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Ischemic Lesions (ischemic + lesion)
Kinds of Ischemic Lesions Selected AbstractsImproved dynamic susceptibility contrast (DSC)-MR perfusion estimates by motion correctionJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2007Robert K. Kosior BSc Abstract Purpose To investigate the effect of patient motion on quantitative cerebral blood flow (CBF) maps in ischemic stroke patients and to evaluate the efficacy of a motion-correction scheme. Materials and Methods Perfusion data from 25 ischemic stroke patients were selected for analysis. Two motion profiles were applied to a digital anthropomorphic brain phantom to estimate accuracy. CBF images were generated for motion-corrupted and motion-corrected data. To correct for motion, rigid-body registration was performed. The realignment parameters and mean CBF in regions of interest were recorded. Results All patient data with motion exhibited visibly reduced intervolume misalignment after motion correction. Improved flow delineation between different tissues and a more clearly defined ischemic lesion (IL) were achieved in the motion-corrected CBF. A significant difference occurred in the IL (P < 0.05) for patients with severe motion with an average difference between corrupted and corrected data of 4.8 mL/minute/100 g. The phantom data supported the patient results with better CBF accuracy after motion correction and high registration accuracy (<1 mm translational and <1° rotational error). Conclusion Motion degrades flow differentiation between adjacent tissues in CBF maps and can cause ischemic severity to be underestimated. A registration motion correction scheme improves dynamic susceptibility contrast (DSC)-MR perfusion estimates. J. Magn. Reson. Imaging 2007;26:1167,1172. © 2007 Wiley-Liss, Inc. [source] Protein phosphatase 2A,negative regulation of the protective signaling pathway of Ca2+/CaM-dependent ERK activation in cerebral ischemiaJOURNAL OF NEUROSCIENCE RESEARCH, Issue 12 2008Jie Zhao Abstract Extracellular-signal-regulated kinase (ERK) undergoes rapid inactivation following the intense activation evoked by cerebral ischemia and reperfusion. However, the precise mechanism of this inactivation has not been elucidated. To investigate how phosphatases regulate the ERK cascade following ischemia, the PP2A inhibitors cantharidin and okadaic acid were administrated to the CA1 subregion of the rat hippocampus. The resulting sustained ERK activity implies that PP2A is a major phosphatase contributing to the rapid inactivation, but not activation, of ERK following cerebral ischemia. The increase in PP2A activity induced by ceramide has a weak effect on the activation of Raf via dephosphorylation of Ser259 in response to ischemia. In contrast, ketamine (Keta) and cyclosporine A (CsA), two chemicals that block calcium signal in ischemia, decrease ERK activity by blocking Raf dephosphorylation of Ser259. We also observed that activation of an upstream protein, Ras-GRF, leads to calcium/calmodulin-dependent activation of the ERK signaling cascade in response to ischemic stimuli. In addition, the activity of cyclic AMP response element-binding protein (CREB) and estrogen receptor , (ER,), target proteins of ERK and protective elements against ischemic lesion, parallels the activity of ERK. These data indicate that PP2A plays a significant role in blocking the protective effect induced by the ERK kinase pathway and that fast inactivation of ERK is the result of cross talk between calcium/calmodulin-dependent, positively regulated signal cascades and a ceramide-dependent negative signaling pathway. © 2008 Wiley-Liss, Inc. [source] Heterogeneous hyperactivity and distribution of ischemic lesions after focal cerebral ischemia in Mongolian gerbilsNEUROPATHOLOGY, Issue 4 2006Noriko Katsumata Various types of poststroke hyperactivity exist in humans, but studies of each mechanism using animal models are scarce. We aimed to analyze the heterogeneity of postischemic hyperlocomotion and to identify the ischemic lesions responsible for postischemic hyperlocomotion in rodent models of focal ischemia. Mongolian gerbils underwent right common carotid artery occlusion (CCAO) for 10 or 20 min. At 24 h, 2 days, and 7 days postischemia, we performed quantitative and qualitative locomotor analysis and correlated these results with the extent of ischemic lesions. Intermittent explosive hyperlocomotion was induced transiently in a 10-min CCAO group at 24 h after ischemia and continual unexplosive hyperlocomotion persisted for 7 days in the 20-min CCAO animals. Selective neuronal death, confined to the hippocampal cornu ammonis 1 (CA1), was observed in the 10-min CCAO group and widespread cortical and basal ganglia infarction was observed in the 20-min CCAO group. Amyloid precursor protein was transiently observed in the hippocampus at 24 h postischemia in the 10-min CCAO animals, while it was widely distributed over the ischemic regions throughout the 7 days postischemia in the 20-min CCAO animals. Incidence maps and correlation analysis revealed hippocampal neuronal death of the CA1 sector and widespread hemispheric infarction, including the cortex, as the region responsible for the 10-min and 20-min CCAO-induced hyperactivity, respectively. Two distinct types of locomotor hyperactivity were observed that varied with regard to the distribution of the ischemic lesion, that is, hippocampal neuronal death and widespread infarction involving the cortex. These two types of locomotor hyperactivity appear to be models of the different types of poststroke hyperactivity seen in stroke patients. [source] Sodium imaging intensity increases with time after human ischemic stroke,ANNALS OF NEUROLOGY, Issue 1 2009Muhammad S. Hussain MD Objective Establishing time of onset is important in acute stroke management. Current imaging modalities do not allow determination of stroke onset time. Although correlations between sodium magnetic resonance imaging signal intensity within ischemic lesions and time of onset have been shown in animal models, the relation to onset time has not been established in human stroke. Utilizing high-quality sodium images, we tested the hypothesis that sodium signal intensity increases with time from symptom onset in human ischemic stroke. Methods Twenty-one stroke patients (63 ± 15 years old) were scanned 4 to 104 hours after symptom onset. Follow-up images were obtained in 10 patients at 23 to 161 hours after onset, yielding a total of 32 time points. A standard stroke imaging protocol was acquired at 1.5 Tesla, followed by sodium magnetic resonance imaging at 4.7 Tesla. Relative sodium signal intensity within each lesion was measured with respect to the contralateral side. Results The sodium image quality was sufficient to visualize each acute lesion (lesion volume range, 1.7,217cm3). Relative sodium signal intensity increased nonlinearly over time after stroke onset. Sodium images acquired within 7 hours (n = 5) demonstrated a relative increase in lesion intensity of 10% or less, whereas the majority beyond 9 hours demonstrated increases of 23% or more, with an eventual leveling at 69 ± 18%. Interpretation Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55,62 [source] Negative fluid-attenuated inversion recovery imaging identifies acute ischemic stroke at 3 hours or less,ANNALS OF NEUROLOGY, Issue 6 2009Götz Thomalla MD Objective o evaluate the use of fluid-attenuated inversion recovery (FLAIR) imaging as surrogate marker of lesion age within the first 6 hours of ischemic stroke. Methods e analyzed FLAIR and diffusion-weighted imaging (DWI) sequences performed within 6 hours of symptom onset in 120 consecutive patients with ischemic stroke with known symptom onset. The visibility of acute ischemic lesions on FLAIR images was judged in two steps (on FLAIR alone and with knowledge of DWI) and compared with DWI. Results egative FLAIR in the case of positive DWI allocated ischemic lesions to a time window 3 hours or less with a high specificity (0.93) and a high positive predictive value (0.94), whereas sensitivity (0.48) and negative predictive value (0.43) were low. Lesion visibility on FLAIR images alone (35.6%) and with knowledge of DWI (62.5%) was lower than on DWI (97.1%). The sensitivity of FLAIR increased with increasing time from symptom onset from 27.0/50.0% , 3 hours to 56.7/93.3% after 3 to 6 hours (FLAIR alone/with knowledge of DWI). Multivariate regression analysis spotted longer time from symptom onset and larger size of the ischemic lesion as independent predictors of lesion visibility on FLAIR images. Interpretation "mismatch" between positive DWI and negative FLAIR allows the identification of patients that are highly likely to be within the 3-hour time window. Within the first 6 hours of stroke, the sensitivity of FLAIR sequences for acute ischemic lesions increases with time from symptom onset elapsing, approximating 100% after 3 to 6 hours. Ann Neurol 2009;65:724,732 [source] Prevalence of Anti-cardiolipin, Anti-,2 Glycoprotein I, and Anti-prothrombin Antibodies in Young Patients with EpilepsyEPILEPSIA, Issue 1 2002R. Cimaz Summary: ,Purpose: To measure anti-cardiolipin (aCL), anti-,2 glycoprotein I (anti-,2GPI), and anti-prothrombin (aPT) antibodies in young patients with epilepsy, and to correlate their presence with demographic data, clinical diagnoses, laboratory and neuroradiologic findings, and antiepileptic drugs (AEDs). Methods: Sera from one hundred forty-two consecutive patients with epilepsy with a median age of 10 years were tested for aCL and anti-,2GPI autoantibodies by solid-phase assays. aPT antibodies also were assayed in sera from 90 patients. Positive results were confirmed after a minimum of 6 weeks. Antinuclear antibodies (ANAs) and antibodies against extractable nuclear antigens (ENAs) also were tested. Results: An overall positivity of 41 (28.8%) of 142 sera was found. Fifteen patients were positive for aCL, 25 for anti-,2GPI, and 18 for aPT antibodies. Several patients (12%) displayed more than one specificity in their serum. Only one of these patients had a concurrent positivity for ANAs and ENAs. A predominance of younger patients was found in the antibody-positive group. All types of epilepsy were represented in the positive group. No relation between antibody positivity and AEDs was found. Diffuse ischemic lesions at computed tomography (CT)/magnetic resonance imaging (MRI) scans were present in higher percentages in patients who were antibody positive. No positive patient had a history of previous thrombosis or other features related to systemic lupus erythematosus (SLE), and no patient was born of a mother with SLE. Conclusions: Our study suggests a relation between epilepsy and aPL in young patients. A pathogenetic role for these autoantibodies cannot be excluded, and their determination might prove useful even from a therapeutic point of view. [source] Brain Apparent Water Diffusion Coefficient Magnetic Resonance Image During a Prolonged Visual AuraHEADACHE, Issue 6 2010Robert Belvís MD (Headache 2010;50:1045-1049) Background., Reversible changes in brain magnetic resonance imaging (MRI) weighted in diffusion-weighted images (DWI) and apparent water diffusion coefficient (ADC) maps have been reported in acute stroke, epilepsy, eclampsia, and hypoglycemia, but they are contradictory regarding to migraine aura. Objective., A 41-year-old woman with known basilar migraine for 5 years consulted about a persistent visual aura (visual snow phenomenon) plus bilateral paresthesias in the extremities for 4 days. The headache was treated with success with 10 mg of wafer rizatriptan and 600 mg of ibuprophen. Methods., The neurologic and ophthalmologic examination were normal. An urgent brain MRI detected no lesions in T1, T2, fluid-attenuated inversion recovery, and DWI, but an abnormal signal appeared in the left occipital lobe in ADC and (r)ADC maps. The brain MRI angiography, carotid ultrasound study, transesophageal echocardiography, 24-hour cardiac Holter monitoring, and thrombophilia study were normal. Results., A new brain MRI 8 days after did not show any previous lesion in the same sequences. Conclusions., We present a patient with migraine and transitory abnormal signals in the ADC map of an occipital region during persistent visual aura. The clinical-radiological relationship is congruent. Some similar cases have showed these MRI signals during the aura, suggesting cytotoxic edema, without ischemic lesions in the MRI controls. Theses ADC images probably appear in complex auras. [source] Subcortical lesions after transient thread occlusion in the rat: T2 -weighted magnetic resonance imaging findings without corresponding sensorimotor deficitsJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2005Susanne Wegener MD Abstract Purpose To investigate infarct evolution and functional consequences of exclusive subcortical or cortico-subcortical strokes, transient middle cerebral artery occlusion (MCAO) was conducted in Wistar rats. Materials and Methods MCAO was induced in male Wistar rats (260,300 g) for 60 minutes. Lesion volumes and absolute T2 times on magnetic resonance imaging (MRI) were assessed 1 and 14 days after MCAO using a 4.7-T MRI animal scanner in conjunction with functional testing (adhesive tape removal, cylinder test, and ledged beam walking). Results Functional test scores were not distinguishable between sham-operated animals (N = 5) and those with exclusive caudoputaminal infarct (N = 8; group cp), but showed significant deficits in animals with cortico-subcortical infarction (N = 10; group cp+). The cp group had lower absolute T2 times and a more pronounced reduction in T2 lesion volume over time than the subcortical component in the cp+ group. There was no correlation of T2 lesion size or absolute T2 times and functional impairment in either group. Conclusion When judged from functional tests alone, subcortical ischemic lesions may not be diagnosed reliably. Furthermore, T2 -weighted (T2 -w) MRI does not well anticipate functional deficits in primarily striatal lesions. J. Magn. Reson. Imaging 2005;21:340,346. © 2005 Wiley-Liss, Inc. [source] Delirium due to Brain Microembolism: Diagnostic Value of Diffusion-Weighted MRIJOURNAL OF NEUROIMAGING, Issue 2 2007Pablo Irimia MD ABSTRACT Delirum is a common complication in hospitalized patients and it is characterized by acute disturbances of consciousness, attention, cognition, and perception. Despite the frequency with which it is observed, ischemic stroke is generally considered as an unusual cause of delirium. A subtype of brain embolism is characterized by multiple small emboli in different vascular territories, a condition known as "brain microembolism." Given the high contrast of acute ischemic lesions in diffusion weighted imaging (DWI) this technique is particularly helpful to detect these small infarctions. We present here a patient with pulmonary metastases who was treated with bronchial artery embolization and who subsequently developed delirium due to brain microembolism. The embolic material crossed through pulmonary arteriovenous fistulas, producing multiple areas of cerebral ischemia. The ischemic lesions could be visualized only on DWI, and they affected the periventricular region, caudate nucleus, thalamus, and cerebellum. [source] Bilateral Internal Carotid Artery Dissection Mimicking Inflammatory Demyelinating DiseaseJOURNAL OF NEUROIMAGING, Issue 4 2003C. Lie MD ABSTRACT Background and Purpose. Internal carotid artery (ICA) dissection (ICAD) may be extremely difficult to diagnose only on the basis of historical information and clinical signs, and even standard brain imaging (computed tomography [CT], T2-weighted magnetic resonance imaging [MRI]) may not be sufficient to delineate the underlying pathology clearly, as shown in this case. Methods. The clinical presentation and parenchymal lesion pattern on CT were suggestive of inflammatory demyelinating disease, and additional multiparametric MRI was per-formed. Results. Diffusion-weighted MRI, magnetic resonance angiography, and perfusion-weighted MRI revealed acute ischemic lesions, bilateral ICA obstruction, and bilateral hypoperfusion in the middle cerebral artery territories. Bilateral ICAD was confirmed by Doppler and duplex ultrasound, and anticoagulation therapy was initiated. A follow-up examination showed recanalization of the obstructed ICAs and the normalization of cerebral perfusion. Conclusion. This case illustrates the importance of demonstrating the pathology and the value of multiparametric MRI techniques for the diagnosis and monitoring of ICAD and its hemodynamic consequences. [source] Moyamoya-disease-related ischemic stroke in the postpartum periodJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 5 2009Kei Miyakoshi Abstract Stroke during pregnancy or the puerperium is an extremely rare yet serious cause of perinatal morbidity and mortality. Moyamoya disease, a cerebrovascular occlusive pathology with a female predominance, may become symptomatic for the first time in association with pregnancy. A 36-year-old woman with postpartum pre-eclampsia suddenly developed hemiparesis in the left arm with dysarthria after the initiation of antihypertensive measures. Cranial magnetic resonance imaging and angiography revealed acute ischemic lesions in the right hemisphere along with the steno-occlusive lesions of bilateral terminal portions of the internal carotid artery, indicating Moyamoya disease. With anti-platelet medication, the patient recovered gradually and was diagnosed as having Moyamoya disease using conventional angiography 3 months postpartum. In this case, the fluctuations in blood pressure in association with pre-eclampsia appear to have exacerbated the clinical symptoms of Moyamoya disease. As such, Moyamoya disease should be considered as an underlying disease of ischemic stroke associated with pregnancy. [source] Corticobasal degeneration as cause of progressive non-fluent aphasia: Clinical, radiological and pathological study of an autopsy caseNEUROPATHOLOGY, Issue 6 2006Masaki Takao A Japanese male developed gradual loss of spontaneous speech at age 60. Three years later meaningful speech had deteriorated to the point that it had become restricted to monotonous utterances. Neuropsychological examination at age 62 showed that he had severe non-fluent aphasia. A brain MRI demonstrated mild cortical atrophy with ischemic lesions in the cerebral white matter. He was diagnosed as having primary progressive aphasia. At age 63, he was admitted to the hospital to reevaluate the neurological condition. Neurologic examination showed severe non-fluent aphasia, hyperreflexia, snout and sucking reflexes. No alien hand was observed. He was able to walk, dress, wash himself and use chopsticks as well as name real objects. At age 65, 99mTc-hexamethylpropyleneamine oxime single photon emission computed tomography (HMPAO-SPECT) revealed diffuse cerebral hypoperfusion that was particularly prominent in the left frontal lobe. An MRI showed progressive cortical atrophy with the definite atrophy of the left paracentral gyrus. The hippocampal formation and putamen were also atrophic. He died of pneumonia at age 67. The brain weighed 810 g with atrophy of the frontal lobe, globus pallidus, enlargement of the lateral ventricles and depigmentation of the substantia nigra. Microscopic examination showed severe neuronal loss and gliosis in the cerebral cortex, globus pallidus interna and substantia nigra. Ballooned neurons were observed in the cerebral cortex. Gallyas-Braak method revealed numerous astrocytic plaques and argentophilic threads in the cerebrum. Clinical diagnosis of corticobasal degeneration sometimes is difficult in individuals with atypical clinical presentations. More exact clinical and radiological criteria may warrant a diagnosis of corticobasal degeneration. [source] Heterogeneous hyperactivity and distribution of ischemic lesions after focal cerebral ischemia in Mongolian gerbilsNEUROPATHOLOGY, Issue 4 2006Noriko Katsumata Various types of poststroke hyperactivity exist in humans, but studies of each mechanism using animal models are scarce. We aimed to analyze the heterogeneity of postischemic hyperlocomotion and to identify the ischemic lesions responsible for postischemic hyperlocomotion in rodent models of focal ischemia. Mongolian gerbils underwent right common carotid artery occlusion (CCAO) for 10 or 20 min. At 24 h, 2 days, and 7 days postischemia, we performed quantitative and qualitative locomotor analysis and correlated these results with the extent of ischemic lesions. Intermittent explosive hyperlocomotion was induced transiently in a 10-min CCAO group at 24 h after ischemia and continual unexplosive hyperlocomotion persisted for 7 days in the 20-min CCAO animals. Selective neuronal death, confined to the hippocampal cornu ammonis 1 (CA1), was observed in the 10-min CCAO group and widespread cortical and basal ganglia infarction was observed in the 20-min CCAO group. Amyloid precursor protein was transiently observed in the hippocampus at 24 h postischemia in the 10-min CCAO animals, while it was widely distributed over the ischemic regions throughout the 7 days postischemia in the 20-min CCAO animals. Incidence maps and correlation analysis revealed hippocampal neuronal death of the CA1 sector and widespread hemispheric infarction, including the cortex, as the region responsible for the 10-min and 20-min CCAO-induced hyperactivity, respectively. Two distinct types of locomotor hyperactivity were observed that varied with regard to the distribution of the ischemic lesion, that is, hippocampal neuronal death and widespread infarction involving the cortex. These two types of locomotor hyperactivity appear to be models of the different types of poststroke hyperactivity seen in stroke patients. [source] MRI monitoring of focal cerebral ischemia in peroxisome proliferator-activated receptor (PPAR)-deficient miceNMR IN BIOMEDICINE, Issue 3 2007Jean-Baptiste Pialat Abstract Peroxisome proliferator-activated receptors (PPARs) are a potential target for neuroprotection in focal ischemic stroke. These nuclear receptors have major effects in lipid metabolism, but they are also involved in inflammatory processes. Three PPAR isotypes have been identified: ,, , (or ,) and ,. The development of PPAR transgenic mice offers a promising tool for prospective therapeutic studies. This study used MRI to assess the role of PPAR, and PPAR, in the development of stroke. Permanent middle cerebral artery occlusion induced focal ischemia in wild-type, PPAR, -null mice and PPAR, -null mice. T2 -weighted MRI was performed with a 7 T MRI scan on day 0, 1, 3, 7 and 14 to monitor lesion growth in the various genotypes. General Linear Model statistical analysis found a significant difference in lesion volume between wild-type and PPAR-null mice for both , and , isotypes. These data validate high-resolution MRI for monitoring cerebral ischemic lesions, and confirm the neuroprotective role of PPAR, and PPAR, in the brain. Copyright © 2007 John Wiley & Sons, Ltd. [source] Sodium imaging intensity increases with time after human ischemic stroke,ANNALS OF NEUROLOGY, Issue 1 2009Muhammad S. Hussain MD Objective Establishing time of onset is important in acute stroke management. Current imaging modalities do not allow determination of stroke onset time. Although correlations between sodium magnetic resonance imaging signal intensity within ischemic lesions and time of onset have been shown in animal models, the relation to onset time has not been established in human stroke. Utilizing high-quality sodium images, we tested the hypothesis that sodium signal intensity increases with time from symptom onset in human ischemic stroke. Methods Twenty-one stroke patients (63 ± 15 years old) were scanned 4 to 104 hours after symptom onset. Follow-up images were obtained in 10 patients at 23 to 161 hours after onset, yielding a total of 32 time points. A standard stroke imaging protocol was acquired at 1.5 Tesla, followed by sodium magnetic resonance imaging at 4.7 Tesla. Relative sodium signal intensity within each lesion was measured with respect to the contralateral side. Results The sodium image quality was sufficient to visualize each acute lesion (lesion volume range, 1.7,217cm3). Relative sodium signal intensity increased nonlinearly over time after stroke onset. Sodium images acquired within 7 hours (n = 5) demonstrated a relative increase in lesion intensity of 10% or less, whereas the majority beyond 9 hours demonstrated increases of 23% or more, with an eventual leveling at 69 ± 18%. Interpretation Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55,62 [source] Negative fluid-attenuated inversion recovery imaging identifies acute ischemic stroke at 3 hours or less,ANNALS OF NEUROLOGY, Issue 6 2009Götz Thomalla MD Objective o evaluate the use of fluid-attenuated inversion recovery (FLAIR) imaging as surrogate marker of lesion age within the first 6 hours of ischemic stroke. Methods e analyzed FLAIR and diffusion-weighted imaging (DWI) sequences performed within 6 hours of symptom onset in 120 consecutive patients with ischemic stroke with known symptom onset. The visibility of acute ischemic lesions on FLAIR images was judged in two steps (on FLAIR alone and with knowledge of DWI) and compared with DWI. Results egative FLAIR in the case of positive DWI allocated ischemic lesions to a time window 3 hours or less with a high specificity (0.93) and a high positive predictive value (0.94), whereas sensitivity (0.48) and negative predictive value (0.43) were low. Lesion visibility on FLAIR images alone (35.6%) and with knowledge of DWI (62.5%) was lower than on DWI (97.1%). The sensitivity of FLAIR increased with increasing time from symptom onset from 27.0/50.0% , 3 hours to 56.7/93.3% after 3 to 6 hours (FLAIR alone/with knowledge of DWI). Multivariate regression analysis spotted longer time from symptom onset and larger size of the ischemic lesion as independent predictors of lesion visibility on FLAIR images. Interpretation "mismatch" between positive DWI and negative FLAIR allows the identification of patients that are highly likely to be within the 3-hour time window. Within the first 6 hours of stroke, the sensitivity of FLAIR sequences for acute ischemic lesions increases with time from symptom onset elapsing, approximating 100% after 3 to 6 hours. Ann Neurol 2009;65:724,732 [source] MAP2 and neurogranin as markers for dendritic lesions in CNS injury.APMIS, Issue 2 2000An immunohistochemical study in the rat We compared two staining methods for the demonstration of dendrites under normal and pathological conditions of the rat central nervous system. MAP2- and neurogranin immunohistochemistry was applied to samples from normal tissue, spinal cord subjected to graded compression trauma, cerebral cortex following contusion trauma, and brains with focal ischemic lesions induced by occlusion of the middle cerebral artery (MCAO). Normal rats showed MAP2 immunoreactivity in nerve cell bodies and dendrites of brain and spinal cord. However, neurogranin staining was present only in nerve cell bodies and dendrites of the normal brain, and not in the spinal cord. Reduction of MAP2 immunoreactivity was seen in lesions of spinal cords subjected to compression trauma. Neurogranin staining was of no value in this experimental condition since it was not present under normal conditions. The brain contusions showed loss of both MAP2- and neurogranin immunoreactivity at the site of the lesion. MCAO resulted in an extensive loss of MAP2- and neurogranin staining in the ipsilateral hemisphere. In conclusion, our study shows that MAP2 immunostaining is a sensitive method for identifying dendritic lesions of various CNS injuries in the rat. Neurogranin immunostaining is an alternative method for investigations of dendritic pathology in the brain but not in the spinal cord. [source] Apraxia related with subcortical lesions due to cerebrovascular diseaseACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010N. E. Tabaki Tabaki NE, Vikelis M, Besmertis L, Vemmos K, Stathis P, Mitsikostas DD. Apraxia related with subcortical lesions due to cerebrovascular disease. Acta Neurol Scand: 2010: 122: 9,14. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, To examine whether ideomotor apraxia exists in patients with subcortical ischemic lesions. Patients and Methods,,, A matched-control, prospective and multi-centered research design was used. Ideomotor apraxia, anxiety and depression were assessed by the Movement Imitation Test and the Hamilton scales, respectively. Results,,, Forty two consecutive patients with subcortical ischemic stroke and an equal number of healthy participants, matched in age and sex were included. Paired-sample t-tests showed that patients had significantly more apractic elements in their movements (t = 5.03, P < 0.01), higher anxiety (t = ,2.55, P = 0.0014) and depression levels (t = ,2.61, P = 0.012) than their healthy matched participants. Participants with higher anxiety and depression scores performed worse on the Movement Imitation Test. Conclusions,,, Ischemic damage of subcortical modular systems may affect praxis. [source] | ||||||||||