Angiogenesis, Neurogenesis and Neuroplasticity in Ischemic Stroke

Only very little is know about the neurovascular niche after cardioembolic stroke. Three processes implicated in neurorepair: angiogenesis, neurogenesis and synaptic plasticity, would be naturally produced in adult brains, but also could be stimulated through endogen neurorepair phenomena. Angiogenesis stimulation generates new vessels with the aim to increase collateral circulation. Neurogenesis is controlled by intrinsic genetic mechanisms and growth factors but also ambiental factors are important. The leading process of the migrating neural progenitor cells (NPCs) is closely associated with blood vessels, suggesting that this interaction provides directional guidance to the NPCs. These findings suggest that blood vessels play an important role as a scaffold for NPCs migration toward the damaged brain region. DNA microarray technology and blood genomic profiling in human stroke provided tools to investigate the expression of thousands of genes. Critical comparison of gene expression profiles after stroke in humans with those in animal models should lead to a better understanding of the pathophysiology of brain ischaemia. Probably the most important part of early recovery after stroke is limited capacity of penumbra/infarct neurones to recover. It became more clear in the last years, that penumbra is not just passively dying over time but it is also actively recovering. This initial plasticity in majority contributes towards later neurogenesis, angiogenesis and final recovery. Penumbra is a principal target in acute phase of stroke. Thus, the origin of newly formed vessels and the pathogenic role of neovascularization and neurogenesis are important unresolved issues in our understanding of the mechanisms after stroke. Biomaterials for promoting brain protection, repair and regeneration are new hot target. Recently developed biomaterials can enable and increase the target delivery of drugs or therapeutic proteins to the brain, allow cell or tissue transplants to be effectively delivered to the brain and help to rebuild damaged circuits. These new approaches are gaining clear importance because nanotechnology allows better control over material-cell interactions that induce specific developmental processes and cellular responses including differentiation, migration and outgrowth

Transient Global Amnesia Associated with an Acute Infarction at the Cingulate Gyrus

Background. Transient global amnesia (TGA) is a syndrome of sudden, unexplained isolated short-term memory loss. In the majority of TGA cases, no causes can be identified and neuroimaging, CSF studies and EEG are usually normal. We present a patient with TGA associated with a small acute infarct at the cingulate gyrus. Case Report. The patient, a 62 year-old man, developed two episodes of TGA. He had hypertension and hypercholesterolemia. He was found to have an acute ischemic stroke of small size (15 mm of maximal diameter) at the right cerebral cingulate gyrus diagnosed on brain magnetic resonance imaging. No lesions involving other limbic system structures such as thalamus, fornix, corpus callosum, or hippocampal structures were seen. The remainder of the examination was normal. Conclusion. Unilateral ischemic lesions of limbic system structures may result in TGA. We must bear in mind that TGA can be an associated clinical disorder of cingulate gyrus infarct

Transient global amnesia associated with an acute infarction at the cingulate gyrus.

Journal Article;Background. Transient global amnesia (TGA) is a syndrome of sudden, unexplained isolated short-term memory loss. In the majority of TGA cases, no causes can be identified and neuroimaging, CSF studies and EEG are usually normal. We present a patient with TGA associated with a small acute infarct at the cingulate gyrus. Case Report. The patient, a 62 year-old man, developed two episodes of TGA. He had hypertension and hypercholesterolemia. He was found to have an acute ischemic stroke of small size (15 mm of maximal diameter) at the right cerebral cingulate gyrus diagnosed on brain magnetic resonance imaging. No lesions involving other limbic system structures such as thalamus, fornix, corpus callosum, or hippocampal structures were seen. The remainder of the examination was normal. Conclusion. Unilateral ischemic lesions of limbic system structures may result in TGA. We must bear in mind that TGA can be an associated clinical disorder of cingulate gyrus infarct.Ye

Transient global amnesia associated with an acute infarction at the cingulate gyrus.

Journal Article;Background. Transient global amnesia (TGA) is a syndrome of sudden, unexplained isolated short-term memory loss. In the majority of TGA cases, no causes can be identified and neuroimaging, CSF studies and EEG are usually normal. We present a patient with TGA associated with a small acute infarct at the cingulate gyrus. Case Report. The patient, a 62 year-old man, developed two episodes of TGA. He had hypertension and hypercholesterolemia. He was found to have an acute ischemic stroke of small size (15 mm of maximal diameter) at the right cerebral cingulate gyrus diagnosed on brain magnetic resonance imaging. No lesions involving other limbic system structures such as thalamus, fornix, corpus callosum, or hippocampal structures were seen. The remainder of the examination was normal. Conclusion. Unilateral ischemic lesions of limbic system structures may result in TGA. We must bear in mind that TGA can be an associated clinical disorder of cingulate gyrus infarct.Ye

Papel de las placas complejas de ateroma aórtico en la recurrencia del infarto cerebral de etiología incierta

Introducción y objetivos. En un subgrupo de pacientes con infarto cerebral, las exploraciones diagnósticas no invasivas no permiten establecer un diagnóstico etiológico. Hemos estudiado su evolución y el valor del ecocardiograma transesofágico en el diagnóstico del ateroma complejo aórtico en pacientes con infarto cerebral de etiología incierta que presentan recurrencia. Pacientes y método. Al evaluar a 1.840 pacientes consecutivos con un primer infarto cerebral mediante un protocolo restrictivo para la ecocardiografía transesofágica, en 248 no pudo establecerse un diagnóstico etiológico. Durante 1 año de seguimiento con fármacos antiplaquetarios, se practicó un ecocardiograma transesofágico en caso de nuevo episodio isquémico cerebral. Se comparó la prevalencia de placas complejas aórticas en estos pacientes con recurrencia respecto a la de los infartos cerebrales de etiología incierta del French Study of Aortic Plaques in Stroke que no presentaron un segundo infarto cerebral. Resultados. Presentaron un segundo infarto cerebral 17 de los 248 pacientes con etiología incierta (6,9%). El ecocardiograma transesofágico estableció la etiología en 15 de ellos (88,2%), que fue atribuida a placas complejas de ateroma aórtico en 14 casos (82,4%). En cambio, entre los pacientes del French Study con infarto cerebral de etiología incierta que no presentaron reinfarto cerebral durante el primer año de seguimiento, la prevalencia de placas complejas aórticas fue del 21,1% (p < 0,0001). Conclusiones. Durante el primer año de seguimiento con antiagregantes, la mayoría de los pacientes con infarto cerebral de etiología incierta no presenta recurrencia. En el subgrupo con recurrencia isquémica cerebral, el ecocardiograma transesofágico permite establecer el diagnóstico definitivo en el 88,2% de los casos; la principal etiología implicada es la ateromatosis avanzada de la aorta torácica