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Biomedical subjects

C Dohmen

Publications and source records attributed to C Dohmen.

12 recordsLinked to original sources
PubMed2006

[Post-stroke-depression. Algorithm for a standardized diagnostic approach in clinical routine].

Depression is a frequent and important complication after stroke. The occurrence of a post-stroke-depression (PSD) has a significant impact on the functional and cognitive deficit, on mortality and on quality of life after stroke. In contrast to the clinical importance, PSD is often ignored in routine management of stroke patients and remains often untreated if diagnosed. The diagnostic uncertainty is aggravated by the lack of appropriate diagnostic criteria for PSD in the International Classification of Diseases (ICD-10) used in Germany. For the first time, we present an algorithm, which allows for a standardized examination of stroke patients on the presence of PSD. All stroke patients should be examined initially by a short and simple screening tool and are subjected to more extensive procedures only if PSD is assumed based on the screening result. Furthermore potentials and limitations to convert the diagnosis of PSD into a diagnostic related group (DRG) that is used to calculate the hospital's reimbursement are highlighted. Finally pharmacological treatment options for PSD are discussed.

Algorithms↗
PubMed2006

Stroke after initiation of interferon-beta treatment for relapsing-remitting disseminated white matter disease.

BACKGROUND: Interferon-beta (INF-beta) is effective and used in reducing exacerbation frequency and disease progression in multiple sclerosis. In certain circumstances, INF-beta can lead to rare side effects. AIMS OF THE STUDY: We report the case of a 34-year-old female patient satisfying the McDonald criteria of multiple sclerosis without showing typical pathologic changes in cerebrospinal fluid (CSF). After introduction of INF-beta treatment, she quickly developed further progression of her disseminated neurological symptoms and finally an ischemic cerebral infarction. METHODS: Evaluation of the patient included arterial angiography, magnetic resonance and positron emission tomography, histopathological assessment as well as a broad spectrum of serum and CSF analysis. RESULTS: All diagnostic evaluations and the clinical course revealed evidences for a primary angiitis of the CNS. We discuss the possible worsening due to inappropriate INF-beta treatment in cerebral angiitis promoting severe cerebrovascular insufficiency. CONCLUSION: The authors suggest that all diagnostic multiple sclerosis criteria including typical CSF findings should be ascertained before INF-beta treatment is initiated.

Adjuvants, Immunologic↗
PubMed2004

Which time-to-peak threshold best identifies penumbral flow? A comparison of perfusion-weighted magnetic resonance imaging and positron emission tomography in acute ischemic stroke.

BACKGROUND AND PURPOSE: In acute ischemic stroke, the hypoperfused but viable tissue is the main therapeutic target. In clinical routine, time-to-peak (TTP) maps are frequently used to estimate the hemodynamic compromise and to calculate the mismatch volume. We evaluated the accuracy of TTP maps to identify penumbral flow by comparison with positron emission tomography (PET). METHODS: Magnetic resonance imaging (MRI) and PET were performed in 11 patients with acute ischemic stroke (median 8 hours after stroke onset, 60 minutes between MRI and PET imaging). The volumes defined by increasing TTP thresholds (relative TTP delay of >2, >4, >6, >8, and >10 seconds) were compared with the volume of hypoperfusion (<20 mL/100 g per min) assessed by 15O-water PET. In a volumetric analysis, each threshold's sensitivity, specificity, and predictive values were calculated. RESULTS: The median hypoperfusion volume was 34.5 cm3. Low TTP thresholds included large parts of the hypoperfused but also large parts of normoperfused tissue (median sensitivity/specificity: 93%/60% for TTP >2) and vice versa (50%/91% for TTP >10). TTP >4 seconds best identifies hypoperfusion (84%/77%). The positive predictive values increased with the size of hypoperfusion. CONCLUSIONS: This first comparison of quantitative PET-CBF with TTP maps in acute ischemic human stroke indicates that the TTP threshold is crucial to reliably identify the tissue at risk; TTP >4 seconds best identifies penumbral flow; and TTP maps overestimate the extent of true hemodynamic compromise depending on the size of ischemia. Only if methodological restrictions are kept in mind, relative TTP maps are suitable to estimate the mismatch volume.

Adult↗
PubMed2004

[Cerebral microdialysis in stroke].

Cerebral microdialysis is an invasive technique for neurochemical monitoring that has been established for neuro-critical disorders such as subarachnoid hemorrhage and severe brain injury. We present data on cerebral microdialysis in stroke patients which were obtained in an ongoing study supported by the German Ministry for Education and Research. So far, 50 patients have been included who required critical care due to massive stroke of the middle cerebral artery territory. By correlating the microdialysis results with follow-up CT scans, we could define the neurochemical characteristics of three different brain compartments: (1) noninfarcted brain tissue with normal microdialysis values, (2) brain areas adjacent to the infarct core which were not hypodense in CT scans but caused reversible neurochemical alterations, and (3) the infarct core with massive concentration changes which did not normalize over the measuring period of 3 to 5 days. Microdialysis values averaged over time and correlated with initial PET scans helped to describe neurochemical predictors of a malignant, i.e., life-threatening, space-occupying course of the ischemic stroke. We discuss the value of this method in guiding therapy and predicting clinical outcome in the context of other neurological critical care disorders and describe the pros and cons of cerebral microdialysis as an invasive monitoring technique.

Brain Edema↗
PubMed2003

Significant shrinkage of extracellular space during global cerebral ischemia: differences in gray and white matter ischemia.

Brain extracellular space (ECS) provides an important microenvironment for neurons and glial cells. In the present study, we investigated differences in ischemic changes of ECS in gray and white matter during global ischemia in cats (n = 8). Diffusion capacity of tetramethylammonium ion (TMA+, 74.1Da) was evaluated by measuring extracellular TMA+ concentration applied via microdialysis. In both gray and white matter, TMA+ concentration significantly increased within 10 minutes after the induction of ischemia, and sustained during 120 min of ischemia. The increase, however, was slower and smaller in white matter than in gray matter. In other two animals, volume fraction and tortuosity of ECS were determined by iontophoresis during global ischemia. After 30 min of ischemia induction, volume fraction was decreased and tortuosity was increased in both gray and white matter. In white matter, decrease in volume fraction and increase in tortuosity were smaller than in gray matter. The present study demonstrates that cerebral ischemia induces not only significant shrinkage of ECS volume but also restricts molecular diffusion within. Smaller changes of diffusion capacity within white matter ECS during ischemia may be relevant for lower ischemic vulnerability of the region.

Animals↗
PubMed2003

Identification of malignant brain edema after hemispheric stroke by PET-imaging and microdialysis.

Cerebral blood flow (CBF) and extent of irreversible tissue damage as well as the time course of extracellular concentration of amino acids, substrates of energy metabolism, and purine metabolites, intracranial pressure and tissue oxygen tension were assessed in 34 patients with large strokes covering more than 50% of the MCA territory. The results were compared to findings in the experimental model of transient (for 3 hours) MCA occlusion in cats. In the experimental model as well as in the clinical setting development of malignant brain infarcts (due to formation of space occupying brain edema) was predicted by the size of critically hypoperfused tissue and the volume of irreversibly damaged tissue. The course of malignant infarcts was characterized by progressive increase in concentrations of excitatory amino acids, lactate, pyruvate, glycerol, hypoxanthine and in intracranial pressure, while cerebral perfusion pressure and tissue oxygen tension decreased. These results clearly differentiate a malignant from a benign course of large hemispheric infarction. The methods can be used to identify patients at risk for formation of space occupying edema and to select patients who could benefit from invasive therapeutic strategies.

Amino Acids↗
PubMed2001

Elevation of extracellular glutamate in the final, ischemic stage of progressive epidural mass lesion in cats.

Epidural mass lesions may cause ischemia due to progressive intracranial hypertension. In order to investigate the impact of intracranial pressure on accumulation of neuroactive substances, we gradually raised intracranial pressure in five halothane anesthetized cats by inflation of an epidural balloon. We evaluated in the parietal cortex contralateral to the site of balloon inflation, alterations of extracellular glutamate and purine catabolites and of the lactate/pyruvate ratio in relation to changes of intracranial, cerebral perfusion and mean arterial blood pressure. In a complementary experiment, regional cerebral blood flow was assessed by sequential positron emission tomography. In this simplified mass lesion model, extracellular glutamate increased in all cats at a late, critical stage after tentorial herniation, when intracranial pressure had increased to more than 90 mm Hg, cerebral perfusion pressure had decreased below 40-50 mm Hg. Positron emission tomography assessments revealed that the ischemic threshold for glutamate accumulation was in the range of 15-20 mL/100 g/min. Purine catabolites and the lactate/pyruvate ratio increased somewhat earlier than glutamate, but also after reaching the critical, terminal stage. We conclude that in this model of progressive epidural compression, glutamate-mediated excitotoxic processes at sites remote from the initial focal lesion depend on processes such as delayed ischemia in combination with tentorial herniation and systemic hypotension. These processes seem to be initiated by a decrease of cerebral perfusion pressure below a threshold of 40-50 mm Hg.

Animals↗
PubMed2001

Adenosine in relation to calcium homeostasis: comparison between gray and white matter ischemia.

In vitro studies suggest that adenosine may attenuate anoxic white matter damage as an intrinsic protective substance. The authors investigated ischemic alterations of purines in relation to tissue depolarization and extracellular calcium and amino acid concentrations in vivo using microdialysis and ion-selective electrodes in cortical gray and subcortical white matter of 10 cats during 120 minutes of global brain ischemia. Immediately on induction of ischemia, regional cerebral blood flow ceased in all cats in both gray and white matter. The direct current potential rapidly decreased, the decline being slower and shallower in white matter. Extracellular calcium levels decreased in gray matter. In contrast, they first increased in white matter and started to decrease below control levels only after approximately 30 minutes. Adenosine levels transiently increased in both tissue compartments; the peak was delayed by 30 minutes in white matter. Thereafter, levels declined faster in gray than in white matter and remained elevated in the latter tissue compartment. Inosine and hypoxanthine elevations were progressive in both regions but smaller in white matter. Levels of gamma-aminobutyric acid, another putatively protective agent, steadily increased, starting immediately in gray matter and delayed by almost 1 hour in white matter. The delayed and prolonged accumulation of adenosine correlates with a slower adenosine triphosphate breakdown in white matter ischemia and may result in protection of white matter by suspending cellular calcium influx.

Adenosine↗
PubMed2001

Predictive value of neurochemical monitoring in large middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Space-occupying brain edema is a life-threatening complication in patients with large hemispheric stroke. Early identification of patients at risk is necessary to decide on invasive therapies such as decompressive hemicraniectomy or hypothermia. To assess potential predictors of malignant brain edema by measurement of intracranial pressure (ICP) and microdialysis in patients with large hemispheric stroke and different clinical course. METHODS: In an ongoing prospective clinical study, an ICP and microdialysis probe were placed into the parenchyma of the ipsilateral frontal lobe of 10 patients. Extracellular concentrations of glutamate, lactate, pyruvate, and glycerol were measured continuously. Repeated cranial CT scans were scrutinized for size of infarction and presence of mass effect. RESULTS: The dynamics of the different substances varied in accordance with the clinical course, size of infarction, and local brain edema: Increase in ICP and in glutamate concentration and lactate-pyruvate ratio was followed by massive edema and large infarcts; generally low and stable ICP and substrate concentrations were found in patients without progressive space-occupying infarcts. CONCLUSIONS: In patients with large hemispheric infarction, bedside monitoring with microdialysis is feasible and might be helpful together with ICP recording to follow the development of malignant brain edema.

Adult↗
PubMed1999

Breakdown of calcium homeostasis in relation to tissue depolarization: comparison between gray and white matter ischemia.

In vitro studies suggest that ischemic injury of cerebral white matter is mediated by nonsynaptic cellular mechanisms, such as Ca2+ entry into axons through reversal of the Na+ -Ca2+ exchanger. The authors investigated extracellular Ca2+ concentration in relation to tissue depolarization (direct current potential) in vivo using ion-selective electrodes in cortical gray and subcortical white matter of alpha-chloralose-anesthetized cats during 120 minutes of global cerebral ischemia. On induction of ischemia, regional CBF, as measured by hydrogen clearance, ceased. The direct current potential decreased rapidly within minutes in gray matter and with little time delay in white matter. Extracellular Ca2+ concentration decreased just as quickly in gray matter. In white matter, in contrast, extracellular Ca2+ increased in the first 20 to 30 minutes, and a delayed and much slower decline, compared with gray matter, was observed thereafter, reaching a minimal level only about 60 minutes after occlusion. Our results suggest that smaller and delayed transmembrane shifts of Ca2+ are correlates of delayed ischemic membrane dysfunction in central white matter tracts, which may be explained by a lack of synaptic mechanisms.

Action Potentials↗
PubMed1990

Effect of medial arterial calcification on O2 supply to exercising diabetic feet.

We investigated whether medial arterial calcification (MAC) impairs O2 supply to the exercising foot in diabetic patients with foot lesions. Transcutaneous O2 tension (tcPO2) was monitored at the dorsum of the foot before and after bicycle exercise in 11 diabetic patients with peripheral ischemic vascular disease (PIVD) with or without concomitant existence of MAC, 10 patients with MAC but without PIVD, 10 diabetic control subjects, and 6 nondiabetic control subjects. The mean preexercise tcPO2 level was comparable in these four groups. However, tcPO2 decreased significantly with exercise in feet with PIVD (mean +/- SE -17.9 +/- 2.7%, P less than 0.01, n = 11), regardless of presence or absence of vascular calcification. On the other hand, the value increased significantly with exercise in feet with MAC but without PIVD (21.2 +/- 3.5%, P less than 0.01, n = 10) and in those of diabetic control subjects (14.9 +/- 3.6%, P less than 0.01), respectively. The tcPO2 remained unchanged in the feet of nondiabetic control subjects (1.7 +/- 1.1%). The results suggest that MAC is not associated with reduced O2 supply to the exercising foot in diabetic patients.

Adult↗