Following stroke, complete cellular death in the ischemic brain area may ensue, with remaining brain areas undergoing tissue remodelling to various degrees. Experience-dependent brain plasticity exerted through an enriched environment (EE) promotes remodelling after central nervous system injury, such as stroke. Post-stroke tissue reorganization is modulated by growth inhibitory molecules differentially expressed within the ischemic hemisphere, like chondroitin sulfate proteoglycans found in perineuronal nets (PNNs). PNNs in the neocortex predominantly enwrap parvalbumin-containing GABAergic (PV/GABA) neurons, important in sensori-information processing. Here, we investigate how extracellular matrix (ECM) proteases and their inhibitors may participate in the regulation of PNN integrity during stroke recovery. Rats were subjected to photothrombotic stroke in the motor cortex, and functional deficits were assessed at 7 days of recovery. Sham and stroked rats were housed in either standard or EE conditions for 5 days, and infarct volumes were calculated. PNNs were visualized by immunohistochemistry and counted in the somatosensory cortex of both hemispheres. mRNA expression levels of ECM proteases and protease inhibitors were assessed by RT-qPCR and their activity analyzed by gel zymography. PNNs and protease activity were also studied in brains from stroke patients where similar results were observed. EE starting 2 days after stroke and continuing for 5 days stimulated behavioral recovery of limb-placement ability without affecting infarct size. EE promoted a decrease of PNNs around PV/GABA neurons and a concomitant modulation of the proteolytic activity and mRNA expression of ECM proteases and protease inhibitors in the somatosensory cortex. This study provides molecular targets for novel therapies that could support rehabilitation of stroke patients.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-017-0461-2) contains supplementary material, which is available to authorized users.
Background
Parkinsonian variant of multiple system atrophy is a neurodegenerative disorder frequently misdiagnosed as Parkinson’s disease. No early imaging biomarkers currently differentiate these disorders.
Methods
Simple visual imaging analysis of the substantia nigra and locus coeruleus in neuromelanin-sensitive magnetic resonance imaging and nigrosome 1 in susceptibility-weighted sequences was performed in thirty patients with parkinsonian variant of multiple system atrophy fulfilling possible/probable second consensus diagnostic criteria. The neuromelanin visual pattern was compared to patients with Parkinson’s disease with the same disease duration (n = 10) and healthy controls (n = 10). Substantia nigra semi-automated neuromelanin area/signal intensity was compared to the visual data.
Results
Groups were similar in age, sex, disease duration, and levodopa equivalent dose. Hoehn & Yahr stage was higher in parkinsonian multiple system atrophy patients, 69% of whom had normal neuromelanin size/signal, significantly different from Parkinson’s disease patients, and similar to controls. Nigrosome 1 signal was lost in 74% of parkinsonian multiple system atrophy patients. Semi-automated neuromelanin substantia nigra signal, but not area, measurements were able to differentiate groups.
Conclusions
In patients with parkinsonism, simple visual magnetic resonance imaging analysis showing normal neuromelanin substantia nigra and locus coeruleus, combined with nigrosome 1 loss, allowed the distinction of the parkinsonian variant of multiple system atrophy from Parkinson’s disease and healthy controls. This easy and widely available method was superior to semi-automated measurements in identifying specific imaging changes in substantia nigra and locus coeruleus.
Ménière's disease (MD) is a clinical syndrome characterized by recurrent episodes of spontaneous vertigo, unilateral fluctuating sensorineural hearing loss, tinnitus, and aural fullness. Endolymphatic hydrops is recognized as the pathophysiological substrate of the disease, having been demonstrated in anatomical pathological studies and more recently by magnetic resonance imaging (MRI). The current criteria of the disease, however, remain symptom based and do not include the demonstration of endolymphatic hydrops. The authors review MRI techniques and diagnostic criteria of endolymphatic hydrops and the role of MRI in MD is discussed.
Background: Menière's disease (MD) is an inner ear disorder characterized by recurrent episodes of spontaneous vertigo, unilateral low-frequency sensorineural hearing loss, tinnitus, and aural fullness. Current diagnosis still often has to rely on subjective and audiometric criteria only, although endolymphatic hydrops is recognized as the pathophysiological substrate of the disease, having been demonstrated in anatomical pathological studies and by magnetic resonance (MRI). The modiolus has a close functional and anatomical relationship with the cochlear nerve and membranous labyrinth and can be evaluated with MRI but no data exist on the modiolar size in MD.Purpose: Our purpose is to examine the following hypothesis. Is cochlear modiolus smaller in symptomatic ears in MD?Methods: We used a retrospective 3 Tesla MR study (heavily T2-weighted 3D fast asymmetric spin-echo images and 0.5 mm slice thickness) comparing the mean modiolar area (MMA) in the index and best ears of eight patients with definite MD based on audiometric data. The obtained MMA values were compared against the audiometric data and the presence of vestibular endolymphatic hydrops.Results: No differences were seen in MMA between best and worst ears. Ears with a pure tone average (PTA) ≥25 dB and more pronounced endolymphatic hydrops showed lower MMA (not statistically significant). Two patients with extreme endolymphatic hydrops showed a noteworthy ipsilateral decrease in the cochlear modiolus area.Conclusion: No differences were seen in MMA between best and worst ears in definite MD. Worse hearing function (PTA ≥ 25dB) and more pronounced endolymphatic hydrops seem to be associated with lower MMA. This might be related to bone remodeling as a consequence of endolymphatic hydrops. Further research is needed to corroborate and explore these findings.
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