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Norbert Galldiks,
Silke Nolden-Hoverath,
Christoph M Kosinski,
Ulrike Stegelmeyer,
Sylvia Schmidt,
Christian Dohmen,
Jens Kuhn,
Kathrin Gerbershagen,
Heiko Bewermeyer,
Peter Walger,
Rolf Biniek, Michael Neveling,
Andreas H Jacobs,
Walter F Haupt
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ABSTRACT: Wound infections due to Clostridium botulinum in Germany are rare and occur predominantly in heroin injectors, especially after subcutaneous or intramuscular injection of heroin ("skin popping"), which is contaminated with spores of C. botulinum. We report a rapid geographical clustering of cases in Germany in a region between Cologne, Bonn, and Aachen with wound botulism and consecutive systemic C. botulinum intoxication in intravenous drug users (IDUs) within 6 weeks in October and November 2005.
A group of 12 IDUs with wound botulism after "skin popping."
Clinical data were available in 11 (92%) of 12 patients; in 7 (58%) of the 12 cases, there was cranial nerve involvement including mydriasis, diplopia, dysarthria, and dysphagia, followed by progressing symmetric and flaccid paralysis of proximal muscles of the neck, arms, trunk, and respiratory muscles. Mechanical respiratory support was necessary. Five of the IDUs were treated with antitoxin, but mechanical respiratory support could not be avoided. The mean ventilation duration was 27.4 days (range 6-77 days). In 4 patients (33%), mechanical ventilation could be avoided; two were treated with antitoxin.
This report describes rapid geographical clustering of wound botulism with severe respiratory complications in IDUs after "skin popping," which has not previously been reported either in Germany or any other European country. Based on these observations and those in other European countries, we conclude that there is a trend towards "skin popping," suggesting a change in injection practices in IDUs. Secondly, we conclude that the total number of cases with wound botulism is likely to increase because "skin popping" is the main risk factor.
Neurocritical Care 02/2007; 6(1):30-4. · 2.47 Impact Factor
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Jan Sobesky,
Monika Frackowiak,
Olivier Zaro Weber,
Moritz Hahn,
Walter Möller-Hartmann,
Jobst Rudolf, Michael Neveling,
Martin Grond,
Susanne Schmulling,
Andreas Jacobs,
Wolf-Dieter Heiss
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ABSTRACT: Predictors of outcome and safety in intravenous thrombolysis within 3 h in clinical routine is a matter of ongoing debate. Available reports contain small patient numbers or summarize heterogeneous multicenter data.
Four hundred and fifty patients received intravenous thrombolysis within 3 h after stroke. Pretreatment NIHSS score and detailed medical history were analyzed. Noncontrast CT was performed before thrombolysis, 24-36 h later and in case of clinical deterioration. Symptomatic intracranial hemorrhage (SICH; any bleeding with an NIHSS increase of > or =4 points) and clinical outcome (modified Rankin Scale, mRS) after 3 months were recorded. Logistic regression identified parameters predictive of independence (mRS 0-2) and SICH.
Median onset to admission, door to needle and onset to treatment time was 75, 50 and 135 min, respectively. Direct presentation by emergency service (64%) was the fastest way of referral. Median pretreatment NIHSS was 11 points. Independence (mRS 0-2) was reached by 53%. Mortality was 11% (7% intracerebral, 4% extracerebral complications). Logistic regression identified low NIHSS, low age and absent diabetes as predictors of independence. Overall hemorrhagic complications and SICH were found in 18 and 4% of the patients, respectively. Extracerebral bleeding complications and allergic reactions were found in 3 and 1%, respectively.
This largest single center report presents a sample in the range of the 3 h rt-PA cohort of all randomized controlled trials. Outcome was comparable to randomized studies with a higher rate of independence and a lower rate of mortality and SICH.
Cerebrovascular Diseases 02/2007; 24(1):56-65. · 2.72 Impact Factor
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ABSTRACT: Brain tissue hypoattenuation on early computed tomography is frequently included in decision making in acute stroke management. However, its pathophysiological counterpart needs further evaluation.
By comparative imaging with diffusion-weighted imaging and 15O-water positron emission tomography we aimed to interpret early (<6 h) hypoattenuation.
In 11 patients, the hypoattenuation corresponded to a decreased proton diffusion (median 115.9% relative DWI value) measured by magnetic resonance imaging and to a severe hypoperfusion (below 12 ml/100 g/ min) assessed by positron emission tomography. The volume of parenchymal hypoattenuation correlated to the tissue with disturbed diffusion (Spearman's rho=0.73), but largely underestimated the hypoperfusion below 20 ml/100 g/min.
Early hypoattenuation reflects the coupling of the severity of ischemia and resulting diffusion changes. It allows an estimate of the infarct core but underestimates the penumbral hypoperfusion.
Cerebrovascular Diseases 01/2006; 21(5-6):336-9. · 2.72 Impact Factor
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ABSTRACT: In ischemic stroke, diffusion-weighted (DW) and perfusion-weighted (PW) magnet resonance imaging (MRI) is used to define the mismatch as the therapeutic target. With positron emission tomography (PET), we characterized the metabolic patterns of tissue compartments identified by MRI and compared the volumes of mismatch to those of PET-defined penumbra.
In 6 acute (median, 5.2 hours) and 7 chronic (median, 10 days) stroke patients in whom a mismatch was defined by PW/DW MRI, PET was performed (median, 120-minute delay). Cerebral blood flow (CBF), oxygen metabolism (CMRO2), and oxygen extraction fraction (OEF) was determined in the areas of DWI lesion, mismatch, and oligemia. Then, the mismatch volume was compared with the volume of penumbra.
DWI lesions showed impaired tissue integrity (low CMRO2 and low OEF). Mismatch areas were viable (normal CMRO2) but showed largely varying OEF. Oligemic areas had metabolic patterns comparable to normal tissue. A mismatch volume was found in all 13 patients. However, only 8 of 13 had a corresponding penumbra volume that covered only a part of the mismatch.
Our comparative PET/MRI study confirmed the current pathophysiological hypothesis for the DWI lesion and for the oligemic areas. However, the mismatch area did not reliably detect elevated OEF and overestimated the penumbra defined by PET.
Stroke 06/2005; 36(5):980-5. · 5.73 Impact Factor
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ABSTRACT: Cerebral cavernous malformations (CCMs) are congenital vascular anomalies that can cause seizures, intracranial hemorrhages, focal neurological deficits, and migrainelike headaches. Magnetic resonance (MR) imaging has substantially facilitated diagnosis of CCM. It is now widely accepted that familial clustering with an autosomal dominant inheritance pattern should be suspected in cases of multiple lesions.
To determine by MR imaging the penetrance of cavernous malformations in a 3-generation family that included 5 members with typical clinical signs and diagnostic findings.
All family members underwent routine MR T1-weighted and T2-weighted spin-echo sequences in addition to MR T2-weighted gradient-echo sequences.
Four family members had been symptomatic with either brainstem bleeding, headaches, or focal neurological signs. The gradient-echo sequences yielded a dramatically higher sensitivity with regard to lesion number and distribution. As in previous reports of familial CCM, an increase in lesion number with increasing age, changes in lesion characteristics, de novo occurrence in serial MR imaging over time, and the phenomenon of anticipation could be confirmed in this family.
Magnetic resonance gradient-echo sequences should be considered the method of choice for diagnosis of familial CCM.
Archives of Neurology 05/2005; 62(4):653-8. · 7.58 Impact Factor
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ABSTRACT: Space-occupying brain edema is a life-threatening complication in patients with large middle cerebral artery (MCA) infarction. To determine predictors of this detrimental process, we investigated alterations of extracellular non-transmitter amino acid concentrations in peri-infarct tissue.
Thirty-one patients with infarctions covering >50% of the MCA territory in early cranial CT scans were included in the study. Probes for microdialysis, intracranial pressure, and tissue oxygen pressure were placed into the noninfarcted ipsilateral frontal lobe. Positron emission tomography imaging was performed in 16 of these patients to measure cerebral blood flow in the tissue around the neuromonitoring probes.
Fourteen of the 31 patients developed a malignant MCA infarction, and 17 did not. The patients in the malignant group had significantly lower extracellular concentrations of non-transmitter amino acids than those in the benign group in the first 12 hours of neuromonitoring. At this time, CBF values determined in regions of interest around the probes by positron emission tomography and tissue oxygen pressure showed that the monitored tissues were not yet infarcted, and no differences in transmitter amino acids concentrations were found between the 2 groups. Furthermore, extracellular concentrations of non-transmitter amino acids were negatively correlated with size of infarction.
We assume that reduction of non-transmitter amino acid concentrations reflects an expansion of the extracellular space by vasogenic edema formation in peri-infarct tissue of patients with malignant MCA infarction. Our findings facilitate early prediction of malignant edema formation and may help to increase knowledge of the pathophysiology of the peri-infarct zone of large MCA infarction.
Stroke 01/2004; 34(12):2908-13. · 5.73 Impact Factor
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ABSTRACT: To predict malignant course in patients with large middle cerebral artery (MCA) infarction, we combined PET imaging and neuromonitoring, including microdialysis.
Thirty-four patients with stroke of >50% of the MCA territory in early cerebral CT scan were included. Probes for microdialysis and measurement of intracranial pressure and tissue oxygen pressure (Pto2) were placed into the ipsilateral frontal lobe. PET was performed with 11C-flumazenil to assess CBF and irreversible neuronal damage.
PET measurements within 24 hours after stroke showed larger volumes of ischemic core (mean, 144.5 versus 62.2 cm3) and larger volumes of irreversible neuronal damage (157.9 versus 47.0 cm3) in patients with malignant course (ie, edema formation with midline shift) than in patients with benign course. Mean cerebral blood flow values within the ischemic core were significantly lower and the volume of the ischemic penumbra was smaller in the malignant than in the benign group. In patients with malignant course, cerebral perfusion pressure dropped to <50 to 60 mm Hg 22 to 72 hours (mean, 52.0 hours) after onset of symptoms; subsequently, Pto2 dropped and glutamate increased, indicating secondary ischemia. Maximal changes in the monitored variables reached significant levels for glutamate, aspartate, GABA, glycerol, lactate-to-pyruvate ratio, hypoxanthine, intracranial pressure, cerebral perfusion pressure, and Pto2.
PET allowed prediction of malignant MCA infarction within the time window suggested for hemicraniectomy. Neuromonitoring helped to classify the clinical courses by characterizing pathophysiological sequelae of malignant edema formation. In contrast to PET, however, it did not predict fatal outcome early enough for successful implementation of invasive therapies.
Stroke 09/2003; 34(9):2152-8. · 5.73 Impact Factor
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ABSTRACT: Pneumonia has been estimated to occur in about one third of patients after acute stroke. Only limited data are available on stroke-associated pneumonia (SAP) in specialized neurological intensive care units (NICUs).
We enrolled 124 patients with acute stroke who were treated at our university hospital NICU in a prospective observational study. Incidence rates and risk factors of SAP and long-term clinical outcome were determined.
SAP incidence was 21% with a spectrum of pathogens, which is comparable to previously published data on general ICU patients. Mechanical ventilation, multiple location, and vertebrobasilar stroke, as well as dysphagia and abnormal chest x-ray findings, were identified as risk factors for the disease. SAP patients showed higher mortality rates than nondiseased subjects (acute, 26.9% versus 8.2%; long-term, 35.3% versus 14.3%) and a significantly poorer long-term clinical outcome (Barthel Index, 50.5+/-42.4 versus 81.5+/-27.8; Rankin Scale, 3.5+/-1.7 versus 2.2+/-1.6).
Our data underline the considerable epidemiological and prognostic impact of SAP for the treatment of acute stroke patients in a specialized NICU setting. They demonstrate that the occurrence of SAP deteriorates clinical outcome in these patients. Our results allow us to identify high-risk stroke patients at time of NICU admission in whom the use of preventive treatment strategies is most promising.
Stroke 05/2003; 34(4):975-81. · 5.73 Impact Factor
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ABSTRACT: □ HintergrundArt und Ausmaß klinischer Kaliummangelsymptome korrelieren nicht streng mit dem Grad der im Serum gemessenen Hypokaliämie,
so daß auch bei Extremwerten abortive klinische Verlaufsformen beobachtet werden.
□ FalldarstellungIm Zusammenhang mit einer Gastroenteritis entwickelte ein 47jähriger Patient eine Schwäche in den Muskeln des Schulter- und
Beckengürtels sowie schmerzhafte Parästhesien in beiden Beinen, welche zur stationären Aufnahme führten. Bei der neurologischen
Untersuchung bestanden symmetrische, proximal betonte Paresen der Extremitäten, ferner lebhaftes Faszikulieren der Oberschenkelmuskulatur.
Das Serumkalium zum Aufnahmezeitpunkt lag bei 1,7 mmol/l. Im EKG wurde langsamer Sinusrhythmus mit regelrechter Kammerde-
und_-repolarisation ohne relevante Rhythmusstörungen registriert. Die Ätiologie der Hypokaliämie lag einerseits in einer langjährigen
Diuretikatherapie einer Herzinsuffizienz (Furosemid 80 mg/d ohne Elektrolytkontrollen) bei gleichzeitigem langjährigen mißbräuchlichen
Laxanzienkonsum, andererseits in einem akuten Elektrolytverlust infolge der Gastroenteritis. Trotz hochdosierter Kaliumsubstitution
ließ sich der Serumspiegel zunächst nur geringfügig anheben, erst nach zusätzlicher Gabe des Aldosteronantagonisten Spironolacton
stabilisierten sich die Serumspiegel im unteren Normalbereich. Parallel zum Anstieg des Serumkaliums berichtete der Patient
einen Rückgang der sensiblen Mißempfindungen sowie eine Zunahme der Kraft der Extremitäten. Im EMG wurde eine Besserung des
auch initial nur gering ausgeprägten myopathischen Musters dokumentiert.
□ SchlußfolgerungLeitsymptom der Hypokaliämie war die dyskaliämische Lähmung mit ihrer typischen Symptomatik, nicht die bei derart niedrigen
Serumkaliumspiegeln häufigeren EKG-Veränderungen und Rhythmusstörungen. Die Bedeutung dieser Beobachtung liegt in der isolierten
neurologischen Symptomatik einer extremen Hypokaliämie ohne die zu erwartenden Entgleisungen vegetativer und kardialer Natur.
□ BackgroundClinical signs of hypokalemia are not directly related to the extent of the electrolyte imbalance, and therefore monosymptomatic
cases may be observed.
□ Case ReportFollowing an acute gastroenteritis with considerable diarrhea, a 47-year-old male patient was admitted to hospital for progressive
painful paraparesis. Upon admission, the patient complained of painful paresthesias in both legs, and a moderate flaccid paraparesis
with widespread fasciculations and loss of leg tendon reflexes was found. Serum potassium level on admission was 1.7 mmol/l.
Other signs of hypokalemia were absent, and the ECG showed a slow sinus rhythm without disturbances of de- or repolarisation
or cardiac arrhythmias. Hypokalemic paralysis was diagnosed and was considered to be primarily drug-induced, as the patient
had a history of laxative abuse and was on a continuous medication with furosemide (80 mg/d) without regular assessment of
serum electrolytes. The additional electrolyte loss following the gastroenteritis precipitated the development of clinical
signs of hypokalemia. In parallel to the rise in serum potassium levels, both painful paresthesias and muscle weakness disappeared,
and electromyography documented the amelioration of the myopathic syndrome.
□ ConclusionThe prominent clinical symptom of hypokalemia was a dyskalemic paralysis in the absence of other sequelae of electrolyte imbalance,
such as cardiac arrhythmias or vegetative disturbances.
05/1999; 94(7):391-394.
-
Lupus, v.15, 240-243 (2006).
-
Prävention atherosklerotischer Erkrankungen, 140-148 (2007).
-
Stroke, v.35, 2843-2847 (2004).
-
Stroke, v.34, 2908-2913 (2003).
-
Archives of Neurology, v.62, 653-658 (2005).
-
Stroke, v.36, 980-985 (2005).
-
Stroke, v.34, 975-981 (2003).
-
Stroke, v.34, 254-254 (2003).
-
Neurology, v.63, 1976-1976 (2004).
-
Stroke, v.38, 498-498 (2007).
-
Stroke, v.34, 975-981 (2003).
