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Biomedical subjects

Michael G Hennerici

Publications and source records attributed to Michael G Hennerici.

At least 19 recordsLinked to original sources
PubMed2006

Pathophysiology of stroke rehabilitation: the natural course of clinical recovery, use-dependent plasticity and rehabilitative outcome.

Even though the disruption of motor activity and function caused by stroke is at times severe, recovery is often highly dynamic. Recuperation reflects the ability of the neuronal network to adapt. Next to an unmasking of latent network representations, other adaptive processes, such as excitatory metabolic stress, an imbalance in activating and inhibiting transmission, leading to salient hyperexcitability, or the consolidation of novel connections, prime the plastic capabilities of the system. Rehabilitative interventions may modulate mechanisms of neurofunctional plasticity and influence the natural course after stroke, both positively, but potentially also acting detrimentally. Though routine rehabilitative procedures are an integral part of stroke care, evidence as to their effectiveness remains equivocal. The present review describes the natural course of motor recovery, focusing on ischemic stroke, and discusses use- and training-dependent adaptive effects. It complements a prior article which highlighted the pathophysiology of plasticity. Though the interaction between rehabilitation and plasticity remains elusive, an attempt is made to clarify how and to what extent rehabilitative therapy shapes motor recovery.

Brain↗
PubMed2006

Writing good abstracts.

INTRODUCTION: Writing an abstract means to extract and summarize (AB - absolutely, STR - straightforward, ACT - actual data presentation and interpretation). Thousands of abstracts are submitted to stroke conferences each year. The following suggestions may improve the chances of your work being selected for presentation, and to communicate results in the most efficient and unambiguous way. TITLE AND STRUCTURE: Make the title dynamic and informative, rather than descriptive. Structure the abstract following the IMRaD (Introduction, Methods, Results and Discussion) principle for your future original paper where background would become Introduction and conclusions would enter Discussion. Select the appropriate category for submission carefully. This determines which experts grade the abstract and the session where your competitors represent their work. If selected appropriately, your abstract is more likely to be graded by peers with similar interests and familiarity with your work or field. Methods should describe the study design and tools of data acquisition shortly, not data. RESULTS: Provide data that answer the research question. Describe most important data with numbers and statistics. Make your point with data, not speculations and opinions. Abbreviations should be avoided and only be used after they have been spelled out or defined. Common mistakes include failure to state the hypothesis, rationale for the study, sample size and conclusions. Highlight the novelty of your work by carefully chosen straightforward wording. CONCLUSIONS: Conclusions have to be based on the present study findings. Make sure your abstract is clear, concise and follows all rules. Show your draft to colleagues for critique, and if you are not a native English speaker show it to a person who can improve/correct your text. Remember that accepted abstracts of completed original research should be followed by published original papers - if this is not intended or fails, it may indicate an impaired ability to succeed in scientific writing and an academic career.

Abbreviations as Topic↗
PubMed2006

Intravenous ancrod for acute ischaemic stroke in the European Stroke Treatment with Ancrod Trial: a randomised controlled trial.

BACKGROUND: Intravenous tissue plasminogen activator is the only approved specific treatment for acute ischaemic stroke. Ancrod, a natural defibrinogenating agent from snake venom, has proved to have a favourable effect when given within 3 h after an acute ischaemic stroke. The European Stroke Treatment with Ancrod Trial was undertaken to assess the effects of ancrod when given within 6 h. METHODS: 1222 patients with an acute ischaemic stroke were included in this randomised double-blind placebo-controlled trial. Brain CT scans were done to exclude intracranial haemorrhages and large evolving ischaemic infarctions. Patients were randomly assigned ancrod (n=604) or placebo (n=618). The primary outcome was functional success at 3 months (survival, Barthel Index of 95 or 100, or return to prestroke level). The analysis was by intention-to-treat. This trial is registered with ClinicalTrials.gov, trial number NCT00343174. FINDINGS: Functional success at 3 months did not differ between patients given ancrod (42%) and those given placebo (42%) (p=0.94, OR=0.99, 95% CI, 0.76-1.29). INTERPRETATION: On the basis of our findings, ancrod should not be recommended for use in acute ischaemic stroke beyond 3 h.

Aged↗
PubMed2006

Brain temperature during 340-kHz pulsed ultrasound insonation: a safety study for sonothrombolysis.

BACKGROUND AND PURPOSE: Because ultrasound is used for improving thrombolysis of cerebral infarction but continuous ultrasound insonation also has significant thermal effects, we evaluated brain temperature increase and tissue destruction during pulsed ultrasound emission. METHODS: We examined 340-kHz pulsed ultrasound effects in male Wistar rats. Ultrasound was applied transcranially for 30 minutes on different power levels (1 to 7 W/cm2). Temperature was measured at different locations (brain, in the focus of ultrasound beam, inner ear, temporalis muscle, and rectum). The cooling time after 30-minute insonation for every power level was recorded, and animals were examined by postmortem brain histology (TUNEL and hematoxylin/eosin). RESULTS: Brain temperature increased within 2 to 5 minutes of insonation. Brain temperature increase and cooling time were in proportion to power level, and even with the highest intensity of 7 W/cm2 for 30 minutes, the maximum elevation of mean brain temperature was 0.9 degrees C, with the highest cooling time of 40 minutes. No deleterious side effects of this treatment could be found in histological examination. CONCLUSIONS: Using a pulsed ultrasound design, only a moderate temperature increase could be observed with no histopathological abnormalities. Deleterious side effects of mid-kilohertz ultrasound (eg, intracerebral hemorrhage) are therefore not a consequence of local brain temperature increase.

Animals↗
PubMed2006

Is hypoperfusion an important cause of strokes? If so, how?

Traditionally hypoperfusion and embolism are considered separate important causes of stroke in patients with arterial occlusive disease. However, although hypoperfusion and embolism differ in mechanisms and location, they generally coincide in severe obstructive lesions and cause washout disturbances of embolism in low perfusion territories distal to stenosis. Unless the collateral blood supply is sufficient to prevent ischemia, multiple remote spot-like infarctions occur within the hypoperfused brain territory. In border-zone distributed infarction - long suspected to result from hemodynamic compromise alone - complementary interaction of embolisation and hypoperfusion territories has to be considered. Thus hypoperfusion with embolism or embolism alone are the most common explanations for stroke, the former often associated with less severe clinical deficits than the latter.

Arterial Occlusive Diseases↗
PubMed2006

Tirofiban for the treatment of ischaemic stroke.

Tirofiban is one of three glycoprotein IIb/IIIa receptor antagonists approved by the US FDA, beside abciximab and eptifibatide. The approval of tirofiban covers conservative treatment of myocardial infarction and unstable angina, as well as percutaneous coronary intervention, for which treatment with tirofiban is recommended in moderate-to-high-risk patients. The efficacy of glycoprotein IIb/IIIa antagonists in myocardial infarction indicated that these agents may also be helpful in the treatment of acute ischaemic stroke. Although experimental data are lacking, observational studies are promising. In recent years, increasing effort in studying glycoprotein IIb/IIIa antagonists has been made, mostly for treatment with abciximab. However, there is one Phase II trial that investigated treatment with tirofiban.

Animals↗
PubMed2006

Protein S-100B--a prognostic marker for cerebral damage.

The assessment of S-100B in acute neurological disorders such as global hypoxia, ischaemic or haemorrhagic stroke and traumatic brain injury reflects severity of symptoms and outcome. However, the temporal profile of S-100B release depends on topography, intensity and pathophysiology of the damage e.g. immediate release after traumatic brain injury following the acute destruction of neuronal tissue or delayed release after ischaemic stroke in which gradual breakdown of the blood-brain barrier plays a crucial role. In chronic brain diseases, knowledge about the clinical value of quantification of S-100B is scarce and further evaluations are needed. This review considers both conditions for S-100B measurement and illustrates advantages and limitations in comparison with clinical and neuroimaging data.

Animals↗
PubMed2005

Vascular diagnosis and acute stroke: what, when and why not?

Even within the 3-hour time window, the less the delay to thrombolysis, the more likely it is to be effective. Delays caused by unnecessary examinations based on physicians' uncertainty about the relevance of vascular diagnostics must be overcome if acute therapy is to be administered efficiently. Only defined information concerning inclusion and exclusion criteria, a CT or preferably an MRI of the brain and limited additional data should be achieved prior to treatment and as quickly as possible, preferably within 1 h. All other information is to be gathered after the start of treatment, to assess the possible etiology of stroke, to classify the prognosis, and to recognize the possible need for early intervention such as in carotid stenosis. A primary diagnostic approach with MRI-guided treatment decision should be limited to cases with uncertain or 3- to 9-hour time window to improve selection of patients potentially at benefit from specific treatment and stroke unit/ICU care.

Acute Disease↗
PubMed2005

Pathophysiology of stroke rehabilitation: temporal aspects of neuro-functional recovery.

Stroke almost always causes an impairment of motor activity and function. Clinical recovery, though usually incomplete, is often highly dynamic and reflects the ability of the neuronal network to adapt. Mechanisms that underlie neuro-functional plasticity are now beginning to be understood. Albeit the enormous efforts undertaken to support the natural course of re-convalescence through rehabilitation, little has been done to relate possible effects of these therapeutic approaches to mechanisms of adaptive pathophysiology. The review presented here focuses on these mechanisms during the course of recovery post stroke. Next to an unmasking of latent network representations, other adaptive processes, such as excitatory metabolic stress, an imbalance in activating and inhibiting transmission, leading to salient hyperexcitability or mechanisms that consolidate novel connections prime the system's plastic capabilities. These pathophysiological processes potentially interact with rehabilitative interventions. They therefore form the foundation of positive, but possibly also negative recuperation under therapy.

Brain↗
PubMed2005

Transcranial low-frequency ultrasound-mediated thrombolysis in brain ischemia: increased risk of hemorrhage with combined ultrasound and tissue plasminogen activator: results of a phase II clinical trial.

BACKGROUND: Clinical studies using ultrasound at diagnostic frequencies in transcranial Doppler devices provided encouraging results in enhancing thrombolysis with tissue plasminogen activator (tPA) in acute stroke. Low-frequency ultrasound does not require complex positioning procedures, penetrates through the skull better, and has been demonstrated to accelerate thrombolysis with tPA in animal experiments in wide cerebrovascular territories without hemorrhagic side effects. We therefore conducted the first multicenter clinical trial to investigate safety of tPA plus low-frequency ultrasound (300 kHz). METHODS: Acute stroke patients within a 6-hour time window were included (National Institutes of Health Stroke Scale scores >4). Magnetic resonance imaging (MRI) was used to document vascular occlusion and to rule out cerebral hemorrhage. Patients were allocated to combination therapy alternately; the first patient received tPA only, the second patient received tPA plus ultrasound, etc. Follow-up included serial MRI directly thereafter and 24 hours later to confirm recanalization and tissue imaging. Clinical recovery was measured after treatment and 3 months later. RESULTS: 26 patients (70.4+/-9.7 years) entered the trial (12 tPA, 14 tPA plus ultrasound). The study was prematurely stopped because 5 of 12 patients from the tPA only group but 13 of 14 patients treated with the tPA plus ultrasound showed signs of bleeding in MRI (P<0.01). Within 3 days of treatment, 5 symptomatic hemorrhages occurred within the tPA plus ultrasound group. At 3 months, neither morbidity nor treatment-related mortality or recanalization rates differed between both groups. CONCLUSIONS: This study demonstrated bioeffects from low-frequency ultrasound that caused an increased rate of cerebral hemorrhages in patients concomitantly treated with intravenous tPA.

Aged↗
PubMed2004

Early motor evoked potentials in acute stroke: adjunctive measure to MRI for assessment of prognosis in acute stroke within 6 hours.

BACKGROUND: In acute stroke, a magnetic resonance (MR) perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) mismatch (PWI>DWI mismatch) may indicate tissue at risk for infarction and poor prognosis. However, different to early enthusiasm about this surrogate marker, its validity has shown several drawbacks in individual patients. Rather than relying on imaging, we evaluated motor evoked potentials (MEP) as a measure of cerebral function in the acute stroke setting. METHODS: Thirteen patients with acute hemiparetic stroke underwent time to peak PWI and DWI within 6 h after onset as well as recordings of early MEP of first dorsal interosseous muscles. Outcome was assessed by the Unified Neurological Stroke Scale and Barthel Index at day 42. RESULTS: Of 8 patients with PWI>DWI mismatch, 4 patients with normal MEP had a good clinical outcome and 4 patients with absent or pathological MEP had an unfavourable outcome (p < 0.05, Fisher's exact test). In all patients without PWI>DWI mismatch, MEP findings predicted clinical outcome. Normal MEP at day 0--but not PWI/DWI findings--significantly correlated with a good clinical outcome. CONCLUSIONS: Early MEP recordings in acute stroke patients provide valid prognostic information; they may become more useful for specific treatment decisions than presently available MRI surrogate parameters.

Acute Disease↗
PubMed2004

Dystonia in the Mohr-Tranebjaerg syndrome responds to GABAergic substances.

Mutations in the X-linked deafness-dystonia peptide 1 (DDP1) gene cause Mohr-Tranebjaerg syndrome (MTS), a rare form of deafness associated with dystonia. In the patient presented here, improvement of dystonic symptoms upon treatment with alcohol and GABAergic substances is demonstrated for the first time.

Adult↗
PubMed2004

The unstable plaque.

Ischaemic strokes and transient ischaemic attacks are commonly caused by cerebral embolism originating from formation of a platelet-rich thrombus superimposed on an atherosclerotic plaque or by atherothrombotic plaque rupture in a carotid or intracranial artery. Despite advances made through ultrasound imaging in our understanding of atherosclerotic plaque progression and regression, the issue of whether differences in plaque structure alone can distinguish between lesions that become symptomatic and others that remain clinically silent continues to be debated. Recent biochemical and imaging studies have identified characteristics that may reflect a high risk of vulnerability, such as outward, abluminal plaque remodelling, the presence of intra-plaque haemorrhage, inflammation, severe flow disturbances around the encroaching lesion, plaque cap thinning and ulceration, and abnormal plaque motion. Plaque stability may be improved through management of traditional cardiovascular risk factors or with biological or pharmacological agents that target pathways involved in plaque pathophysiology. Unstable plaques place patients at risk of unpredictable ischaemic events and in patients with such lesions, specific preventive treatment beyond long-term antiplatelet therapy can be used to prevent new or recurrent events.

Carotid Artery Diseases↗
PubMed2003

Deviations from the diffusion tensor model as revealed by contour plot visualization using high angular resolution diffusion-weighted imaging (HARDI).

The standard diffusion tensor model is limited in its ability to provide detailed information about multidirectional fiber architecture in human white matter. Additional directional acquisition of diffusivity properties with high angular resolution diffusion-weighted imaging (HARDI) acquisition schemes may deliver more information on areas with fiber crossings than standard DTI. However, representation of the additional information and the rating and visualization of fiber complexity is challenging. We used projection 2D-plots in combination with a HARDI acquisition scheme of 129 diffusion directions and compared the spherical diffusion variance index (SDI) with the relative anisotropy index (RAI). In normal controls, white matter areas with unidirectional fiber arrangement and areas with more complex fiber composition were identified with this approach. HARDI confirms and can visualize deviations from the tensor-like representation, thereby providing information on fiber structure complexity, which may be of considerable interest for clinical studies.

Anisotropy↗