Acute Phase Of Cerebral Infarction Research Articles

Midkine in repair of the injured nervous system

Midkine (MK) is a growth factor with neurotrophic and neurite outgrowth activities. It was expressed in the peri-ischaemic area in the acute phase of cerebral infarction in rat brains. Astrocytes were the origin of MK in this occasion. MK has been assessed in terms of its effects on neural injury. The administration of MK into the lateral ventricle immediately prior to ischaemia prevented cell death in the hippocampal CA1 neurons degenerated by transient forebrain ischaemia in gerbils. MK administration was also beneficial in rats with neural injury, especially after kainic acid-induced seizures. Gene therapy with mouse MK cDNA using an adenovirus was effective in reducing the cerebral infarction volume and in increasing the number of neuronal precursor cells in the subventricular zone of the rat brain. MK mRNA and MK protein were found in spinal cord motor neurons of the anterior horn in both the acute phase of sciatic nerve injury and 3 weeks later. MK immunoreactivity was also found in the proximal side of a sciatic nerve-injured site in sciatic nerve axons. MK receptors were expressed in Schwann cells after injury, suggesting crosstalk between axons and Schwann cells. MK was also present in nerve terminals and influenced ACh receptor clustering during neuromuscular development in Xenopus. Thus, MK may also be involved in reinforcing and maintaining the synapse. All these findings indicate the therapeutic potential of MK for promoting repair of the nervous system after injury.Linked ArticlesThis article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4

Efficacy of Superficial Temporal Artery-Middle Cerebral Artery Double Anastomoses in a Patient with Rapidly Progressive Moyamoya Disease: Case Report

Moyamoya disease can be associated with a rapidly progressive course in young patients. This report describes a patient with moyamoya disease who experienced rapid disease progression, resulting in cerebral infarction and a wide area of diminished cerebral perfusion. Double superficial temporal artery (STA)-middle cerebral artery (MCA) anastomoses were utilized to immediately increase cerebral perfusion in the affected area. This case involved a 5-year-old girl who had been diagnosed with moyamoya disease and had undergone STA-MCA anastomosis with indirect bypass in the right hemisphere at the age of 3. At the time of presentation, magnetic resonance (MR) imaging showed cerebral infarction at the left frontal lobe, and MR angiography showed rapidly progressive narrowing of the left MCA that had not been present 3 months prior. N-isopropyl-p-[I123] iodoamphetamine single-photon emission computed tomography (IMP-SPECT) showed markedly decreased uptake in the left hemisphere. She underwent emergent STA-MCA double anastomoses with indirect bypass on the left side. IMP-SPECT showed marked increase in uptake in the left hemisphere. The anterior cerebral artery (ACA) territory adjacent to the cerebral infarction also showed increased uptake on the SPECT. Postoperatively, there were no clinical or radiographic indications of ischemic or hemorrhagic complications. Double anastomoses are effective in quickly and significantly increasing blood flow. The postoperative course in this case was uneventful. Double anastomoses are a surgical option for patients with moyamoya disease who show rapid disease progression, even in those in the acute phase of cerebral infarction.

脳梗塞急性期における片麻痺上肢への促通反復療法と持続的低周波電気刺激法の同時併用療法による運動機能と浮腫の改善

目的：脳梗塞急性期の片麻痺上肢への促通反復療法を持続的低周波電気刺激下で行う同時併用療法が麻痺と浮腫，関節可動域に及ぼす影響について検討した．対象：対象は2011 年4 月から2 年間に当院に入院した急性期脳梗塞片麻痺患者で，片麻痺と麻痺側手に浮腫があった患者30 名である．方法：単盲検無作為化比較試験を用い，促通反復療法と持続的低周波電気刺激との同時併用療法群（介入群）と関節可動域訓練群（対照群）に割付け，それぞれの治療を30 分，2 週間実施した．効果の評価はUpper Limb Fugl-Meyer Assessment（FMA），浮腫の測定，関節可動域テストを治療の前後に行った．結果：治療によって，介入群は全ての評価が有意に改善した．対照群はFMAに有意な改善を認めたが浮腫と関節可動域は改善がなく，改善度も介入群がFMAと浮腫，関節可動域で対照群より有意に大きかった．結語：促通反復療法と持続的低周波電気刺激の同時併用療法は，急性期片麻痺上肢の運動麻痺回復と麻痺側手の浮腫軽減を促進する．

The lower safety level of blood pressure evaluated by123I-IMP single-photon emission computed tomography in acute cerebral infarction patients

SUMMARY Aims: At the acute phase of cerebral infarction, the autoregulation of cerebral blood flow (CBF) is compromised. In this study, we explored the lower safety level of blood pressure (BP) for maintaining optimal CBF in acute cerebral infarction patients. Patients & methods: Acute middle cerebral artery territorial infarctions were screened. Patients who had single-photon emission computed tomography performed within 7 days following onset were enrolled (n = 30). The CBF ratio (ischemic:intact) was calculated at the border zone of the middle cerebral artery. Vascular lesions were assessed by magnetic resonance angiography. Results: The lowest BP level that maintained the CBF ratio ≥0.6 was 109 mmHg in patients with mild-to-moderate stenosis and 142/79 mmHg in patients with occlusion at the lesion side and stenosis at the intact side by the linear regression analysis. Conclusion: BP control should be carefully managed in acute stroke patients with occlusion and stenosis in the main arteries of the brain.

Relevance between quality craft and safe medication of Shuxuetong injection

Shuxuetong (SXT) injection is the first animal original injection in traditional Chinese medicine, the main component are the leech and the earthworm. SXT has got five national invention patents, and is recognized as the most potent medicine expelling blood stasis agent, which indication is the only one be clearly approved by SFDA as the acute phase of cerebral infarction. Modern biological extraction technology is adopted to prepare SXT, the entire production process using only saline as a solvent. Patented product process is induced to maximize the retention of medicinal components and activity, as well as to remove invalid substances as variant protein,high molecular weight substances which causes allergic reactions. SXT have been isolated and identified class 7 of56 compounds, the molecular weight is from 100 to 1 700 Da, mainly including peptides, glycopeptides, endogenous small molecules.

Study of Hemostatic Biomarkers in Acute Ischemic Stroke by Clinical Subtype

We studied the usefulness of hemostatic biomarkers in assessing the pathology of thrombus formation, subtype diagnosis, prognosis in the acute phase of cerebral infarction, and differences between various hemostatic biomarkers. Our study included 69 patients with acute cerebral infarction who had been hospitalized within 2 days of stroke onset. Fibrin monomer complex (FMC), soluble fibrin (SF), D-dimer, thrombin-antithrombin III complex, fibrinogen, antithrombin III, and fibrin/fibrinogen degradation products (FDPs) were assayed as hemostatic biomarkers on days 1, 2, 3, and 7 of hospitalization. In the cardioembolic (CE) stroke group, FMC and SF levels were significantly higher on days 1 and 2 of hospitalization, and D-dimer levels were significantly higher on day 1 of hospitalization, compared to the noncardioembolic (non-CE) stroke group. FDP levels were significantly higher at all times in the CE group compared to the non-CE group. Neither the National Institute of Health Stroke Scale (NIHSS) used during hospitalization nor the modified Rankin Scale (mRS) used at discharge found any significant correlations to hemostatic biomarkers, but the NIHSS score during hospitalization was significantly higher in the CE group than in the non-CE group. Measurements of hemostatic biomarkers, such as FMC, SF, and D-dimer on the early stage of cerebral infarction are useful for distinguishing between CE and non-CE stroke.

Predictors of poor outcome in patients with acute cerebral infarction.

Background and PurposePlasma D-dimer levels are elevated during the acute phase of cerebral infarction (CI). We investigated whether the D-dimer level on admission and other clinical characteristics could be used to predict the poor outcome of patients with acute CI.MethodsThe clinical characteristics and plasma D-dimer levels measured within 3 days of onset were compared according to outcome among patients with acute CI.ResultsIn total, 359 consecutive patients (mean age, 71.8 years) were examined, of which 174 had a poor outcome [score on the modified Rankin scale (mRS) ≥3] at 30 days after hospitalization. The mean mRS score was higher and a poor outcome was observed more frequently among women than among men (p<0.001 for each). The proportions of women, cardioembolism, atrial fibrillation, advanced age (≥75 years), prior history of CI or transient ischemic attack, and elevated D-dimer level (≥1.0 µg/mL) were significantly higher among patients with a poor outcome than among those with a good outcome. A multivariate analysis showed that elevated D-dimer level [≥1.0 µg/mL; odds ratio (OR), 2.45; 95% confidence interval (95% CI), 1.52-3.89; p<0.01], advanced age (OR, 1.93; 95% CI, 1.21-3.07; p<0.01), and female gender (OR, 1.75; 95% CI, 1.08-2.83; p=0.02) were independent predictors of a poor outcome.ConclusionsCertain clinical characteristics (gender and advanced age) and an elevated D-dimer level upon admission can be used to predict the outcome of patients with acute CI at 30 days after hospitalization.

Neurovascular intervention in the acute phase of cerebral infarction

Background and purpose Endovascular therapies in acute ischaemic stroke may offer benefits to patients that are not eligible for standard use of intravenous tissue activator plasminogen (iv t-PA) or when this is not effective. Our aim is to present the initial experience in with endovascular techniques in the Community of Madrid. Methods We present data from our registry of acute ischaemic strokes treated with endovascular re-perfusion therapies in five University Hospitals in Madrid (Spain) during the period 2005–2009. We recorded demographic data, vascular risk factors, risk severity with the NIHSS (National Institute of Health Stroke Scale), endovascular techniques, complications and mortality rates. Functional outcome and neurological disability at 90 days was defined by the modified Rankin scale (mRs). Results A total of 41 patients were treated with endovascular therapies. Mean age was 58.6 ± 19.9, and 56.1% were males. Of those 22 patients had an anterior circulation stroke and 19 had a posterior circulation stroke. Baseline NIHSS score was: median, 17 [range, 2–34]; 7 patients had previously received IV t-PA. The following endovascular techniques were performed: mechanical disruption (26 patients), intra-arterial infusion of t-PA (26 patients), angioplasty and stenting (5 patients), mechanical use of MERCI device (3 patients). Partial or total re-canalization was achieved in 32 patients (78%). Only one patient had a symptomatic cerebral haemorrhage. Three months after stroke, 53.6% of the patients were independent (mRs = 2) and overall mortality rate was 19.5%. Conclusions Acute ischaemic stroke is a potentially treatable medical emergency within the first hours after the onset of symptoms. Stroke endovascular procedures constitute an alternative for patients with IV t-PA exclusion criteria or when this is not effective.

Evaluation of Factors Associated With Elevated Levels of Platelet-Derived Microparticles in the Acute Phase of Cerebral Infarction

Platelet-derived microparticles (PDMPs) have attracted attention as blood coagulation-promoting, endothelial cell-activating factors. The objective of this study was to determine the parameters associated with elevated PDMP levels and examine their relationship with atherosclerotic lesions of main intracranial and extracranial arteries. Participants included a control group (C) of 61 patients with no apparent cerebral vascular lesions and 110 patients with acute-phase cerebral infarction, consisting of a small-vessel occlusion group (S) of 34 patients, a large-artery atherosclerosis group (L) of 41 patients, a cardioembolism group (CE) of 20 patients, and a stroke of undetermined etiology group (U) of 15 patients. Platelet-derived microparticle levels were measured using enzyme-linked immunosorbent assay (ELISA) at the time of admission, and the patients were reclassified into group CP (control level PDMPs), consisting of 70 patients with control PDMP levels, and group HP (high PDMPs), consisting of 40 patients with elevated PDMP levels. All patients underwent cranial magnetic resonance (MR) and carotid ultrasound examinations. Platelet-derived microparticle levels were significantly higher in groups S and L than in group C (P < .01). Concomitant intima-media thickness (IMT; odds ratio [OR] = 1.29, P < .05) and concomitant intracranial stenosis (OR = 3.95, P < .01) were significantly correlated with elevated PDMP levels. Fibrinogen and high-sensitivity CRP levels were significantly higher in group HP than in group CP. Alterations in PDMP levels correlated with the presence of atherothrombotic lesions, and PDMP levels are expected to be useful as a clinical indicator, reflecting the presence of intracranial atherosclerotic lesions in the acute phase of cerebral infarction.

Hypoadiponectinemia in Patients with Cerebral Infarction: Comparison with Other Atherosclerotic Disorders

The present study was undertaken to determine serum adiponectin level in patients with cerebral infarction and to further analyze any difference in serum adiponectin levels among atherosclerotic disorders. One hundred fifty-two subjects with atherosclerotic disorders were enrolled, 110 males and 42 females, with the age of 67.0 +/- 9.9 years (mean +/- SD). They were divided into 62 patients with cerebral infarction, 48 patients with ischemic heart disease, and 42 patients with arteriosclerosis obliterans. Thirty-two subjects matched by age, gender, and body mass index served as controls. Serum adiponectin levels were 7.2 +/- 0.6 microg/mL (mean +/- SE) in the patients with cerebral infarction, 7.2 +/- 0.8 microg/mL in those with ischemic heart disease, and 6.9 +/- 0.9 microg/mL in those with arteriosclerosis obliterans. They were significantly less than the level of 12.6 +/- 1.9 microg/mL in the control group (P < 0.01). However, there was no difference in serum adiponectin level among three groups of atherosclerotic disorders. In the patients with acute cerebral infarction, serum adiponectin level was temporarily reduced from 7.3 +/- 0.9 to 6.2 +/- 0.8 microg/mL 14 days after the hospitalization (P < 0.01), followed by recovery to the basal value. The present findings indicate that serum adiponectin levels are equivalently reduced in patients with atherosclerotic disorders, and that serum adiponectin is changeable under acute phase of cerebral infarction.

Circadian rhythm abnormalities in the acute phase of cerebral infarction correlate with poor prognosis in the chronic phase

The aim of this study was to determine circadian rhythm abnormalities in patients with acute cerebral infarction and their relationship with prognosis in the chronic phase. The subjects were 50 patients who were admitted within 48 h of onset. Rectal temperature and wrist motor activity were recorded during the acute phase. Time-series data were assayed by MEM spectral analysis. Functional prognosis (degree of handicap) was assessed at 3 months after stroke onset by the modified Rankin Scale. Ambulatory patients tended to exhibit circadian rhythm in rectal temperature and/or wrist activity rhythms, whereas non-ambulatory patients did not ( P < 0.001) in the acute phase of ischemic stroke. Our findings suggest the biological rhythms of rectal temperature and wrist activity during the acute stroke phase might be a possible prognostic indicator of their chronic phase.

Relationship between blood pressure changes in acute phase of cerebral infarction and its prognosis

目的 了解脑梗死发病急性期血压变化与预后的关系.方法收集广州医学院第二附属医院2001年1月至12月收住院的发病时间少于24 h的脑梗死患者232例的临床资料,其中男127例,女105例,平均年龄(68±10)岁;记录其发病时的血压以及住院第1～3天的平均血压,出、入院时的Barthel指数(Barthel Index,BI)评分、改良Rankin量表评分(Modification of Rankin Scale,MRS)、美国国立卫生研究所脑卒中评分(National Institute of Health Stroke Scale,NIHSS)和改善的分值以及住院天数,并对数据进行分析.结果脑梗死急性期合并原发性高血压的患者易出现高血压(P＜0.01),未合并原发性高血压的患者多出现低血压(P＜0.01).脑梗死急性期血压水平正常或者轻度升高的患者出院时NIHSS改善程度分别是(1±4)、(5±2)分,明显高于其余两组(P＜0.05).急性期明显低血压组患者的死亡率和继发症发生率明显高于其余各组(P＜0.05).结论脑梗死发病的急性期血压过低或者过高均有可能加重病情,而发病时血压偏低是脑梗死预后不良的原因之一.脑梗死急性期注意血压监护以及调整血压保持在正常或轻度升高水平具有重要意义。

Elevated Factor VIII: C Level Is a Risk Factor for Cerebral Infarction.

To explore the association between the risk of cerebral infarction (CI) and markers of coagulation and fibrinolytic systems. A prospective case-control study was carried out in PUMCH, in which 124 unselected patients with CI as well as 91 control patients were studied. Blood samples in acute phase of CI were obtained within 10 days from onset, and the convalescent smples were obtained at least 6 months after onset. Factor VII, FVIII:C, FX, vWF, AT-III, PC, PS, FPS,protein Z( PZ), D-dimer and TAT levels were measured. Associtions were assessed by multiple logistic regression analyses. Compared with control group, levels of FVIII:C, vWF, FVII, DD, TAT in patients with acute CI were marked elevated (FVIII:C194.6±48.6% vs 91.1±26.9%, p=0.000; vWF 123.2±28.8% vs 90.0±20.5%, p=0.003; FVII 98.7±25.2% vs 82.3±25.3%, p=0.002; DD 0.41±0.61 mg/l vs 0.12±0.10 mg/l, p=0.008; TAT 40.9±73.3 ng/ml vs 12.3±11.5 ng/ml, p=0.028, whereas level of FX was not changed significantly. Levels of anticoagulation proteins were decreased. Levels of PZ was 0.41μg/ml lower than cortrol (1.32±0.83μg/ml vs 1.73 ±0.55μg/ml, p=0.004) The result of logistic regression analysis showed levels of FVIII:C and vWF in acute phase were related with CI, with OR 1.143, 95%CI 1.099~1.189, P<0.01 and OR 1.040, 95%CI 1.003~1.082, P<0.05 for FVIII:C and vWF respectively. Compared with acute phase, levels of FVIII:C, DD and TAT in convalescent phase were reduced (FVIII:C 144.3±37.2% vs 193.5±46.2%, P=0.000; DD 0.21±0.20 mg/l vs 0.41±0.78 mg/l,p=0.025; TAT 15.2±10.3 ng/ml vs 42.9±72.6 ng/ml, p=0.030). However, the levels of FVIII:C, vWF and FVII were still higer than that of control(FVIII: C 144.3±47.2%, vs 91.1±26.9%, vWF 110.7±23.2% vs 90.0±20.5%, FVII 93.6±25.5% vs 82.3±25.3%, P<0.05). Level of PZ was elevated by 0.33μg/ml. The result of multiple logistic regression analyses indicated FVIII:C, vWF were the independent risk factors for CI

Neuroprotective effect of NS-7, a novel Na + and Ca 2+ channel blocker, in a focal ischemic model in the rat

NS-7 is a novel, voltage-dependent Na + and Ca 2+ channel blocker. This study evaluated the in vivo neuroprotective effect of NS-7 in a rat transient focal ischemic model when administered during occlusion. Left middle cerebral artery occlusion was induced in adult male Sprague–Dawley rats for 120 min using an intraluminal thread method. The rats received a single intravenous injection of NS-7 or saline (control group) just after the onset of ischemia, and at 30, 60 and 120 min after ischemia. Their brains were removed after 48 h reperfusion, sectioned, and stained with hematoxylin and eosin. Animals were evaluated by neurological examination at 120 min ischemia and 48 h reperfusion. Infarcted cortex and striatum were measured quantitatively and infarction volumes were calculated. Cortical infarction volumes were 128±74 (NS-7) and 214±64 mm 3 (control) immediately after the ischemia group, 155±48 (NS-7) and 225±12 mm 3 (control) after the 30 min group, 160±54 (NS-7) and 225±48 mm 3 (control) after the 60 min group, and 176±43 (NS-7) and 223±38 mm 3 (control) after the 120 min group. Cortices in NS-7-treated groups were significantly less infarcted than in control groups at all treatment times. There was no significant difference in the striatal infarction volume between the treatment and control groups. Neurological examination showed that hemiparesis and abnormal posture of the NS-7 groups were significantly more improved at 48 h reperfusion than those of the control groups without posture examination in the 120 min group. These observations suggest that NS-7 may be a new potential therapeutic agent for the acute phase of cerebral infarction.

Neurosonology in Cerebral Ischemia: Future Application of Transcranial Doppler in Acute Stroke

Transcranial Doppler (TCD) has become a general practice in recent years in the diagnostic study of patients with cerebral ischemia. This is due to the fact that it is a rapid, noninvasive, reproducible and dynamic examination of intracranial circulation. In the acute phase of cerebral infarction, it can detect MCA occlusion with a good correlation with angiographic findings and, what is even more important, the patients who will later suffer lacunar infarctions almost always show a normal Doppler examination. Acute abnormalities can also demonstrate the mechanism of the clinical signs; the examination informs us of the existence of collaterals and severe occlusions or stenoses of the extracranial arteries, and can change the priority in the search for the etiological diagnosis. The diagnosis of intracranial stenoses as a cause of clinical signs is another immediate application of TCD, right from the acute phase. If in the future anticoagulation is shown to be an optimum treatment for secondary prophylaxis in intracranial stenoses, TCD will probably become the diagnostic technique of choice. The ability to predict the prognosis based on parameters obtained by TCD opens up the possibility of using it as an auxiliary technique for the selection of patients for reperfusion treatment, having in its favor that it is quick and easy to perform, and therefore suitable for treatment monitoring. It seems clear that the data obtained by Doppler in the first 6 h are a good predictor of both spontaneous improvement and early impairment, which could help to avoid treatment in patients in whom a rapid improvement can be expected. Finally, the hemodynamic data of the TCD could be of inestimable value in the assessment and monitoring of intracranial hypertension treatments and for hemodynamic management of the patient, allowing the treatment margins of the acute phase of arterial hypertension to be reliably established without compromising the perfusion pressure. In conclusion, TCD will possibly be more widely used in the future in the acute phase of cerebral infarction as a guide to diagnostic procedures, for treatment selection and for monitoring of cerebral hemodynamics.

Aspirine et accidents ischémiques cérébraux

At the acute phase of cerebral infarction, two recent large studies found that the use of aspirin reduces both mortality and the risk of the recurrence of stroke. In primary prevention, aspirin nearly halves the risk of myocardial infarction but does not reduce that of stroke. Concerning the secondary prevention of atherothrombotic brain infarcts, aspirin has been the most extensively studied drug, and is efficient between 50 mg and 1.3 g. In spite of the efficacy of other antiplatelets in this indication--ticlopidine (500 mg), clopidogrel (75 mg) and dipyridamole (400 mg)--aspirin remains the most cost-effective, doses between 100 and 300 mg being the most widely used. Cardiac diseases with a high embolic risk require the use of oral anticoagulation. In nonvalvular atrial fibrillation, the choice of antithrombotic drugs depends on risk stratification: oral anticoagulants are indicated in high-risk subjects, whereas aspirin is recommended in low-risk subjects and when oral anticoagulants are contraindicated. Studies with associations of aspirin and other antiplatelets are required to increase the yield of this medication in high-risk subjects, in parallel with efforts to detect and to treat the vascular risk factors.

INHIBITION OF COLLAGEN-INDUCED PLATELET AGGREGATION BY ARGATROBAN IN PATIENTS WITH ACUTE CEREBRAL INFARCTION

Platelet aggregation induced by collagen is enhanced in patients with cerebral thrombosis [1], and platelet aggregates and activation products such as beta-thromboglobulin appear in the circulation, particularly during the acute phase [2]. It is known that the presence of activated platelets markedly amplifies thrombin generation by the prothrombinase complex. Platelet aggregation, for which thrombin is the most potent stimulator, is effected by the activation of the thrombin receptor. Activated platelets likely provide the principal surfaces on which intrinsic coagulation factors and prothrombinase assemble in vivo. Moreover, the blood coagulation cascade is simultaneously enhanced during the acute phase of cerebral infarction, resulting in thrombin production and fibrin formation [3]. Cerebral arterial thrombosis is thought to be initiated by rupture of atherosclerotic plaque. Platelets adhere to the constituents of the plaque, and platelet aggregation and the formation of thrombin occur rapidly. The presence of activated platelets involving thrombin generation in cerebral infarction remains to be further clarified. The present study in patients with acute cerebral infarction was undertaken to determine whether argatroban, a direct thrombin inhibitor, is effective in inhibiting collagen-induced platelet aggregation. It is well known that argatroban inhibits not only thrombin cleavage of fibrinogen with a Ki of 19 nM, but also thrombin-mediated platelet activation with a Ki of 40 nM [4]. We evaluated whether the sensitivity of platelets to collagen is increased in the presence of a trace amount of thrombin associated on platelets, at a concentration that does not induce platelet aggregation in acute cerebral infarction. The study also measured the inhibitory effect, if any, of the addition of argatroban during platelet hyperactivation induced by collagen.

Neuroexcitatory amino acids and their relation to infarct size and neurological deficit in ischemic stroke.

The participation of excitatory amino acids (EAAs) in the pathogenesis of ischemic neuronal lesion has been experimentally demonstrated, but clinical experience is scarce. Our objective was to examine EAA levels during the acute phase of cerebral infarction in relation to infarct size and intensity of neurological deficit. Using high-performance liquid chromatography, we determined the glutamate, aspartate, taurine, and glycine concentrations in the plasma and cerebrospinal fluid (CSF) of 128 patients with ischemic cerebral infarction confirmed by CT and 43 control subjects. Blood and CSF samples were obtained on admission within the first 24 hours from symptom onset. The severity of the neurological deficit was assessed with the Canadian Stroke Scale immediately after these tests and at 48 hours after inclusion in the study. Infarct volume was determined in a second CT performed between the 4th and 7th day after the patient's inclusion. The concentration of plasmatic glutamate was 121.39 +/- 80.89 mumol/L in the control group and 163.71 +/- 103.13 mumol/L in the patient group (P = .015); in CSF it was 3.46 +/- 1.20 mumol/L in control subjects and 6.55 +/- 4.65 mumol/L in patients (P < .0001). The concentration of glycine in plasma was 158.02 +/- 32.15 mumol/L in control subjects and 189.37 +/- 74.04 mumol/L in patients (P = .007); in CSF it was 6.18 +/- 2.28 mumol/L in control subjects and 11.23 +/- 6.96 mumol/L in patients (P < .0001). The concentrations of glutamate in plasma and in CSF were significantly higher in patients with large cerebral infarcts and in those with cortical infarcts. Levels of glutamate and glycine in plasma and CSF were significantly higher in patients with a higher degree of neurological deficit. Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.

Course of blood pressure after cerebral infarction and transient ischemic attack

In 63 patients, admitted for cerebral infarction or transient ischemic attack (TIA), the blood pressure course was studied. The blood pressure before the event was studied retrospectively; 32 patients were normotensive, in 31 patients existed hypertension, with antihypertensive treatment in 15 of these cases. The blood pressure after the event was studied prospectively, and turned out to be risen in 67% of the patients on the day of admission. It fell in the first day after infarction or TIA, mainly on the second day, to a plateau level reached on the fifth day. Only 3 patients (5%) remained hypertensive until discharge from the hospital. In 48 patients blood pressure values were available as measured two to six months after discharge, without a change in antihypertensive medication. Blood pressure was increased compared to the value measured before discharge. In 14 patients (29%) hypertensive blood pressure figures were measured at that time. It is concluded that blood pressure is elevated in the acute phase of cerebral infarction and TIA, but falls spontaneously in the first days to normotensive levels in most patients; because blood pressure may increase again, measurements of blood pressure within the first months after discharge are needed.

Neurological complications of sickle cell anemia.

A variety of neurological complications occur with sickle cell hemoglobinopathy. The most striking and most common is cerebral infarction. It is also the most devastating. Because of the high recurrence rate in untreated patients, cerebral infarction is the most debilitating neurological complication. The observed frequency varies from 6% to as high as 34% in different reports. The pathogenesis, clinical features, and demography are discussed. Diagnostic procedures should include a spinal tap to rule out potentially treatable lesions. CT scan and cerebral angiography may also be helpful in certain cases. Transfusion therapy remains the mainstay of management in the acute phase of cerebral infarction. There is considerable evidence to indicate that long-term transfusion programs are effective in the prevention of recurrences. Intracranial hemorrhage, spinal cord infarction, isolated neuropathies due to anatomical proximity to infarcted bones, lead neuropathy, auditory problems, and ocular manifestations are other neurological problems which can affect patients with sickle cell disease.