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PubMed2006

Activation of leukocyte-endothelial interactions and reduction of selective neuronal death after global cerebral ischemia.

The role of leukocyte-endothelial interactions (LEI) as part of the inflammatory response after global cerebral ischemia (GCI) is hardly understood and may be detrimental as well as beneficial. Objective of the current study was to investigate the cause-effect relationship of activated leukocytes for the development of ischemic brain damage. Mongolian gerbils were subjected to 15 min of global cerebral ischemia. A cranial window was implanted for quantitative analysis of the pial microcirculation focusing on leukocyte-endothelium interactions by intravital fluorescence microscopy up to 3 h of reperfusion. Subsequently the animals were daily screened for neurological deficits and the evolving brain damage was assessed histologically after 4 days. After global cerebral ischemia the number of rolling and adherent leukocytes increased 20- and >23-fold, respectively upon 3 h of reperfusion as compared to controls (P<0.05). Ischemic animals developed neurological deficits and showed a significant loss of neurons in selective vulnerable areas of the brain. The extent of leukocyte activation, i.e. the maximum number of rollers and stickers directly correlated to the number of viable neurons on day 4 in hippocampus, cortex, and striatum. We conclude that there is a relationship between activation of leukocyte-endothelium interactions and the reduction of ischemic brain damage after global cerebral ischemia. Activation of leukocytes may have neuroprotective potential or indicate regenerative processes.

Animals↗
PubMed2006

Mitochondrial membrane potential and ischemic neuronal death.

Mitochondria are intracellular organelles in which high energy phosphate is produced. Ischemia causes depletion of the materials necessary to produce this phosphate and strongly affects the electron transport chain. Apoptosis commences during and after ischemia. As such, it is likely that a significant relationship exists between inactivation of electron transport and apoptosis. Mitochondrial membrane potential (MMP) reflects performance of the electron transport chain and can indicate a pathological disorder of this system. In an experimental setting, oxygen-glucose depletion (OGD) in neuronal cell culture has been employed to simulate an ischemic condition. The relationship between MMP and subsequent neuronal death during and after OGD has been examined. MMP dissipation and concomitant neuronal death have been reported, but recent studies have demonstrated mitochondrial hyperpolarization preceding neuronal death. The direction of MMP polarization depends on the extent of OGD. Long OGD results in depolarization, while shorter OGD induces hyperpolarization. Neurons are still viable during hyperpolarization, but the process may switch on the apoptotic cascade. Meanwhile, dissipation of MMP seems to be a consequence of severe energy deficit, leading to necrosis. MMP may be a marker of subsequent apoptosis, although a causal relationship remains to be determined.

Animals↗
PubMed2006

Regional cerebral blood flow changes in a patient with delusional parasitosis before and after successful treatment with risperidone: a case report.

The pathophysiology and appropriate pharmacological interventions for delusional parasitosis (DP) remain unknown. Here, we present a case of DP following brain infarction of the right temporoparietal region. Pharmacotherapy with risperidone resulted in a dramatic therapeutic response over a short period. In a sequential N-isopropyl-p-[(123)I]-iodoamphetamine single photon emission computed tomography ([(123)I]-IMP SPECT) study, post-treatment SPECT images revealed a marked increase of rCBF in the large areas including the bilateral frontal and left temporoparietal regions, the right parietal operculum and the bilateral basal ganglia, in contrast to pre-treatment SPECT images showing a global decrease of rCBF. Our clinical outcome suggests the efficacy and safety of risperidone for treatment of DP and that both dopaminergic and serotonergic dysfunction may play a role in DP. Our sequential SPECT findings suggest that psychiatric improvement of DP is associated with increased rCBF.

Aged, 80 and over↗
PubMed2004

Lesion lateralization in patients with epilepsy and precocious destructive insults.

Destructive brain lesions that occur early in development are often unilateral or asymmetric. We analyzed the lateralization of lesions among a previously reported series of 51 patients with three kinds of destructive lesions based on their topography: specific arterial territory (AT), arterial borderzone territory (Bdz), hemispheric (H). Five patients (all from group Bdz) had bilateral nonlateralizing lesions. The distributions of left- and right-sided lesions were distinct among the groups (P=0.014): in group H, all patients except one presented with right-sided lesions (89%); in group Bdz, left-sided lesions (53%) were more frequent than right-sided lesions (17.7%); in group AT, left- and right-sided lesions were more equally distributed (56 and 44%). Our study suggests that there is a trend toward lesion lateralization among patients with different patterns of precocious destructive lesions. Differences in cerebral maturation and vulnerability between the hemispheres is a possible factor explaining lesion lateralization in early life insults.

Adolescent↗
PubMed1998

Multiplane transesophageal echocardiography and stroke.

Transesophageal echocardiography (TEE) is considered a basic tool in the diagnostic and follow-up evaluation of stroke patients, since up to 40% of cerebral ischemic events are presumed to have a cardiac origin. TEE offers a superior resolution of the posterior cardiac structures, such as left atrium and appendage and atrial septum, as well as of the aorta. By means of TEE, evidence has accumulated that some cardiovascular abnormalities (left-sided thrombi, tumors and vegetative lesions, complicated plaques of the aortic arch) are associated with ischemic stroke. Nevertheless, some issues remain unresolved. Will exclusion of atrial thrombus by multiplane TEE preclude embolism after cardioversion of atrial fibrillation? If anticoagulation before and after cardioversion is needed to provide adequate protection against embolism, will TEE be indicated in all patients? Moreover, can the detection of spontaneous echo contrast or enlarged and hypokinetic left atrial appendage in atrial fibrillation modify the therapeutic strategy? Is atrial septal aneurysm (ASA) a real embolic source, particularly when a right-to-left shunt is not associated? Considering the high prevalence of patent foramen ovale (PFO) in normal subjects, how can we identify patients at higher risk of embolism? Furthermore, methodologic points have to be taken into account when we analyze data from the literature. First, most studies are retrospective; a sole prospective study demonstrated that atherosclerotic plaques >4 mm thick in the aortic arch are significant predictors of recurrent brain infarction and other cardiovascular events in patients > or =60 years of age. Second, the association between the aforementioned cardiac abnormalities (mainly ASA and PFO) and cardiogenic embolism is biased by the patient-enrollment criteria used in those studies so that their pathogenetic role has not yet been established. Prospective studies with the enrollment of appropriate control groups will be necessary to define what can be considered a marker of embolic risk; the diagnosis "cardiogenic embolism" will not be a definitive diagnosis in most cases.

Atrial Fibrillation↗
PubMed1999

Right ventricular thrombosis early after bidirectional Glenn shunt.

Thrombosis in the right ventricle occurred early after bidirectional superior cavopulmonary shunt in 2 patients with pulmonary atresia with intact ventricular septum and major right ventricular coronary artery communication, and perioperative brain infarction occurred in 1 patient. Clinicians should be aware of the hazards of this potentially lethal complication, and transfusion of platelets and fresh plasma should be minimized. Although the hemodynamic state is good, echocardiography should be performed frequently and strict anticoagulation should be started as early as possible.

Coronary Vessel Anomalies↗
PubMed1997

Hypercortisolism after stroke--partly cytokine-mediated?

Increased activity of the hypothalamic-pituitary-adrenal (HPA) axis is common early after stroke. Hypercortisolism is a prominent manifestation. Normally the secretion of cortisol is regulated by adrenocorticotrophic hormone (ACTH), but recently an ACTH/cortisol dissociation after stroke was reported. Cytokines may influence the HPA axis, and plasma IL-6 levels are elevated following stroke. We investigated correlations between cortisol, ACTH, and cytokines, and between blood pressure and blood hormone levels early after stroke in seven stroke patients. All had neurological symptoms secondary to brain infarctions. Blood samples for analysis of cortisol, ACTH, IL-6, TNF alpha, norepinephrine, and epinephrine were collected four times daily, and 24-h blood pressure was measured. Plasma IL-6, but not ACTH, correlated significantly to serum cortisol. Catecholamine levels correlated with cytokine and cortisol levels. This study suggests that several routes for HPA-axis dysregulation is present early after stroke. Cytokine release may play an important role in this situation.

Adrenocorticotropic Hormone↗
PubMed1997

Simultaneous bilateral contrast transcranial doppler monitoring in patients with intracardiac and intrapulmonary shunts.

The prevalence of a right-to-left intracardiac shunt, demonstrated by echocardiography and transcranial Doppler sonography has been shown to be higher in stroke patients than in normal controls. The aim of this study was to assess the sensitivity and specificity of contrast transcranial Doppler sonography in comparison to transesophageal echocardiography in the detection and differentiation of intracardiac and intrapulmonary shunts and to correlate the transcranial Doppler findings with clinical outcome and morphological findings. Forty five consecutive stroke patients with suspected paradoxical embolism were entered into the study. In all 25 patients with middle cerebral artery stroke of the left (56%) or right (44%) territory and echocardiographic demonstrated patent foramen ovale (80%) or intrapulmonary shunt (20%), simultaneous bilateral transcranial Doppler sonography of the middle cerebral arteries was performed after contrast medium injection during rest and valsalva straining under standardized and optimized conditions. Overall sensitivity for the detection of a right-to-left shunt by contrast transcranial Doppler sonography was 97% and overall specificity was 70%. Bilateral appearance of microbubbles, microbubble count and time delay of microbubble appearance significantly increased after valsalva straining. In patients with intracardiac shunts, a significantly higher microbubble count (32 vs. 13 in patients with an intrapulmonary shunt) and a shorter time interval of microbubble appearance (11 vs. 14 s in patients with intrapulmonary shunts) was observed. There was no correlation between the side and numerical distribution of microbubble count and the location and severity of the current clinical symptoms, as well as between microbubble count and presence and hemispherical distribution of brain infarcts. Transcranial Doppler sonography is a highly sensitive method for the detection of right-to-left shunts, whether of cardiac or pulmonary location. However. no correlation was found between the side and number of microbubbles counted and the clinical symptomatology.

Adolescent↗
PubMed1999

Fragmentation of the Golgi apparatus of Betz cells in patients with amyotrophic lateral sclerosis.

The Golgi apparatus (GA) of the large pyramidal motor neurons in the cerebral cortex (Betz cells), was examined in sixteen patients with sporadic amyotrophic lateral sclerosis (ALS), in one patient with familial ALS (FALS), and in ten non-ALS age matched controls including one patient with Huntington's disease and one patient with a brain infarct. The GA was immunostained with an antibody against the MG-160 protein, a conserved sialoglycoprotein of the medial cisternae of the organelle. In ALS, 13.2% of counted Betz cells had fragmented GA in contrast to 0.6% in the ten non-ALS controls. The fragmentation of the GA of Betz cells was identical to that previously reported in spinal cord motor neurons from patients with sporadic ALS and in transgenic mice expressing the G93A mutation of the gene encoding the Cu/Zn superoxide dismutase. The striking morphological similarity between the fragmentation of the GA observed in Betz cells and in spinal cord motor neurons suggests that a similar pathogenic mechanism is responsible for both, and that the fragmentation of the GA of the spinal cord motor neurons is not a consequence of deafferentation due to the degeneration of the Betz cells.

Adult↗
PubMed1996

A valveless high stroke volume counterpulsation device restores hemodynamics in patients with congestive heart failure and intractable cardiogenic shock awaiting heart transplantation.

The paraaortic counterpulsation device is a round pumping chamber with one valveless opening 20 mm in diameter and a 100 ml stroke volume. The paraaortic counterpulsation device was implanted on the ascending aorta of three male patients with intractable cardiogenic shock. Patients were assisted for 4 hours and 8 and 54 days, respectively; the first patient died as a result of nonresponding peripheral vasodilation and the other two died of septic shock. The two patients who were assisted for 8 and 54 days were conscious and able to function in a limited manner during the mechanical assistance. Discontinuation of the mechanical support for a few seconds was followed by low systolic arterial pressure (30 to 60 mm Hg) and syncopal episodes. Biochemical tests and autopsy results in these patients showed no evidence of blood cell destruction, thrombus formation, brain infarction, or other distal emboli. In conclusion, satisfactory hemodynamic effects, excellent biocompatibility, and simplicity of the implantation procedure in these patients encourage the use of the paraaortic counterpulsation device as a bridge to heart transplantation.

Adult↗
PubMed1999

The older man's heart and heart disease.

CAD is the most common cause of death in older men and was present in 44% of 664 men, mean age 80 years. Independent risk factors for new coronary events in older men include increasing age, prior CAD, cigarette smoking, hypertension, diabetes mellitus, high serum total cholesterol, and low serum HDL cholesterol. In older men with hypertension, echocardiographic LVH is a powerful independent predictor of new coronary events, atherothrombotic brain infarction, and CHF. In 554 older men with a mean age of 80 years, two-dimensional and Doppler echocardiography demonstrated that the prevalence of aortic stenosis was 14%, 1 + aortic regurgitation or greater was 31%, rheumatic mitral stenosis was 0.4, 1 mitral regurgitation or greater was 32%, mitral annular calcium was 35%, hypertrophic cardiomyopathy was 3%, idiopathic dilated cardiomyopathy was 1%, left atrial enlargement was 29%, LVH was 41%, and abnormal LVEF was 29%. The prevalence and incidence of CHF increase with age in older persons. The prevalence of a normal LVEF associated with CHF as a result of prior myocardial infarction or hypertension was 22% in men aged 60 to 69 years, 33% in men aged 70 to 79 years, 41% in men aged 80 to 89 years, and 47% in men aged 90 years or older.

Aged↗
PubMed1993

Abnormalities of hemostasis in ischemic stroke.

Despite important new diagnostic laboratory and imaging technologies, the cause of brain infarction remains unexplained in 20% to 40% of subjects. Most stroke patients do not require extensive evaluations of coagulation, but hypercoagulability may account for a significant proportion of unexplained strokes. Hemostatic abnormalities associated with stroke may be broadly classified as familial or acquired. Principal among the familial thrombotic coagulopathies are deficiencies in concentration or function in protein-C, protein-S, and antithrombin III, but other hereditary abnormalities include sickle cell disease, homocystinuria, and dysfibrinogenemia. The acquired disorders of hemostasis associated with stroke probably constitute a larger proportion of the important stroke-related coagulopathies. In particular, the aPL antibody syndrome is now strongly associated with thrombotic events including stroke, although neither the mechanism of thrombosis nor effective therapies for this syndrome have been clearly elucidated. Many of the acquired hemostatic abnormalities exist within a special clinical setting such as with malignancy or with myeloproliferative diseases, nephrotic syndrome, and liver disease. Presumably many of these share common pathways of coagulation activation or dysfunction with the inherited disorders. Most of the hemostatic disorders in stroke are associated with dysfunction of vascular endothelium and abnormalities of or interference with the natural anticoagulant proteins: protein-C, protein-S, and antithrombin III. Improved understanding of these relationships should lead to better diagnosis and treatment for people at risk of stroke.

Antithrombin III Deficiency↗
PubMed2005

Angioplasty and stenting of the cervical carotid bifurcation under filter protection: a prospective study in a series of 53 patients.

The aim of this study is to assess safety, reliability, ease of use and usefulness of filter protection devices during angioplasty and stenting of stenotic lesions of the cervical carotid bifurcation. Over a period of 42 months, 53 patients harboring a cervical carotid bifurcation stenotic lesion were treated, by angioplasty and/or stenting using filter protection devices of different kinds. The stenosis was atherosclerotic in 48 cases, post-surgical in four and post-radiation in one case. In all cases, the treatment was successful, with good restoration of the luminal diameter. There were three major strokes (5.6%) and one minor stroke (1.9%). Two of these (one major, one minor) occurred a few hours after the stenting procedure and both seemed by all evidence due to a hemorrhagic hyperperfusion syndrome. One hemiparesis and dysphasia occurred two days after the procedure, secondary to subacute thrombosis with occlusion of the stent. One patient complained of three episodes of decrease in visual acuity of the eye ipsilateral to the stenting in the two weeks following treatment. In conclusion, in our experience, use of the devices adds only few minutes to the procedure time; direct lesions of the arterial wall, such as dissections or intraluminal thrombi, related to the use of filters were never observed, and spasm of the distal I.C.A. also proved rapidly regressive. The content of all filters, if any, was histologically examined, but plaque material was found only in one case, probably owing to our primary stenting technique without use of pre-dilation. The major technical drawback is in-filter coagulation, which occurred in 16 cases, occluding the membrane of the filter and thus slowing or blocking intracranial flow. Such an event can be counteracted by a more aggressive anti-coagulation protocol, which could, however, be responsible for the two complications with hemorrhagic brain infarction. Furthermore, we observed two other major neurological events, which bring the incidence of neurological complications in this series as high as 7.5%. Therefore, it is our opinion that safety of filters is not yet proven, and consequently great care must be taken in their use.

Aged↗
PubMed1998

Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy.

BACKGROUND/AIMS: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirrhosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis. METHODS: Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood. RESULTS: Five out of six patients demonstrated increased signal intensity in the basal ganglia. Overt portal-systemic encephalopathy was not noted prior to or at the time of evaluation. Normal EEG results were recorded in all patients. Only one of the six patients had pathological results in at least two out of four psychometric tests. This latter patient had had a large right-sided brain infarction. Arterial ammonia concentrations were normal in four of the six patients; one patient with increased ammonia levels had concomitant renal insufficiency with azotemia. The other four patients had no relevant concomitant diseases. Serum manganese levels were non-significantly increased compared with a control group (p=0.06), but they were significantly correlated to basal ganglia signal intensity (R=0.88; p=0.02). CONCLUSIONS: Our results demonstrate that bright basal ganglia primarily represent shunt-induced alterations. They are not directly associated with disturbed liver function nor with portal-systemic encephalopathy.

Adult↗
PubMed1994

[Cerebrovascular complications of non-bacterial thrombotic endocarditis: value of transesophageal echocardiography].

Non bacterial thrombotic endocarditis is a frequent cause of cerebrovascular complications in patients with cancer. Clinical features are often misleading and symptoms are hardly linked to valvular thrombosis in the absence of systemic embolism. We describe here a case mainly illustrating two aspects: clinical and neuroradiological manifestations of multiple distal brain infarcts and the value of transoesophageal echocardiography for the diagnosis.

Cerebral Infarction↗
PubMed1977

Kinking of the carotid artery: indications for surgery and surgical procedure.

In seven patients surgical correction of kinking with stenosis of the extracranial part of the carotid artery was performed. The indications for surgical treatment of carotid kinking are discussed in detail. The following criteria for surgical correction are applied: 1. symptoms of cerebral ischemia must be present; 2. position or motion of head and neck can provoke symptoms; 3. definite stenosis of the corresponding carotid artery at the level of kinking; 4. no other causes of cerebral ischemia; 5. no irreversible brain infarction. A simple and effective surgical procedure as a routine method for correction of carotid kinking is described. Only in special circumstances a more extensive open arterial reconstruction might be necessary.

Aged↗
PubMed2003

Antiserum against human glucose transporter 5 is highly specific for microglia among cells of the mononuclear phagocyte system.

Human monocytes and a variety of tissue macrophages, including microglia, were studied immunohistochemically to determine the expression of a novel microglial marker, human glucose transporter 5 (hGLUT5), in these cells. The hGLUT5 was not expressed in most peripheral macrophages in the normal state, but weakly expressed in some foamy macrophages in atherosclerotic lesions. There was no hGLUT5 reactivity in blood monocytes. In the lesions of brain infarcts, foamy macrophages (predominantly monocyte-derived cells) in the ischemic core were mostly negative for hGLUT5, while activated and phagocytic microglia in the transitional zone were consistently positive. The present study indicated that unlike other microglial markers, hGLUT5 is rarely present in peripheral macrophages, and that hGLUT5 immunohistochemistry is useful in distinguishing microglia-derived macrophages from monocyte-derived macrophages in acute necrotic lesions.

Glucose Transporter Type 5↗
PubMed1999

Hypoglossal motoneurons are postsynaptically inhibited during carbachol-induced rapid eye movement sleep.

The obstructive sleep apnea syndrome is characterized by the occurrence of cyclic snoring and frequent apneic episodes during sleep, with consequent hypoxia and hypercapnia. Obstructive sleep apnea syndrome is associated with excess daytime sleepiness, depression, and an increased incidence of ischemic cardiopathy, cardiac arrhythmias, systemic hypertension and brain infarction. Hypoglossal motoneurons, which innervate extrinsic and intrinsic muscles of the tongue, play a key role in maintaining the patency of the upper airway and in the pathophysiology of obstructive sleep apnea syndrome. Based on data obtained by using extracellular recording techniques, there is a consensus that hypoglossal motoneurons cease to discharge during rapid eye movement sleep, because they are disfacilitated. Since other somatic motoneurons are known to be postsynaptically inhibited during rapid eye movement sleep, we sought to determine, by the use of intracellular recording techniques during cholinergically induced rapid eye movement sleep, whether postsynaptic inhibitory mechanisms act on hypoglossal motoneurons. We found that, during this state, a powerful glycinergic premotor inhibitory system acts to suppress hypoglossal motoneurons. This finding opens new avenues for the treatment of obstructive sleep apnea syndrome, and provides a foundation to explore the neural and pharmacological control of respiration-related motoneurons during rapid eye movement sleep.

Action Potentials↗