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  • 1
    Article
    Article
    In: Notfallmedizin up2date, 2017, Vol.12(01), pp.79-91
    Description: Bewusstseinsstörungen kommen in der neurologischen Notfall- und Intensivmedizin häufig vor und erfordern eine schnelle Diagnostik und zielgerichtete Therapie, da sonst irreversible Schäden des zentralen Nervensystems drohen. Beides ist im Rettungsdienst nur eingeschränkt möglich und reduziert sich auf die wesentlichen Maßnahmen.
    ISSN: 1611-6550
    E-ISSN: 1862-6955
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  • 2
    In: The New England Journal of Medicine, 2015, Vol.372(15), pp.1476-1478
    Description: The authors report a fatal case of progressive multifocal leukoencephalopathy in a 54-year-old woman in whom lymphocytopenia developed after treatment with delayed-release dimethyl fumarate for multiple sclerosis. To the Editor: We report the case of a 54-year-old woman with multiple sclerosis who was treated with delayed-release dimethyl fumarate (DMF; Tecfidera, Biogen Idec) and who died on October 13, 2014, from complications related to aspiration pneumonia and progressive multifocal leukoencephalopathy (PML) with severe, prolonged lymphocytopenia. The patient, who had received the diagnosis of multiple sclerosis in 1996 and had been treated with glatiramer acetate, was randomly assigned to the placebo group in the 2-year Determination of the Efficacy and Safety of Oral Fumarate in Relapsing–Remitting Multiple Sclerosis (DEFINE) trial.1 She subsequently received delayed-release DMF (at a dose of . . .
    Keywords: Medicine;
    ISSN: 0028-4793
    E-ISSN: 1533-4406
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  • 3
    Language: English
    In: Intensive Care Medicine, 2001, Vol.27(7), pp.1231-1234
    Description: Objective : Perfusion abnormalities are an overall phenomenon in severe sepsis and septic shock, leading to organ dysfunction. We investigated whether carbon dioxide (CO 2 )-induced vasomotor reactivity (VMR) is impaired in septic patients, compared with values obtained outside sepsis. Design : Prospective, clinical study. Setting : Six-bed neurologic critical care unit of a university hospital. Patients and participants : Eight consecutive patients with severe sepsis and septic shock. Measurements and results : CO 2 -reactivity was measured during and outside a period of severe sepsis or septic shock according to ACCP/SCCM criteria by means of transcranial Doppler sonography and near-infrared spectroscopy (NIRS). VMR was calculated as the percentage change of cerebral blood flow velocity (normalized CO 2 -reactivity, NCR) and absolute changes in concentration of oxygenated hemoglobin, deoxygenated hemoglobin, total hemoglobin (HbO 2 , Hb, HbT) and Hbdiff (difference between HbO 2 and Hb) in µmol/l per 1% increase in end-tidal CO 2 (CR-HbO 2 , CR-Hb, CR-HbT, CR-Hbdiff). NCR and NIRS-reactivities were significantly reduced during severe sepsis and septic shock compared with values outside sepsis (mean, SD, Wilcoxon): NCR 11.0 (7.1) versus 30.7 (13.0), p 〈0.02; CR-HbO 2 0.70 (0.61) versus 2.33 (1.11), p 〈0.02; CR-Hb –0.17 (0.74) versus –1.42 (1.28), p 〈0.04; CR-HbT 0.53 (0.48) versus 1.05 (0.40), p 〈0.03; CR-Hbdiff 0.91 (1.33) versus 3.75 (2.33), p 〈0.02. This indicates a severely disturbed VMR. Conclusions : In the advent of a disturbed cerebral autoregulation, critical drops in blood pressure during sepsis are transferred directly into the vascular bed, leading to cerebral hypoperfusion. This mechanism might contribute to the pathogenesis of septic encephalopathy.
    Keywords: Sepsis Spectroscopy, near-infrared Ultrasonography, Doppler, transcranial Vasomotor reactivity
    ISSN: 0342-4642
    E-ISSN: 1432-1238
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  • 4
    Language: English
    In: Journal of Medical Case Reports, Jan 22, 2010, Vol.4, p.19
    Description: Introduction Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo. Case presentation A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise. Conclusion Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.
    Keywords: Optic Nerve Diseases -- Risk Factors ; Optic Nerve Diseases -- Diagnosis ; Optic Nerve Diseases -- Care And Treatment ; Optic Nerve Diseases -- Patient Outcomes ; Optic Nerve Diseases -- Case Studies ; Subdural Hematoma -- Risk Factors ; Subdural Hematoma -- Diagnosis ; Subdural Hematoma -- Care And Treatment ; Subdural Hematoma -- Patient Outcomes ; Subdural Hematoma -- Case Studies ; Anticoagulants -- Usage ; Anticoagulants -- Health Aspects
    ISSN: 1752-1947
    Source: Cengage Learning, Inc.
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  • 5
    Language: English
    In: Journal of Medical Case Reports, Jan 22, 2010, Vol.4, p.19
    Description: Introduction Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo. Case presentation A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise. Conclusion Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.
    Keywords: Optic Nerve Diseases -- Risk Factors ; Optic Nerve Diseases -- Diagnosis ; Optic Nerve Diseases -- Care And Treatment ; Optic Nerve Diseases -- Patient Outcomes ; Optic Nerve Diseases -- Case Studies ; Subdural Hematoma -- Risk Factors ; Subdural Hematoma -- Diagnosis ; Subdural Hematoma -- Care And Treatment ; Subdural Hematoma -- Patient Outcomes ; Subdural Hematoma -- Case Studies ; Anticoagulants -- Usage ; Anticoagulants -- Health Aspects
    ISSN: 1752-1947
    Source: Cengage Learning, Inc.
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  • 6
    Language: English
    In: Journal of Medical Case Reports, 01 January 2010, Vol.4(1), p.19
    Description: Abstract Introduction Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy...
    Keywords: Medicine
    ISSN: 1752-1947
    E-ISSN: 1752-1947
    Source: Directory of Open Access Journals (DOAJ)
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  • 7
    Language: English
    In: Journal of medical case reports, 22 January 2010, Vol.4, pp.19
    Description: Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo. A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise. Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.
    Keywords: Case Report;
    E-ISSN: 1752-1947
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  • 8
    Language: English
    In: Epilepsy Research, 2010, Vol.89(2), pp.355-359
    Description: The clinical differentiation between stroke and seizure is usually straightforward but postictal neurological deficits can be mistaken for stroke in case no detailed medical history is available. Up to now, the imaging findings of Todd's paresis are not well described. This case report demonstrates that postictal paresis can be accompanied by a reversible global hemispheric hypoperfusion as measured with perfusion MRI indicating transient but profound cerebrovascular dysfunction in postictal paresis. Extensive postictal perfusion changes must be discriminated from emerging stroke to avoid potentially harmful therapy like thrombolysis. Further investigations are warranted to clarify the role of cerebrovascular dysfunction in the pathophysiology of postictal paresis.
    Keywords: Mri ; Epilepsy ; Perfusion Imaging ; Medicine ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0920-1211
    E-ISSN: 1872-6844
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  • 9
    Language: English
    In: JAMA, 24 February 2015, Vol.313(8), pp.824-36
    Description: Although use of oral anticoagulants (OACs) is increasing, there is a substantial lack of data on how to treat OAC-associated intracerebral hemorrhage (ICH). To assess the association of anticoagulation reversal and blood pressure (BP) with hematoma enlargement and the effects of OAC resumption. Retrospective cohort study at 19 German tertiary care centers (2006-2012) including 1176 individuals for analysis of long-term functional outcome, 853 for analysis of hematoma enlargement, and 719 for analysis of OAC resumption. Reversal of anticoagulation during acute phase, systolic BP at 4 hours, and reinitiation of OAC for long-term treatment. Frequency of hematoma enlargement in relation to international normalized ratio (INR) and BP. Incidence analysis of ischemic and hemorrhagic events with or without OAC resumption. Factors associated with favorable (modified Rankin Scale score, 0-3) vs unfavorable functional outcome. Hemorrhage enlargement occurred in 307 of 853 patients (36.0%). Reduced rates of hematoma enlargement were associated with reversal of INR levels 〈1.3 within 4 hours after admission (43/217 [19.8%]) vs INR of ≥1.3 (264/636 [41.5%]; P 〈 .001) and systolic BP 〈160 mm Hg at 4 hours (167/504 [33.1%]) vs ≥160 mm Hg (98/187 [52.4%]; P 〈 .001). The combination of INR reversal 〈1.3 within 4 hours and systolic BP of 〈160 mm Hg at 4 hours was associated with lower rates of hematoma enlargement (35/193 [18.1%] vs 220/498 [44.2%] not achieving these values; OR, 0.28; 95% CI, 0.19-0.42; P 〈 .001) and lower rates of in-hospital mortality (26/193 [13.5%] vs 103/498 [20.7%]; OR, 0.60; 95% CI, 0.37-0.95; P = .03). OAC was resumed in 172 of 719 survivors (23.9%). OAC resumption showed fewer ischemic complications (OAC: 9/172 [5.2%] vs no OAC: 82/547 [15.0%]; P 〈 .001) and not significantly different hemorrhagic complications (OAC: 14/172 [8.1%] vs no OAC: 36/547 [6.6%]; P = .48). Propensity-matched survival analysis in patients with atrial fibrillation who restarted OAC showed a decreased HR of 0.258 (95% CI, 0.125-0.534; P 〈 .001) for long-term mortality. Functional long-term outcome was unfavorable in 786 of 1083 patients (72.6%). Among patients with OAC-associated ICH, reversal of INR 〈1.3 within 4 hours and systolic BP 〈160 mm Hg at 4 hours were associated with lower rates of hematoma enlargement, and resumption of OAC therapy was associated with lower risk of ischemic events. These findings require replication and assessment in prospective studies. clinicaltrials.gov Identifier: NCT01829581.
    Keywords: Blood Pressure ; Anticoagulants -- Adverse Effects ; Cerebral Hemorrhage -- Chemically Induced ; Hematoma -- Physiopathology
    ISSN: 00987484
    E-ISSN: 1538-3598
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  • 10
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