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Biomedical subjects

W Hacke

Publications and source records attributed to W Hacke.

At least 163 records · Page 9Linked to original sources
PubMed1997

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

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 < 7 in five patients, 7 to 12 in 11 patients, and > 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.

Adult↗
PubMed1997

Bolus injection of MR contrast agents: hemodynamic effects evaluated by intracerebral laser Doppler flowmetry in rats.

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.

Animals↗
PubMed1997

Neurocritical care for acute ischemic stroke.

Treatment strategies for acute ischemic stroke include general and specific measures. The rationale for these strategies is discussed, and the current practice in the acute phase of ischemic stroke is presented. Special attention is given to the patient requiring intensive care.

Adult↗
PubMed1996

The association of leukocyte count, fibrinogen and C-reactive protein with vascular risk factors and ischemic vascular diseases.

In 154 subjects (age 63 +/- 11 years; 63 women and 91 men) randomly selected from the population, we tested the hypothesis that inflammatory parameters are associated with vascular risk factors and particularly with a history of ischemic vascular diseases. The subjects were part of the control group (n = 197) in a case-control study investigating recent infection as a risk factor for acute cerebrovascular ischemia and had been matched for sex and age with patients suffering from acute ischemic stroke or transient ischemic attack. Subjects with malignant or inflammatory diseases, with recent trauma, surgery or vascular diseases (n = 43) were excluded from the present analysis. In multivariate analysis, current smoking, diabetes mellitus, age > or = 65 years, and a history of stroke independently increased the leukocyte count. Hypertriglyceridemia, peripheral arterial disease, and diabetes mellitus were positively associated with C -reactive protein (CRP). Age > or = 65 years and diabetes mellitus independently increased fibrinogen. (p < 0.05, respectively) Subjects with a history of cerebrovascular, cardiovascular or peripheral arterial disease had higher leukocyte counts, fibrinogen and CRP than subjects without vascular risk factors and higher leukocytes and fibrinogen than subjects with one or more risk factors. Subjects under the age of 65 with vascular risk factors but without ischemic diseases had higher leukocyte count, fibrinogen and CRP and subjects older than 65 with risk factors had higher CRP than subjects without risk factors or ischemic diseases in the same age group. (p < 0.05, respectively) These results support the hypotheses that low-grade inflammation is associated with vascular risk factors and that inflammatory mechanisms may contribute to the risk of organ ischemia.

Adolescent↗
PubMed1996

'Malignant' middle cerebral artery territory infarction: clinical course and prognostic signs.

BACKGROUND: Although the clinical features of space-occupying ischemic stroke are well known, there are limited prospective data on the clinical course of complete middle cerebral artery territory infarction and on the predisposing factors leading to subsequent herniation and brain death. METHODS: The clinical course of patients with complete middle cerebral artery territory infarction, defined by computed tomography and vascular imaging, was evaluated. Initial clinical presentation was assessed by the Scandinavian Stroke Scale and the Glasgow Coma Scale. Serial computed tomography with measurement of midline and septum pellucidum shift and data on the presence and location of vascular occlusion by angiography or Doppler ultrasound were obtained directly after admission. Time course and outcome were analyzed with regard to the clinical findings on admission and at follow-up. The functional status of surviving patients was assessed using the Barthel Index. RESULTS: Fifty-five patients with complete middle cerebral artery territory infarction caused by occlusion of either the distal intracranial carotid artery or the proximal middle cerebral artery trunk were studied. In all patients, embolic infarction was presumed. The mean Scandinavian Stroke Scale score on admission was 20, and the time course of deterioration varied between 2 and 5 days. Forty-nine patients required ventilator assistance during the acute stage of disease. Only 12 patients (22%) survived the infarct. The cause of death was transtentorial herniation with subsequent brain death in 43 patients. Survivors had a mean Barthel Index score of 60 (range, 45 to 70). CONCLUSIONS: The prognosis of complete middle cerebral artery territory stroke is very poor and can be estimated by early clinical and neuroradiological data within the first few hours after the onset of symptoms. A space-occupying mass effect develops rapidly and predictably over the initial 5 days after presentation. Herniation occurred as an end point in 43 (78%) of these patients.

Adult↗
PubMed1996

Excess glutamate levels in the cerebrospinal fluid predict clinical outcome of bacterial meningitis.

BACKGROUND: The clinical course of bacterial meningitis still is characterized by a high mortality and frequent neurological deficits in survivors. In addition to other potentially neurotoxic mediators of inflammation, the excitatory amino acid glutamate, which has been implicated in neuronal death in a variety of other neurological diseases, may also be involved in the pathological process of bacterial meningitis. OBJECTIVES: To investigate the prognostic value of the glutamate concentration in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. PATIENTS AND METHODS: Thirty consecutive patients with bacterial meningitis were included in a prospective study. The clinical severity of the disease was assessed on admission and 14 days after the beginning of antibiotic treatment by means of the Glasgow Coma Scale. Studies of CSF were performed on admission and after 3 to 6 days. In addition to standard CSF investigations, including cell count, cytologic findings, protein analysis, glucose and lactate levels, and microbiological tests, the concentration of glutamate in the CSF was measured by an enzymatic assay. RESULTS: At admission, both CSF cell count and concentration of glutamate correlated well with the severity of the disease. After treatment, glutamate concentrations decreased significantly to normal or only slightly elevated levels in 23 patients. However, in 7 patients glutamate levels remained markedly increased. In this group, clinical outcome was significantly worse than in the group of patients with low glutamate levels in the second CSF analysis. CONCLUSIONS: A prolonged increase of glutamate levels in the CSF may predict poor clinical outcome in patients with bacterial meningitis, possibly because of the sustained neurotoxic effects of this excitatory neurotransmitter.

Adolescent↗
PubMed1996

[Infectious diseases as a cause and risk factor for cerebrovascular ischemia].

Cerebrovascular ischemia can be caused by infectious diseases which involve cerebral arteries or the heart, including infectious endocarditis, bacterial and fungal meningitis, neurosyphilis, neuroborreliosis, herpes zoster, the acquired immunodeficiency syndrome, cat scratch disease and other rare infectious diseases. Presently, there is increasing evidence that infection in general and mainly respiratory infection is a risk factor for ischemic stroke. Case reports and smaller case series reported an association of cerebrovascular ischemia and recent infection in children and younger adults. Two case control studies from Helsinki (54 patients under the age of 50) and from Heidelberg (197 patients aged 80 or less) identified recent infection as an important risk factor for ischemic stroke. Febrile, bacterial and respiratory infections were most important in this respect. In the study from Heidelberg, the neurological deficit was more severe and cardioembolism was more frequent in infection-associated stroke than in stroke without preceding infection. This review summarizes the association of infectious diseases and cerebrovascular ischemia and discusses potential pathogenetic mechanisms linking both diseases.

Adult↗
PubMed1996

[Epidural cerebrospinal fluid pressure measurement and therapy of intracranial hypertension in "malignant" middle cerebral artery infarct].

BACKGROUND AND PURPOSE: A permanent elevation of ICP after severe brain injury for instance in subarachnoid or intracerebral hemorrhage or neurotrauma is associated with a poor clinical outcome. Although increasingly being used in the intensive care of patients with elevated ICP, continuous epidural ICP monitoring in ischemic stroke has not been firmly established yet. PATIENTS AND METHODS: We prospectively evaluated the clinical course and outcome of patients with raised ICP due to space occupying ischemic middle cerebral artery (MCA) infarction as seen in CT, who underwent continuous ICP monitoring. Epidural ICPprobes were inserted ipsilaterally (all patients) and contralaterally (additional in 7 patients) to the side of infarctation. Glasgow Coma and Scandinavian Stroke Scales (GCS and SSS) were obtained initially and in the further clinical course. All patients were subjected to a standardized treatment protocol for raised ICP. ICP values were correlated with clinical presentation at the time point of deterioration, with outcome and CT findings. Effectiveness of different treatment modalities to lower ICP were analyzed and discussed. RESULTS: 9 of 48 patients survived the MCA infarct (19%), with the cause of death being transtentorial herniation with subsequent brain death in all 39 patients. Mean SSS at admission was 20.6 (survivors 21.5 +/- 5.6, nonsurvivers 19.8 +/- 6.5). All patients showed clinical signs of herniation before the increase of ICP. All 39 patients who died developed ICP values higher than 35 mmHg and no patient with ICP values of more than 35 mmHg survived. CCT changes dit not necessarily reflect the absolute measured ICP values. All treatment modalities for raised ICP including osmotherapy, controlled hyperventilation, tromethamol and barbiturates were initially effective, but only in a minority of patients ICP control could be sustained. CONCLUSIONS: We conclude that ICP monitoring in large hemispheric infarction may predict clinical outcome. ICP monitoring was not helpful in guiding long term treatment of ICP. It remains doubtful, whether ICP monitoring has a positive influence on clinical outcome of acute severe ischemic stroke.

Adult↗
PubMed1996

Excess glutamate in the cerebrospinal fluid in bacterial meningitis.

We investigated possible neurotoxic components in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. On murine cerebellar neuronal cell cultures, CSF exerted a dose-dependent toxic effect, which was attenuated by the NMDA receptor antagonist MK-801. Glutamate concentrations in the CSF of patients with bacterial meningitis were measured by an enzymatic assay and found to be significantly elevated (p < 0.001) as compared to viral meningitis and non-inflammatory neurological diseases. The concentration of glutamate in the CSF of patients with bacterial meningitis varied considerably and correlated with the severity of the disease as scored by the Glasgow Coma Scale. Cells in the CSF, mainly comprising polymorphonuclear granulocytes, did not release any glutamate into the culture medium, whereas blood monocytes produced remarkable amounts. These findings implicate an important role of monocytic inflammatory cells in bacterial meningitis by the release of glutamate, which may contribute to neuronal cell death.

Adult↗
PubMed1996

[Paraneoplastic cerebellar degeneration: case report of a patient with breast carcinoma].

Case Report on a Breast Cancer Patient: A description of medical history, diagnosis and therapy of a patient with breast cancer is presented. The patient showed primary symptoms of vertigo and truncal and gait ataxia. The cause of this cerebellar disorder was a paraneoplastic cerebellar degeneration (PCD) characterized by anti-Purkinje cell antibodies (anti-Yo) directed against specific epitops shared by Purkinje and tumour cells. The presence of these antibodies in some patients suggests an autoimmune mechanism, although their role in pathogenesis has not been established. Usually malignancies of the breast and the ovaries are associated with anti-Yo positive PCD. The intensive search for the underlying neoplasma led to the identification of a malignant tumour of the right breast. Tumour excision of subsequent immunosuppressive treatment resulted in a progression of PCD. Antibody titers remained nearly unchanged during the course of the disease.

Autoantibodies↗
PubMed1996

Critical illness polyneuropathy: clinical findings and outcomes of a frequent cause of neuromuscular weaning failure.

OBJECTIVE: To describe clinical and electrophysiologic features and outcomes of critically ill patients with neuromuscular causes of failure to wean from mechanical ventilator support. DESIGN: A prospective, consecutive, case series. SETTING: Neurological, neurosurgical, and medical intensive care units in a university hospital. PATIENTS: Seven patients during a 3-yr period with failure to wean from mechanical ventilation not explained by pulmonary complications. INTERVENTIONS: Muscle and nerve biopsy in three patients. MEASUREMENTS AND MAIN RESULTS: Detailed electrodiagnostic studies were done in all patients 3 to 6 wks (median 4.5) after the onset of the acute illness and were repeated 3 months to 3.5 yrs later in those patients who survived. Primary illnesses included various intracranial and medical conditions. All patients had moderate-to-severe limb weakness with marked muscle atrophy. Tendon reflexes were decreased in three patients, exaggerated in two patients with intracranial lesions, and absent in two patients. Electromyography demonstrated severe acute denervation, with striking involvement of proximal muscles. Muscle and nerve biopsies showed severe neurogenic atrophy and axonal degeneration without inflammation. There was no evidence of primary myopathy. Two patients died of complications of sepsis. Of the survivors, three patients had no further weakness at the time of reexamination, except for peroneal nerve palsy in one patient. Two patients, still in the recovery period, showed markedly improved conditions but still showed slight weakness of the proximal muscles. By electrophysiology, signs of chronic neurogenic damage were demonstrable in all survivors at follow-up. CONCLUSIONS: Critical illness polyneuropathy is a frequent cause of neuromuscular weaning failure in critically ill patients, regardless of the type of primary illness. Involvement of proximal (including facial and paraspinal) muscles is striking. Tendon reflexes are often preserved. Patients with central nervous system injury may likewise develop critical illness polyneuropathy. In these latter patients, tendon reflexes may even be exaggerated. Recovery from critical illness polyneuropathy is usually rapid and clinically complete, although incomplete on electrodiagnostic study. Residual peripheral nerve lesion, generally of the peroneal nerve, is the most frequent feature of incomplete recovery. The need for careful electrophysiologic testing is emphasized to clarify the nature and extent of neuromuscular disturbances in critically ill patients. Failure to recognize the development of neuropathy in these patients may lead to erroneous conclusions about the ability to wean them from the ventilator.

Adult↗
PubMed1996

Vertebrobasilar thrombosis: diagnosis, management, and the use of intra-arterial thrombolytics.

OBJECTIVES: To review the diagnosis and management of vertebrobasilar thrombosis and to discuss the use of thrombolytics in the treatment of this disease. DATA SOURCES: Selected references discussing epidemiology, anatomy, pathophysiology, diagnosis, therapy, and rehabilitation of vertebrobasilar occlusive disease. STUDY SELECTION: Studies addressing acute intervention and outcome in the therapy of vertebrobasilar thrombosis were reviewed. DATA EXTRACTION: Only those studies with angiographic documentation of arterial thrombosis and, in the case of thrombolysis, recanalization, were considered valid. DATA SYNTHESIS: Thrombosis of the vertebrobasilar system is a highly fatal disease and should be treated as a neurologic emergency. The key to effective management depends on early recognition of the symptom complex and a thorough understanding of the anatomy and pathophysiology of the disease process. CONCLUSIONS: A timely, integrated, multidisciplinary approach to the patient with vertebrobasilar thrombosis can improve outcome. The use of thrombolytics in the treatment of vertebrobasilar occlusion holds promise but the benefits have not yet been proven in a controlled, randomized study.

Humans↗
PubMed1996

Lubeluzole in acute ischemic stroke. A double-blind, placebo-controlled phase II trial. Lubeluzole International Study Group.

BACKGROUND AND PURPOSE: We aimed to assess the safety and efficacy of lubeluzole in patients with a clinical diagnosis of acute (< 6 hours) ischemic stroke in the carotid artery territory. METHODS: A randomized, double-blind, placebo-controlled multicenter trial was conducted in 232 patients. Because treatment was administered within 6 hours and a CT scan was not mandatory before the start of treatment, 39 patients with either an intracerebral hemorrhage or ischemic stroke in the vertebrobasilar circulation were excluded from the primary efficacy analysis as prespecified in the protocol. Of the 193 patients with acute ischemic stroke in the carotid artery territory (target population), 61 received placebo, 66 lubeluzole 7.5 mg over 1 hour followed by 10 mg/d for 5 days, and 66 lubeluzole 15 mg over 1 hour followed by 20 mg/d for 5 days. RESULTS: The trial, initially aimed at a patient inclusion of 270, was terminated prematurely according to the advice of the Safety Committee because of an imbalance in mortality between the treatment groups. Mortality rates at the final follow-up of 28 days for placebo, lubeluzole 10 mg/d, and lubeluzole 20 mg/d were, respectively, 18%, 6%, and 35% in the target population, results that were confirmed in the intent-to-treat population. Multivariate logistic regression analysis showed that the lower mortality in the lubeluzole 10 mg/d group was significantly in favor of the 10 mg/d treatment (P = .019). The higher mortality rate in the 20 mg/d group could be explained, at least in part, by an imbalance at randomization that led to a higher number of patients in that group with severe ischemic stroke. A total of 26 of 66 patients (39%) who received lubeluzole 10 mg/d had a score on the Barthel Index of > 70 at day 28, indicating no or mild disability, compared with 21 of 61 (34%) in the placebo group and 19 of 66 (29%) in the lubeluzole 20 mg/d group (P = NS). CONCLUSIONS: In patients with acute ischemic stroke, the dosage regimen of 7.5 mg over 1 hour followed by 10 mg/d of intravenous lubeluzole is safe and statistically significantly reduced mortality. Further clinical trials in a larger number of patients are ongoing to confirm efficacy.

Acute Disease↗
PubMed1996

Thrombolytic therapy of acute basilar artery occlusion. Variables affecting recanalization and outcome.

BACKGROUND AND PURPOSE: Thrombolysis may reduce mortality after acute basilar artery (BA) occlusion. We intended to find variables affecting recanalization and clinical outcome in patients with BA occlusion undergoing thrombolytic therapy. METHODS: We analyzed in retrospect the clinical and angiographic data of a consecutive series of 51 patients treated with intra-arterial urokinase (n = 44; 0.3 to 1.5 mIU) or intravenous or intra-arterial recombinant tissue plasminogen activator (n = 7; 22 to 100 mg). We identified effective variables by multiple logistic regression analyses and univariate tests. RESULTS: Sites of occlusion were the caudal (n = 23), middle (n = 18), and distal (n = 10) segments of the BA. The pathogenesis was embolism in 35 and local atherothrombosis in 16 patients. Collateral circulation was good in 32 patients and poor or absent in 19 patients. Recanalization was achieved in 26 of 51 (51%) patients and was associated with occlusions of embolic etiology (P = .0025). Mortality was 46% (12/26) in the recanalization group and 92% (23/25) in the nonrecanalization group (P = .0004). Other independent variables affecting mortality were length of BA obstruction (P = .0011), age (P = .0008), and collateral state (P = .0454). After follow-up (median, 32 months), 10 of the 16 survivors were only minimally impaired, with a Barthel Index score of 95 or greater; 5 patients were moderately and 1 severely disabled. CONCLUSIONS: Recanalization of acute BA occlusion reduces mortality significantly. Length of BA obstruction and state of the collaterals are additional independent variables affecting survival. Young patients with monosegmental embolic occlusion of the BA seem to have the best chance to considerably profit from thrombolysis.

Adolescent↗