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  • 1
    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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  • 2
    Language: English
    In: Behavioural Brain Research, Sept 1, 2013, Vol.252, p.110(7)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.bbr.2013.05.048 Byline: Elisabeth Sens, Christin Knorr, Christoph Preul, Winfried Meissner, Otto W. Witte, Wolfgang H.R. Miltner, Thomas Weiss Abstract: acents Motor performance significantly increased during TFD in stroke patients. acents Somatosensory sensitivity significantly increased during TFD in stroke patients. acents Sensorimotor performance did not increase during TFD in healthy subjects. acents The pretest of stroke patients showed a significant deficit in GOT and SSDT. acents TFD might become an additional tool in motor rehabilitation of post stroke patients. Author Affiliation: (a) Biological & Clinical Psychology, Friedrich Schiller University, Jena, D-07743, Germany (b) Department of Neurology, Jena University Hospital, Jena, D-07747, Germany (c) Department of Anesthesiology and Intensive Care, Jena University Hospital, Jena, D-07747, Germany (d) Center for Sepsis Control and Care CSCC, Jena University Hospital, Jena, D-07747, Germany Article History: Received 7 May 2013; Revised 24 May 2013; Accepted 26 May 2013
    Keywords: Stroke Patients
    ISSN: 0166-4328
    Source: Cengage Learning, Inc.
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  • 3
    In: Stroke A Journal of Cerebral Circulation, 2011, Vol.42(5), pp.1363-1370
    Description: BACKGROUND AND PURPOSE—: Reduced somatosensation is a common impairment after stroke. This somatosensory deficit is known to be a reliable predictor of poor rehabilitation outcome. Several methods of physical therapy have addressed this problem, but with only moderate success. Here, we used a new neural plasticity-based approach, ie, a simple, inexpensive, pharmacologically induced temporary functional deafferentation (TFD) of the forearm to investigate whether TFD might result in beneficial effects on the somatosensory sensibility and motor capacity of the stroke-affected hand. METHODS—: Examination was performed over 2 consecutive days of an efficient rehabilitation program for stroke patients referred to as constraint-induced movement therapy. Patients were deafferented on one of these days but not on the other (placebo session). The order of deafferentation and nondeafferentation was counterbalanced across patients. TFD of the stroke-affected forearm was realized using an anesthetic cream. Somatosensory abilities were assessed by a Grating orienting task, and a shape-sorter drum task was used to test motor performance. Both tests were performed each day before and after the constraint-induced movement therapy training session. RESULTS—: We found significantly better outcomes for Grating orienting task and shape-sorter drum task after TFD on the forearm as compared to placebo, indicating increased somatosensory abilities and motor performance in stroke patients using the simple TFD procedure. CONCLUSIONS—: The improvement was achieved during the course of one of the best established poststroke rehabilitation programs, suggesting that TFD on the more affected forearm might become an efficient additional tool in stroke rehabilitation.
    Keywords: Medicine;
    ISSN: 0039-2499
    E-ISSN: 15244628
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  • 4
    Language: English
    In: Behavioural Brain Research, 01 September 2013, Vol.252, pp.110-116
    Description: Temporary functional deafferentation is of interest to become an additional tool in neurorehabilitative treatments. Temporary functional deafferentation is known to improve sensory and motor outcomes in chronic stroke patients and healthy subjects. The present study soughts to indicate differences in the efficiency of pharmacologically induced temporary functional deafferentation between chronic stroke patients and matched healthy subjects. 46 chronic stroke patients and 20 age- and gender-matched healthy subjects were deafferented on one forearm by an anesthetic cream. Somatosensory performance was assessed using von-Frey Hair testing and Grating orientation task; motor performance was assessed by means of a shape-sorter-drum task. Grating orientation task and shape-sorter-drum task were significantly improved during temporary functional deafferentation in stroke patients but not in healthy subjects. Von-Frey Hair testing revealed no improvement of absolute tactile thresholds during temporary functional deafferentation in both groups. Furthermore, the stroke patients showed deficits at baseline measurement in all assessments except the von-Frey Hair test. Temporary functional deafferentation of a forearm by an anesthetic cream results in improvements of motor performance and somatosensory discrimination in stroke patients but not in healthy subjects. Therefore, it is reasonable to test in a next step whether temporary functional deafferentation might become an additional tool in motor rehabilitation of post stroke patients.
    Keywords: Stroke ; Temporary Functional Deafferentation ; Sensorimotor Improvement ; Cortical Plasticity ; Rehabilitation ; Anatomy & Physiology
    ISSN: 0166-4328
    E-ISSN: 0166-4328
    E-ISSN: 18727549
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  • 5
    Language: English
    In: Journal of neurology, April 2005, Vol.252(4), pp.441-7
    Description: To evaluate the role of MR morphometry in the characterization of cerebral microangiopathy (CMA) in relation to clinical and neuropsychological impairment. 3D MR images of 27 patients and 27 age-matched controls were morphometrically analysed for regional thickness. The normalized values were related to the patients' clinical and neuropsychological scores. The patients were categorised according to the amount of structural MR signal changes. A ventricle index reflecting internal atrophy was related to MR morphology and cortical thickness as an indicator for external atrophy. Cortical thickness was significantly reduced in the patients group (3.03 mm +/- 0.26 vs. 3.22 mm +/-0.13 in controls, p=0.001). The severest loss of cortical thickness occurred in severe CMA. Internal and external atrophy evolved in parallel and both showed a significant relationship with structural MR-abnormalities (p〈0.05; r=-0.7; r=0.67; r=-0.74, respectively). Neuropsychological performance correlated strongly with the loss of cortical thickness. Cortical thickness was identified as the most sensitive parameter to characterize CMA. A strong correlation was found of morphometric parameters to the severity of CMA based on a score derived from T2-weighted MRI. The degree of cortical atrophy was directly related to the degree of neuropsychological impairment. Our findings suggest that the cortical thickness is a valid marker in the structural and clinical characterization of CMA.
    Keywords: Cerebral Cortex -- Pathology ; Cerebrovascular Disorders -- Pathology
    ISSN: 0340-5354
    E-ISSN: 14321459
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  • 6
    In: Brain, 2016, Vol. 139(12), pp.3267-3280
    Description: Deficits of simultaneous perception (simultanagnosia) are common in posterior cortical atrophy (PCA), but the precise underlying mechanism is unclear. By testing patients with PCA owing to Alzheimer’s disease, Neitzel et al. show that simultanagnosia reflects an impairment of visual processing speed caused by white matter atrophy within the left superior parietal lobe. Deficits of simultaneous perception (simultanagnosia) are common in posterior cortical atrophy (PCA), but the precise underlying mechanism is unclear. By testing patients with PCA owing to Alzheimer’s disease, Neitzel et al. show that simultanagnosia reflects an impairment of visual processing speed caused by white matter atrophy within the left superior parietal lobe. Posterior cortical atrophy is dominated by progressive degradation of parieto-occipital grey and white matter, and represents in most cases a variant of Alzheimer’s disease. Patients with posterior cortical atrophy are characterized by increasing higher visual and visuo-spatial impairments. In particular, a key symptom of posterior cortical atrophy is simultanagnosia i.e. the inability to perceive multiple visual objects at the same time. Two neuro-cognitive mechanisms have been suggested to underlie simultanagnosia, either reduced visual short-term memory capacity or decreased visual processing speed possibly resulting from white matter impairments over and above damage to cortical brain areas. To test these distinct hypotheses, we investigated a group of 12 patients suffering from posterior cortical atrophy with homogenous lesion sides in parieto-occipital cortices and varying severity of grey and white matter loss. More specifically, we (i) tested whether impaired short-term memory capacity or processing speed underlie symptoms of simultanagnosia; (ii) assessed the link to grey and white matter damage; and (iii) integrated those findings into a neuro-cognitive model of simultanagnosia in patients with posterior cortical atrophy. To this end, simultaneous perception of multiple visual objects was tested in patients with posterior cortical atrophy mostly with positive Alzheimer’s disease biomarkers and healthy age-matched controls. Critical outcome measures were identification of overlapping relative to non-overlapping figures and visuo-spatial performance in tests sensitive to simultanagnosia. Using whole report of briefly presented letter arrays based on the mathematically formulated ‘Theory of Visual Attention’, we furthermore quantified parameters of visual short-term memory capacity and visual processing speed. Grey and white matter atrophy was assessed by voxel-based morphometry analyses of structural magnetic resonance data. All patients showed severe deficits of simultaneous perception. Compared to controls, we observed a specific slowing of visual processing speed, while visual short-term memory capacity was preserved. In a regression analysis, processing speed was identified as the only significant predictor of simultaneous perception deficits that explained a high degree of variance (70–82%) across simultanagnosia tasks. More severe slowing was also indicative for more severe impairments in reading and scene comprehension. Voxel-based morphometry yielded extensive reductions of grey and white matter in parieto-occipital and thalamic brain areas. Importantly, the degree of individual atrophy of white matter in left superior parietal lobe, but not of any grey matter region, was associated with processing speed. Based on these findings, we propose that atrophy of white matter commonly observed in posterior cortical atrophy leads to slowing of visual processing speed, which underlies the overt clinical symptoms of simultanagnosia.
    Keywords: Posterior Cortical Atrophy ; Atypical Alzheimer’s Disease ; Simultanagnosia ; Theory Of Visual Attention ; Voxel - Based Morphometry
    ISSN: 0006-8950
    E-ISSN: 1460-2156
    Source: Oxford University Press
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  • 7
    Language: English
    In: Neuropsychologia, May 2010, Vol.48(6), pp.1735-1741
    Description: An influential single case study (Calder, Keane, Manes, Antoun, & Young, 2000, , 1077–1078) recently showed a marked multimodal impairment in the recognition and experience of disgust in a patient with a left-hemispheric lesion of the basal ganglia and the insular cortex. Here, we investigated whether a similar deficit will be observed in a patient with a comparable lesion of the insula and basal ganglia in the right hemisphere. Remarkably, the patient showed no impairments in the recognition or experience of disgust and also no notable impairments in the recognition and experience of other emotions, across a range of stimuli, as compared to healthy comparison subjects. Thus, either deficits in disgust processing are not reliably observed in patients with lesion of the insula and basal ganglia regardless of the laterality of the lesion; or right-hemispheric lesions, in contrast to left-hemispheric lesions, do not seem to induce impairments in the processing of disgust.
    Keywords: Brain ; Hemispheres ; Lateralization ; Emotion ; Medicine
    ISSN: 0028-3932
    E-ISSN: 1873-3514
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  • 8
    Language: English
    In: NeuroImage, 01 October 2010, Vol.52(4), pp.1314-1327
    Description: Regional structural brain changes are among the most robust biological findings in schizophrenia, yet the underlying pathophysiological changes remain poorly understood. Recent evidence suggests that abnormal neuronal/dendritic plasticity is related to alterations in membrane lipids. We examined whether serum activity of membrane lipid remodelling/repairing cytosolic phospholipase A (PLA ) were related to regional brain structure in magnetic resonance images (MRI). The study involved 24 schizophrenia patients, who were either drug-naïve or off antipsychotic medication, and 25 healthy controls. Using voxel-based morphometry (VBM) analysis of T1-high-resolution MRI-images, we correlated both gray matter and white matter changes with serum PLA -activity. PLA activity was increased in patients, consistent with previous findings. VBM group comparison of patients vs. controls showed abnormalities of frontal and medial temporal cortices/hippocampus, and left middle/superior temporal gyrus in first-episode patients. Group comparison of VBM/PLA -correlations revealed a distinct pattern of disease-related interactions between gray/white matter changes in patients and PLA -activity: in first-episode patients ( = 13), PLA -activity was associated with structural alterations in the left prefrontal cortex and the bilateral thalamus. Recurrent-episode patients ( = 11) showed a wide-spread pattern of associations between PLA -activity and structural changes in the left (less right) prefrontal and inferior parietal cortex, the left (less right) thalamus and caudate nucleus, the left medial temporal and orbitofrontal cortex and anterior cingulum, and the cerebellum. Our findings demonstrate a potential association between membrane lipid biochemistry and focal brain structural abnormalities in schizophrenia. Differential patterns in first-episode vs. chronic patients might be related to PLA -increase at disease-onset reflecting localized regenerative activity, whereas correlations in recurrent-episode patients might point to less specific neurodegenerative aspects of disease progression.
    Keywords: Schizophrenia ; Imaging ; Mri ; Gray Matter ; White Matter ; Morphometry ; Phospholipids ; Membrane Lipids ; Marker ; Medicine
    ISSN: 1053-8119
    E-ISSN: 1095-9572
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  • 9
    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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  • 10
    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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