RESUMEN
The heart and brain are constantly interacting under normal physiological conditions. This interaction is under the control of the autonomic nervous system with parasympathetic and sympathetic nerve fibers including the participating brain structures. Pathological conditions, such as epilepsy and ischemic cerebral stroke influence heart function, especially the frequency and may result in severe arrhythmia. An asymmetric influence of the left and right brain hemispheres on the heart rate is still under debate. Conversely, the influence of the heart in cases of acute cardiac arrest on brain function is equally relevant and a common clinical problem after resuscitation. We review the damaging cascade of global cerebral hypoxia and the value of different diagnostic procedures as well as the ethical problem of the point in time of termination of consciousness and the instruments for estimating the prognosis.
Asunto(s)
Sistema Nervioso Autónomo/fisiopatología , Encefalopatías/complicaciones , Encefalopatías/fisiopatología , Encéfalo/fisiopatología , Muerte Súbita Cardíaca/etiología , Corazón/inervación , Corazón/fisiopatología , Humanos , Modelos Cardiovasculares , Modelos NeurológicosRESUMEN
BACKGROUND: The term "aseptic meningitis" encompasses cases of meningitis with negative bacterial CSF culture, which predominantly are of viral etiology. While the clinical course is usually benign, complications such as encephalitic involvement resulting in a more severe clinical course may occur. Dysfunction of the blood-brain-barrier (BBB), which is a prerequisite for viral entry into the brain parenchyma, can be approximated using the CSF/serum albumin ratio, readily obtainable in routine CSF analysis. OBJECITVES: Analysis of CSF patterns in patients with aseptic meningitis/meningoencephalitis with a focus on BBB dysfunction as a marker for encephalitic involvement. STUDY DESIGN: Retrospective chart review of patients admitted to our hospital between 2004 and 2016 with a diagnosis of aseptic meningitis/meningoencephalitis. RESULTS: Patients with aseptic meningitis displaying clinical, MR-tomographic or electroencephalographic signs of encephalitic involvement were significantly older than patients without these features (47.4 vs. 35.5 yrs., p=0.002). In patients with meningoencephalitis, CSF analysis revealed a more severe disruption of BBB, approximated by the CSF/serum albumin ratio (p=0.002). Compromised BBB function correlated positively with length of hospitalization (p=0.007), indicative of a more severe clinical course. The number of CSF lymphocytes was found to predict the severity of the BBB disruption, which additionally was more frequently observed when herpesviridae were identified as infectious agents. CONCLUSIONS: We suggest that the CSF/serum albumin ratio as an estimate for BBB function should be attended to in the evaluation of patients with aseptic meningitis. Severe BBB dysfunction, older age and infection with herpesviridae appear to raise the risk for encephalitic involvement.
Asunto(s)
Barrera Hematoencefálica/fisiopatología , Meningitis Aséptica/diagnóstico , Meningoencefalitis/diagnóstico , Adulto , Factores de Edad , Anciano , Biomarcadores/sangre , Barrera Hematoencefálica/virología , Femenino , Infecciones por Herpesviridae/complicaciones , Infecciones por Herpesviridae/virología , Hospitalización , Humanos , Imagen por Resonancia Magnética , Masculino , Meningitis Aséptica/sangre , Meningitis Aséptica/líquido cefalorraquídeo , Meningoencefalitis/sangre , Meningoencefalitis/líquido cefalorraquídeo , Meningoencefalitis/virología , Persona de Mediana Edad , Estudios Retrospectivos , Albúmina Sérica/líquido cefalorraquídeo , Adulto JovenRESUMEN
BACKGROUND: Acute ischemic stroke patients may occasionally suffer from concomitant acute coronary syndrome (ACS). Troponin I and T are established biomarkers to detect ACS. Recently introduced high-sensitive cardiac troponin (hs-TNI and hs-TNT) assays are increasingly used to identify ACS in stroke patients even without signs or symptoms of ACS. These new test systems very often detect elevated values of hs-troponin, although clinical relevance and consequences of elevated hs-TNI values in these patients are unclear so far. PATIENTS AND METHODS: We examined hs-TNI values in 834 consecutive ischemic stroke patients admitted to our Comprehensive Stroke Center during a 1-year period. hs-TNI was measured immediately after admission and after 3 h if initial hs-TNI was elevated above the 99th percentile of normal values (>0.045 ng/ml). Patients with elevated values were divided into two groups: (1) constant and (2) dynamic hs-TNI values. The dynamic approach was defined as a 30% rise or fall of the hs-TNI value above the critical value within 3 h. All patients received stroke diagnostic and continuous monitoring according to international stroke unit standards, including a 12-lead ECG, blood pressure, body temperature and continuous ECG monitoring, as well as regular 6-hourly neurological and general physical examination (including NIHSS scores). The cardiologists - as members of the Stroke Unit team - evaluated clinical symptoms/examination, as well as laboratory, echocardiographic and ECG findings for the diagnosis of ACS. RESULTS: 172/834 (20.6%) patients showed elevated hs-TNI levels on admission. Patients with elevated hs-TNI values exhibited a significantly (p < 0.001) increased rate of hypertension (89 vs. 77.2%), history of stroke (24.4 vs. 14.8%), history of coronary artery disease (65.7 vs. 34.1%), history of myocardial infarction (22.1 vs. 7.6%), heart failure (12.8 vs. 5.7%) and atrial fibrillation (44.2 vs. 23.6%). 82/136 patients showed constant and 54/136 patients dynamic hs-TNI values: among the latter, 5 patients were diagnosed with ST segment elevation myocardial infarction (STEMI) and 24 with non-STEMI (NSTEMI). CONCLUSION: Our data demonstrate that hs-TNI was elevated in about 20.6% of acute ischemic stroke patients but therapeutically relevant ACS was diagnosed only in the dynamic group. hs-TNI elevations without dynamic changes may occur in stroke patients without ACS due to different reasons that stress the heart. Therefore, we suppose that hs-TNI is a sensitive marker to detect high-risk patients but serial measurements are mandatory and expert cardiological workup is essential for best medical treatment and to accurately diagnose ACS in acute ischemic stroke patients.
Asunto(s)
Síndrome Coronario Agudo/diagnóstico , Infarto del Miocardio/diagnóstico , Accidente Cerebrovascular/sangre , Troponina I/sangre , Síndrome Coronario Agudo/sangre , Anciano , Anciano de 80 o más Años , Angiotensina Amida , Biomarcadores/sangre , Electrocardiografía/métodos , Femenino , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Medición de Riesgo , Factores de Riesgo , Accidente Cerebrovascular/diagnóstico , Troponina T/sangreRESUMEN
OBJECTIVE: Neuropsychological sequelae are common after aneurysmal subarachnoid hemorrhage (aSAH) and may be associated with or caused by supposed hypothalamic-pituitary dysfunction. We evaluated the incidence of neuro-endocrine and neuropsychological deficits after aSAH and their interrelations in a standardized manner. METHODS: 26 patients (20 females) were prospectively screened for neuro-endocrine and neuropsychological deficits 3 and 6 months after aSAH. We measured GH, IGF-1, prolactin, LH, FSH, estradiol, TSH, fT4, total T3, testosterone, ACTH as well as cortisol before and after ACTH-stimulation. Neuropsychological analysis covered verbal comprehension, short term and working memory, visuospatial construction, figural memory, psychomotor speed, attention, and concentration. RESULTS: After 3 months central hypogonadism was observed in 2 patients accompanied by central hypothyroidism in 1 male subject. Central hypogonadism resolved spontaneously after 6 months in both. After 3 months, neuropsychological deficits were detected in 57% of the examined patients (44% attention deficits, 38% memory impairment, 12% psychomotor deficits). Neuropsychological deficits were still present in 53% after 6 months. CONCLUSION: We found a low prevalence of neuro-endocrine and a high prevalence of neuropsychological deficits in patients 3 and 6 months after aSAH. Thus, the absent co-incidence of central hormonal and psychological dysfunction leaves a causal association questionable.
Asunto(s)
Enfermedades del Sistema Endocrino/epidemiología , Enfermedades del Sistema Endocrino/etiología , Trastornos Mentales/epidemiología , Trastornos Mentales/etiología , Hemorragia Subaracnoidea/complicaciones , Hemorragia Subaracnoidea/diagnóstico , Adolescente , Adulto , Anciano , Estudios de Cohortes , Enfermedades del Sistema Endocrino/diagnóstico , Femenino , Estudios de Seguimiento , Humanos , Incidencia , Masculino , Trastornos Mentales/diagnóstico , Persona de Mediana Edad , Sistemas Neurosecretores/fisiopatología , Pronóstico , Hemorragia Subaracnoidea/epidemiología , Hemorragia Subaracnoidea/cirugía , Resultado del Tratamiento , Adulto JovenRESUMEN
Focused ultrasound-induced opening of the blood-brain barrier (BBB) in the presence of ultrasound contrast agents is a promising strategy for a targeted drug delivery to the brain. The aim of our study was to identify whether brain molecular stress pathways are targeted by ultrasound treatment. Using an upper level of acoustic pressures in combination with microbubbles, which have been previously reported as reliable for BBB opening without causing tissue damage, we found that ultrasound leads to an increased ubiquitinylation of proteins in neuronal (11+/-3 ubiquitin-overexpressing cells per optical field) but not glial cells 6 h post-insonation, increasing to 16 (+/-4) labelled cells after 24 h. No changes in the expression of Hsp70 and Hsc70 were detected over 24 h. Ultrasound treatment was followed by limited apoptosis after 24 h (32+/-6 cleaved-caspase 3-positive cells per optical field) in the insonated areas. Only neurons were identified in the apoptotic population. Although these observations may not be applicable for all acoustic parameters useful for BBB opening, they demonstrate that insonation of the rat brain with the parameters used in our experiments is a useful tool for BBB opening and induces specific cellular stress response restricted to neuronal cells.
Asunto(s)
Barrera Hematoencefálica/fisiología , Encéfalo/metabolismo , Neuroglía/metabolismo , Neuronas/metabolismo , Sonicación , Ubiquitina/biosíntesis , Animales , Apoptosis , Encéfalo/citología , Sistemas de Liberación de Medicamentos , Regulación de la Expresión Génica , Proteínas del Choque Térmico HSC70/biosíntesis , Proteínas del Choque Térmico HSC70/genética , Proteínas HSP70 de Choque Térmico/biosíntesis , Proteínas HSP70 de Choque Térmico/genética , Imagenología Tridimensional , Masculino , Microburbujas , Microscopía Confocal , Proteínas del Tejido Nervioso/biosíntesis , Proteínas del Tejido Nervioso/genética , Ratas , Ratas Wistar , Factores de TiempoRESUMEN
Combined 2-MHz ultrasound (US) and second-generation, sulfur hexafluoride microbubbles (MB) treatment (US+MB) was performed in a permanent middle cerebral artery (MCA) occlusion model in rats to evaluate possible effects on the ischemic cascade. We used 16 Wistar rats and the MCA occlusion model for stroke induction. Glutamate, pyruvate, lactate and glycerol levels were measured by intracerebral microdialysis before and after stroke induction and after US+MB application (n = 8) for 20 h. After 24 h, brain infarct volume, apoptosis and IL-6 and TNF-alpha levels were evaluated. The infarct volume was significantly reduced (p < 0.05) in the US+MB-treated group compared with control animals. In additional, glutamate levels were significantly lower in US+MB-treated animals, and these animals showed a higher rate of apoptotic cell death in the infarcted area. The levels of IL-6 and TNF-alpha concentrations were not different in both groups, and there was no apoptotic cell death outside the infarction in animals treated with US+MB. The results demonstrate that US+MB with second generation microbubbles does not have a harmful effect on ischemic stroke in an MCA occlusion model of the rat.
Asunto(s)
Isquemia Encefálica/terapia , Arteria Cerebral Media/diagnóstico por imagen , Terapia Trombolítica/métodos , Animales , Biomarcadores/sangre , Isquemia Encefálica/sangre , Isquemia Encefálica/diagnóstico por imagen , Ácido Glutámico/sangre , Glicerol/sangre , Infarto de la Arteria Cerebral Media/sangre , Infarto de la Arteria Cerebral Media/diagnóstico por imagen , Infarto de la Arteria Cerebral Media/terapia , Ácido Láctico/sangre , Masculino , Microburbujas , Microdiálisis , Modelos Animales , Ácido Pirúvico/sangre , Ratas , Ratas Wistar , Hexafluoruro de Azufre , UltrasonografíaRESUMEN
Intima-media thickness (IMT) is increasingly used as a surrogate end point of vascular outcomes in clinical trials aimed at determining the success of interventions that lower risk factors for atherosclerosis and associated diseases (stroke, myocardial infarction and peripheral artery diseases). The necessity to promote further criteria to distinguish early atherosclerotic plaque formation from thickening of IMT and to standardize IMT measurements is expressed through this updated consensus. Plaque is defined as a focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the surrounding IMT value or demonstrates a thickness >1.5 mm as measured from the media-adventitia interface to the intima-lumen interface. Standard use of IMT measurements is based on physics, technical and disease-related principles as well as agreements on how to perform, interpret and document study results. Harmonization of carotid image acquisition and analysis is needed for the comparison of the IMT results obtained from epidemiological and interventional studies around the world. The consensus concludes that there is no need to 'treat IMT values' nor to monitor IMT values in individual patients apart from exceptions named, which emphasize that inside randomized clinical trials should be performed. Although IMT has been suggested to represent an important risk marker, according to the current evidence it does not fulfill the characteristics of an accepted risk factor. Standardized methods recommended in this consensus statement will foster homogenous data collection and analysis. This will help to improve the power of randomized clinical trials incorporating IMT measurements and to facilitate the merging of large databases for meta-analyses.
Asunto(s)
Arterias Carótidas/diagnóstico por imagen , Enfermedades de las Arterias Carótidas/diagnóstico por imagen , Túnica Íntima/diagnóstico por imagen , Túnica Media/diagnóstico por imagen , Adulto , Anciano , Enfermedades Cardiovasculares/etiología , Enfermedades de las Arterias Carótidas/complicaciones , Ensayos Clínicos como Asunto/métodos , Humanos , Interpretación de Imagen Asistida por Computador , Persona de Mediana Edad , Proyectos de Investigación , Factores de Riesgo , Ultrasonografía/métodos , Ultrasonografía/normasRESUMEN
OBJECTIVE: The aim of this study was to evaluate number and kind of neurological patients in comparison with other patients on a medical ICU. METHODS: Over a period of one year, all neurological intensive care patients on a medical ICU were evaluated according to age, sex, diagnosis, mortality, diagnostic methods, ventilation and referral to other hospitals and general wards. RESULTS: Comparable to a specialist neurological ICU a wide spectrum of neurological diseases could be observed on an interdisciplinary ICU. In comparison to other patient groups, patients with neurological disease had a higher rate of ventilation, a longer hospital stay and a higher mortality. CONCLUSION: Our data also demonstrate the relevant amount of neurological patients (19 % measured by bed assignment) in comparison to all patients, and the specific neurological procedures were applicable on a medical/interdisciplinary ICU. A higher interest for neurological patient on a medical ICU would therefore be essential.
Asunto(s)
Unidades de Cuidados Intensivos/estadística & datos numéricos , Enfermedades del Sistema Nervioso/epidemiología , Adulto , Factores de Edad , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Tiempo de Internación , Masculino , Persona de Mediana Edad , Enfermedades del Sistema Nervioso/fisiopatología , Enfermedades del Sistema Nervioso/terapia , Derivación y Consulta , Respiración Artificial , Mecánica Respiratoria/fisiología , Estudios RetrospectivosRESUMEN
Intima-media thickness (IMT) is increasingly used in clinical trials as a surrogate end point for determining the success of interventions that lower risk factors for atherosclerosis. The necessity for unified criteria to distinguish early atherosclerotic plaque formation from thickening of IMT and to standardize IMT measurements is addressed in this consensus statement. Plaque is defined as a focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the surrounding IMT value or demonstrates a thickness of > or =1.5 mm as measured from the media-adventitia interface to the intima-lumen interface. Standard use of IMT measurements is recommended in all epidemiological and interventional trials dealing with vascular diseases to improve characterization of the population investigated. The consensus concludes that there is no need to 'treat IMT values' nor to monitor IMT values in individual patients apart from few exceptions. Although IMT has been suggested to represent an important risk marker, it does not fulfill the characteristics of an accepted risk factor. Standardized methods recommended in this consensus statement will foster homogenous data collection and analysis. This will help to improve the power of studies incorporating IMT measurements and to facilitate the merging of large databases for meta-analyses.
Asunto(s)
Arterias Carótidas/diagnóstico por imagen , Túnica Íntima/diagnóstico por imagen , Túnica Media/diagnóstico por imagen , Ultrasonografía/normas , Arteriosclerosis/diagnóstico por imagen , HumanosRESUMEN
The key goal in the treatment of acute ischemic stroke is fast vessel recanalization. Thrombolysis with recombinant tissue plasminogen activator (rt-PA) is efficient in humans but mean time for recanalization is within hours. Ultrasound bio-effects has been shown to facilitate rt-PA mediated thrombolysis in peripheral arteries. We used an embolic stroke model in the rat. In all rats we induced an ischemic stroke by a selective occlusion of the middle cerebral artery with whole blood clots. From an entire collective of 54 rats 47 completed the protocol (n = 7 died early). Four different groups (no treatment n = 6; full dose rt-PA treatment only [10 mg/kg per body weight] n = 14, half dose rt-PA treatment plus ultrasound n = 10, and full dose rt-PA treatment plus ultrasound n = 17) were investigated. We found a significant reduction of absolute as well as relative infarct volume in the full dose rt-PA plus ultrasound group (81+/-72 mm(3); P< 0.05) in comparison to untreated rats (253+/-159 mm(3); P < 0.05) as well as in comparison to rats treated with full dose rt-PA only (167+/-91 mm(3); P < 0.05). There were five intracranial bleedings giving a bleeding rate of 9.3%. In summary: ultrasound treatment in addition to rt-PA is more effective than single rt-PA treatment in reducing infarct volume and safe with regard to bleeding.
Asunto(s)
Hipoxia-Isquemia Encefálica/terapia , Infarto de la Arteria Cerebral Media/terapia , Terapia Trombolítica/métodos , Terapia por Ultrasonido/métodos , Animales , Terapia Combinada , Modelos Animales de Enfermedad , Relación Dosis-Respuesta a Droga , Hipoxia-Isquemia Encefálica/patología , Hipoxia-Isquemia Encefálica/fisiopatología , Infarto de la Arteria Cerebral Media/patología , Infarto de la Arteria Cerebral Media/fisiopatología , Infarto de la Arteria Cerebral Media/prevención & control , Hemorragia Posoperatoria/prevención & control , Ratas , Ratas Sprague-Dawley , Ratas Wistar , Proteínas Recombinantes de Fusión/farmacología , Terapia Trombolítica/tendencias , Activador de Tejido Plasminógeno/farmacología , Resultado del Tratamiento , Terapia por Ultrasonido/tendenciasAsunto(s)
Isquemia Encefálica/complicaciones , Parálisis/diagnóstico , Parálisis/etiología , Anciano , Anticonvulsivantes/uso terapéutico , Electroencefalografía , Femenino , Predicción , Humanos , Imagen por Resonancia Magnética , Parálisis/tratamiento farmacológico , Accidente Cerebrovascular/etiologíaRESUMEN
BACKGROUND AND PURPOSE: Excessive release of nitric oxide (NO) has been implicated in the pathophysiology of neurodegeneration in ischemic stroke. We compared intracerebral release of indicators of NO generation at the acute and subacute stages of transient focal cerebral ischemia. METHODS: In vivo microdialysis in the rat striatum was performed at the acute (first hours) and subacute (after 24 or 48 hours) stages of cerebral ischemia or sham operation to monitor intracerebral release of the stable NO metabolites nitrite and nitrate. RESULTS: Whereas only a nonsignificant trend toward increased release of these NO metabolites was evidenced in acute cerebral ischemia, a significant NO generation was observed subacutely, 48 hours after induction of cerebral ischemia. Aminoguanidine, a selective inhibitor of inducible NO synthase, suppressed this delayed release of nitrite and nitrate. CONCLUSIONS: Whereas these observations do not support a major NO generation in acute cerebral ischemia, they indicate an inducible NO synthase-dependent NO generation predominantly at the subacute phase of ischemic neurodegeneration. Therefore, NO generation may play a pathophysiological role in delayed ischemic neurodegeneration.
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Isquemia Encefálica/metabolismo , Cuerpo Estriado/metabolismo , Óxido Nítrico/biosíntesis , Animales , Isquemia Encefálica/fisiopatología , Cuerpo Estriado/fisiopatología , Inhibidores Enzimáticos/farmacología , Guanidinas/farmacología , Microdiálisis , Degeneración Nerviosa/etiología , Nitratos/análisis , Óxido Nítrico Sintasa/antagonistas & inhibidores , Óxido Nítrico Sintasa de Tipo II , Nitritos/análisis , Ratas , Factores de TiempoRESUMEN
Timing and extent of trauma-induced release of interleukin-1beta (IL-1beta) in extracellular fluid of the CNS were analyzed. In brain tissue perfusates obtained by in vivo microdialysis a marked release of IL-1beta was unexpectedly detected within less than 60 min. At such an early stage of neurotrauma, mRNA expression of IL-1beta was detected whereas immunoreactivity for the IL-1beta protein was negative. Concentrations of extracellularly secreted IL-1beta protein gradually increased, peaked at day 2 and decreased thereafter. Drugs acting on mononuclear phagocytes significantly modulated IL-1beta secretion. This so far unrecognized acuity of IL-1beta release demonstrated here, may represent a precondition for the orchestrating role of this mediator in the cascade of inflammatory host response.
Asunto(s)
Lesiones Encefálicas/metabolismo , Interleucina-1/metabolismo , Proteínas Virales , Animales , Encéfalo/citología , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Cloroquina/farmacología , Colchicina/farmacología , Inmunohistoquímica , Inflamación/metabolismo , Interferón gamma/farmacología , Interleucina-1/genética , Lipopolisacáridos/farmacología , Masculino , Microdiálisis , Microglía/efectos de los fármacos , Microglía/metabolismo , ARN Mensajero/análisis , ARN Mensajero/genética , Ratas , Ratas Wistar , Serpinas/farmacología , Factores de TiempoRESUMEN
The clinical value of determination of CNS-specific proteins in peripheral blood at the acute phase of ischemic stroke is unclear. S-100 protein and neurone specific enolase were serially quantified in peripheral blood at the acute and subacute phase of ischemic stroke (hours 4, 8, 10, 24 and 72 after onset of symptoms). Whereas S-100 protein was detected in none of the matched control subjects. this protein was observed in 17/24 of the stroke patients. Patients with detectable S-100 protein had significantly larger infarctions. Cortical infarctions had already significantly increased S-100 concentrations at days 1 and 3 compared to subcortical or brainstem infarctions. Patients with volumes of brain lesion of >5 ccm exhibited significantly increased serum levels of S-100 at hours 10, 24 and 72 compared to those with lesion volumes of <5 ccm. At hours 10, 24 and 72, concentrations of S-100 correlated with scores of neurological outcome. Although kinetics of release of neurone specific enolase showed a similar pattern of release in blood, no significant association to outcome or extent of brain damage was observed. These results suggest that S-100 protein and not NSE may represent a useful serum marker of brain damage in acute stroke.
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Isquemia Encefálica/diagnóstico , Trastornos Cerebrovasculares/diagnóstico , Fosfopiruvato Hidratasa/sangre , Proteínas S100/sangre , Anciano , Anciano de 80 o más Años , Encéfalo/irrigación sanguínea , Encéfalo/fisiopatología , Química Encefálica , Isquemia Encefálica/sangre , Isquemia Encefálica/complicaciones , Trastornos Cerebrovasculares/sangre , Trastornos Cerebrovasculares/etiología , Femenino , Humanos , Cinética , Estudios Longitudinales , Masculino , Proteínas del Tejido Nervioso/sangre , Valor Predictivo de las Pruebas , Factores de Tiempo , Resultado del TratamientoRESUMEN
The release of circulating isoforms of selectin- (L-selectin, ELAM-1) and immunoglobulin-type- (ICAM-1) adhesion molecules, responsible for accumulation of leukocytes at sites of tissue injury was studied in CSF and serum of 21 patients with bacterial meningitis and in healthy subjects. Their concentrations were compared with the intrathecal leukocyte recruitment and release of inflammatory cytokines. In contrast to serum concentrations of the leukocyte-derived adhesion molecule, sL-selectin, serum concentrations of endothelial-derived adhesion molecules, sELAM-1 and sICAM-1, were significantly increased in meningitis. No intrathecal synthesis of these adhesion molecules was observed. Serum levels of sELAM-1 were associated with extent of CSF pleocytosis and with concentrations of proinflammatory cytokines IL-1beta and TNF alpha in CSF, but not in serum. Therefore, expression of endothelial adhesion molecules i.e. ELAM-1 may be responsible for the massive intrathecal recruitment of potentially harmful leukocytes in patients with bacterial meningitis. Intrathecally released proinflammatory cytokines may represent the inducing signals for their endothelial upregulation.