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PubMed2003

Radical "visual capture" observed in a patient with severe visual agnosia.

We report the case of a 79-year-old female with visual agnosia due to brain infarction in the left posterior cerebral artery. She could recognize objects used in daily life rather well by touch (the number of objects correctly identified was 16 out of 20 presented objects), but she could not recognize them as well by vision (6 out of 20). In this case, it was expected that she would recognize them well when permitted to use touch and vision simultaneously. Our patient, however, performed poorly, producing 5 correct answers out of 20 in the Vision-and-Touch condition. It would be natural to think that visual capture functions when vision and touch provide contradictory information on concrete positions and shapes. However, in the present case, it functioned in spite of the visual deficit in recognizing objects. This should be called radical visual capture. By presenting detailed descriptions of her symptoms and neuropsychological and neuroradiological data, we clarify the characteristics of this type of capture.

Aged↗
PubMed1996

Middle cerebral artery occlusion in the rat by intraluminal suture. Neurological and pathological evaluation of an improved model.

BACKGROUND AND PURPOSE: The purpose of the present study was to evaluate a modified method of intraluminal suture occlusion of the middle cerebral artery (MCA) on the volume of brain infarction and on neurobehavioral function in rats subjected to a temporary focal ischemic insult. METHODS: Male Sprague-Dawley rats were anesthetized with halothane and subjected to 60 minutes or 2 hours of temporary MCA occlusion (MCAo) by an intraluminal thread. In one group of rats, the suture was coated with poly-L-lysine, while in a second group, a conventional uncoated suture was used. Behavioral function was evaluated at 50 to 60 minutes after occlusion and during a 3-day period after MCAo. Three days after MCAo brains were perfusion-fixed and infarct volumes were measured. RESULTS: In rats with 60-minute MCAo, only 3 of 7 animals with uncoated sutures had infarcts, whereas in the group with poly-L-lysine-coated sutures, all rats (n = 7) exhibited infarction (P = .009, Fisher's exact test). With 2 hours of MCAo, total infarct volume (corrected for brain edema) was significantly larger in rats with poly-L-lysine-coated sutures than in the group with uncoated sutures (mean +/- SEM, 122.1 +/- 4.8 versus 67.0 +/- 18.2 mm3, respectively; P = .03; n = 4 in each group). In the 2-hour MCAo study, infarct volumes in the uncoated-suture group tended to be variable and inconsistent (coefficient of variation, 54%) compared with the group in which sutures were coated with poly-L-lysine, in which a highly consistent infarct was produced (coefficient of variation of infarct volume, 8%). CONCLUSIONS: Reversible MCAo in which a poly-L-lysine-coated intraluminal suture was used proved to be a reliable and effective modification of this technique, yielding consistently larger infarcts and greatly reduced interanimal variability.

Animals↗
PubMed2001

[Mechanisms of delayed neuronal death in experimental acute cerebral ischemia].

Delayed neuronal death or incomplete brain infarction was firstly described by two independent groups of researchers, which noted that in case of middle cerebral artery permanent and temporary occlusion two different types of lesions develop in the brain. Permanent occlusion results in infarction and coagulation necrosis. Significantly different brain lesion appears after short-term (< 30 min) middle cerebral artery occlusion followed by a long-term survival (up to 28 days). In these experiments the volume of incomplete infarction or the size of selective neuronal damage depends on time elapsed after the occlusion is removed. The authors suggest that the selective neuronal death in the areas of incomplete infarction is caused by apoptosis. Applying various methods of neuroimaging and ultrastructural study of tissue damage, the authors concluded that neuronal death in the ischemic penumbra occurs by two different mechanism. Necrosis develops promptly in the center, while apoptosis happens later in the margin of the penumbra. In experimental ischemic models, production of interleukin-1 beta and tumor necrosis factor-alpha activate the macrophagal NO-synthase (NOS-2), that leads to long-lasting NO generation. The latter causes necrosis or apoptosis depending on place of NO generation, on concentration, on glucose and growth factor quantities in paracrine media and at last on interaction and ratio between NO and superoxide anione (NO/O2-) ion concentration. NO mediated apoptosis comprises the upregulation of tumor suppressor protein P-53, activation of caspases, chromatin condensation, ladder-like fragmentation of DNA and alterations in the expression of apoptosis-associated proteins which belong to BCL-2 family. The activation of caspases is the critical signal for apoptosis. Experimental studies proved, that inhibition of caspases blocks neuronal death and diminishes the size of infarction in temporary and permanent focal cerebral ischemic rat models. If we combine antiexcitotoxic and antiapoptotic strategies by application of caspase we would significantly enlarge therapeutic window and such combinations has to become the central area of further investigations.

Acute Disease↗
PubMed2006

Aortic arch atheroma: stroke reduction in cardiac surgical patients.

Cardiac surgery is increasingly performed on elderly patients with extensive coronary artery abnormalities who have impaired left ventricular function, decreased physiologic reserve, and multiple comorbid conditions. Considerable numbers of these patients develop perioperative neurologic complications ranging from subtle cognitive dysfunction to more evident postoperative confusion, delirium, and, less commonly, clinically apparent stroke. Magnetic resonance imaging studies have elucidated that a considerable number of patients have new ischemic brain infarcts, particularly after conventional coronary artery bypass graft surgery. Mechanisms of cerebral injury during and after cardiac surgery are discussed. Intraoperative transesophageal echocardiography and epiaortic scanning for detection of atheromatous disease of the proximal thoracic aorta is paramount in identifying patients at high risk from neurologic injury. It is important to recognize that our efforts to minimize neurologic injury should not be limited to the intraoperative period. Particular efforts should be directed to temperature management, glycemia control, and pharmacologic neuroprotection extending into the postoperative period. Preoperative magnetic resonance angiography may be of value for screening patients with significant atheroma of the proximal thoracic aorta. It is likely that for patients with no significant atheromatous disease, conventional coronary artery revascularization is the most effective long-term strategy, whereas patients with atheromatous thoracic aorta may be better managed with beating heart surgery, hybrid techniques, or medical therapy alone. Patient stratification based on the aortic atheromatic burden should be addressed in future trials designed to tailor treatment strategies to improve long-term outcomes of coronary heart disease and reduce the risks of perioperative neurologic injury.

Animals↗
PubMed2000

Visual neglect as a predictor of functional outcome one year after stroke.

OBJECTIVE: The aim was to study the role of visual neglect in acute right hemisphere brain infarct as a predictor of poor functional outcome during the first year after stroke. In particular, we were interested in the additional value of neglect measures besides hemiparesis, hemianopia, cognitive deficits and age. PATIENTS AND METHODS: A consecutive series of 57 patients with a neuroradiologically verified right hemisphere infarct was examined within 10 days of the stroke. Fifty patients were followed up for 1 year. Neglect was measured with the Conventional and the Behavioural subtests of the Behavioural Inattention Test (BITC and BITB, respectively). The predictors were determined at the 10-day examination. Functional outcome was assessed 3, 6 and 12 months after the onset with the Frenchay Activities Index. RESULTS: Neglect in BITB was the best single predictor, which together with high age formed the best combination of predictors for poor functional outcome at each follow-up. Hemiparesis was also included in this prediction model at the 3-month follow-up, but hemianopia, BITC, or visuoconstructional and memory deficits showed no additional predictive value. However, neglect usually recovered soon. When neurological and cognitive deficits were assessed at the same time as the outcome, hemiparesis rather than neglect was the strongest correlate of poor outcome. CONCLUSION: Neglect in acute stroke is an important predictor of poor functional recovery. Residual neglect, which could be compensated in the follow-up tests, may nevertheless restrict patients' real-life activities and hobbies.

Acute Disease↗
PubMed2005

Identification of embolic stroke patterns by diffusion-weighted MRI in clinically defined lacunar stroke syndromes.

BACKGROUND: A number of clinical syndromes describing the presentation of deep brain infarcts are called lacunar syndromes resulting from small vessel occlusion (SVO). To verify the reliability of the clinical diagnosis "lacunar syndrome," the value was investigated with diffusion-weighted MRI (DWI). METHODS AND RESULTS: A total of 73 patients (mean age 66 years; range 35 to 83 years) with sudden onset of a classical lacunar syndrome were enrolled. On the basis of the DWI findings, patients were divided into 3 groups: group 1, single subcortical lesion (<15-mm lesion; 43 patients; 59%); group 2, large (> or =15 mm) or scattered lesions in 1 vascular territory (16 patients; 22%); and group 3, multiple lesions in multiple vascular territories (14 patients; 19%). A stroke mechanism other than SVO could be identified in 17 (23%) patients. Cardiac work-up revealed a cardiac embolic source in 8 patients (11%). Duplex sonography revealed symptomatic stenosis in 9 patients (12%). Based on the work-up information, 29 patients (40%) were found to have a potential cause of stroke other than SVO. A significant correlation with >1 single lesion on DWI-MRI and a clinical proven embolic source was observed (P=0.002). In 9 patients with MRI suspicious for a pathomechanism other than SVO, no embolic source was found. CONCLUSIONS: The use of DWI-MRI improves the accuracy of the subtype diagnosis of stroke. Inaccuracy has to be expected in approximately one third if lacunar diagnosis is based on clinical and computed tomography findings. Most of these "false-positive" cases are attributable to large artery or cardiogenic embolic stroke.

Adult↗
PubMedDate not supplied

Calcium antagonists reduce the extent of infarction in rat middle cerebral artery occlusion model as determined by quantitative magnetic resonance imaging.

The appearance and evolution of brain infarcts over 3 days following proximal occlusion of the left middle cerebral artery (MCA) in SHR rats were measured non-invasively by magnetic resonance imaging (MRI). Infarcts were clearly visible in coronal, T2 weighted brain sections, 24, 48 and 72 h after MCA occlusion in the left hemisphere, as areas of increased NMR signals. The infarcts were quantified by pixel counting in each section, the sum of 4 sections representing an accurate estimate of the total infarct size. The location and extent of infarction, determined by MRI, were found to be highly reproducible and correlated well with post-mortem histological and biochemical data. A neurological score, made every 24 h, paralleled the evolution of the infarct size, which culminated after 48 h. Pre- or post-treatment of MCA occluded rats with the dihydropyridine calcium antagonist PN 200-110 resulted in a substantial reduction of infarct size, determined by MRI 24, 48 and 72 h after infarction, compared to vehicle treated controls. These findings were corroborated by corresponding improvements of the neurological scores as well as histological and biochemical data. Post-treatment with nimodipine showed qualitatively similar effects. These results support the notion that calcium antagonists, through vascular and/or metabolic mechanisms, are effective in treating acute stroke. Since they were obtained in a chronic, relevant model of stroke with a method directly applicable also to humans, they should encourage further clinical studies with calcium antagonists.

Animals↗
PubMedDate not supplied

Compartmentation of acid-base balance in brain during complete ischemia.

During near complete hyperglycemic brain ischemia, brain lactate levels rise in excess of 16-18 mmol/K and are associated with severe brain infarction. Analyses of pHo, Pt(CO2), and total brain lactate under these circumstances suggest that H+, HCO3, and lactate become unequally distributed between cells and the interstitial space and, perhaps, even between different types of brain cells. In addition, to whatever physiological advantages it may generate, such compartmentalization may be a factor leading to cell death in brain ischemia.

Acid-Base Equilibrium↗
PubMed1998

Dye dilution and oximetry for detection of patent foramen ovale.

OBJECTIVES: Patent foramen ovale (PFO) is a risk factor for stroke of undetermined (cryptogenic) origin. Low cost and non-invasive bedside tests for detection of PFO are needed as alternatives to contrast transesophageal echocardiography. We investigated whether dye dilution curves and oximeter recordings are useful for detecting PFO and what is the prevalence of PFO in patients with cryptogenic stroke determined with these bedside methods. We also studied whether stroke risk factors, number of brain lesions, and stroke recurrence rates were different in patients with an unexplained stroke with and without PFO. MATERIAL AND METHODS: Dye dilution curves and oximeter recordings with non-invasive earpiece apparatus were obtained in 59 patients aged under 50 years who had had a cryptogenic brain infarction. The number of ischemic lesions in the brain was counted by MRI. RESULTS: PFO was found in 24 (41%) of 59 patients. There was a 100% concordance in results obtained by dye dilution and by oximetry. Risk factors for stroke were similar in subjects with PFO and those without PFO. No significant association was found between PFO and Valsalva-like activity at stroke onset. Those with PFO did not have more ischemic lesions detected by MRI nor did they have more recurrent ischemic episodes. CONCLUSION: Dye dilution and oximetry are cheap and useful methods for detection of PFO and could be used for screening of the risk of paradoxical embolism. Because these 2 methods were not compared with the golden standard, transesophageal echocardiography, the specificity and sensitivity of the tests remain unsettled.

Adolescent↗
PubMed2002

Spontaneous ischemic events in the brain and heart adapt the hearts of severely atherosclerotic mice to ischemia.

To investigate if spontaneous ischemic events in mice with severe multi-organ atherosclerosis could adapt to ischemia, apolipoprotein E/LDL receptor knockout mice were fed an atherogenic diet for 7 to 9 months. Signs of spontaneous ischemia occurred. One to two days later, hearts were excised, Langendorff-perfused with induced global ischemia, and compared with mice without signs of disease. In vivo heart or brain infarctions were verified by heart histology and/or increased serum levels of cardiac troponin T and S100B. Hearts of mice with spontaneous ischemic events had improved function and reduced Langendorff-induced infarctions. To investigate the remote preconditioning effect of brain ischemia, bilateral ligation of the internal carotid arteries was performed in C57BL6 mice. Twenty-four hours later, their isolated hearts were protected against induced global ischemia. A possible role of inducible NO synthase (iNOS) was studied in iNOS knock out mice, who were not preconditioned by induced brain ischemia. Cardiac iNOS was unchanged 24 hours after preconditioning, suggesting that NO is a trigger rather than a mediator of protection. These findings suggest that spontaneous ischemic events in the brain and heart adapt the heart to ischemia. This can be mimicked by induced brain ischemia, with iNOS as a key factor of protection.

Animals↗
PubMed1997

S-100 protein and neuron-specific enolase concentrations in blood as indicators of infarction volume and prognosis in acute ischemic stroke.

BACKGROUND AND PURPOSE: Better techniques are needed to monitor infarction volume and predict neurological outcome after ischemic brain infarction. We evaluated the usefulness of serial measurements of S-100 protein versus neuron-specific enolase (NSE) in blood samples from patients with acute stroke. METHODS: Using nonisotopic sandwich immunoassays, we measured plasma concentrations of S-100 protein and NSE on admission and on days 3, 4, 7, and 14 after infarction in 44 patients (age range, 22 to 86 years; mean age, 65.1 years; 12 female, 32 male). Infarct volume was measured by volumetric CT on day 4 after ictus, and clinical outcome was assessed at discharge from hospital with the Activities of Daily Living Scale and 6 months after infarction with the Glasgow Outcome Scale. RESULTS: Peak blood levels of S-100 protein were found on day 2.5 +/- 1.3, and peak levels of NSE were found on day 1.9 +/- 0.8 after infarction. Peak plasma levels of S-100 protein correlated well with infarct volume (r = .75, P < .001) and with clinical outcome assessed with the Glasgow Outcome Scale (r = .51, P < .001). Serum levels of NSE correlated with infarct volume (r = .37, P < .05) but not with clinical outcome (r = .18, P > .05). CONCLUSIONS: The results of our study indicate that measuring blood concentrations of S-100 protein periodically in the first 10 days after cerebral infarction helps to predict infarct volume and the long-term neurological outcome more accurately than periodic measurements of blood concentrations of NSE.

Activities of Daily Living↗
PubMed2004

Secondary prevention of stroke: a practical guide to drug treatment.

Stroke is a disease of the elderly and, as a result of the expected demographic changes in many industrialised countries, its incidence is likely to increase in the future. A first-ever stroke significantly increases the likelihood of further events; thus, secondary prevention is of major importance. Only a minority of recurrent strokes can be prevented by surgical or other invasive methods, meaning that most secondary preventive measures involve drug treatment, which has become increasingly sophisticated in recent years. Ischaemic stroke constitutes the vast majority of all strokes; effective secondary prevention depends on a variety of factors, of which the correct classification in terms of subtypes and aetiological mechanisms is a pivotal prerequisite, as is the assessment of the patient's cardiovascular risk profile. In addition to the evaluation of pathomechanisms, stratification of subtypes of brain infarction is mainly based on morphology seen with brain imaging techniques, which provides additional evidence for the presumed cause of the stroke. Inhibitors of platelet function and anticoagulants are the two major groups of antithrombotic drugs used for the secondary prevention of stroke. Antiplatelet agents are still indicated in the majority of patients after ischaemic stroke, especially if an arterial origin is presumed. In addition to aspirin (acetylsalicylic acid), the position of which as the first-line antiplatelet drug is increasingly being questioned, other compounds with antiplatelet activity have been developed and have proven effective in secondary stroke prevention, including ticlopidine, clopidogrel and dipyridamole. Anticoagulants are principally indicated after cardioembolic ischaemic stroke; however, their inherent bleeding risks render their use in many cases rather difficult, in particular for elderly patients. Patient compliance with the recommended treatment is of major importance, given the somewhat limited efficacy of antithrombotic agents in stroke prevention. Since 'real world' experience does not match the circumstances under which clinical trials are conducted, this article will also deal with problems not covered by specific studies, such as risk stratification for anticoagulant treatment and how to proceed in cases of unknown stroke aetiology. The management of major cardiovascular risk factors is the other mainstay of secondary stroke prevention. Recent evidence indicates that antihypertensive treatment may be as effective as antithrombotic drugs for secondary prevention of stroke. This still needs to be proven for the treatment of other cardiovascular risk factors, such as diabetes mellitus and hypercholesterolemia. Nevertheless, the results of recent studies investigating the effect of HMG-CoA reductase inhibitors ('statins') on cardiovascular events strongly suggest a stroke-preventive effect.

Anticoagulants↗
PubMed1976

[Experimental model of transient cerebral circulatory disorders by way of embolization of cerebral arteries with fresh blood clots].

A total of 85 experimental animals received through the blood flux of the carotid arteries clots of autogenic blood of 1 hour age. A histomorphological study after 40 minutes following an embolism there were revealed clots in the cerebral arteries in 13 out of 14 animals. After 1.5 hours in 1 of 17, and after 24 hours in none of the 10 animals. Directly following the administration of clots in all the 20 animals of this series, there were symptoms of focal brain lesions: hemipareses, ptosis and myosis, a "trot around circles", etc. In all 20 animals there was a complete regress of the symptom at different times (from 10 min to 18 hours). In all cases there was an increased amount of lactic acid in the cerebral blood outflow while subsequently was reduced, correlating with the time of clot lysis. The morphological control did not depict brain infarctions. It is assumed that the reason of brain dysfunctions is an obturation by blood clots of cerebral arteries, while their normalization is due to a spontaneous lysis of the embols which obturated the cerebral arteries.

Animals↗
PubMed1986

[Lateralized periodic activity and cerebral infarct].

A series of EEG recordings shows the evolution of a periodic activity (PA) in a 57-year-old man with acute cerebral infarction. The complexes ranged from 100 to 150 microV, the duration was 750 msec; the periodic occurrence repeated itself every 2 sec. PA is obliterated during the onset of electroclinical seizures. The CT scan shows temporal brain infarction.

Brain↗
PubMed2005

Functional activation within the PI-DWI mismatch region in recovery from ischemic stroke: preliminary observations.

In this study, we sought to investigate if brain tissue affected by ischemia can accommodate areas of activation related to restoration of brain function following ischemic stroke. In two patients perfusion imaging (PI) and diffusion weighted imaging (DWI) obtained in the acute phase after stroke was coregistered with BOLD imaging of brain functions acquired when profound recovery had occurred. Both patients suffered from thrombembolic brain infarction due to dissection of the internal carotid artery (ICA) characterized by a severe PI-DWI mismatch in the acute stage of stroke. Following ICA recanalization and clinical recovery BOLD imaging showed task-specific activation adjacent to the infarct lesion within the former PI-DWI mismatch area. The data in these two stroke patients provide evidence that brain tissue at risk of infarction as shown by the PI-DWI mismatch can survive and, thereby, constitute the major site underlying post-ischemic recovery.

Adult↗
PubMedDate not supplied

[Cost of the treatment of acute cerebrovascular insufficiency causing cerebral infarction].

Many countries are interested in the cost of therapy of the acute cerebral flow insufficiency leading to brain infarction. Total costs include: drugs, laboratory tests, nursing care, the cost of patients' food, equipment, amortization, hospital administration etc. The total expenditure for a 10-15-day treatment of the acute neurological incident depended on the severity of the disease and was 8 million ++ złoty in case of mildly ill patient, 9 million in case of moderately severe disease, and 21 million złoty in case of severely ill patient. If the costs of such tests as CT and TCD-scanning will be added, total cost will increase significantly.

Acute Disease↗
PubMed2004

[Angiogenesis and its regulatory factors in brain tissue of neonatal rat hypoxic-ischemic encephalopathy].

OBJECTIVE: To investigate possible mechanism of angiogenesis in brain tissue of neonatal rat hypoxic-ischemic encephalopathy (HIE). METHODS: Forty seven-day old neonatal rats were randomly assigned to hypoxic-ischemic (Model group) or sham treatment (Sham group), each group had 20 rats. Five rats from each group were sacrificed on days 1, 3, 7 and 14 after hypoxia-ischemia. Paraffin sections of the brain were stained with anti-endothelial cell, anti-proliferating cell nuclear antigen (PCNA) or anti-vascular endothelial growth factor (VEGF) by using single or double immunohistochemistry. The brain capillary density index (BCDI), brain proliferating capillary density index (BPCDI) and the expression of VEGF were analyzed under the microscope. The expression of VEGF and hypoxia-inducible factor-1alpha (HIF-1alpha) mRNA in hypoxic-ischemic side of the brain was measured by RT-PCR. RESULTS: BCDI around infarct brain tissue in the model group began to rise on day 3 and remained higher than that of the sham group from day 3 to day 14 [day 3: (9.80 +/- 1.05)/HPF vs. (4.90 +/- 0.66)/HPF, P < 0.01;day 14: (13.29 +/- 3.90)/HPF vs. (6.08 +/- 1.50)/HPF, P < 0.01]. Occasional proliferating capillary was found in brain tissue of normal neonatal rats. The density of proliferating brain capillary on day 3 and day 7 of Model group [(0.54 +/- 0.15)/HPF vs. (0.90 +/- 0.25)/HPF] were significantly higher than those of Sham group [(0.12 +/- 0.05)/HPF vs. (0.13 +/- 0.07)/HPF, P < 0.01]. VEGF was mainly expressed in the cytoplasm of neurons, capillary endothelial cells and pial cells. Viable neurons and endothelial cells in the infarct areas also expressed VEGF. The expression of VEGF mRNA in hypoxic-ischemic brain tissue was significantly higher than that of normal control (P < 0.01) and temporally preceded angiogenesis. The expression of VEGF mRNA at 12 hours of HIE model was significantly higher than that of normal control (1.56 +/- 0.27 vs. 0.95 +/- 0.21, P < 0.05). It reached its peak on day 1 and day 3 (1.85 +/- 0.31 vs. 1.86 +/- 0.39), significantly higher than that of normal control (P < 0.01), and decreased by day 7 and day 14, without significant difference compared with normal control (P > 0.05). The expression of HIF-1alpha mRNA was also up-regulated after hypoxic-ischemic treatment. The expression of HIF-1alpha mRNA (1.07 +/- 0.21) was significantly higher than that of normal control (0.64 +/- 0.28, P = 0.048) at 3-hour of HIE model, reached its peak on day 1 (1.73 +/- 0.42, P < 0.01), remained at high expression level on day 3 (1.44 +/- 0.36, P < 0.05) and began to decline by day 7 and day 14 when it was not significantly different from normal control. CONCLUSIONS: Angiogenesis exists in the brain tissue of neonatal rat HIE model. Up-regulation of VEGF expression mediated by HIF-1 may play an important role in the process of angiogenesis.

Animals↗
PubMed1979

[Cerebral strokes. Incidence and mortality].

The paper presents data concerning the incidence of brain strokes and the mortality rate. These indices were received for the first time on a large population by the method of brain stroke register. The frequency of brain strokes during one year equaled to 2.5 cases, the mortality rate 1 case per 1000 population. Genuine indices of the incidence and mortality rates for different age groups were established. They appeared to be relatively high in people over 60 years. The mortality coefficient is higher in females. In brain infarctions the frequency and mortality is higher than in brain and subarachnoidal hemorrhages.

Adult↗