Background: The results of recent studies on cognitive disability after traumatic brain injury-associated diffuse axonal injury (DAI) are inconsistent. In these studies, the diagnosis of DAI relied on cranial computed tomography. Objective: To further clarify the extent and severity of a possibly DAI-associated cognitive impairment by the use of magnetic resonance imaging (MRI) and detailed neuropsychological testing. Design and Participants: From a databank of 299 patients with traumatic brain injury, 18 patients (age range, 17-50 years; median initial Glasgow Coma Scale score, 5) who showed an MRI lesion pattern compatible with pure DAI were identified. All of the patients had undergone MRI on a 3-T system. Pure DAI was defined by the findings of traumatic microbleeds on T2*-weighted gradient-echo images in the absence of otherwise traumatic or nontraumatic MRI abnormalities. Main Outcome Measures: Neuropsychological performance in the categories of attention and psychomo-tor speed, executive functions, spans, learning and memory, and intelligence 4 to 55 months (median, 9 months) after traumatic brain injury. Results: All of the patients showed impairments of 1 or more cognitive subfunctions, and no cognitive domain was fundamentally spared. Memory and executive dysfunctions were most frequent, the former reaching a moderate to severe degree in half of the patients. In comparison, deficits of attention, executive functions, and short-term memory were mostly mild. Correlations between the amount of traumatic microbleeds and specific or global cognitive performance were absent. Conclusions: An MRI lesion pattern compatible with isolated DAI is associated with persistent cognitive impairment. The traumatic microbleed load is no sufficient parameter for the assessment of DAI severity or functional outcome.
Stereotactic surgery is based on a high degree of accuracy in defining and localising intracranial targets and placing surgical tools. Brain shift can influence its accuracy significantly. Deep brain stimulation of the subthalamic nucleus can markedly change the quality of life of patients with advanced Parkinson's disease, but the outcome depends on the quality of electrode placement. A patient is reported in whom the placement of the second electrode was not successful. Deformation field analysis of pre- and postoperative three dimensional magnetic resonance images showed an intraoperative brain movement of 2 mm in the region of the subthalamic nucleus (the target point). Electrode repositioning resulted in efficient stimulation effects. This case report shows the need to reduce risk factors for intraoperative brain movement and demonstrates the ability of deformation field analysis to quantify this complication
Somatosensory signals modulate activity throughout a widespread network in both of the brain hemispheres: the contralateral as well as the ipsilateral side of the brain relative to the stimulated limb. To analyze the ipsilateral somatosensory brain areas that are engaged during limb stimulation, we performed functional magnetic resonance imaging (fMRI) in 12 healthy subjects during electrical median nerve stimulation using both a block- and an event-related fMRI design. Data were analyzed through the use of model-dependent (SPM) and model-independent (ICA) approaches. Beyond the well-known positive blood oxygenation level-dependent (BOLD) responses, negative deflections of the BOLD response were found consistently in several ipsilateral brain areas, including the primary somatosensory cortex, the supplementary motor area, the insula, the dorsal part of the posterior cingulate cortex, and the contralateral cerebellum. Compared to their positive counterparts, the negative hemodynamic responses showed a different time course, with an onset time delay of 2.4 s and a peak delay of 0.7 s. This characteristic delay was observed in all investigated areas and verified by a second (purely tactile) event-related paradigm, suggesting a systematic difference for brain areas involved in the processing of somatosensory information. These findings may indicate that the physiological basis of these deactivations differs from that of the positive BOLD responses. Therefore, an altered model for the negative BOLD response may be beneficial to further model-dependent fMRI analyses.
Position-dependent effects on brain structure may undermine the accuracy of neuronavigational and other neurosurgical procedures. Furthermore, in longitudinal MR volumetric studies, gravitational effects should be kept in mind and the scanning position should be rigidly controlled for.
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.
Following stroke, many patients suffer from chronic motor impairment and reduced somatosensation in the stroke-affected body parts. Recent experimental studies suggest that temporary functional deafferentation (TFD) of parts of the stroke-affected upper limb or of the less-affected contralateral limb might improve the sensorimotor capacity of the stroke-affected hand. The present study sought evidence of cortical reorganization and related sensory and motor improvements following pharmacologically induced TFD of the stroke-affected forearm.Examination was performed during 2 d of Constraint-Induced Movement Therapy. Thirty-six human patients were deafferented on the stroke-affected forearm by an anesthetic cream (containing lidocaine and prilocaine) on one of the 2 d, and a placebo cream was applied on the other. The order of TFD and placebo treatment was counterbalanced across patients. Somatosensory and motor performance were assessed using a Grating orienting task and a Shape-sorter-drum task, and with somatosensory-evoked magnetic fields. Evoked magnetic fields showed significant pre-to postevaluation magnitude increases in response to tactile stimulation of the thumb of the stroke-affected hand during TFD but not following placebo treatment. We also observed a rapid extension of the distance between cortical representations of the stroke-affected thumb and little finger following TFD but not following placebo treatment. Moreover, somatosensory and motor performance of the stroke-affected hand was significantly enhanced during TFD but not during placebo treatment. Thus, pharmacologically induced TFD of a stroke-affected forearm might improve the somatosensory and motor functions of the stroke-affected upper limb, accompanied by cortical plasticity.
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