ABSTRACT
Existen pocos estudios evaluando los factores de riesgo para el desarrollo de epilepsia posterior a un ictus isquémico arterial (IIA) en la infancia. Objetivo: Evaluar los predictores clínicos y radiológicos para epilepsia post-ictus (EPI) en una cohorte de niños chilenos con un primer IIA. Metodología: Estudio analítico longitudinal observacional prospectivo de una cohorte de niños con diagnóstico de IIA entre 1 mes y 18 años, enrolados de forma consecutiva en la base de datos de Patología Cerebrovascular del Hospital Clínico de la Pontificia Universidad Católica de Chile entre los años 2003 y 2013. Todos los participantes con imágenes por resonancia magnética encefálica al momento del diagnóstico. Las variables estudiadas incluyeron características clínicas y radiológicas del evento agudo asociadas a EPI según estudios previos. Creamos un modelo multivariado por regresión logística para estimar los Odds Ratios (ORs) y sus respectivos intervalos de confianza al 95% (ICs) de cada variable estudiada para EPI (significancia <0,05). Resultados: De 81 niños reclutados, 41 (50,6%) con EPI. El análisis multivariado determinó que los predictores independientes de EPI incluyen edad menor al momento del IIA (OR=0,81; IC=0,69-0,95), ocurrencia de crisis sintomáticas agudas (OR=8,63; IC=2,03-36,7), infarto cortical (OR=17,2; IC=3,12-95,3) y arteriopatías del sistema nervioso central (OR=12; IC=1,47-97,8). Conclusiones: las crisis agudas, menor edad, infarto cortical y arteriopatías son factores de riesgo independientes para EPI en niños con un primer IIA. Palabras clave: accidente vascular encefálico pediátrico; epilepsia postictal, ictus isquémico, arteriopatía, infarto cortical.
Abstract. There are few studies evaluating the risk factors for the development of epilepsy after an arterial ischemic stroke (IIA) in childhood. Objective: To assess the clinical and radiological predictors for epilepsy post-stroke (EPI) in a cohort of Chilean children with a first IIA. Methodology: prospective observational longitudinal analytical study of a cohort of children with a IIA diagnosis, from 1 month to 18 years old, consecutively enrolled in the brain stroke database of the Hospital of the Pontificia Universidad Católica de Chile between 2003 and 2013. All participants had a brain magnetic resonance performed at the time of the diagnosis. The variables studied included clinical and radiological features of the acute event associated to EPI according to previous studies. We created a multivariate logistic regression model to estimate the Odds Ratios (ORs) and their respective intervals of confidence 95% (ICs) of each variable studied for EPI (significance < 0,05). Results: of 81 children recruited, 41 (50.6%) had EPI. The multivariate analysis determined that the independent predictors of PPE include: younger age at the time of the IIA (OR = 0. 81; IC = 0, 69-0, 95), occurrence of acute symptomatic crisis (OR = 8, 63; IC = 2, 03-36, 7), cortical infarction (OR = 17, 2; IC = 3, 12-95, 3) and arteriopathies of the central nervous system (OR = 12; IC = 1, 47-97, 8). Conclusions: acute crises, younger age, cortical infarction and arterial disease are independent risk factors for EPI in children with a first IIA.Key words: Pediatric brain vascular accident; epilepsy postictal, ischemic stroke, arterial disease, cortical infarction
ABSTRACT
Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.
ABSTRACT
Predominant involvement of a particular group of fingers due to a central nervous system lesion has been described as pseudoperipheral palsy. Two patients visited our hospital with isolated weakness of a particular group of fingers due to small cortical infarctions. A 51-year-old woman suddenly developed weakness in her left index and middle fingers. The brain MRI showed a small infarct in the right frontal cortex. A 67-year-old man was sudden difficulty using his chopsticks and had weakness in his right thumb and index finger. The brain MRI showed a small infarct in the left precentral cortex.
Subject(s)
Aged , Female , Humans , Middle Aged , Brain , Central Nervous System , Fingers , Infarction , Magnetic Resonance Imaging , Paralysis , ThumbABSTRACT
Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.
ABSTRACT
Foot drop usually results from lesions affecting the peripheral neural pathway related to dorsiflexor muscles, especially the peroneal nerve. Although a central nervous system lesion is suspected when there is a lack of clinical evidence for a lower motor neuron lesion, such cases are extremely rare. We describe a patient with sudden isolated foot drop caused by a small acute cortical infarction in the high convexity of the precentral gyrus. This report indicates that a cortical infarction may have to be considered as a potential cause of foot drop.
Subject(s)
Humans , Central Nervous System , Cerebral Infarction , Foot , Infarction , Motor Neurons , Muscles , Neural Pathways , Peroneal NerveABSTRACT
Small cortical infarctions can produce isolated motor paresis in the upper extremities. Several cases of isolated hand or finger paresis have been reported, but isolated shoulder weakness is extremely rare. We report here a patient who developed isolated shoulder weakness due to a small cortical infarction in the medial precentral gyrus.
Subject(s)
Humans , Fingers , Hand , Infarction , Paresis , Shoulder , Upper ExtremityABSTRACT
Small cortical strokes can produce predominant isolated weakness in a particular group of fingers: radial or ulnar. The traditional views are of point-to-point representations of each finger to neurons located in the precentral gyrus of the motor cortex such that the neurons of the radial fingers are located laterally and those of the ulnar fingers are located medially. We present a case of isolated weakness of middle, ring, and little fingers due to a small cortical infarction in the medial precentral gyrus.
Subject(s)
Fingers , Infarction , Motor Cortex , Neurons , StrokeABSTRACT
With the development of electrophysiologic technique, a more detailed topographical organizations of motor cortex, especially hand area have been introduced in animal experiment. To the best our knowledge, in cerebral infarction, only one patient with isolated weakness of intrinsic hand muscles has been reported. We present two patients with cerebral infarction who showed isolated weakness in their intrinsic hand. Patient 1; A 76-year-old woman with coronary artery obstructive disease developed abrupt weakness in flexion of right thumb, index, middle finger and in adduction of thumb. Brain MRI showed a small discrete lesion in the posterior bank of left precentral gyrus. An angiography revealed an occlusion of left central sulcus artery. Prominent thumb adduction weakness was remained 11 days later. Patient 2; A 57-year-old hypertensive man was admitted because of recurrent TIA and decreased grasp power of right hand, especially flexion and adduction of thumb, index finger and middle finger. Brain MRI showed focal lamina necrosis in left precentral gyrus. An angiography revealed an occlusion of left internal carotid artery. Findings in our patients suggest that the similar arrangement of efferent zone for cortical hand area found in monkeys also may exist in human beings.