Showing papers by "Werner Hacke published in 1997"

Acute stroke: usefulness of early CT findings before thrombolytic therapy.

Abstract: PURPOSE: To determine whether the extent of subtle parenchymal hypoattenuation detected on computed tomographic (CT) scans obtained within 6 hours of ischemic stroke is a factor in predicting patients' response to thrombolytic treatment. MATERIALS AND METHODS: The baseline CT scans of 620 patients, who received either recombinant tissue plasminogen activator (rt-PA) or a placebo, in a double-blind, randomized multicenter trial were prospectively evaluated and assigned to one of three categories according to the extent of parenchymal hypoattenuation: none, 33% or less (small), or more than 33% (large) of the middle cerebral artery territory. The association between the extent of hypoattenuation on the baseline CT scans and the clinical outcome in the placebo-treated and the rt-PA-treated groups after 3 months was analyzed. RESULTS: In 215 patients with a small hypoattenuating area, treatment increased the chance of good outcome. In 336 patients with a normal CT scan and in 52 patients with a large hypoatte...

Intraventricular brain-derived neurotrophic factor reduces infarct size after focal cerebral ischemia in rats.

Abstract: Brain-derived neurotrophic factor (BDNF), acting through the high-affinity receptor tyrosine kinase (TrkB), is widely distributed throughout the central nervous system and displays in vitro trophic effects on a wide range of neuronal cells, including hippocampal, cerebellar, and cortical neurons. In vivo, BDNF rescues motorneurons, hippocampal, and substantia nigral dopaminergic cells from traumatic and toxic brain injury. After transient middle cerebral artery occlusion (MCAO), upregulation of BDNF-mRNA in cortical neurons suggests that BDNF potentially plays a neuroprotective role in focal cerebral ischemia. In the current study, BDNF (2.1 micrograms/d) in vehicle or vehicle alone (controls) was delivered intraventricularly for 8 days, beginning 24 hours before permanent middle cerebral artery occlusion by intraluminal suture in Wistar rats (n = 13 per group). There were no differences in physiological variables recorded during surgery for the two groups. Neurological deficit (0 to 4 scale), which was assessed on a daily basis, improved in BDNF-treated animals compared with controls (P < 0.05; analysis of variance and Scheffe's test). There were no significant differences in weight in BDNF-treated animals and controls during the experiment. After elective killing on day 7 after MCAO, brains underwent 2,3,5-triphenyltetrazolium chloride staining for calculation of the infarct volume and for histology (hematoxylin and eosin and glial fibrillary acid protein). The mean total infarct volume was 83.1 +/- 27.1 mm3 in BDNF-treated animals and 139.2 +/- 56.4 mm3 in controls (mean +/- SD; P < 0.01, unpaired, two-tailed t-test). The cortical infarct volume was 10.8 +/- 7.1 mm3 in BDNF-treated animals and 37.9 +/- 19.8 mm3 in controls (mean +/- SD; P < 0.05; unpaired, two-tailed t-test), whereas ischemic lesion volume in caudoputaminal infarction was not significantly different. These results show that pretreatment with intraventricular BDNF reduces infarct size after focal cerebral ischemia in rats and support the hypothesis of a neuroprotective role for BDNF in stoke.

Brain temperature monitoring and modulation in patients with severe MCA infarction

Abstract: Article abstract-Background: Brain temperature has been measured only occasionally in humans. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3 degrees C degrees higher in the brain has been reported. Elevated temperature facilitates neuronal injury after ischemia. At present, no information concerning changes in brain temperature after acute stroke is available. Methods: In 15 patients who had suffered severe ischemic stroke in the MCA territory, intracerebral temperature was recorded with use of two different thermocouples, with intraventricular, epidural, and parenchymatous measurements. Body-core temperature (Foley catheter temperature) and jugular bulb temperature (n = 5) were recorded simultaneously. Measures for reducing brain temperature were compared. Results: In all patients, brain temperature exceeded body-core temperature by at least up to 1 degrees C (range, 1.0 to 2.1 degrees C). Temperature in the ventricles exceeded epidural temperature by up to 2.0 degrees C. Brain temperature modulation was independent of single pharmacologic (paracetamol, metamizol) treatments. Only systemic cooling was effective and sustained hypothermic (33 to 34 degrees C) brain temperatures. Conclusion: After MCA stroke, human intracerebral temperature is higher than central body-core temperature. There is also a temperature gradient within the brain, with the ventricles warmer than the surface. Mild hypothermia in the treatment of severe cerebral ischemia with use of cooling blankets is both easy to perform and effective in the therapy of severe hemispheric infarction. NEUROLOGY 1997;48: 762-767

Prognosis of stroke patients requiring mechanical ventilation in a neurological critical care unit.

Abstract: Background and Purpose Intubation and mechanical ventilation are sometimes necessary during treatment of acute stroke. Indications include neurological deterioration, pulmonary complications, and elective intubation for procedures and surgery. Prognosis in severe stroke patients requiring mechanical ventilation has often been reported to be poor. This study was performed to prospectively assess the prognosis of stroke patients who require ventilation in a neurological intensive care unit and to determine factors that may influence outcome. Methods Analysis was made of 124 consecutive stroke patients who required mechanical ventilation over a 2-year period. We determined the survival rate at 1 year after admission. Initial clinical data, history of previous diseases, and indication for intubation were analyzed for prognostic significance by univariate and multiple logistic regression analysis. Results The 1-year survival rate was 33.1% (n=41). Sixty-five patients (52%) died in the neurological intensive ca...

Serum neuron-specific enolase as early predictor of outcome after cardiac arrest.

Abstract: Objective: To examine the prognostic value of serum neuron-specific enolase for early prediction of outcome in patients at risk for anoxic encephalopathy after cardiac arrest. Design: Prospective study. Setting: Coronary intensive care unit of the University of Heidelberg. Patients: Forty-three patients (66.8 ± 12.7 [SD] yrs, range 33 to 85) who had had either primary or secondary cardiac arrest, followed by cardiopulmonary resuscitation (CPR). Interventions: Serial blood samples and clinical examinations. Measurements and Main Results: Serum neuron-specific enolase concentrations were determined after CPR on 7 consecutive days. Twenty-five patients remained comatose and subsequently died; 18 patients survived the first 3 months and had no relevant functional deficit at 3-month follow-up. Neuron-specific enolase concentrations were correlated with neurologic outcome. Concentrations of >33 ng/mL predicted persistent coma with a high specificity (100%) and a positive predictive value of 100%. Overall sensitivity was 80%, with a negative predictive value of 78%. Serum concentrations of neuron-specific enolase exceeded this cutoff value no more than 3 days after cardiac arrest in 95% of patients in whom these concentrations had exceeded 33 ng/mL. Conclusions: In patients who have been resuscitated after cardiac arrest, serum neuron-specific enolase concentrations of >33 ng/mL predict persistent coma with a high specificity. Values below this cutoff level do not necessarily indicate complete recovery, because this method has a sensitivity of 80%.

Barbiturate coma in severe hemispheric stroke Useful or obsolete

Abstract: Barbiturates are administered in a variety of clinical conditions to control elevated intracranial pressure (ICP). However, their routine use to treat elevated ICP has been questioned because it may cause severe side effects. We therefore investigated the effect of high-dose barbiturate therapy on ICP and outcome in patients with severe brain edema after severe middle cerebral artery (MCA) or hemispheric infarction. Barbiturate coma was induced with thiopental infusion in 60 patients with critically increased ICP due to large hemispheric or MCA territory infarction, defined by CT. ICP was monitored in all patients during barbiturate therapy. Barbiturate coma was induced after a standardized treatment protocol for increased ICP after failure of osmotherapy and mild hyperventilation. During barbiturate administration, cerebral perfusion pressure (CPP) and mean arterial pressure were recorded. Clinical outcome of these patients and the individual effect on ICP were analyzed. Only five of 60 patients who were treated with barbiturate coma survived (8%). All other patients died after transtentorial herniation with subsequent brain death. Barbiturate infusion was followed by a drop in ICP in 50 patients and showed no effect on ICP values in 10 patients. CPP decreased with a mean of 9 mm Hg (range, 5 to 20 mm Hg). Although barbiturates were initially effective, only in some patients was ICP control sustained. Severe side effects of barbiturate therapy, besides arterial hypotension, were seen in 15 patients (25%). Barbiturate coma in the therapy of increased ICP after severe ischemic hemispheric stroke can lower critically elevated ICP levels. However, it seems to have no positive effect on neurologic outcome.

Superoxide Dismutase Activity in Serum of Patients With Acute Cerebral Ischemic Injury Correlation With Clinical Course and Infarct Size

Abstract: Background and Purpose Superoxide dismutase (SOD) is one of the major free radical scavenging systems that might play a role in both degenerative and acute diseases of the central nervous system. Methods We measured SOD activity in the serum of 41 patients with acute ischemic stroke with a chemiluminometric assay based on the generation of oxygen free radicals by xanthine and xanthine oxidase. Results SOD activity was significantly lower in patients with ischemic stroke than in age-matched control patients with nonvascular, neurological illnesses (n=24; P <.034, Wilcoxon rank test). The activity was inversely correlated with the size of infarction on CT ( P =.01, Spearman correlation) and the severity of neurological deficits ( P <.001, Spearman correlation). The decreased SOD activity recovered within 5 days after stroke to values found in serum of control patients. Conclusions Our data suggest that the SOD activity in serum is reduced in stroke patients, and replacement of antioxidative activity could be beneficial in the acute treatment of cerebral ischemia.

Craniectomy: An aggressive treatment approach in severe encephalitis

Abstract: Article abstract-Background and objective: Focal encephalitis may be associated with brain edema, which is often fatal. The control of intracranial pressure (ICP) is therefore crucial for further therapeutic strategies in space-occupying edema following encephalitis. However, aggressive treatment strategies such as hemicraniectomy have not been described in a larger series of patients. Patients and methods: We describe the clinical course and outcome in six patients who developed severe brain edema associated with acute encephalitis. All received maximum medical treatment for elevated ICP, but with signs of brainstem compression emerging, hemicraniectomy was performed to control ICP. Results: All patients had a very severe encephalitic syndrome and were treated over the course of weeks in the neurocritical care unit (NCCU). However, all patients recovered almost completely and showed only mild or no neurologic deficit when reexamined after 4 months to 3 years. Conclusion: Hemicraniectomy should be considered in patients with severe brain edema following encephalitis as a potentially lifesaving therapeutic measure. Moreover, the initial neurologic deficit seems to have no impact on the long-term clinical outcome. NEUROLOGY 1997;48: 412-417

Plasma Insulin-like Growth Factor I and IGF Binding Protein 3 Levels in Patients With Acute Cerebral Ischemic Injury

Abstract: Background and Purpose The insulin-like growth factors (IGF) are synthesized in the brain and are involved in fetal brain development. An increased expression of IGF-I and IGF-II occurs in cerebral regions with neuronal damage after experimental hypoxic injury. Furthermore, the expression of mRNAs coding for IGF-I and the binding proteins IGFBP-2 and IGFBP-3 is augmented in response to unilateral ischemia in animal models. The secretory dynamics of IGF-I in human cerebral ischemia have not yet been investigated. Methods Plasma IGF-I and IGFBP-3 were measured sequentially in 20 patients with acute ischemic stroke (within 24 hours and 3, 5, and 10 days thereafter). For analysis the patients were assigned to three groups according to the diameter of the infarct area as measured on CT scan: small ( 5 cm). Eight age-matched patients with nonvascular, neurological illnesses served as controls. Results Plasma IGF-I and IGFBP-3 plasma concentrations after acute cerebral ischemia were strikingly lower than those in control subjects and healthy individuals reported in the literature. Plasma IGF-I levels in patients with large infarcts were significantly statistically lower than those in control subjects ( P <.05), and plasma IGFBP-3 levels were significantly lower than those in control subjects on days 5 and 10. Conclusions IGF-I and IGFBP-3 plasma levels are decreased in patients after cerebral ischemia. After acute ischemic stroke, increased demand for growth factors, altered tissue distribution, and accelerated metabolic clearance rate or central inhibition of the somatotrophic axis may contribute to these low plasma concentrations. Growth factors such as IGF-I and IGFBP-3 may play an important role in the pathophysiology of acute cerebral ischemia, and growth factors may have a considerable effect on future therapeutic regimens.

Infection-Associated Cervical Artery Dissection Three Cases

Abstract: Background The pathogenesis of cervical artery dissection remains unknown. Infection-mediated damage of the arterial wall may be one contributing mechanism. We present three male patients with respiratory infection prior to cervical artery dissection. Case Descriptions Case 1: During an upper respiratory tract infection, a 49-year-old patient developed bilateral carotid and vertebral artery dissection with complete vessel restitution. Case 2: Within 3 years, a 40-year-old patient experienced two episodes of bilateral internal carotid artery dissection, both preceded by febrile upper respiratory tract infection. Case 3: A 52-year-old patient developed right-sided and, 2 years later, left-sided internal carotid artery dissection, each following upper respiratory tract infection. Conclusions Infection may be a trigger factor in the pathogenesis of cervical artery dissection.

Hemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction.

Abstract: Surgical decompression to alleviate raised intracranial pressure has been reported repeatedly in the past decades in small series of patients. Only recently have there been indications from larger trials that surgical decompression may be beneficial in treating space-occupying hemispheric infarction. However, surgical requirements for the procedure to be effective have not yet been defined. Based on theoretical criteria, the authors operated on 43 patients with medically uncontrollable hemispheric infarctions. The craniectomies were planned to be as large as possible and performed in combination with a subtemporal decompression. Postoperative computerized tomography scans were evaluated for these criteria. The mean survival rate for the group of 43 patients was 72.1% and no surviving patient ended up in a vegetative state. The mean area of craniectomy was found to be 84.3 ± 16.5 cm2 and the mean distance of the inferior craniectomy margin to the middle fossa was 1.8 ± 1.3 cm. Comparison of survivors and n...

Predominant involvement of motor fibres in patients with critical illness polyneuropathy.

Abstract: Critical illness polyneuropathy (CIP) is a recognized cause of muscle weakness and failure of weaning from a ventilator. In order to characterize the features of CIP, we have examined 28 consecutive surgical patients with severe sepsis using bedside electrophysiology. Of the 28 patients (median APACHE II score 31), 20 developed moderate to severe CIP, as shown by the presence of moderate to severe denervation activity on resting EMG. The median nerve compound muscle action potential (CMAP) amplitudes were reduced to 3.24 (SEM 0.48) mV, while sensory nerve action potential (SNAP) amplitudes obtained from the same nerve were normal (13.1 (1.9) microV). In approximately 50% of these patients, the reduction in CMAP exceeded 50% of the lower limit of normal. Similar results were obtained from stimulation of the ulnar nerve. We conclude that CIP is a major complication in patients with severe sepsis and prolonged artificial ventilation. It predominantly involves motor fibres and thus markedly interferes with weaning from the ventilator.

Quantitation of herpes simplex virus type 1 DNA in cells of cerebrospinal fluid of patients with herpes simplex virus encephalitis

Abstract: We used a nested polymerase chain reaction assay to quantitate the number of viral copies in cells of CSF of eight patients with herpes simplex virus encephalitis (HSVE). The viral load was monitored in serial CSF samples during the course of disease and correlated to clinical symptoms, radiologic manifestations, efficacy of acyclovir treatment, and overall clinical outcome. Before treatment, HSV type 1 (HSV-1) copies were detected at a mean value of 1,786/10(5) (range, 5 to 8,333/10(5) cells; median, 81/10(5) cells). During therapy, HSV-1 DNA decreased gradually to a mean value of 6 copies/10(5) cells (range, 0 to 33 copies/10(5) cells; median, 0 copies/10(5) cells) within 6 to 21 days and disappeared or was barely detectable before treatment completion in most cases. The HSV-1 burden in the CSF did not clearly correlate with the severity of clinical signs or the degree of cranial imaging findings and overall outcome. Quantitation of HSV-1 copies allows rapid and reliable monitoring of antiviral therapy. The absence of a clear correlation between viral load in the CSF and morbidity may suggest a role for indirect mechanisms of brain injury in HSVE.

Brain temperature monitoring and modulation in patients with severe MCA infarction

Abstract: BACKGROUND Brain temperature has been measured only occasionally in humans. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3 degrees C degrees higher in the brain has been reported. Elevated temperature facilitates neuronal injury after ischemia. At present, no information concerning changes in brain temperature after acute stroke is available. METHODS In 15 patients who had suffered severe ischemic stroke in the MCA territory, intracerebral temperature was recorded with use of two different thermocouples, with intraventricular, epidural, and parenchymatous measurements. Body-core temperature (Foley catheter temperature) and jugular bulb temperature (n = 5) were recorded simultaneously. Measures for reducing brain temperature were compared. RESULTS In all patients, brain temperature exceeded body-core temperature by at least up to 1 degrees C (range, 1.0 to 2.1 degrees C). Temperature in the ventricles exceeded epidural temperature by up to 2.0 degrees C. Brain temperature modulation was independent of single pharmacologic (paracetamol, metamizol) treatments. Only systemic cooling was effective and sustained hypothermic (33 to 34 degrees C) brain temperatures. CONCLUSION After MCA stroke, human intracerebral temperature is higher than central body-core temperature. There is also a temperature gradient within the brain, with the ventricles warmer than the surface. Mild hypothermia in the treatment of severe cerebral ischemia with use of cooling blankets is both easy to perform and effective in the therapy of severe hemispheric infarction.

Basilar artery embolism Clinical syndrome and neuroradiologic patterns in patients without permanent occlusion of the basilar artery

Abstract: The objective of this study was to clarify the clinical and radiologic features, risk factors, and prognosis of basilar embolism without permanent basilar artery occlusion. Forty-five patients (mean age, 59 years) with basilar artery embolism participated in the study. Patients with basilar artery occlusion were excluded. The Glasgow Coma Scale (GCS) score on admission was 12 in 29 patients. Etiologic factors were cardiac arrhythmia (17 patients), vertebral artery occlusion (12 patients), cervical spine trauma (4 patients), embolism following angiography (2 patients), and surgery (1 patient). MRI was performed in 17 patients and CT in 39 patients. Radiologic examinations were initially normal in 14 patients and remained normal in three patients. Final infarct localization was the thalamus (36 patients), cerebellum (20 patients), posterior cerebral artery territory (21 patients), midbrain (12 patients), and pons (8 patients). Eight to 12 weeks after stroke 12 patients were without clinical signs (Glasgow Outcome Scale [GOS] 1), 15 patients had minor neurologic deficits (GOS 2), 10 were severely disabled (GOS 3), and eight patients had died (GOS 5). Outcome correlated with GCS on admission (p < 0.0001) and with the number of ischemic lesions (p = 0.0001). The typical syndrome is an acute loss of consciousness followed by multiple brainstem symptoms. Usually, clinical symptoms improve rapidly and, in some patients, completely. Compared with basilar occlusion, basilar embolism has a relatively low mortality and outcome is frequently excellent.

Magnetic resonance imaging in Creutzfeldt-Jakob disease: evidence of focal involvement of the cortex

Abstract: Creutzfeldt-Jakob disease is a prion disease clinically characterised by rapidly progressing dementia, cerebellar and extrapyramidal signs, and myoclonus. Cerebral imaging procedures are considered to be of little value for definite premortem diagnosis, which still depends on brain biopsy. Corresponding to cognitive deficits neuropathological changes mostly affect the cerebral cortex, and less severely other grey matter areas such as the caudate, putamen, and thalamus.1 The following case report suggests that MRI using a fluid attenuated inversion recovery (FLAIR) sequence might detect pathological changes in the cerebral cortex. A 45 year old man presented with a three month history of progressive memory deficit, listlessness, and loss of speech. He repeatedly lost his orientation in the forest where he had worked as a wood cutter for many years. His history was remarkable for bulbectomy of the right eye at the age of 15 months, probably due to retinoblastoma. On examination he complied with simple requests, only. He spoke very little with multiple perseverations. Severe deficits of memory and orientation were obvious. Pronounced irritability with bursts of aggressiveness made neuroleptic therapy necessary. Deep tendon reflexes were brisk but plantar responses were flexor. Rigidity affecting all limbs and hypomimia indicated involvement of …

Haematoma evacuation does not improve outcome in spontaneous supratentorial intracerebral haemorrhage: A case-control study

Abstract: Surgical intervention in supratentorial intracerebral haemorrhage (ICH) is still controversial. We assessed the value of haematoma evacuation with a case-control study. 145 consecutive patients with supratentorial spontaneous ICH without tumour or vascular abnormalities were analysed. Haematoma evacuation was performed in 24 patients. Age, sex, Glasgow Coma Scale (GCS), level of consciousness, pupillary reaction on admission, localisation, aetiology and volume of the haematoma, presence of ventricular blood, and Glasgow Outcome Scale (GOS) on discharge were analysed. From statistical analysis 40 patients >80 years and with haematoma volume <10ml, who were always treated conservatively, were excluded. Prognostic factors retained from a multiple regression model with the dichotomised GOS scale (GOS 1–3, 4+5) as response variable were GCS, haematoma volume and location. The only difference between all medically treated and “operated” patients was haematoma volume, which was larger in the “operated” patients. All 24 evacuated cases could be matched to a medically treated control regarding age, haematoma volume and location, GCS, and pupillary reaction. Significant differences between the two groups could not be detected. Outcome was not different between the two groups. After separating the sample into patients with and without ventricular haemorrhage, there was no different outcome between the two groups either. We conclude that haematoma evacuation did not improve outcome in supratentorial spontaneous ICH. Since haematomas were evacuated mainly in clinically deteriorating patients, our data suggest that the only effect of haematoma evacuation is to stop progressive deterioration rather than to improve overall clinical outcome.

Neurogene Störungen der Herz- und Lungenfunktion bei akuten zerebralen Läsionen

Abstract: Incidence and clinical significance of cardiopulmonary complications of acute cerebral lesions are still unclear. Neurogenic pulmonary edema (NPE) is characterized as an acute, protein-rich lung edema occurring shortly after cerebral lesions associated with an acute rise of intracranial pressure. NPE is infrequently diagnosed, usually in association with head trauma. Pathophysiological mechanisms include a rise of the pulmonary vascular hydrostatic pressure either due to sympathetic innervation with pulmonary vasoconstriction or increased left-atrial pressure following systemic arterial hypertension or an increase in pulmonary capillary permeability. In contrast to NPE, cardiac complications are frequently observed, most consistently in patients with subarachnoid hemorrhage. Typical ECG changes are repolarization abnormalities, similar to those observed in coronary heart disease, and cardiac arrhythmias. The CK-MB may be slightly elevated; echocardiographic findings show a depressed left-ventricular function. Pathological examination reveals myofibrillar necrosis. Cardiac complications are explained with overactivity of the sympathetic innervation and high levels of circulating catecholamines. For adequate treatment, close cardiac monitoring is required in all patients with acute cerebral lesions.

Acute and Critical Care in Neurology

Abstract: The diagnostic and therapeutic management of selected neurological diseases requiring intensive treatment is summarized with special regard for current standards and new developments in therapy. Ischemic stroke is an emergency since the outcome can be improved by immediate and adequate general supporting as well as specific (thrombolytic) therapy in specialized stroke units. Surgical evacuation of supratentorial intracerebral hemorrhage is still controversial. We give an overview of conditions in which surgical therapy such as cerebellar hemorrhage and large, nondominant ganglionic hemorrhage might be advisable. Cerebral venous thrombosis is treated with full-dose intravenous heparin even if hemorrhage is present. In acute bacterial meningitis, early treatment of foci and empiric antibiotic therapy is crucial in order to prevent complications. The outcome of herpes simplex encephalitis can be favorably influenced by treatment with aciclovir and aggressive therapy of elevated ICP and seizures. Acute Guillain-Barre syndrome requires daily monitoring of vital functions in order to recognize the need for intensive care; intravenous immunoglobulins and plasmapheresis are equally recommended for clinical and financial reasons.

Bolus Injection of MR Contrast Agents: Hemodynamic Effects Evaluated by Intracerebral Laser Doppler Flowmetry in Rats

Abstract: PURPOSE To determine the effects on arterial blood pressure and cerebral blood flow of intravenous bolus injection of three MR contrast agents: gadopentetate dimeglumine, polylysine-Gd-DTPA, and superparamagnetic iron particles (SPIO). METHODS A single-fiber laser Doppler flowmetry probe was placed intracerebrally in 56 anesthetized rats. Cerebral blood flow and mean arterial blood pressure were measured before (baseline), during, and up to 30 minutes after intravenous bolus administration of the three contrast agents: 0.1 mmol/kg and 0.3 mmol/kg gadopentetate dimeglumine (n = 18 per group), 0.3 mmol/kg polylysine-Gd-DTPA (n = 10), and 0.03 mmol/kg SPIO (n = 10). RESULTS Neither the higher nor lower dose of gadopentetate dimeglumine had any statistically significant effect on cerebral blood flow, and there was no change in blood pressure during administration of either dose of gadopentetate dimeglumine. Administration of polylysine-Gd-DTPA caused a transient drop in blood pressure in two animals, marked in one (decrease to 21% of baseline values) and mild in the other (84% of baseline). After administration of SPIO, a significant decrease in blood pressure occurred in one animal (41% of baseline). Despite this decrease in mean arterial blood pressure, there were no statistically significant changes in cerebral blood flow after administration of polylysine-Gd-DTPA or SPIO. CONCLUSION Our results suggest that bolus injection of these contrast agents at clinically relevant doses causes no significant alteration in cerebral blood flow. We conclude that gadopentetate dimeglumine is well suited for cerebral MR perfusion imaging without inherent influence on cerebral blood flow and that the same is probably true for polylysine-Gd-DTPA and SPIO.

rtPA in acute ischemic stroke European perspective

Abstract: Since the two randomized studies of recombinant tissue plasminogen activator (rtPA) in acute stroke, the National Institute of Neurological Disorders and Stroke (NINDS) study and the European Cooperative Acute Stroke Study (ECASS) were published, the relevance of the results of both trials has been the subject of controversy. The overall positive results of the 3-h NINDS trial finally led to the approval of rtPA at a dose of 0.9 mg/kg in the United States. The negative result of the ECASS intent-to-treat (ITT) analysis, in which a 1.1-mg dosage of rtPA with a longer time window had been used, created a more reluctant attitude in Europe. This article reviews the results of the two trials. In addition, a short report of the main points of a roundtable discussion held during the Fourth Conference on Thrombolytic Therapy in Acute Ischemic Stroke, in June of 1996 in Copenhagen, are given. Review of the ECASS and the NINDS results. In autumn of 1995, the results of two large, placebo-controlled trials testing the efficacy and safety of intravenous rtPA were published.1,2 ECASS allowed a 6-hour time window and used an rtPA dose of 1.1-mg/kg.1 The NINDS stroke trial used 90- and 180-minute time windows and tested a lower dose of rtPA (0.9 mg/kg).2 One prominent feature of the ECASS trial was the introduction of subtle, pre-defined CT exclusion criteria which were used to identify the so-called "target population." It should be emphasized that the target population was defined in the protocol, served as a basis for the sample size calculations, and that the identification of protocol violations …

Management of Acute Ischaemic Stroke - Is There a Consensus?

Abstract: Although there is currently no generally accepted consensus on the management of acute ischaemic stroke, several organisations are working towards producing guidelines for this disease. A major step i