Impact of Early Blood Pressure Lowering in Patients Presenting with Acute Ischemic Stroke.

PURPOSE OF REVIEW: In this review article we will discuss the acute hypertensive response in the context of acute ischemic stroke and present the latest evidence-based concepts of the significance and management of the hemodynamic response in acute ischemic stroke. RECENT FINDINGS: Acute hypertensive response is considered a common hemodynamic physiologic response in the early setting of an acute ischemic stroke. The significance of the acute hypertensive response is not entirely well understood. However, in certain types of acute ischemic strokes, the systemic elevation of the blood pressure helps to maintain the collateral blood flow in the penumbral ischemic tissue. The magnitude of the elevation of the systemic blood pressure that contributes to the maintenance of the collateral flow is not well established. The overcorrection of this physiologic hemodynamic response before an effective vessel recanalization takes place can carry a negative impact in the final clinical outcome. The significance of the persistence of the acute hypertensive response after an effective vessel recanalization is poorly understood, and it may negatively affect the final outcome due to reperfusion injury. Acute hypertensive response is considered a common hemodynamic reaction of the cardiovascular system in the context of an acute ischemic stroke. The reaction is particularly common in acute brain embolic occlusion of large intracranial vessels. Its early management before, during, and immediately after arterial reperfusion has a repercussion in the final fate of the ischemic tissue and the clinical outcome.

Transradial Access Results in Faster Skin Puncture to Reperfusion Time than Transfemoral Access in Posterior Circulation Mechanical Thrombectomy.

BACKGROUND: Successful mechanical embolectomy for acute embolic arterial occlusion in the posterior cerebral circulation can potentially result in less neurologic disability and mortality. The transradial approach can potentially offer more direct navigation into the posterior circulation than the transfemoral approach and can result in faster recanalization time. OBJECTIVE: To compare procedural metrics and the technical and clinical outcomes of transradial versus transfemoral access for mechanical embolectomy in the posterior cerebral circulation. MATERIAL AND METHODS: Single-center retrospective review of a prospectively maintained neurointerventional database from a large volume neurointerventional service in a tertiary academic center. Patients presenting with acute disabling symptoms due to embolic occlusion of a large intracranial artery in the posterior that underwent to endovascular treatment in our institution from January 2017 to January 2019 were included in the present study. RESULTS: Between January 2018 and January 2019 a total of 10 subjects underwent a mechanical embolectomy for acute embolic occlusion on the posterior circulation via transradial access; and between January 2017 and January 2018 a total of 10 subjects underwent a mechanical embolectomy for acute embolic occlusion on the posterior circulation via transfemoral access. Subjects in the transradial access group had a shorter skin puncture to recanalization time compared to the transfemoral group (29.2 ± 17.6 in the transradial group vs. 63.9 ± 56.7 in the transfemoral group respectively). CONCLUSIONS: This is the first study comparing transradial versus transfemoral access for mechanical embolectomy in patients with acute embolic occlusion in the posterior cerebral circulation. Transradial access resulted in a safe, effective, and faster endovascular route for recanalization in the acute embolic occlusion of the posterior circulation.

Infarto hemisférico maligno de la arteria cerebral media. Consideraciones diagnósticas y opciones terapéuticas / Malignant hemispheric infarction of the middle cerebral artery. Diagnostic considerations and treatment options

Introducción: El infarto hemisférico maligno (IHM) constituye un tipo específico y devastador de ictus isquémico. Usualmente afecta el territorio completo de la arteria cerebral media, aunque a veces involucra además otros territorios, presentando evolución clínica frecuentemente catastrófica, cuando solo se aplica tratamiento médico convencional. Objetivo: El propósito de esta revisión es analizar la evidencia científica disponible sobre el tratamiento de esta entidad. Desarrollo: El IHM tiene una morbimortalidad elevada. Clínicamente se caracteriza por deterioro neurológico temprano y síndrome hemisférico severo. Su sello distintivo es el desarrollo de edema cerebral ocupante de espacio, entre el primer y tercer día del inicio de los síntomas. El efecto de masa provoca desplazamientos, distorsiones y herniaciones de las estructuras encefálicas, aun en ausencia inicial de hipertensión endocraneal. Hasta hace pocos años, el IHM era considerado una entidad fatal e intratable, ya que la mortalidad asociada al tratamiento convencional podía superar el 80%. En este contexto desfavorable, la hemicraniectomía descompresiva ha resurgido como una alternativa terapéutica eficaz en casos seleccionados, reportándose un descenso de la mortalidad entre un 15-40%. Conclusiones: En los últimos años diversos estudios clínicos aleatorizados han demostrado el beneficio de la hemicraniectomía descompresiva en los pacientes con IHM, la cual no solo ha disminuido la mortalidad sino que también ha mejorado los resultados funcionales

Introduction: Malignant hemispheric infarction (MHI) is a specific and devastating type of ischemic stroke. It usually affects all or part of the territory of the middle cerebral artery although its effects may extend to other territories as well. Its clinical outcome is frequently catastrophic when only conventional medical treatment is applied. Objective: The purpose of this review is to analyse the available scientific evidence on the treatment of this entity. Development: MHI is associated with high morbidity and mortality. Its clinical characteristics are early neurological deterioration and severe hemispheric syndrome. Its hallmark is the development of space-occupying cerebral oedema between day 1 and day 3 after symptom onset. The mass effect causes displacement, distortion, and herniation of brain structures even when intracranial hypertension is initially absent. Until recently, MHI was thought to be fatal and untreatable because mortality rates with conventional medical treatment could exceed 80%. In this unfavourable context, decompressive hemicraniectomy has re-emerged as a therapeutic alternative for selected cases, with reported decreases in mortality ranging between 15% and 40%. Conclusions: In recent years, several randomised clinical trials have demonstrated the benefit of decompressive hemicraniectomy in patients with MHI. This treatment reduces mortality in addition to improving functional outcome

Malignant hemispheric infarction of the middle cerebral artery. Diagnostic considerations and treatment options. / Infarto hemisférico maligno de la arteria cerebral media. Consideraciones diagnósticas y opciones terapéuticas.

INTRODUCTION: Malignant hemispheric infarction (MHI) is a specific and devastating type of ischemic stroke. It usually affects all or part of the territory of the middle cerebral artery although its effects may extend to other territories as well. Its clinical outcome is frequently catastrophic when only conventional medical treatment is applied. OBJECTIVE: The purpose of this review is to analyse the available scientific evidence on the treatment of this entity. DEVELOPMENT: MHI is associated with high morbidity and mortality. Its clinical characteristics are early neurological deterioration and severe hemispheric syndrome. Its hallmark is the development of space-occupying cerebral oedema between day 1 and day 3 after symptom onset. The mass effect causes displacement, distortion, and herniation of brain structures even when intracranial hypertension is initially absent. Until recently, MHI was thought to be fatal and untreatable because mortality rates with conventional medical treatment could exceed 80%. In this unfavourable context, decompressive hemicraniectomy has re-emerged as a therapeutic alternative for selected cases, with reported decreases in mortality ranging between 15% and 40%. CONCLUSIONS: In recent years, several randomised clinical trials have demonstrated the benefit of decompressive hemicraniectomy in patients with MHI. This treatment reduces mortality in addition to improving functional outcomes.

Does dementia increase risk of thrombolysis?: a case-control study.

BACKGROUND: Dementia represents a potential challenge when thrombolysis is a treatment option. In this study, we assess the impact of dementia on the rate of intracerebral hemorrhage (ICH) and hospital mortality associated with acute ischemic stroke (AIS) in patients treated with thrombolysis. METHODS: A cohort of patients with AIS was identified from the National Inpatient Sample database for the years 2000 to 2007. Vascular and degenerative types of dementia were identified by the International Classification of Diseases-9-CM codes. A matched random sample without dementia was selected from a pool of those with AIS and treated with thrombolysis. RESULTS: In this analysis, 35,557 patients with diagnosis of dementia were included; 207 (0.56%) received thrombolysis. In-hospital mortality (17.48% vs 8.63%) and ICH (5.80% vs 0.38%) were higher in the thrombolysis group (p < 0.0001) compared to those who did not receive thrombolysis. Multivariate analysis showed that thrombolysis was associated with increased hospital mortality (odds ratio [OR] 16.15; 95% confidence interval [CI] 8.54-30.53) and ICH (OR 2.80; 95% CI 1.82-4.32). Compared to a matched population of patients without dementia treated with thrombolysis (n = 621), those who had dementia and were treated with thrombolysis had similar risks of ICH (5.80% vs 4.51%, p = 0.45) and mortality (17.39% vs 14.49%, p = 0.31) rates. With thrombolysis, ICH remained a predictor of mortality for both dementia and control groups (OR 2.25; 95% CI 1.02-4.99). CONCLUSION: The administration of thrombolysis for AIS in patients with dementia was not associated with increased risk of ICH or death compared to the counterparts without dementia. ICH remained as predictor of mortality.

Predictors of recurrent stroke in African Americans.

BACKGROUND: Stroke incidence and mortality are disproportionately higher among African Americans than among whites. OBJECTIVE: To describe the recurrent stroke characteristics and determine the predictability of known vascular risk factors for stroke recurrence in African Americans. METHODS: The authors followed 1,809 African Americans in the African-American Antiplatelet Stroke Prevention Study with recent noncardioembolic ischemic stroke for recurrent stroke, recurrent stroke subtype, and disability. RESULTS: Of the subjects, 10.6% experienced a recurrent stroke during follow-up. The mean interval between eligibility and recurrent stroke was 325 days (median 287 days, SD = 224 days). Stroke recurrence resulted in an average 1.5-point increase in the National Institute of Health Stroke Scale (p < 0.001) and a 3.5-point decrease in modified Barthel Index (p < 0.001). Of previously nondisabled subjects, 48% became disabled or died after stroke recurrence (p < 0.0001). Longitudinal analysis resulted in a hazard for recurrent stroke for each 10-mm Hg increase in systolic blood pressure of 1.103 (95% CI: 1.031 to 1.179, p = 0.004), pulse pressure 1.123 (95% CI: 1.041 to 1.213, p = 0.003), and mean arterial pressure 1.123 (95% CI: 1.001 to 1.260, p = 0.048). Multivariate analysis revealed increases in the recurrent stroke hazard for increases in baseline Glasgow Outcome Score (1.449, 95% CI: 1.071 to 1.961, p = 0.016) and increases in longitudinal pulse pressure (1.009, 95% CI: 1.001 to 1.017, p = 0.029). CONCLUSION: Recurrent stroke leads to disability and disability predicts recurrent stroke. Hypertension is the most predictive modifiable stroke risk factor.

Angioplasty for intracranial artery stenosis.

BACKGROUND: Intracranial artery stenosis causes up to 10% of all ischaemic strokes. The rate of recurrent vascular ischaemic events is very high. Angioplasty with or without stent placement is a feasible procedure to dilate the vessel affected. However, its safety and efficacy have not been systematically studied. OBJECTIVES: To determine the efficacy and safety of angioplasty combined with best medical treatment compared with best medical treatment alone in patients with acute ischaemic stroke or transient ischaemic attack (TIA) resulting from intracranial artery stenosis for preventing recurrent ischaemic strokes, death, and vascular events. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched March 2006). In addition we searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 1, 2006), MEDLINE (1966 to March 2006), EMBASE (1980 to February 2006) and Science Citation Index (1945 to March 2006). To identify further published, unpublished and ongoing trials we searched reference lists of relevant articles and contacted authors and experts in the field. SELECTION CRITERIA: Randomised or otherwise controlled studies comparing best medical care plus angioplasty of the intracranial cerebral arteries, with or without stent placement, with best medical care alone. Studies were only included if data for clinical significant endpoints such as recurrent ischaemic stroke, haemorrhagic stroke and death were available. DATA COLLECTION AND ANALYSIS: Two review authors selected trials for inclusion, and independently assessed trial quality and extracted data. Calculation of relative treatment effects with subgroup analysis was done if possible. MAIN RESULTS: No randomised controlled trials were found. There were 79 articles of interest consisting of open-label case series with three or more cases. The safety profile of the procedure showed an overall perioperative rate of stroke of 7.9% (95% confidence intervals (CI) 5.5% to 10.4%), perioperative death of 3.4% (95% CI 2.0% to 4.8%), and perioperative stroke or death of 9.5% (95% CI 7.0% to 12.0%). No comments can be made on the effectiveness of the procedure. AUTHORS' CONCLUSIONS: At present there is insufficient evidence to recommend angioplasty with or without stent placement in routine practice for the prevention of stroke in patients with intracranial artery stenosis. The descriptive studies show that the procedure is feasible although carries a significant morbidity and mortality risk. Evidence from randomised controlled trials is needed to assess the safety of angioplasty and its effectiveness in preventing recurrent stroke.

Position-dependent levitation of the dominant arm after left parietal stroke: an unreported feature of posterior alien limb syndrome?

We describe a patient with an unreported feature of posterior alien limb phenomenon characterized by position-dependent levitation of the dominant arm exacerbated by tactile stimulation and associated with low-amplitude tremor of the fingers of the right hand in addition to a sensation of strangeness in the arm, secondary to a left parietal stroke.

Fou rire prodromique and history of pathological laughter in the XIXth and XXth centuries.

Fou rire prodromique (prodrome of crazy laughter) is a rarely described nosological entity. In 1903, Charles Féré, a French neurologist, introduced the term fou rire prodromique to describe pathological laughter heralding an apoplectic event. He was also among the first to describe gelastic epilepsy. His description was influenced by Edouard Brissaud, who supported the existence of a thalamic center for laughter regulation and suggested that spasmodic laughter and crying were due to lesions of the faisceau psychique (anterior internal capsule) or to irritation of the faisceau géniculé (corticobulbar tract). One hundred Years later, we review the evolution of the theories about pathological laughter and crying from Charles Bell in the early XIXth Century, up to the seminal works of Kinnier Wilson and James Papez and the era of modern neuroscience.

Intracerebral hemorrhage associated with Sneddon's syndrome: is ischemia-related angiogenesis the cause? Case report and review of the literature.

Sneddon's syndrome is characterized by livedo reticularis and multiple ischemic infarcts often associated with antiphospholipid antibodies. Intracerebral hemorrhage (ICH) is unusual in Sneddon's syndrome and has not been reported as the presenting complaint. We report a 38-year-old woman with a history of two miscarriages, Raynaud's phenomenon and livedo reticularis who presented acutely with ICH. Angiography showed prominent leptomeningeal and transdural anastomoses (pseudoangiomatosis). Anticardiolipin antibodies were positive. A right frontal brain biopsy failed to reveal vasculitis and a skin biopsy was nonspecific. MRI showed residual intracerebral hemorrhage (ICH), diffuse atrophy, multiple small white matter infarcts and leptomeningeal enhancement. This is the first report of Sneddon's syndrome presenting with an ICH. It shares features with the Divry-van Bogaert syndrome. We discuss the cause of the pseudoangiomatosis pattern and its role in the genesis of the hemorrhage and suggest that cerebral angiography should be done in every patient with Sneddon's syndrome, as it could impact therapy.

Surgical decompression for cerebral oedema in acute ischaemic stroke.

BACKGROUND: The high mortality that follows a large cerebral infarction is in part due to brain oedema. Oedema causes mass-effect with raised intracranial pressure and herniation. Medical therapies are used to reduce intracranial pressure but outcome is poor in spite of treatment. Decompressive surgical techniques that attempt to relieve high intracranial pressure due to oedema have been described, but their efficacy in reducing case fatality and disability is uncertain. OBJECTIVES: To compare medical therapy plus decompressive surgery with medical therapy alone on the outcomes death and 'death or dependency' in patients with an acute ischaemic stroke complicated by clinical and radiologically confirmed cerebral oedema. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (4 October 2001). In addition, we searched the following electronic databases: the Cochrane Controlled Trials Register (Cochrane Library, issue 3, 2001), MEDLINE (1966 - April 2002), EMBASE (1980 - April 2002), and SCISEARCH (to April 2002). We also searched the reference lists of all relevant articles retrieved and contacted individual investigators and experts in the field. SELECTION CRITERIA: Randomised controlled studies comparing the outcome of treatment with decompressive surgical intervention with treatment not involving surgery. We aimed to include only those studies with low or moderate risk of bias. DATA COLLECTION AND ANALYSIS: Titles retrieved by searching were assessed for relevance by one author. Data were extracted independently by two authors with discussion to resolve differences. Relevant sub-group analyses were planned and we planned to calculate Peto odds ratios with 95% confidence intervals. MAIN RESULTS: Over 9000 citations were retrieved and inspected for relevance. We identified no randomised-controlled trials to include in a meta-analysis. Five observational studies reporting comparative data were found along with a number of small series and single case reports. Two ongoing randomised-controlled trials were identified. REVIEWER'S CONCLUSIONS: There is no evidence from randomised-controlled trials to support the use of decompressive surgery for the treatment of cerebral oedema in acute ischaemic stroke. Evidence from randomised-controlled trials is needed to accurately assess the effect of decompressive surgery.

"Fou rire prodromique" as the presentation of pontine ischaemia secondary to vertebrobasilar stenosis.

"Fou rire prodromique" (prodrome of crazy laughter) is a rare form of pathological laughter of uncertain pathophysiology. A patient is presented with pathological laughter as the first manifestation of pontine ischaemia due to vertebrobasilar stenosis. A 65 year old man developed uncontrollable and unemotional laughter for almost an hour followed by transient right facial-brachial paresis. He had fluctuation of laughter, right facial brachial paresis, and occasional crying. Magnetic resonance imaging, magnetic resonance angiogram (MRA), and an angiogram showed small left pontine and cerebellar infarcts, left vertebral artery occlusion, and right vertebral and basilar artery stenosis. His condition deteriorated to bilateral brain stem infarction and he died. Necropsy confirmed the extensive brain stem infarction. Pathological laughter can be the very first presenting manifestation of ischaemia of the ventrotegmental junction of the upper pons. It is hypothesised that the pathological laughter in this patient was secondary to ischaemic ephaptic stimulation of the descending corticopontine/ bulbar pathways.

Massive cerebral edema after recanalization post-thrombolysis.

BACKGROUND: Intravenous thrombolysis with tissue plasminogen activator is an approved and effective therapy for acute ischemic stroke within the first 3 hours from onset. In addition to the risk of hemorrhage, there is a risk of postrecanalization cerebral edema. The authors present the case of a patient with an ischemic stroke treated successfully with intra-arterial thrombolysis who subsequently developed massive brain edema in the face of clinical improvement. CASE: An 81-year-old man presented within 1 hour of developing a full right middle cerebral artery (MCA) syndrome. Computed tomography (CT) was normal. A cerebral angiogram demonstrated an occlusion of the M1 segment of the right MCA. The patient was treated with intra-arterial urokinase 750,000 units. He recovered during the procedure. Serial CT scans demonstrated progressive edema with mass effect in the right MCA distribution. The patient remained asymptomatic except for a mild sensory deficit. DISCUSSION: Postrecanalization cerebral edema is an uncommon but potentially lethal complication of thrombolysis. It is postulated that the edema is due to ischemic injury aggravated by reperfusion with vasogenic edema. The presence of this massive edema is usually associated with clinical worsening. The present case illustrates that this disorder can be associated with good outcome.

Sumatriptan can alleviate headaches due to carotid artery dissection.

Cluster headaches can be mimicked by a spontaneous carotid artery dissection. We report a 45-year-old man with a spontaneous carotid artery dissection whose unilateral headache responded to sumatriptan. An oral dose of 50 mg of sumatriptan relieved 90% of the pain after 2 hours. A second dose the next day achieved similar results within 4 hours. The diagnosis of dissection was made later by magnetic resonance angiogram and conventional angiography. This case illustrates that a positive response to a triptan can not be used to distinguish the first attack of cluster headache from a carotid artery dissection.

Isolated vertigo as a manifestation of vertebrobasilar ischemia.

OBJECTIVE: We sought to demonstrate that isolated episodes of vertigo can be the only manifestation of vertebrobasilar ischemia. BACKGROUND: Isolated persistent vertigo is classically ascribed to labyrinthine disorders and is only rarely considered to reflect vertebrobasilar ischemia. METHODS: We retrospectively analyzed all of the records of the Saint Louis University Stroke Registry between January 1, 1992 and September 1, 1993. We set out to identify those patients discharged with a diagnosis of transient ischemic attack (TIA) in the vertebrobasilar system. We reviewed their clinical records and the results of their diagnostic studies. RESULTS: We screened 600 admissions and found 29 patients with vertebrobasilar circulation TIAs. Of these, five men and one woman had episodic vertigo for at least 4 weeks as their only presenting symptom. All six patients had one of two abnormal patterns on magnetic resonance angiography (MRA): focal basilar stenosis or widespread vertebrobasilar slow flow. In three patients, the MRA findings were confirmed by cerebral angiography. Five patients were treated with warfarin and one with aspirin. Two patients developed brainstem infarctions, one of them fatal. CONCLUSIONS: Isolated vertigo can be the only manifestation of vertebrobasilar ischemia. Its frequency may be underestimated in clinical practice. Noninvasive testing is helpful both for diagnosis and follow-up.

Cerebrovascular hemodynamic inefficiency of premature ventricular contractions.

Transcranial Doppler (TCD) measurements of middle cerebral artery (MCA) blood flow velocities were recorded and synchronized with electrocardiographic (EKG) recordings in 52 EKG/TCD complexes in 4 patients. Thirty-seven normal sinus beats and 13 conductive and 2 nonconductive premature ventricular contractions (PVCs) were examined. Mean velocities averaged 45 +/- 4 cm/sec for normal sinus rhythm (NSR) vs 26 +/- 4 cm/sec in the PVC group (P = 0.007). Peak systolic velocities averaged 74 +/- 6 cm/sec for the NSR and 45 +/- 7 cm/sec in the PVC group (P = 0.016). The latency between the QRS complexes and corresponding TCD wave forms (QRS-SU) averaged 0.12 +/- 0.03 sec in NSR AND 0.17 +/- 0.04 sec for the PVC group (P < 0.001). In addition, QRS-SU was inversely related to all velocities. PVCs appeared to be less hemodynamically efficient than NSR. The lower blood flow velocities and increased QRS-SU may result from lower stroke volume and delayed ventricular contraction associated with the aberrant QRS complex.

Sinus arrest after administration of intravenous metoclopramide.

BACKGROUND: Sinus arrest is a rare complication of metoclopramide administration. CASE DESCRIPTION: A 51-year-old woman developed Guillain-Barre syndrome and severe dysautonomia. Metoclopramide was administered for the treatment of gastroparesis. Sinus arrest followed drug administration on several occasions and on rechallenge. CONCLUSIONS: After reviewing the literature and discussing possible etiologies for this unusual adverse drug reaction in this setting, we recommend that metoclopramide be used with caution in patients prone to develop bradyarrythmias, particularly those with dysautonomias and Guillain-Barre syndrome.