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Biomedical subjects

K Einhäupl

Publications and source records attributed to K Einhäupl.

At least 19 recordsLinked to original sources
PubMed2006

Risk and predictors of early epileptic seizures in acute cerebral venous and sinus thrombosis.

We assessed the risk and determined predictors of early epileptic seizures (ES) in patients with acute cerebral venous and sinus thrombosis (CVST). A prospective series of 194 consecutive patients with acute CVST admitted to neurological wards in two German university hospitals was analysed for frequency of ES and in-hospital mortality. Demographic, clinical and radiological characteristics during the acute stage were retrospectively analysed for significant association with ES in univariate and multivariate analyses. During the acute stage, 19 patients (9.8%) died. Early symptomatic seizures were found in 86 patients (44.3%). Status epilepticus occurred in 11 patients (12.8%) of whom four died. Amongst patients with epileptic seizures, mortality was three times higher in those with status than in those without (36.4% and 12%, respectively). In multivariate logistic regression analysis, motor deficit [odds ratio (OR) 5.8; 95% CI 2.98-11.42; P < 0.001], intracranial haemorrhage (OR 2.8; 95% CI 1.46-5.56; P = 0.002) and cortical vein thrombosis (OR 2.9; 95% CI 1.43-5.96; P = 0.003) were independent predictors of early epileptic seizures. Status epilepticus was an important source of morbidity and early mortality in patients with CVST in this study. Patients with focal motor deficits, cortical vein thrombosis and intracranial haemorrhage carried the highest risk for ES. Prophylactic antiepileptic treatment may be an option for these patients.

Adolescent↗
PubMed2006

EFNS guideline on the treatment of cerebral venous and sinus thrombosis.

Cerebral venous and sinus thrombosis (CVST) is a rather rare disease which accounts for <1% of all strokes. Diagnosis is still frequently overlooked or delayed due to the wide spectrum of clinical symptoms and the often subacute or lingering onset. Current therapeutic measures which are used in clinical practice include the use of anticoagulants such as dose-adjusted intravenous heparin or body weight-adjusted subcutaneous low-molecular-weight heparin (LMWH), the use of thrombolysis, and symptomatic therapy including control of seizures and elevated intracranial pressure. We searched MEDLINE (National Library of Medicine), the Cochrane Central Register of Controlled Trials (CENTRAL) and the Cochrane Library to review the strength of evidence to support these interventions and the preparation of recommendations on the therapy of CVST based on the best available evidence. Review articles and book chapters were also included. Recommendations were reached by consensus. Where there was a lack of evidence, but consensus was clear we stated our opinion as good practice points. Patients with CVST without contraindications for anticoagulation should be treated either with body weight-adjusted subcutaneous LMWH or dose-adjusted intravenous heparin (good practice point). Concomitant intracranial haemorrhage related to CVST is not a contraindication for heparin therapy. The optimal duration of oral anticoagulation after the acute phase is unclear. Oral anticoagulation may be given for 3 months if CVST was secondary to a transient risk factor, for 6-12 months in patients with idiopathic CVST and in those with 'mild' hereditary thrombophilia. Indefinite anticoagulation (AC) should be considered in patients with two or more episodes of CVST and in those with one episode of CVST and 'severe' hereditary thrombophilia (good practice point). There is insufficient evidence to support the use of either systemic or local thrombolysis in patients with CVST. If patients deteriorate despite adequate anticoagulation and other causes of deterioration have been ruled out, thrombolysis may be a therapeutic option in selected cases, possibly in those without intracranial haemorrhage (good practice point). There are no controlled data about the risks and benefits of certain therapeutic measures to reduce an elevated intracranial pressure (with brain displacement) in patients with severe CVST. Antioedema treatment (including hyperventilation, osmotic diuretics and craniectomy) should be used as life saving interventions (good practice point).

Anticoagulants↗
PubMed2004

Cerebral venous and sinus thrombosis.

Cerebral venous and sinus thrombosis (CVST) can present with a variety of clinical symptoms ranging from isolated headache to deep coma. Prognosis is better than previously thought and prospective studies have reported an independent survival of more than 80% of patients. Although it may be difficult to predict recovery in an individual patient, clinical presentation on hospital admission and the results of neuroimaging investigations are--apart from the underlying condition--the most important prognostic factors. Comatose patients with intracranial haemorrhage (ICH) on admission brain scan carry the highest risk of a fatal outcome. Available treatment data from controlled trials favour the use of anticoagulation (AC) as the first-line therapy of CVST because it may reduce the risk of a fatal outcome and severe disability and does not promote ICH. A few patients deteriorate despise adequate AC which may warrant the use of more aggressive treatment modalities such as local thrombolysis. The risk of recurrence is low (< 10%) and most relapses occur within the first 12 months. Analogous to patients with extracerebral venous thrombosis, oral AC is usually continued for 3 months after idiopathic CVST and for 6-12 months in patients with inherited or acquired thrombophilia but controlled data proving the benefit of long-term AC in patients with CVST are not available.

Cerebral Veins↗
PubMed2003

Risk of recurrence of cerebral venous and sinus thrombosis during subsequent pregnancy and puerperium.

OBJECTIVE: To assess the risk of recurrence of cerebral venous and sinus thrombosis (CVST) during subsequent pregnancy and puerperium in women with previous cerebral venous occlusive disease. METHODS: The authors retrospectively studied the relapse rate of CVST and the incidence of extracerebral venous thrombosis during subsequent pregnancies in 39 women (from 125 patients with CVST) who suffered a CVST at childbearing age. RESULTS: Mean follow up was 10.25 years (range 1 to 20). Twenty two pregnancies and 19 births were observed in 14 women without evidence of either recurrence of CVST or extracerebral venous thrombosis. One pregnancy occurred during oral anticoagulation and was interrupted and two pregnancies ended with spontaneous abortions. Low dose heparin had been given during five pregnancies. CONCLUSIONS: The risk of recurrence for CVST during pregnancy seems to be low and these data do not justify a negative advice on pregnancy in women with previous CVST. Further studies are needed to evaluate the need for a prophylactic anticoagulation during pregnancy and puerperium.

Adolescent↗
PubMed2001

Sulfonylurea drugs do not influence initial stroke severity and in-hospital outcome in stroke patients with diabetes.

BACKGROUND AND PURPOSE: Sulfonylurea drugs inhibit ATP-dependent potassium channels and may increase mortality after myocardial infarction. Sulfonylurea drugs also inhibit ischemic preconditioning in experimental models of brain ischemia and in clinical studies in the human heart. METHODS: In the present study we examined the impact of sulfonylurea drugs on in-hospital mortality and the immediate neurological deficit of diabetic stroke patients. From a larger stroke data bank, we studied 146 diabetic patients with acute hemispheric ischemic stroke. Sixty patients were using sulfonylurea drugs. RESULTS: Major baseline characteristics such as age, blood pressure, admission glucose level, HbA(1c), distribution of cardiovascular risk factors, and presumed stroke etiology (Trial of Org 10172 in Acute Stroke Treatment [TOAST] criteria) were not different. Mortality (15% versus 14%; P=0.86) and initial stroke severity (Canadian Neurological Scale score, 7.4 versus 7.5; P=0.79) were not significantly different between patients with and without sulfonylurea drugs. Further end points such as Rankin Scale score, deteriorating stroke, duration of hospital stay, type of infarcts on CT/MRI, requirement of intensive care, and complications were not different. In a stepwise logistic regression model, sulfonylurea drugs were not independent predictors for increased mortality, deteriorating stroke, or stroke severity. CONCLUSIONS: In the present hospital-based study, sulfonylurea drugs in patients with diabetes and stroke are not associated with increased stroke severity, mortality, or a worse in-hospital outcome.

Aged↗
PubMed2000

Spontaneous low frequency oscillations of cerebral hemodynamics and metabolism in human adults.

UNLABELLED: We investigated slow spontaneous oscillations in cerebral oxygenation in the human adult's visual cortex. The rationale was (1) to demonstrate their detectability by near infrared spectroscopy (NIRS); (2) to analyze the spectral power of as well as the phase relationship between the different NIRS parameters (oxygenated and deoxygenated hemoglobin and cytochrome-oxidase; oxy-Hb/deoxy-Hb/Cyt-ox). Also (3) influences of functional stimulation and hypercapnia on power and phase shifts were investigated. The results show that-in line with the literature-low frequency oscillations (LFO) centred around 0.1 s(-1) and even slower oscillations at about 0.04 s(-1) (very low frequency, VLFO) can be distinguished. Their respective power differs between oxy-Hb, deoxy-Hb, and Cyt-ox. Either frequency (LFO and VLFO) is altered in magnitude by functional stimulation of the cortical area examined. Also we find a change of the phase shift between the vascular parameters (oxy-Hb, tot-Hb) and the metabolic parameter (Cyt-ox) evoked by the stimulation. It is shown that hypercapnia attenuates the LFO in oxy-Hb and deoxy-Hb. CONCLUSIONS: (1) spontaneous vascular and metabolic LFO and VLFO can be reproducibly detected by NIRS in the human adult. (2) Their spectral characteristics and their response to hypercapnia are in line with those described in exposed cortex (for review see (Hudetz et al., 1998)) and correspond to findings with transcranial doppler sonography (TCD) (Diehl et al., 1995) and fMRI (Biswal et al., 1997). (3) The magnitude of and phase relation between NIRS-parameters at the LFO may allow for a local noninvasive assessment of autoregulatory mechanisms in the adult brain.

Adult↗
PubMed1999

Antiplatelet therapy: views from the experts.

Antiplatelet therapy is recommended for stroke prevention in persons with a history of thromboembolic stroke or transient ischemic attack (TIA) that is not of cardiac origin. Aspirin was the first antiplatelet agent to be used in this context and is still the most frequently prescribed preventive treatment for ischemic stroke. However, because the results of clinical studies with aspirin have been inconsistent, the dose of aspirin required for stroke prevention in persons with cerebrovascular disease has been a subject of debate among stroke neurologists. In the present discussion, low-dose aspirin is generally regarded by the experts as equivalent in effectiveness to high-dose aspirin, and its higher tolerability has the potential to significantly increase compliance with long-term therapy. Higher aspirin doses may have clinical utility in particular settings, but this requires further study. Despite the controversy, aspirin is now recognized as the treatment standard against which other antiplatelet agents are compared. Antiplatelet agents that may be more effective than aspirin have now been developed. Although each of these agents has been directly compared with aspirin in a large, randomized clinical trial, the lack of direct comparisons among these alternative antiplatelet therapies complicates decisions regarding long-term care of patients with cerebrovascular disease. An international panel of stroke neurologists reports that their selection of antiplatelet therapies for patients with prior history of TIA or stroke depends most heavily on drug efficacy and safety issues and is limited by availability (approval status of alternatives).

Humans↗
PubMed1999

Treatment of ischaemic stroke.

Stroke is a neurological emergency that requires rapid diagnostic workup and immediate treatment. Basic medical management such as maintenance of a high level of systemic blood pressure, provision of an optimal supply of oxygen, and correction of hyperthermia, hyperglycaemia and hypovolemia can contribute to a more favourable clinical outcome of stroke patients. Neuroprotective drugs have shown to be effective in reducing cerebral infarct size in several animal species but their clinical benefit in stroke patients remains to be proven. Neither heparin nor aspirin can improve neurological outcome or significantly reduce death or dependency several months after the ischaemic event, but aspirin is clearly effective in reducing early death or stroke recurrence within the first few weeks. Early anticoagulation should be used for patients at high risk for recurrent cardioembolic stroke and with carotid or vertebral artery dissection, although this recommendation is not based on the results of randomised controlled trials.

Anticoagulants↗
PubMed1997

Noninvasive near infrared spectroscopy monitoring of regional cerebral blood oxygenation changes during peri-infarct depolarizations in focal cerebral ischemia in the rat.

Intermittent peri-infarct depolarizations (PID), which spread from the vicinity of the infarction over the cortex, have been reported in focal ischemia. These depolarizations resemble cortical spreading depression except that they damage the cortex and enlarge the infarct volume possibly because of compromised oxygen delivery. The main purpose of this study was to evaluate the noninvasive technique of near-infrared spectroscopy (NIRS) for the identification of PID and to evaluate its capability for further pathophysiological studies. We used male barbiturate-anesthetized Wistar rats (n = 10) in which middle cerebral artery occlusion had been performed with a surgical thread. Middle cerebral artery occlusion resulted in a drop in parietally measured regional cerebral blood flow (laser Doppler flowmetry) to 31 +/- 8% of baseline flow. Six +/- 4 minutes after the induction of focal ischemia, 5 +/- 2 direct current deflections were recorded during a one-hour measurement period which may be regarded as PID. Measuring regional cerebral blood oxygenation changes with a NIRO 500 revealed dynamic concentration changes in the three chromophores oxyhemoglobin [HbO2], deoxyhemoglobin [Hb], and the oxidized form of cytochrome aa3 [CytO] during PID. Typically, an initial slight decrease of [HbO2] (-6.1 +/- 1.7 arbitrary units [AU] and an increase of [Hb] (+11.5 +/- 7.7 AU) were followed by an increase of [HbO2] (+10.8 +/- 4.7 AU) and a decrease of [Hb] (-4.7 +/- 5.5 AU); [CytO] decreased during the depolarizations (-2.0 +/- 1.2 AU). We conclude that NIRS can detect typical PID-associated changes in blood oxygenation. We hypothesize that during the course of PID, unlike "normal" spreading depression, hypoxygenation precedes hyperoxygenation of the microcirculation in a given cortex volume as the depolarization wave propagates through hemodynamically compromised to intact tissue. This would accord with the known damaging effect of PID. The NIRS "fingerprint" of PID encourages the search for PID during early stroke in patients.

Animals↗
PubMed1994

Detection of oligoclonal IgA in cerebrospinal fluid samples by an isoelectric focusing procedure.

An isoelectric focusing procedure for the detection of oligoclonal IgA in cerebrospinal fluid (CSF) samples is presented. CSF IgA bands were found in 69% of patients with various inflammatory neurological diseases, in 22% of patients with other neurological diseases, but in none of the patients with non-neurological diseases. In patients with inflammatory neurological diseases we examined the relationship between an intrathecal synthesis of oligoclonal IgA and an intrathecal IgA synthesis as proved by a formula recently described by Reiber and Felgenhauer: 83% of patients with an intrathecal IgA synthesis according to the formula of Reiber and Felgenhauer also showed CSF IgA bands whereas 59% of patients without an intrathecal IgA synthesis displayed an intrathecal synthesis of oligoclonal IgA. Seventeen percent of patients with inflammatory neurological diseases were characterized by an intrathecal synthesis of oligoclonal IgA but did not show either an intrathecal IgA synthesis or an intrathecal synthesis of oligoclonal IgG, the detection of oligoclonal IgA therefore being the only evidence of an intrathecal humoral immune response in these patients.

Humans↗
PubMed1994

Cerebral sinus and venous thrombosis in rats induces long-term deficits in brain function and morphology--evidence for a cytotoxic genesis.

The pathophysiology of cerebral venous infarctions is poorly understood, due partially to the lack of a suitable experimental model. Therefore, we developed a model in rats to study acute and long-term changes of brain function and morphology following thrombosis of the superior sagittal sinus. The superior sagittal sinus of rats was exposed, ligated, and injected with thrombogenic material. Thrombosis of the longitudinal sinus and ascending cortical veins was monitored by intravital fluorescence angiography. Histology was studied at 24 h and 4 weeks after thrombosis and changes in intracranial pressure, electroencephalogram (EEG), and tissue impedance were noted. Spontaneous locomotor activity was followed for 4 weeks after thrombosis. The effect of heparin treatment on tissue impedance was evaluated. Thrombosis of the superior sagittal sinus could be regularly induced, although pathological sequelae developed only if ascending veins were affected. Sinus and venous thrombosis was histologically characterized by bilateral, parasagittal infarctions. Thrombosis induction was followed by an increase in intracranial pressure from 4.7 +/- 1.6 to 12.8 +/- 2.4 mm Hg (n = 4) at 1 h after thrombosis, associated with an exponential rise in tissue impedance to 165 +/- 14% (n = 8) of the control. EEG changes were similar to those following global cerebral ischemia and remained pathological for up to 6 months after thrombosis (n = 6). As a permanent behavioral deficit spontaneous locomotor activity was reduced to 60 +/- 10% (n = 6) of the control. Finally, the administration of heparin (1 IU/g body weight) after thrombosis induction was found to reverse the pathological tissue impedance response of the brain. In conclusion, involvement of ascending cortical veins following sinus thrombosis appears to be critical for the development of irreversible tissue damage, such as infarction. Changes in intracranial pressure and tissue impedance suggest that the venous thrombosis was followed by brain edema of a predominantly cytotoxic nature. Venous thrombosis led to long-term changes of brain function, as demonstrated by persistent disturbances of the EEG or of the spontaneous locomoter drive. These deficits may be amenable to treatment with heparin.

Animals↗
PubMed1994

Capillary perfusion of the rat brain cortex. An in vivo confocal microscopy study.

Confocal laser-scanning microscopy was used to visualize subsurface cerebral microvessels labeled with intravascular fluorescein in a closed cranial window model of the anesthetized rat. In noninvasive optical sections up to 250 microns beneath the brain surface, plasma perfusion and blood cell perfusion of individual capillaries were studied. Under resting conditions, in all cerebral capillaries the presence of plasma flow as demonstrated by the appearance of an intravenously injected fluorescent tracer within 20 seconds after injection. Plasma flow was verified even in capillaries that contained stationary erythrocytes or leukocytes; 91.1% of the capillaries contained flowing blood cells, 5.2% contained stationary blood cells, and no blood cells were seen in 3.6%. Mean blood cell velocity was 498.3 +/- 443.9 microns/s, and the mean blood cell supply rate was 35.75 +/- 28.01 cells per second. When capillaries were continuously observed for 1 minute, "on" and "off" periods of blood cell flow were noted. During hypercapnia (increase of PCO2 from 33.25 to 50.26 mm Hg), mean blood cell flux increased from 38.6 +/- 17.2 to 55.5 +/- 12.2 per second (P < .005, paired t test of mean values in six animals), and blood cell velocity increased from 519.5 +/- 254.8 to 828.5 +/- 460.8 microns/s (P = .074, paired t test of mean values in six animals). Homogeneity of blood cell flux increased as indicated by the coefficient of variation decreasing from 44.6% to 22.0%, and the portion of poorly perfused capillaries (blood cell flux, < 40 per second) decreased from 59.2% to 22.4%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up.

OBJECTIVE: The purpose of this study was to determine the value of venous MR angiography as the sole procedure for the diagnosis and follow-up of dural sinus thrombosis. MATERIALS AND METHODS: Forty-two patients with clinical findings suggestive of dural sinus thrombosis were examined with venous MR angiography and spin-echo MR imaging. Maximum-intensity-projection reconstructions and individual sections of the MR angiograms were examined for direct and indirect signs of dural sinus thrombosis by assessing flow signal from the major sinuses, the jugular bulb, upper jugular veins, ascending cortical veins (occlusion or increased flow due to formation of collaterals), diploe (emissary) veins and extracranial veins, and the deep subcortical veins (Galen's and internal cerebral veins). Direct signs of dural sinus thrombosis on MR angiograms included lack of typical high flow signal from a sinus that did not appear aplastic or hypoplastic on single sections from MR angiography and the frayed appearance of the flow signal from a sinus after recanalization. Indirect signs of dural sinus thrombosis included evidence of formation of collaterals, unusually prominent flow signal from deeper medullary veins, cerebral hemorrhage, visualization of emissary veins, and signs of increased intracranial pressure. When available, conventional angiograms were evaluated by analogous criteria as appropriate. Digital subtraction or cut-film angiograms were available for correlation in nine patients. In nine patients, MR angiography was repeated up to eight times during the course of follow-up. The results of MR angiography for all patients were compared with results in 10 control subjects. Confirmation of the diagnosis of dural sinus thrombosis was based either on conventional angiographic findings or on the changes seen in follow-up examinations. RESULTS: Dural sinus thrombosis could be ruled out in 25 of the 42 patients on the basis of clinical and MR angiographic findings. In 17 patients with MR angiographic findings that indicated dural sinus thrombosis, conventional angiography confirmed the diagnosis in nine patients, and changes seen on repeat MR angiograms during follow-up confirmed the diagnosis in nine patients as well (one patient's diagnosis was confirmed by both techniques). Individual frames from two-dimensional fast low-angle shot sequences allowed direct visualization of thrombus. Limited spin-echo sequences as performed here provided inconsistent findings and were insufficient for diagnosis. In the 10 control subjects, attenuation of flow signal was seen in the torcular Herophili in all studies; one subject had a nonpathologic variant of the sinojugular system. CONCLUSION: MR angiography is the technique of choice for diagnostic evaluation and follow-up of dural sinus thrombosis, and it is reliable as the sole examination for this condition. When MR angiographic findings are unremarkable and other abnormalities must be ruled out, routine spin-echo MR imaging should be performed.

Adult↗
PubMed1994

Normal values of cerebrovascular reserve capacity after stimulation with acetazolamide measured by xenon 133 single-photon emission CT.

PURPOSE: To determine whether a standardized stimulation challenge with acetazolamide will be helpful for assessing the vasodilatory capacity in patients with obstructive cerebrovascular disease. METHODS: To establish normative data of the cerebrovascular reserve capacity, a group of 41 control patients was investigated. The regional cerebral blood flow was measured quantitatively before and after stimulation with acetazolamide using the xenon 133 inhalation method and dynamic single-photon emission CT. RESULTS: A significant increase of regional cerebral blood flow was found after administration of 1 g of acetazolamide. By doubling the dose no significant further increase was measured. We found no correlation of either baseline or stimulated flow values with age. However, a linear dependence between the stimulated flow values and their respective baseline values was observed. CONCLUSION: The standardized challenge with acetazolamide seems to be a reliable method to determine cerebrovascular reserve capacity quantitatively.

Acetazolamide↗
PubMed1990

[3D-MR-angiography using Gd-DTPA].

Projection angiograms similar to DSA can be obtained via 3D-gradient echo techniques by subtraction of data sets acquired before and after the intravenous administration of Gd-DTPA (0.1-0.2 mmol/kg body weight). As Gd-DTPA does not penetrate the blood-brain barrier, image subtraction results in complete cancellation of non vascular tissue. In organs without blood-brain barrier Gd-DTPA induced signal enhancement results in modest background superposition of vascular anatomy. With Gd-DTPA angiography vessels are imaged favouring the venous system because of the more constant flow velocity and the lack of ECG synchronization. Gd-DTPA angiography results in high signal-to-noise angiograms and can even be performed with MR imagers which do not meet the hardware requirements for angiography based on flow compensated gradients.

Blood Vessels↗
PubMed1989

B-waves in healthy persons.

The objective of this study was to determine, whether 0.5-2/min oscillations in intracranial pressure ('B-waves') are a physiological phenomenon. In a group of 5 patients 0.5-2/min oscillations of ventricular pressure simultaneous with oscillations in the middle cerebral artery (MCA) flow velocity, as assessed by transcranial Doppler sonography, were observed. Similar oscillations in MCA blood flow velocity were demonstrated in 8 out of 10 healthy subjects with an amplitude of about 10% of the mean flow velocity. We speculate that oscillations both in ventricular pressure and middle cerebral artery blood flow velocity are caused by rhythmic diameter changes of cerebral vessels with concomitant cerebral blood volume oscillations. Our data support the suggestion that B-waves may be physiological.

Adult↗
PubMed1989

Cerebrospinal fluid penetration after single or multiple dosage with ticarcillin/clavulanate.

Penetration of ticarcillin and clavulanate into the cerebrospinal fluid was studied in ten patients with varying degrees of impairment of the blood-brain barrier. In general, penetration of both drugs was relatively low and variable (5.4 +/- 5.8% for clavulanate and 2.0 +/- 4.0% for ticarcillin) but markedly better in those patients with impaired blood/brain barrier.

Adolescent↗