poststroke seizure group (0%). Infarction involving arterial ischemic stroke of anterior circulation were the most common in both the early poststroke seizure (61.9%) and the late poststroke seizure group (57.1%). Epilepsy was the most common sequelae in both the early poststroke seizure (38.1%) and late poststroke seizure group (100%). Children who had initial focal neurological sign (100% vs. 38.1%; P=0.007) or the focal cortical dysfunction on EEG (85.7% vs. 33.3%; P=0.029) were prone to develop late poststroke seizures. Late poststroke seizures had a high risk of developing poststroke epilepsy (100% vs. 38.1%; P=0.007). We conclude that seizures commonly occur in childhood ischemic stroke. Most poststroke seizures developed at an early stage. Infection was the most common etiology that caused early poststroke seizures in childhood ischemic stroke. Initial focal neurological signs and focal cortical dysfunction on EEG are risk factors for developing epilepsy. Poststroke seizures did not affect mortality, but there was a significant difference in normal outcome and epilepsy between those with or without poststroke seizures.     

Poststroke epilepsy: occurrence and predictors--a long-term prospective controlled study (Akershus Stroke Study)

PURPOSE: The aims of the study were to assess the occurrence of poststroke epilepsy (PSE) in patients with ischemic strokes, to identify predictors, and to investigate whether treatment in a stroke unit (SU) influenced the long-term outcomes of epilepsy. METHODS: Patients with PSE, defined as those having two ore more unprovoked epileptic seizures > or = 1 week after an ischemic stroke, were identified from a cohort of 484 patients with ischemic strokes. The patients were prospectively assessed 7-8 years after stroke or until death. Different variables were studied to look for possible predictors. RESULTS: From 484 patients with ischemic strokes, PSE developed in 12 (2.5%) and 15 (3.1%) patients during the first year and 7-8 years after stroke, respectively. Eight (53%) of these patients were treated in a stroke unit (SU), and seven (47%) were treated in a general medical ward (GMW). The mean age of those who developed PSE and those who did not was 74.3 years and 76.3 years, respectively. In a multivariate analysis, a Scandinavian Stroke Scale (SSS) score < 30 on admission was a significant predictor for developing PSE [odds ratio (OR), 4.9; p = 0.004). CONCLUSIONS: The prevalence of PSE, 7 to 8 years after an ischemic stroke, was 3.1%. SSS scores < 30 on admission were a significant predictor for PSE. Neither treatment in SU versus GMW, cortical location, nor age at onset of stroke seemed to influence the risk of developing PSE.     

Post‐stroke depression: can we predict its development from the acute stroke phase?

Objectives – To identify possible predictive factors for post‐stroke depression (PSD) in the acute phase of stroke. Methods – The study design was prospective, observational cohort study of patients with acute cerebral infarction (CI). Neurological and neuropsychological evaluations were conducted within the first 10 days from the onset of stroke and repeated at the 3‐month follow‐up. DSM‐IV criteria were used to define PSD. Results – From a total of 85 patients with CI, 59 patients completed the 3‐month follow‐up and 17 of them (28.8 %) fulfilled PSD criteria at the 3‐month follow‐up. Melancholy index of the Hamilton Depression Rankin Scale (HDRS) was associated with a risk three times greater than that of PSD at the 3‐month follow‐up in the univariate analysis (OR 3.07; 95% CI 1.53–6.16; P = 0.002) with no significant influence of stroke severity or the location of brain infarction (right or left side). The receiver operating characteristic curves pointed to a melancholy index ≥1.5 as the optimal cut‐off level associated with the development of PSD at the 3‐month follow‐up. Conclusions – Melancholy index of the HDRS ≥1.5 could be a useful clinical tool to detect patients with acute stroke at high risk of developing PSD.     

Epilepsy and stroke

Stroke is associated with an increased risk of subsequent seizures and epilepsy. Cerebrovascular lesions are the leading cause of epilepsy in the elderly, ahead of degenerative disorders, brain tumors and head trauma, accounting for up to one-third of newly diagnosed seizures in this population. The frequency of seizures in stroke victims varies from 5 to 20%, but only a minority will develop epilepsy. Based on differences in their presumed pathophysiology, seizures after stroke are usually divided into early and late seizures, according to various definitions. Early seizures are usually defined as those occurring within one or two weeks after stroke; late seizures usually occur within the first year after stroke. Several risk factors of seizures have been identified; stroke subtype and cortical location being the best-characterized predictors of seizure development. The optimal timing and type of anti-epileptic treatment remain debated. Several findings suggest that the majority of first generation anti-epileptic drugs are not the best choice in stroke patients.     

视频脑电监测对脑卒中后癫(癎)的诊断价值

目的 探讨视频脑电监测在脑卒中后癫(癎)的临床诊断价值.方法 回顾性分析68例脑卒中后癫(癎)患者的神经影像学资料、临床发作症状特点和VEEG改变,同时分析脑电图异常放电部位与脑卒中病变部位以及发作类型的对应关系.结果 疑诊脑卒中后癫(癎),视频脑电监测阳性检出率为85.3%,与常规脑电图检出率(30.9%)比较差异有显著性(P<0.05);脑卒中后癫(癎)的发生率与病变部位有明显相关性,脑叶出血或脑梗死累及大脑皮层的发生率较其他部位的病变明显增高; VEEG的异常放电部位、程度与脑卒中病变部位和范围以及发作类型有一定的关联性.结论 VEEG能提高脑卒中后癫(癎)的阳性检出率,并有助于明确其与癫(癎)发作类型与脑卒中病变部位的关系.     

老年人卒中后痫样发作现象的调查研究

This prospective study sought to investigate the clinical,radiological and electroencephalographic(EEG) characteristics of seizures in elderly stroke patients,and their outcomes.Over a 2-year study period,158 consecutive elderly patients with stroke were examined and followed up.Of these patients,32(20%) developed seizures,primarily related to stroke,within a follow up period between 5 months and 2 years.Of these 32 cases,20 experienced infarctions,and 12 experienced hemorrhages.Involvement of cortical regions was detected in most of the patients exhibiting seizures.In these patients,44% of the lesions involved cortical areas exclusively or in addition to subcortical areas observed on computed tomography(CT) images.Twenty-five patients(78%) developed early seizures(within 2 weeks after stroke),and half exhibited immediate post-stroke seizures.None of the patients exhibiting early onset seizures developed recurrent seizures or epilepsy,while 57% of late onset seizures(four cases) developed epilepsy.No specific EEG patterns were apparent in those who later developed epilepsy.Overall,early onset seizures after stroke were found to be relatively common,and did not affect outcome.Late onset seizures were less common,but were associated with chronic epilepsy.     

Post-stroke depression and functional independence: a conundrum

Brown C, Hasson H, Thyselius V, Almborg A‐H. Post‐stroke depression and functional independence: a conundrum.
Acta Neurol Scand: 2012: 126: 45–51.
© 2011 John Wiley & Sons A/S. Objectives – People who suffer a stroke are at risk of developing post‐stroke depression (PSD). Not only does this lower their quality of life but it also increases their risk of another stroke or death. This study aimed to investigate the factors associated with PSD in order to better direct rehabilitation efforts aimed at cutting the incidence of PSD. Material and methods – This study was based on all patients admitted to the stroke unit of a hospital in southern Sweden from 1 October 2003 to 30 November 2005. The total number of patients involved was 181. Measures were collected at 2 ± 1 weeks after discharge from hospital, 3 ± 0.5 months after the occurrence of the stroke and 12 ± 1 months after the occurrence of the stroke. Information collected was results from the Center of Epidemiologic Studies Depression Scale and the Barthel Index together with demographic data including age, sex, time since stroke and relationship status. Results – Those patients involved in the study were mainly men (58–59%) and generally those either married or cohabiting (53–57%). The age of respondents ranged from 32 to 92 years with a mean age of 74.0 (95%CI 72.37–75.63) at 2 ± 1 weeks after discharge. The Barthel Index scores ranged from 15 to 100 with means of between 88.7 and 91.7. Between 15% and 19% of the group were clinically depressed during the time frame of the study. The Barthel Index, measuring functional independence in terms of need for assistance with personal activities of daily living (P‐ADL), was consistently associated with PSD. Conclusions – The differences found in levels of depression between those with lower functional independence after a stroke compared to those more independent in P‐ADL, raise the possibility that attention should be paid to therapeutic rehabilitation for stroke patients to help them recover as much functional independence as possible in order to improve their quality of life and lower their chances of developing PSD.     

Predictive factors for the development of epilepsy after ischemic stroke

ObjectivesIschemic stroke is one of the most common causes of epilepsy in adults. The incidence of post-stroke epilepsy (PSE) is approximately 7%. Risk factors are higher stroke severity, cortical localization, higher National Institute of Health Stroke Scale (NIHSS) upon admission and acute symptomatic seizures. We analyzed the predictive factors of PSE development in our population.Materials and methodsRetrospective observational cohort of adult patients (age ≥ 18 years) with ischemic stroke assessed between January 2012 and June 2020. Patients with personal history of epilepsy and potentially epileptogenic structural injury other than acute or chronic stroke were excluded. Demographic, clinical and imaging variables were evaluated in a multivariate analysis for independent risk factors associated with PSE.ResultsMedical records of 1586 stroke patients were reviewed, 691 met the inclusion criteria and had at least one year of follow-up. Of them, 428 (61.9%) were males. During follow-up, 6.2% had diagnosis of PSE (42/691) with a higher frequency of: previous ischemic stroke, higher NIHSS upon admission, treatment with rt-PA, higher Fazekas scale grade, cortical involvement, hemorrhagic transformation, acute symptomatic seizures, longer hospitalization and higher modified Rankin Scale (mRS) at discharge compared to the group without PSE. In a multivariate analysis, acute symptomatic seizures (OR=3.22, p: 0.033), cortical involvement (OR=0.274, p < 0.05), Fazekas scale score (OR=0.519, p < 0.05) and mRS at discharge (OR=1.33, p: 0.043) were independent risk factors.ConclusionsThe variables related to higher risk of PSE were similar to those reported in the literature, highlighting the importance of neuroimaging findings, acute symptomatic seizures during hospitalization and neurological deficit at discharge. The data obtained will serve as the basis for construction of predictive models, allowing to individualize PSE probability in our population.     

Etiology of late cerebrovascular events after carotid endarterectomy

Background: Progressive carotid artery disease has been shown to cause cerebrovascular events years after a patient’s carotid thromboendarterectomy (CEA). Yet, some late cerebrovascular events in CEA patients are attributable to other etiologies. Objective: We sought to determine frequency and characteristics of late cerebrovascular events in post‐CEA patients attributable to etiologies other than progressive carotid disease. Methods: In a post hoc analysis of data from a CEA‐registry with long‐term follow‐up, all patients with transient ischaemic attack (TIA) or stroke occurring >1 month post‐CEA were identified. The etiologies of these events were dichotomized into the groups large‐artery atherosclerosis (LAA) and that non‐large‐artery atherosclerosis (non‐LAA), i.e. all other etiologies (Trial of Org 10172 in Acute Stroke Trial‐criteria). Frequency and characteristics of both groups were compared. Results: Sixty of 361 post‐CEA patients (16.6%; 95%CI 12.9–20.9%) had late cerebrovascular events after 7 years (median). Thirty patients had ischaemic strokes and 30 had TIAs. These events were attributable to LAA in 48% (29/60) and to non‐LAA in 52% (31/60). In the LAA group, contralateral carotid stenosis (62%; 18/29) was more frequent than recurrent ipsilateral stenosis (38%; 11/29). Amongst non‐LAA patients, cardioembolism (29%; 9/31) and small‐artery‐occlusion (23%; 7/31) were the most frequent causes. LAA and non‐LAA patients did not differ in age, time since CEA, risk factor profile, type of event, and baseline medication. Conclusion: In post‐CEA‐patients, half of the late cerebrovascular events were attributable to etiologies other than LAA. Clinical features did not distinguish LAA‐events from non‐LAA events. Thus, stroke prevention in post‐CEA patients should not be confined to screening for progressive carotid disease but includes efforts to optimize the management of risk factor and cardiac diseases.     

Late-onset seizures and risk of subsequent stroke: A systematic review

Otherwise unexplained late-onset seizures, conventionally defined as epileptic seizures occurring in subjects older than 60 years and in the absence of disorders known to increase the risk of developing epilepsy, have been assumed to be, in most cases, of cerebrovascular origin. We systematically searched the literature to identify the evidence supporting the association between otherwise unexplained late-onset seizures/epilepsy and the risk of subsequent stroke. Most data from the literature indicate that cerebrovascular disease often underlies otherwise unexplained late-onset seizures/epilepsy. Patients presenting with seizures occurring for the very first time in late life and without clinically overt cerebrovascular disease should be considered as at increased risk of stroke. Consequently, these patients should be screened for the presence of vascular risk factors and treated accordingly. Such measures may greatly contribute to prevent strokes in these patients.     

Tissue plasminogen activator does not alter development of acquired epilepsy

Purpose: Tissue plasminogen activator (t‐PA), a proven therapy for acute ischemic stroke, is an endogenous serine protease associated with neuronal activity and synaptic plasticity in the brain. Its expression is enhanced after seizures, and is involved in seizure propagation throughout the brain. Therefore, the increased use of t‐PA to treat stroke may have important implications for the development of poststroke epilepsy. Using experimental and clinical approaches, we investigated the role of t‐PA in the development of epilepsy. Methods: Mice deficient in t‐PA (t‐PA^?/?) or mice transgenically modified to overexpress neuronal t‐PA (T4) underwent amygdala kindling, and seizure threshold and rates of kindling were compared to those in wild‐type mice. For the clinical study, we recruited acute ischemic stroke patients who either received intravenous t‐PA treatment on admission to hospital (n = 177; cases) or did not (n = 158; controls). We then assessed the incidence of early and late onset seizures and epilepsy in these patients. Key Findings: T4 mice were more seizure‐prone than wild‐type mice, exhibiting lower seizure thresholds (p = 0.002), but there were no significant differences observed in the rate of kindling development when comparing either T4 mice, or t‐PA^?/? mice, to their wild‐type controls. Furthermore, we found no significant differences between the proportion of poststroke patients experiencing early or late seizures, or developing epilepsy, between those who received t‐PA and those who did not. Significance: Overexpression of endogenous t‐PA lowers seizure threshold but does not influence kindling epileptogenesis. Moreover, the therapeutic administration of t‐PA in humans does not influence the development of acquired poststroke epilepsy.     

脑卒中继发癫（癎）的临床特征及危险因素分析

目的 探讨脑卒中继发癫（癎）的临床特点及发生癫（癎）的影响因素,为临床防治提供依据.方法 回顾性分析2010-06-2012-06本院收治的76例（病例组）脑卒中后继发癫（癎）的患者资料,同时随机抽取神经内科住院的76例（对照组）未继发癫（癎）的脑卒中患者资料,分析脑卒中后癫（癎）的临床特点和相关危险因素.结果 脑卒中继发癫（癎）发生率7.7%（76/986）,其中缺血性脑卒中82.9%,出血脑卒中17.1%;早发性癫（癎）25.0%,迟发性癫（癎）75.0%;皮质病灶继发癫（（癎））69.7%,皮质下病灶继发癫（（癎））30.3%.单因素分析显示,2组患者脑卒中类型、病灶部位与受累半球侧别等因素比较,差异均有统计学意义（P〈0.05）;多因素分析显示,出血性脑卒中和皮质病灶差异有统计学意义（P〈0.05）.结论 脑卒中继发癫（癎）以迟发性癫（癎）多见.出血性脑卒中和皮质病灶是脑卒中继发癫（癎）的独立危险因素.     

From seizures to epilepsy and its substrates: Neurocysticercosis

Neurocysticercosis (NCC) is the main risk factor for late‐onset seizures in many Taenia solium endemic countries and is also increasingly recognized in high income countries, where it was once thought to have been eliminated. The course and outcome of NCC‐associated seizures and epilepsy are poorly understood. Substrates underlying NCC‐associated seizures and epilepsy are unknown. Another unknown is if there is an association between NCC and hippocampal sclerosis (HS) and if it leads to intractable epilepsy. We review evidence regarding the structural basis of seizures and epilepsy in NCC and its association with HS. There are only a limited number of prospective studies of NCC‐associated seizures and epilepsy. From these, it can be inferred that the risk of seizure recurrence is high following a first seizure, even though seizures are well‐controlled with antiepileptic drugs. The single most important risk factor for ongoing or recurrent seizures is the persistence of either degenerating or residual calcified cysticercus cysts in the brain parenchyma on follow‐up imaging studies. Medically intractable epilepsy requiring surgical treatment appears to be rare in people with NCC. In few cases that have been operated, gliosis around the cysticerci is the principal pathologic finding. Reports of the association between NCC and HS might be categorized into those in which the calcified cysticercus is located within the hippocampus and those in which the calcified cysticercus is located remote from the hippocampus. The former are convincing cases of medically intractable epilepsy with good seizure control following hippocampal resection. In the remaining, it is unclear whether a dual pathology relationship exists between HS and the calcified cysticercus. Carefully planned, follow‐up studies incorporating high‐resolution and quantitative imaging are desirable in order to clarify the outcome, the structural basis of NCC‐associated epilepsy, and also its association with HS.     

Statin on post-stroke epilepsy: A systematic review and meta-analysis

IntroductionRecent research has shown that statins can reduce the incidence of epilepsy after stroke, especially ischemic stroke, but the results are inconsistent. In view of current stroke guidelines do not recommend the use of anti-epileptic drugs (AED) for the prevention of epilepsy after stroke, statins may be a good choice. The purpose of this study was to conduct a systematic review and meta-analysis to determine the effect of statins on the prevention of epilepsy after stroke.MethodsCorrelative cohort studies were identified through search of PubMed, Cochrane Library and Embase databases. The main outcomes included post-stroke epilepsy (PSE) and early-onset seizure (ES). Subgroup analyses and Sensitivity analysis were performed to evaluate the influences of the predefined study characteristics on the outcome.ResultsSeven studies were included (n = 40831). Statin use was associated with a lower risk of PSE (including 6 articles) (odds ratio [OR] 0.60, 95% confidence interval [CI] [0.42, 0.84], p = 0.003), and there is a remarkable effect in ES (including 6 articles) (OR 0.36, 95% CI [0.25, 0.54], p < 0.00001).ConclusionAppropriate use of statins after stroke can reduce the risk of PSE, especially ES.     

Poststroke epilepsy: occurrence, predictors and treatment

Although a well-known clinical phenomenon, there still remain some questions regarding the definitions, pathophysiology and epidemiology of early and late poststroke seizures and of poststroke epilepsy. Poststroke seizures and epilepsy constitute important complications in patients surviving a stroke. Several studies of the prevalence and possible predictors of poststroke seizures and epilepsy have been undertaken during the past few decades. Unfortunately, these studies have not consistently used the established definitions. There are only few studies concerning treatment of poststroke epilepsy in the elderly, especially regarding the effect of the newer antiepileptic drugs. The aim of this article is to give an overview of the latest studies of poststroke seizures, with special emphasis on poststroke epilepsy, by presenting data on occurrence, predictors and treatment. The results from the recent studies on both poststroke seizures (early and late) and poststroke epilepsy are quite consistent. Poststroke epilepsy appears to occur in 2-4% of patients. The most convincing predictors of late poststroke seizures and epilepsy and treatment options are discussed in this review.     

An intravenous insulin protocol for strict glycemic control in acute ischaemic stroke

Background and purpose: There is a J‐shaped association between admission glycemia and outcome. We designed an intravenous insulin protocol aiming at rapid and strict glucose control in hyperglycemic ischaemic stroke patients. Here, we describe the initial experience, safety, and efficacy of this protocol to achieve and maintain euglycemia in the first 48 h. Methods: The protocol is based on parallel scales for adjustment of insulin infusion rate according to current glycemia and the rate of change of glycemia, which was recommended in our stroke unit in 4/2007 in acute ischaemic stroke patients with glycemia > 6 mM. Data were registered in the Acute Stroke Registry and Analysis of Lausanne (ASTRAL). Capillary blood glycemia was measured hourly with fingerprick test at onset of treatment and after each scale change. Target glycemia was 4.0–6.0 mM pre‐prandially (5.5–8.0 mM post‐prandially). Hypokalemia was defined as serum potassium < 3.5 mM and measured every 12 h. Specific algorithms were employed during meals and for patients leaving temporarily the stroke unit for diagnostic or therapeutic workup. Results: In the 90 protocol patients, the first normoglycemia was achieved within 8 h of treatment in 91.1% of patients (median interval 4 h (interquartile range (IQR): 3–6). During the median treatment duration of 25.5 h (IQR: 19.7–37.7), median glucose reduction was 2.5 mM (IQR: 1.3–4.3 mM). The overall rate of hypoglycemias was 4.5% and hypokalemias 18.5%. There was a significant increase in the proportion of hypokalemias on the first on‐treatment measurement compared to admission (24.4% vs. 8.9%, P = 0.002). Conclusions: The proposed intravenous insulin protocol controls acute post‐stroke hyperglycemia but frequently leads to hypokalemia. This issue needs to be addressed for the protocol to be suitable for use in larger, randomized controlled trial to explore its clinical effect.     

Cerebral vasomotor reactivity and dementia after ischemic stroke

Gur AY, Gücüyener D, Korczyn AD, Üzüner N, Gilutz Y, Özdemir G, Bornstein NM. Cerebral vasomotor reactivity and dementia after ischemic stroke.
Acta Neurol Scand: 2010: 122: 383–388.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives – Cerebral hemodynamic features of patients with post‐stroke dementia (PSD) are still obscure. We compared cerebral vasomotor reactivity (VMR) assessed in the acute phase of ischemic stroke (IS) in patients with and without PSD. VMR was also assessed and compared in demented and non‐demented patients in the late phase of IS. Materials and methods – VMR was assessed by transcranial Doppler and the Diamox test (1 g acetazolamide i.v.). PSD was confirmed by the National Institute of Neurological Disorders and Stroke and the Association Internationale pour la Recherche et I’Enseignement en Neurosciences (NINDS‐AIREN) and the Diagnostic and Statistical Manual of Mental Disorders (DSM‐IV) criteria. VMR% values were compared to verify correlation with dementia. Results – Thirty patients with acute IS (AIS) were studied and followed for 3–6 months. An additional group of 37 patients was studied in the late post‐stroke period (PIS). VMR% values in the AIS groups with and without PSD were similar (25.3 ± 20.3% and 36.5 ± 22.4%, respectively, NS). The mean VMR% in the PIS groups with and without PSD were similar (32.3 ± 19.5% and 41.2 ± 24.8%, respectively, NS). Conclusions – VMR cannot predict the development of dementia after AIS and cannot identify patients with dementia in the late phase of stroke.