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Johannes Woitzik,
Nils Hecht,
Alexandra Pinczolits,
Nora Sandow,
Sebastian Major,
Maren K L Winkler,
Steffen Weber-Carstens, Christian Dohmen,
Rudolf Graf,
Anthony J Strong,
Jens P Dreier,
Peter Vajkoczy
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ABSTRACT: OBJECTIVE: To investigate hemodynamic response pattern and spatiotemporal propagation of cortical spreading depolarization in the peri-infarct region of malignant hemispheric stroke. METHODS: In this prospective observational case study we used intraoperative laser speckle technology to measure cerebral blood flow in patients with malignant hemispheric stroke. Additionally, postoperative occurrence of cortical spreading depolarization was monitored using a subdural recording strip for electrocorticography and infarct progression was assessed by serial MRI. RESULTS: In 7 of 20 patients, 19 blood flow changes typical of cortical spreading depolarizations occurred during a 20-minute period. Thirteen events were characterized by increase, 2 by biphasic response, and 4 by decrease of blood flow. Propagation velocity ranged from 1.7 to 9.2 mm/min and propagation area from 0.1 to 4.8 cm2. Intrinsic optical signal alterations preceded and low-frequency vascular fluctuations were suppressed during the hemodynamic responses. A mean number of 56 ± 82 cortical spreading depolarizations per patient was recorded and a mean infarct progression of 30 ± 13 cm3 was detected in 5 of 7 patients. CONCLUSIONS: We visualize the spatiotemporal propagation of spreading depolarizations in the human cerebral cortex intraoperatively. In patients with focal ischemia, multiple cortical spreading depolarizations with either hyperemic or hypoemic flow responses occurred. Our data suggest that, in patients with focal ischemia, cortical spreading depolarizations are associated with both unfavorable and protective hemodynamic responses.
Neurology 02/2013; · 8.31 Impact Factor
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Daniel N Hertle,
Jens P Dreier,
Johannes Woitzik,
Jed A Hartings,
Ross Bullock,
David O Okonkwo,
Lori A Shutter,
Steven Vidgeon,
Anthony J Strong,
Christina Kowoll, Christian Dohmen,
Jennifer Diedler,
Roland Veltkamp,
Thomas Bruckner,
Andreas W Unterberg,
Oliver W Sakowitz
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ABSTRACT: Spreading depolarizations are waves of mass neuronal and glial depolarization that propagate across the injured human cortex. They can occur with depression of neuronal activity as spreading depressions or isoelectric spreading depolarizations on a background of absent or minimal electroencephalogram activity. Spreading depolarizations are characterized by the loss of neuronal ion homeostasis and are believed to damage functional neurons, leading to neuronal necrosis or neurological degeneration and poor outcome. Analgesics and sedatives influence activity-dependent neuronal ion homeostasis and therefore represent potential modulators of spreading depolarizations. In this exploratory retrospective international multicentre analysis, we investigated the influence of midazolam, propofol, fentanyl, sufentanil, ketamine and morphine on the occurrence of spreading depolarizations in 115 brain-injured patients. A surface electrode strip was placed on the cortex, and continuous electrocorticographical recordings were obtained. We used multivariable binary logistic regression to quantify associations between the investigated drugs and the hours of electrocorticographical recordings with and without spreading depolarizations or clusters of spreading depolarizations. We found that administration of ketamine was associated with a reduction of spreading depolarizations and spreading depolarization clusters (P < 0.05). Midazolam anaesthesia, in contrast, was associated with an increased number of spreading depolarization clusters (P < 0.05). By using a univariate odds ratio analysis, we also found a significant association between ketamine administration and reduced occurrence of isoelectric spreading depolarizations in patients suffering from traumatic brain injury, subarachnoid haemorrhage and malignant hemispheric stroke (P < 0.05). Our findings suggest that ketamine-or another N-methyl-d-aspartate receptor antagonist-may represent a viable treatment for patients at risk for spreading depolarizations. This hypothesis will be tested in a prospective study.
Brain 06/2012; 135(Pt 8):2390-8. · 9.46 Impact Factor
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ABSTRACT: Space-occupying brain edema may lead to a malignant course in patients with large middle cerebral artery infarction. Decompressive hemicraniectomy has to be initiated early to prevent further tissue damage. In this retrospective study, we analyzed electroencephalography (EEG) and evoked potentials (EPs), obtained within 24 h after onset of stroke, in 22 patients suffering from a large middle cerebral artery infarction. Our findings indicate a prognostic value of EEG and brainstem auditory EP (BAEP): the absence of delta activity and the presence of theta and fast beta frequencies within EEG-focus predicted a non-malignant course. In contrast, diffuse generalized slowing and slow delta activity in the ischemic hemisphere pointed to a malignant course. Likewise, pathological BAEP were correlated with a malignant course. The coexistence of background slowing and pathological BAEP showed the highest level of significance. In conclusion, our findings implicate an additional early application of electrophysiological methods in stroke patients. EEG and EP deliver useful information to select those patients who develop malignant edema.
Neurological Sciences 04/2012; · 1.32 Impact Factor
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ABSTRACT: In order to determine the impact of the severity of ischemia on malignant edema formation, we investigated various degrees of perfusional deficit by (11)C-flumazenil PET in patients with large middle cerebral artery (MCA) infarction.
17 patients with large MCA stroke were included. Cerebral blood flow (CBF) was measured 15.9 ± 6.4 h after the ictus. Patients were divided into a malignant (n = 9) and a benign group (n = 8) as a function of their clinical courses and edema. Edema was measured as maximal midline shift on follow-up CTs. Total hypoperfusion volume was divided into different subvolumes according to the degree of CBF reduction.
Subvolumes of severe ischemia relative to total ischemic area were significantly larger in the malignant group than in the benign group and were significantly correlated with edema formation. The highest correlation and best predictive values for edema formation with a sensitivity, specificity, and a positive and negative predictive value of 100% were found for subvolumes with severe ischemia. Correlation coefficients and prediction decreased for subvolumes with less severe perfusional deficit, pointing to the risk of misclassifying patients when relying on the volume of total perfusional deficit alone.
Malignant MCA infarction seems to be determined more by the volume of severe perfusional deficit than that of total perfusional deficit. Assessment of severely ischemic areas allows prediction of malignant edema formation and might help to select candidates for hemicraniectomy.
Cerebrovascular Diseases 11/2011; 33(1):1-7. · 2.72 Impact Factor
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Norbert Galldiks,
Lothar Burghaus, Christian Dohmen,
Sven Teschner,
Manfred Pollok,
Josef Leebmann,
Nikolaus Frischmuth,
Peter Hollinger,
Nahed Nazli,
Cordula Fassbender,
Reinhard Klingel,
Thomas Benzing,
Gereon R Fink,
Walter F Haupt
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ABSTRACT: First-line treatment options for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are corticosteroids, intravenous immunoglobulin, and plasma exchange. In a significant number of patients, first-line therapy fails, and long-term maintenance treatment still remains a therapeutic challenge. Immunoadsorption (IA) may be an alternative to classical plasma exchange in the therapy of immune-mediated neurologic diseases. The aim of this investigation was to evaluate efficacy and safety of IA in patients with CIDP with unsatisfactory response to first-line treatment options.
CIDP patients received adjunct IA treatment using tryptophan-immune adsorbers. The inflammatory neuropathy cause and treatment disability (INCAT) score was used to grade disability and monitor treatment effects.
In total, 14 CIDP patients were analyzed. Ten patients were treated in hospital. After one IA treatment series, the INCAT score decreased significantly in all 10 patients. Four of these 14 patients were treated in outpatient clinics using long-term maintenance IA with 1-2 treatments per week. In these 4 patients, effects of long-term maintenance IA resulted in an improvement of overall disability. In all patients, IA was safe, well tolerated, and no severe adverse effects occurred.
IA could be an effective and safe option for CIDP patients with unsatisfactory response to first-line treatment options and for long-term maintenance treatment.
European Neurology 09/2011; 66(4):183-9. · 1.81 Impact Factor
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ABSTRACT: Supported by results of the ECASS III study, intravenous rt-PA thrombolysis is considered a standard therapy for acute stroke within 4.5 h. Still under debate is the use of a more aggressive treatment as that of local intraarterial thrombolysis (LIT) or combining intravenous administration of recombinant tissue plasminogen activator (rt-PA) followed by LIT (bridging concept). Mechanical thrombus removal devices and effective flow achievement by stenting are reported to increase the recanalization rate and patient outcome. Newer reports showed the use of intracranial stents as the latest trend-setting technique. A combined approach hereby appears to achieve the best results consisting of pharmacologic thrombolysis, manual aspiration devices and stenting. We employed a novel removable stent as a new approach in acute stroke, aiming to make the intraarterial thrombolysis through an enhanced thrombus contact surface more effective and to reduce the effective revascularisation time with the possibility of stent removal after re-opening the occluded vessel.
We describe four cases with acute stroke in the anterior and posterior circulation using a newer self-expandable removable stent (Solitaire™ AB) combined with LIT performed in the 'bridging technique', occasionally supported by additional thrombus aspiration.
In all cases, we directly achieved after stenting an effective revascularization with fast recanalization time when using stent implantation first. Stenting was always technically successful without complications.
The easy handling of a removable stent in stent-assisted revascularization combined with thrombolysis (i.v./i.a.) is a newly described technique for acute stroke treatment, which join immediate mechanical recanalization, postulated improved thrombolysis and the possibility of stent removing.
Neuroradiology 04/2011; 53(4):273-82. · 2.82 Impact Factor
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12/2010: pages 481-518;
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Hajime Nakamura,
Anthony J Strong, Christian Dohmen,
Oliver W Sakowitz,
Stefan Vollmar,
Michael Sué,
Lutz Kracht,
Parastoo Hashemi,
Robin Bhatia,
Toshiki Yoshimine,
Jens P Dreier,
Andrew K Dunn,
Rudolf Graf
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ABSTRACT: How does infarction in victims of stroke and other types of acute brain injury expand to its definitive size in subsequent days? Spontaneous depolarizations that repeatedly spread across the cerebral cortex, sometimes at remarkably regular intervals, occur in patients with all types of injury. Here, we show experimentally with in vivo real-time imaging that similar, spontaneous depolarizations cycle repeatedly around ischaemic lesions in the cerebral cortex, and enlarge the lesion in step with each cycle. This behaviour results in regular periodicity of depolarization when monitored at a single point in the lesion periphery. We present evidence from clinical monitoring to suggest that depolarizations may cycle in the ischaemic human brain, perhaps explaining progressive growth of infarction. Despite their apparent detrimental role in infarct growth, we argue that cycling of depolarizations around lesions might also initiate upregulation of the neurobiological responses involved in repair and remodelling.
Brain 07/2010; 133(Pt 7):1994-2006. · 9.46 Impact Factor
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ABSTRACT: Delayed ischemic neurological deficit (DIND) contributes to poor outcome in subarachnoid hemorrhage (SAH) patients. Because there is continuing uncertainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes should be considered. A potential candidate is cortical spreading depolarization (CSD)-induced hypoxia. We hypothesized that recurrent CSDs influence cortical oxygen availability.
Centers in the Cooperative Study of Brain Injury Depolarizations (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery. We used simultaneous, colocalized recordings of electrocorticography and tissue oxygen pressure (p(ti)O(2)) in human cerebral cortex. We screened for delayed cortical infarcts by using sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic resonance imaging.
In a total recording time of 850 hours, 120 CSDs were found in 8 of 9 patients. Fifty-five CSDs ( approximately 46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine ( approximately 75%) of all CSDs occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recurrent CSD. Clusters of CSD occurred simultaneously, with mainly biphasic CSD-associated p(ti)O(2) responses comprising a primary hypoxic and a secondary hyperoxic phase. The frequency of CSD correlated positively with the duration of the hypoxic phase and negatively with that of the hyperoxic phase. Hypoxic phases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic p(ti)O(2) responses changed to monophasic p(ti)O(2) decreases within these clusters. Monophasic hypoxic p(ti)O(2) responses to CSD were found predominantly in DIND patients.
We attribute these clinical p(ti)O(2) findings mainly to changes in local blood flow in the cortical microcirculation but also to augmented metabolism. Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O(2) supply and increase O(2) consumption, and thereby promote DIND.
Annals of Neurology 05/2010; 67(5):607-17. · 11.09 Impact Factor
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Ana I Oliveira-Ferreira,
Denny Milakara,
Mesbah Alam,
Devi Jorks,
Sebastian Major,
Jed A Hartings,
Janos Lückl,
Peter Martus,
Rudolf Graf, Christian Dohmen,
Georg Bohner,
Johannes Woitzik,
Jens P Dreier
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ABSTRACT: In human cortex it has been suggested that the tissue at risk is indicated by clusters of spreading depolarizations (SDs) with persistent depression of high-frequency electrocorticographic (ECoG) activity. We here characterized this zone in the ET-1 model in rats using direct current (DC)-ECoG recordings. Topical application of the vasoconstrictor endothelin-1 (ET-1) induces focal ischemia in a concentration-dependent manner restricted to a region exposed by a cranial window, while a healthy cortex can be studied at a second naïve window. SDs originate in the ET-1-exposed cortex and invade the surrounding tissue. Necrosis is restricted to the ET-1-exposed cortex. In this study, we discovered that persistent depression occurred in both ET-1-exposed and surrounding cortex during SD clusters. However, the ET-1-exposed cortex showed longer-lasting negative DC shifts and limited high-frequency ECoG recovery after the cluster. DC-ECoG recordings of SD clusters with persistent depression from patients with aneurysmal subarachnoid hemorrhage were then analyzed for comparison. Limited ECoG recovery was associated with significantly longer-lasting negative DC shifts in a similar manner to the experimental model. These preliminary results suggest that the ischemic zone in rat and human cortex is surrounded by a normally perfused belt with persistently reduced synaptic activity during the acute injury phase.
Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 03/2010; 30(8):1504-19. · 5.46 Impact Factor
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ABSTRACT: The best treatment of fulminant or progressive cerebral venous and sinus thrombosis (CVST) despite dose-adjusted heparin remains controversial. Local thrombolysis has been successfully performed in several cases. In cases of impending herniation hemicraniectomy has been suggested as ultima ratio. We describe sequential escalation of therapy in "malignant" CVST.
Case report.
We report a case of fulminant CVST in whom sequential escalation of therapy with intravenous heparin, local thrombolysis, and hemicraniectomy was necessitated by the progressive clinical course. The patient survived with a relatively good outcome.
This first description on the combined treatment with local thrombolysis and hemicraniectomy illustrates that even in severely affected individuals, therapeutic nihilism is unwarranted and that all available therapeutic options including local thrombolysis and hemicraniectomy should be taken into consideration.
Neurocritical Care 11/2009; 12(1):98-102. · 2.47 Impact Factor
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ABSTRACT: We report on a case of epilepsia partialis continua with rapid response to intravenous bolus administration of levetiracetam. A 60-year-old woman presented with continuous jerking of the right foot and hallux persisting for more than two days. She had a 9-year history of epilepsy due to a left temporoparietal oligodendroglioma with occasional focal seizures clinically presenting as speech arrest, which was treated with levetiracetam and oxcarbazepine administered orally. After hospital admission, the twitching of the foot and toe was refractory to add-on treatment with lorazepam and diazepam but stopped within 15 min after intravenous bolus administration of 2000 mg levetiracetam. This observation suggests that intravenous bolus administration of levetiracetam may be an effective therapeutic option in epilepsia partialis continua.
Seizure 10/2009; 18(10):716-8. · 1.80 Impact Factor
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Christian Dohmen,
Oliver W Sakowitz,
Martin Fabricius,
Bert Bosche,
Thomas Reithmeier,
Ralf-Ingo Ernestus,
Gerrit Brinker,
Jens P Dreier,
Johannes Woitzik,
Anthony J Strong,
Rudolf Graf
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ABSTRACT: Cortical spreading depression (CSD) and periinfarct depolarization (PID) have been shown in various experimental models of stroke to cause secondary neuronal damage and infarct expansion. For decades it has been questioned whether CSD or PID occur in human ischemic stroke. Here, we describe CSD and PID in patients with malignant middle cerebral artery infarction detected by subdural electrocorticography (ECoG).
Centres of the Co-operative Study of Brain Injury Depolarisations (COSBID) recruited 16 patients with large middle cerebral artery infarction. During surgery for decompressive hemicraniectomy, an electrode strip was placed on the periinfarct region, from which four ECoG channels were acquired.
A total of 1,638 hours was recorded; mean monitoring time per patient was 109.2 hours. A total of 127 CSD and 42 PID events were observed. In CSD, a stereotyped slow potential change spreading between adjacent channels was accompanied by transient depression of ECoG activity. In PID, a slow potential change spread between neighboring channels despite already established suppression of ECoG activity. Most CSDs and PIDs appeared repetitively in clusters. CSD or PID was observed in all but two patients. In these two patients, the electrode strip had been placed over infarcted tissue, and accordingly, no local ECoG or recurrent transient depolarization activity occurred throughout the observation period.
CSD and PID occurred spontaneously with high frequency in this study of patients with malignant middle cerebral artery infarction. This suggests that the large volume of experimental studies of occlusive stroke that implicate spreading depolarizations in its pathophysiology can be translated, with appropriate caution, to patients and their treatment.
Annals of Neurology 07/2008; 63(6):720-8. · 11.09 Impact Factor
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ABSTRACT: To describe a movement disorder characterized by ocular flutter, trunk ataxia, and mild generalized myoclonus associated with anti-GQ1b antibodies.
Case report.
University hospital.
A 37-year-old woman presented with rapid, conjugated, and periodic oscillations of the eyes with a strict preponderance for the horizontal plane (ocular flutter); trunk ataxia; and occasional arrhythmic muscle jerks (myoclonus) most pronounced at the neck.
Brain magnetic resonance imaging results were normal. Cerebrospinal fluid examination revealed mild lymphocytic pleocytosis. Results of extensive serological tests on viral, bacterial, and fungal infections from blood and cerebrospinal fluid samples were unremarkable. Results of screening examinations for neoplasms and paraneoplastic antibodies, including whole-body fludeoxyglucose F18 positron emission tomography, were normal. Positive titers of IgG and IgM anti-GQ1b antibodies were found.
This is the first description of an association between the clinical syndrome of ocular flutter, mild stimulus sensitive myoclonus, and trunk ataxia and anti-GQ1b antibodies. The association with ganglioside antibodies lends further support to the notion of an autoimmune-associated pathology of the syndrome.
Archives of neurology 06/2008; 65(5):659-61. · 6.31 Impact Factor
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Christian Dohmen MD,
Oliver W. Sakowitz MD,
Martin Fabricius MD,
Bert Bosche MD,
Thomas Reithmeier MD,
Ralf-Ingo Ernestus MD,
Gerrit Brinker MD,
Jens P. Dreier MD,
Johannes Woitzik MD,
Anthony J. Strong MD, [......],
Oliver W. Sakowitz,
Martin Fabricius,
Bert Bosche,
Thomas Reithmeier,
Ralf‐Ingo Ernestus,
Gerrit Brinker,
Jens P. Dreier,
Johannes Woitzik,
Anthony J. Strong,
Rudolf Graf
[show abstract]
[hide abstract]
ABSTRACT: Objective
Cortical spreading depression (CSD) and periinfarct depolarization (PID) have been shown in various experimental models of stroke to cause secondary neuronal damage and infarct expansion. For decades it has been questioned whether CSD or PID occur in human ischemic stroke. Here, we describe CSD and PID in patients with malignant middle cerebral artery infarction detected by subdural electrocorticography (ECoG).Methods
Centres of the Co-operative Study of Brain Injury Depolarisations (COSBID) recruited 16 patients with large middle cerebral artery infarction. During surgery for decompressive hemicraniectomy, an electrode strip was placed on the periinfarct region, from which four ECoG channels were acquired.ResultsA total of 1,638 hours was recorded; mean monitoring time per patient was 109.2 hours. A total of 127 CSD and 42 PID events were observed. In CSD, a stereotyped slow potential change spreading between adjacent channels was accompanied by transient depression of ECoG activity. In PID, a slow potential change spread between neighboring channels despite already established suppression of ECoG activity. Most CSDs and PIDs appeared repetitively in clusters. CSD or PID was observed in all but two patients. In these two patients, the electrode strip had been placed over infarcted tissue, and accordingly, no local ECoG or recurrent transient depolarization activity occurred throughout the observation period.InterpretationCSD and PID occurred spontaneously with high frequency in this study of patients with malignant middle cerebral artery infarction. This suggests that the large volume of experimental studies of occlusive stroke that implicate spreading depolarizations in its pathophysiology can be translated, with appropriate caution, to patients and their treatment. Ann Neurol 2008
Annals of Neurology 05/2008; 63(6):720 - 728. · 11.09 Impact Factor
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ABSTRACT: In patients with large middle cerebral artery (MCA) infarction, space-occupying brain edema may lead to a malignant course with up to 80% mortality, under conservative treatment. As interventional treatment strategies must be started before the deterioration occurs, predictors of a malignant course are necessary.
This study reports on the results of evoked potentials (brainstem auditory evoked potentials [BAEP] and median-nerve somatosensory evoked potentials [SEP]) within 24 h after onset of stroke in 30 patients suffering a large MCA infarct (14 patients with a malignant and 16 with a non-malignant course).
Our findings indicate that pathological BAEP indicate a malignant course (P < 0.05).
This study shows that in patients suffering from large MCA infarction early assessment of EP within 24 h after onset of stroke may deliver useful information to select those patients who develop malignant edema.
Neurocritical Care 11/2007; 9(1):13-6. · 2.47 Impact Factor
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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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ABSTRACT: To study cerebrovascular autoregulation and its impact on clinical course in patients with impending malignant middle cerebral artery infarction, we used invasive multimodal neuromonitoring, including measurement of cerebral perfusion pressure, tissue oxygen pressure, and microdialysis.
Fifteen patients with a stroke that involved >50% of the middle cerebral artery territory were included. Probes were placed into the ipsilateral frontal lobe. Autoregulation was assessed by calculation of the cerebral perfusion pressure-oxygen reactivity index (COR) and the correlation coefficient (R) of cerebral perfusion pressure and tissue oxygen pressure at 24 and 72 hours after stroke.
COR and R at 24 hours after stroke were higher in the 8 patients with a malignant course (ie, massive edema formation) compared with the 7 patients with a benign course (COR, 1.99+/-1.46 versus 0.68+/-0.29; R, 0.49+/-0.28 versus 0.06+/-0.31; P<0.05), indicating impaired autoregulation in the malignant course group. At 72 hours, further increases in COR and R were observed in the malignant course group in contrast to the benign course group with stable values over time (COR, 3.31+/-2.38 versus 0.75+/-0.31; R, 0.75+/-011 versus 0.36+/-0.27; P<0.05). With a COR of 0.99, a cutoff value for prediction of a malignant course was found. The lactate-pyruvate ratio was higher in patients with a malignant compared with a benign course at both time points. COR, R, and the lactate-pyruvate ratio showed significant correlations with outcome parameters as a midline shift on cranial computed tomography and score on the modified Rankin scale after 3 months.
We found early impairment of cerebrovascular autoregulation in peri-infarct tissue of patients who developed malignant brain edema, whereas autoregulation was preserved in patients with a benign course. Impaired cerebral autoregulation seems to play a key role for development of a malignant course and might serve as a predictive marker. Impaired cerebral autoregulation also accentuates the need for consequent adjustment of cerebral perfusion pressure in patients with impaired autoregulation.
Stroke 01/2007; 38(1):56-61. · 5.73 Impact Factor
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ABSTRACT: In patients with large middle cerebral artery (MCA) infarction space occupying brain edema may lead to a malignant course with up to 80% mortality under conservative treatment. As interventional treatment strategies must be started before the deterioration occurs predictors of a malignant course are necessary.
This study reports on the results of early electroencephalography (EEG) within 24h after onset of stroke in 25 patients suffering a large MCA infarct (12 patients with a malignant and 13 with a non-malignant course). EEG analysis was performed according well-established indicators for focal as well as global changes.
Our findings indicate that the absence of delta activity and the presence of theta and fast beta frequencies within the focus predict a benign course (p < 0.05), whereas diffuse generalized slowing and slow delta activity in the ischemic hemisphere may point to a malignant course.
This study shows that in patients suffering from large MCA infarction early EEG delivers useful information to select those patients who develop malignant edema.
Clinical Neurology and Neurosurgery 01/2007; 109(1):45-9. · 1.58 Impact Factor
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Stroke 04/2006; 37(3):762-3; author reply 763-4. · 5.73 Impact Factor
