Anosognosia for motor impairment following left brain damage.
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ABSTRACT:
SUBMITTER: Cocchini G
PROVIDER: S-EPMC2672046 | biostudies-other | 2009 Mar
REPOSITORIES: biostudies-other
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Project description:In this paper we review studies that investigated tool use disorders in left-brain damaged (LBD) patients over the last 30 years. Four tasks are classically used in the field of apraxia: Pantomime of tool use, single tool use, real tool use and mechanical problem solving. Our aim was to address two issues, namely, (1) the role of mechanical knowledge in real tool use and (2) the cognitive mechanisms underlying pantomime of tool use, a task widely employed by clinicians and researchers. To do so, we extracted data from 36 papers and computed the difference between healthy subjects and LBD patients. On the whole, pantomime of tool use is the most difficult task and real tool use is the easiest one. Moreover, associations seem to appear between pantomime of tool use, real tool use and mechanical problem solving. These results suggest that the loss of mechanical knowledge is critical in LBD patients, even if all of those tasks (and particularly pantomime of tool use) might put differential demands on semantic memory and working memory.
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Project description:STUDY OBJECTIVES:Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. METHODS:One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index < 15) had polysomnographic sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. RESULTS:A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). CONCLUSIONS:Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. CLINICAL TRIAL REGISTRATION:The study was registered at www.clinicaltrials.gov as NCT01679782.
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Project description:ObjectiveTo test the hypothesis that microvascular brain pathology is associated with late-life motor impairment.MethodsMore than 2,500 persons participating in the Religious Orders Study or the Memory and Aging Project agreed to annual motor assessment and autopsy. Brains from 850 deceased participants were assessed for microvascular pathology including microinfarcts, cerebral amyloid angiopathy, and arteriolosclerosis, and we examined their association with global motor scores proximate to death.ResultsMean age at death was 88.5 years. More than 60% of cases had evidence of 1 or more microvascular pathologies and of these more than half did not have observed macroinfarcts. In separate regression models adjusted for age, sex, and education, microinfarcts and arteriolosclerosis were associated with level of motor function proximate to death (arteriolosclerosis, estimate, -0.027, SE 0.005, p < 0.001; microinfarcts, estimate, -0.017, SE 0.008, p = 0.026). These associations were not attenuated when controlling for vascular risk factors and diseases, postmortem interval, or interval from last clinical examination, and did not vary with level of cognition or presence of dementia proximate to death. When the 3 microvascular pathologies, macroinfarcts, and atherosclerosis were considered together in a single model, more severe arteriolosclerosis (estimate, -0.021, SE 0.005, p < 0.001) and macroinfarcts (estimate, -0.019, SE 0.006, p < 0.001) showed separate effects with the level of motor function proximate to death.ConclusionsMicrovascular brain pathology is common in older adults and may represent an under-recognized, independent cause of late-life motor impairment.
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Project description:Aquired apraxia of speech is a disorder that impairs speech production, despite intact peripheral neuromotor function. Its pathomechanism remains to be established. Neurodegenerative lesion models provide an unequalled opportunity to explore the neural correlates of apraxia of speech, which is present in a subset of patients diagnosed with non-semantic variants of primary progressive aphasia. The normalized pairwise variability index, an acoustic measure of speech motor programming, has shown high sensitivity and specificity for apraxia of speech in cross-sectional studies. Here, we aimed to examine the strength of the pairwise variability index and overall word duration (i.e. articulation rate) as markers of progressive motor programming deficits in primary progressive aphasia with apraxia of speech. Seventy-nine individuals diagnosed with primary progressive aphasia (39 with non-fluent variant and 40 with logopenic variant) and 40 matched healthy controls participated. Patients were followed-up annually (range 1-6 years, median number of visits = 2). All participants completed a speech assessment task and a high-resolution MRI. Our analyses investigated trajectories of speech production (e.g. pairwise variablity index and word duration) and associations with cortical atrophy in the patients. At first presentation, word duration differentiated the nonfluent and logopenic cases statistically, but the range of scores overlapped substantially across groups. Longitudinally, we observed progressive deterioration in pairwise variability index and word duration specific to the non-fluent group only. The pairwise variability index showed particularly strong associations with progressive atrophy in speech motor programming brain regions. Of novelty, our results uncovered a key role of the right frontal gyrus in underpinning speech motor programming changes in non-fluent cases, highlighting the importance of right-brain regions in responding to progressive neurological changes in the speech motor network. Taken together, our findings validate the use of a new metric, the pairwise variability index, as a robust marker of apraxia of speech in contrast to more generic measures of speaking rate. Sensitive/specific neuroimaging biomarkers of the emergence and progression of speech impairments will be useful to inform theories of the pathomechanisms underpinning impaired speech motor control. Our findings justify developing more sensitive measures of rhythmic temporal control of speech that may enable confident detection of emerging speech disturbances and more sensitive tracking of intervention-related changes for pharmacological, neuromodulatory and behavioural interventions. A more reliable detection of speech disturbances has relevance for patient care, with predominance of progressive apraxia of speech a high-risk factor for later diagnosis of progressive supranuclear palsy or corticobasal degeneration.
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Project description:Sense of time is a complex construct, and its neural correlates remain to date in most part unknown. To complicate the frame, physical attributes of the stimulus, such as its intensity or movement, influence temporal perception. Although previous studies have shown that time perception can be compromised after a brain lesion, the evidence on the role of the left and right hemispheres are meager. In two experiments, the study explores the ability of temporal estimation of multi-second actions and non-biological movements in 33 patients suffering from unilateral brain lesion. Furthermore, the modulatory role of induced embodiment processes is investigated. The results reveal a joint contribution of the two hemispheres depending not only on different durations but also on the presence of actions. Indeed, the left hemisphere damaged patients find it difficult to estimate 4500 ms or longer durations, while the right hemisphere damaged patients fail in 3000 ms durations. Furthermore, the former fail when a biological action is shown, while the latter fail in non-biological movement. Embodiment processes have a modulatory effect only after right hemisphere lesions. Among neuropsychological variables, only spatial neglect influences estimation of non-biological movement.
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Project description:Following intestinal perforation in neonatal mice there is an injury to the subventrcular zone stem cell niche. These files are the raw data from mouse brain sections, transecting SVZ in controls and mice with modeled instestinal perforation.
2024-01-24 | GSE254087 | GEO
Project description:Following intestinal perforation in neonatal mice there is an injury to the subventrcular zone stem cell niche. These files are the raw data from mouse SVZ in controls and mice with modeled instestinal perforation.
2023-09-27 | GSE243778 | GEO
Project description:White matter disruption is an important determinant of cognitive impairment after brain injury, but conventional neuroimaging underestimates its extent. In contrast, diffusion tensor imaging provides a validated and sensitive way of identifying the impact of axonal injury. The relationship between cognitive impairment after traumatic brain injury and white matter damage is likely to be complex. We applied a flexible technique-tract-based spatial statistics-to explore whether damage to specific white matter tracts is associated with particular patterns of cognitive impairment. The commonly affected domains of memory, executive function and information processing speed were investigated in 28 patients in the post-acute/chronic phase following traumatic brain injury and in 26 age-matched controls. Analysis of fractional anisotropy and diffusivity maps revealed widespread differences in white matter integrity between the groups. Patients showed large areas of reduced fractional anisotropy, as well as increased mean and axial diffusivities, compared with controls, despite the small amounts of cortical and white matter damage visible on standard imaging. A stratified analysis based on the presence or absence of microbleeds (a marker of diffuse axonal injury) revealed diffusion tensor imaging to be more sensitive than gradient-echo imaging to white matter damage. The location of white matter abnormality predicted cognitive function to some extent. The structure of the fornices was correlated with associative learning and memory across both patient and control groups, whilst the structure of frontal lobe connections showed relationships with executive function that differed in the two groups. These results highlight the complexity of the relationships between white matter structure and cognition. Although widespread and, sometimes, chronic abnormalities of white matter are identifiable following traumatic brain injury, the impact of these changes on cognitive function is likely to depend on damage to key pathways that link nodes in the distributed brain networks supporting high-level cognitive functions.
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