Hannay HJ, Walker A, Dennis M, Kramer L, Blaser S, Fletcher JM. Auditory interhemispheric transfer in relation to patterns of partial agenesis and hypoplasia of the corpus callosum in spina bifida meningomyelocele. Journal of International Neuropsychology Society. 2008 Sep;14(5):771-81.
Department of Psychology, University of Houston, Houston, Texas 77204-5052, USA. jhannay@uh.edu
Spina bifida meningomyelocele with hydrocephalus (SBM) is commonly associated with anomalies of the corpus callosum (CC). We describe MRI patterns of regional CC agenesis and relate CC anomalies to functional laterality based on a dichotic listening test in 90 children with SBM and 27 typically developing controls. Many children with SBM (n = 40) showed regional CC anomalies in the form of agenesis of the rostrum and/or splenium, and a smaller number (n = 20) showed hypoplasia (thinning) of all CC regions (rostrum, genu, body, and splenium). The expected right ear advantage (REA) was exhibited by normal controls and children with SBM having a normal or hypoplastic splenium. It was not shown by children with SBM who were left handed, missing a splenium, or had a higher level spinal cord lesion. Perhaps the right hemisphere of these children is more involved in processing some aspects of linguistic stimuli.
PMID: 18764972
Thursday, January 8, 2009
Partial agenesis of the corpus callosum in spina bifida meningomyelocele and potential compensatory mechanisms.
Hannay HJ, Dennis M, Kramer L, Blaser S, Fletcher JM. (2009) Partial agenesis of the corpus callosum in spina bifida meningomyelocele and potential compensatory mechanisms.
Journal of Clinical and Experimental Neuropsychology. 2009 Feb;31(2):180-94.
After a review of Arthur Benton's conceptual and methodological contributions to the understanding of normal and pathological development, we discuss agenesis of the corpus callosum (CC), criteria for potential neuroanatomical compensatory mechanisms in CC agenesis, and the results of an examination of magnetic resonance imaging (MRI) data of the CC in 193 children with spina bifida meningomyelocele (SBM). There were 26 CC regional patterns. Although complete agenesis did not occur, partial agenesis was observed in 102 children and within 15 CC regional patterns. Only 4.1% had a normal CC. Quantitative assessment of the area of the CC in 26 NC children and 68 children with SBM revealed that all subgroups with CC anomalies had smaller areas than did a subgroup with a normal CC. Areas were especially small in rostral/splenial agenesis and splenial agenesis but larger with rostral agenesis. Subgroups with normal/hypoplastic regions or complete hypoplasia also had CC areas that were smaller than normal but larger than the areas for the splenial agenesis groups. The relative rarity of anterior commissure enlargement (3.1%) and longitudinal bundles of Probst (0.1%) suggest that these particular fiber tract anomalies are unlikely candidates for structural compensatory mechanisms. The hippocampal commissure, enlarged in 13%, may be a more promising candidate. Overall, however, the functionality of anomalous fiber tracts and commissures in SBM is yet to be determined.
PMID: 19052950
Journal of Clinical and Experimental Neuropsychology. 2009 Feb;31(2):180-94.
After a review of Arthur Benton's conceptual and methodological contributions to the understanding of normal and pathological development, we discuss agenesis of the corpus callosum (CC), criteria for potential neuroanatomical compensatory mechanisms in CC agenesis, and the results of an examination of magnetic resonance imaging (MRI) data of the CC in 193 children with spina bifida meningomyelocele (SBM). There were 26 CC regional patterns. Although complete agenesis did not occur, partial agenesis was observed in 102 children and within 15 CC regional patterns. Only 4.1% had a normal CC. Quantitative assessment of the area of the CC in 26 NC children and 68 children with SBM revealed that all subgroups with CC anomalies had smaller areas than did a subgroup with a normal CC. Areas were especially small in rostral/splenial agenesis and splenial agenesis but larger with rostral agenesis. Subgroups with normal/hypoplastic regions or complete hypoplasia also had CC areas that were smaller than normal but larger than the areas for the splenial agenesis groups. The relative rarity of anterior commissure enlargement (3.1%) and longitudinal bundles of Probst (0.1%) suggest that these particular fiber tract anomalies are unlikely candidates for structural compensatory mechanisms. The hippocampal commissure, enlarged in 13%, may be a more promising candidate. Overall, however, the functionality of anomalous fiber tracts and commissures in SBM is yet to be determined.
PMID: 19052950
Neonatal high pressure hydrocephalus is associated with elevation of pro-inflammatory cytokines IL-18 and IFNg in cerebrospinal fluid
Sival DA, Felderhoff-Muser U, Schmitz T, Hoving EW, Schaller C, Heep A. Neonatal high pressure hydrocephalus is associated with elevation of pro-inflammatory cytokines IL-18 and IFNg in cerebrospinal fluid. Cerebrospinal Fluid Research. 2008 Dec 31;5(1):21.
ABSTRACT: BACKGROUND: In human neonatal high pressure hydrocephalus (HPHC), diffuse white matter injury and gliosis predispose to poor neuro-developmental outcome. The underlying mechanism for diffuse white matter damage in neonatal HPHC is still unclear. Analogous to inflammatory white matter damage after neonatal hypoxemia/ischemia, we hypothesized that pro-inflammatory cytokines could be involved in neonatal HPHC. If so, early anti-inflammatory therapy could ameliorate white matter damage in HPHC, before irreversible apoptosis has occurred. In HPHC and control neonates, we therefore aimed to compare cerebrospinal fluid (CSF) concentrations of IL18, IFNgamma and sFasL (interleukin 18, interferon gamma and apoptosis marker soluble-Fas ligand, respectively).
METHODS: In neonatal HPHC (n=30) and controls (n=15), we compared CSF concentrations of IL18, IFNgamma and sFasL using sandwich ELISA. HPHC was grouped according to etiology: spina bifida aperta (n=20), aqueduct stenosis (n=4), and fetal intra-cerebral haemorrhage (n=6). Neonatal control CSF was derived from otherwise healthy neonates (n=15), who underwent lumbar puncture for exclusion of meningitis.
RESULTS: In all three HPHC groups, CSF IL18 concentrations were significantly higher than control values, and the fetal intracranial haemorrhage group was significantly higher than SBA group. Similarly, in all HPHC groups CSF-IFNgamma concentrations significantly exceeded the control group. In both HPHC and control neonates, CSF FasL concentrations remained within the range of reference values.
CONCLUSION: Independent of the pathogenesis, neonatal HPHC is associated with the activation of the pro-inflammatory cytokines (IL-18 and IFNgamma) in the CSF, whereas CSF apoptosis biomarkers (sFasL) were unchanged. This suggests that anti-inflammatory treatment (in addition to shunting) could be helpful to preserve cerebral white matter.
PMID: 19117508
ABSTRACT: BACKGROUND: In human neonatal high pressure hydrocephalus (HPHC), diffuse white matter injury and gliosis predispose to poor neuro-developmental outcome. The underlying mechanism for diffuse white matter damage in neonatal HPHC is still unclear. Analogous to inflammatory white matter damage after neonatal hypoxemia/ischemia, we hypothesized that pro-inflammatory cytokines could be involved in neonatal HPHC. If so, early anti-inflammatory therapy could ameliorate white matter damage in HPHC, before irreversible apoptosis has occurred. In HPHC and control neonates, we therefore aimed to compare cerebrospinal fluid (CSF) concentrations of IL18, IFNgamma and sFasL (interleukin 18, interferon gamma and apoptosis marker soluble-Fas ligand, respectively).
METHODS: In neonatal HPHC (n=30) and controls (n=15), we compared CSF concentrations of IL18, IFNgamma and sFasL using sandwich ELISA. HPHC was grouped according to etiology: spina bifida aperta (n=20), aqueduct stenosis (n=4), and fetal intra-cerebral haemorrhage (n=6). Neonatal control CSF was derived from otherwise healthy neonates (n=15), who underwent lumbar puncture for exclusion of meningitis.
RESULTS: In all three HPHC groups, CSF IL18 concentrations were significantly higher than control values, and the fetal intracranial haemorrhage group was significantly higher than SBA group. Similarly, in all HPHC groups CSF-IFNgamma concentrations significantly exceeded the control group. In both HPHC and control neonates, CSF FasL concentrations remained within the range of reference values.
CONCLUSION: Independent of the pathogenesis, neonatal HPHC is associated with the activation of the pro-inflammatory cytokines (IL-18 and IFNgamma) in the CSF, whereas CSF apoptosis biomarkers (sFasL) were unchanged. This suggests that anti-inflammatory treatment (in addition to shunting) could be helpful to preserve cerebral white matter.
PMID: 19117508
Neurotrophic factor expression in newborns with myelomeningocele: preliminary data.
Chiaretti A, Ausili E, Di Rocco C, Antonelli A, Tabacco F, Focarelli B, Rendeli C. Neurotrophic factor expression in newborns with myelomeningocele: preliminary data. European Journal of Pediatric Neurololgy. 2008 Mar;12(2):113-8.
BACKGROUND: Neurotrophic factors play a crucial role in the stimulation of sprouting, synaptic plasticity and reorganization after spinal cord damage. The aim of this study was to investigate the expression of some neurotrophic factors [brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), and nerve growth factor (NGF)] in the cerebrospinal fluid (CSF) of newborns with myelomeningocele (MMC) and to determine their correlations with this malformation.
METHODS: To measure the expression of BDNF, GDNF, and NGF, we collected CSF samples of six newborns during the neurosurgical operation to correct the open MMC and of 10 matched controls. Endogenous neurotrophic factor levels were quantified using a two-site immuno-enzymatic assay. The statistical analysis was performed using the Mann-Whitney two-tailed two-sample test.
FINDINGS: In the CSF of patients analysis of neurotrophic factor expression showed a significant increase of BDNF, GDNF, and NGF compared to the mean level of the control group (445.8+/-82.3, 86.5+/-2.6, and 59.9+/-6.2 pg/mL, respectively, respect to 10.2+/-5.9, 19.9+/-11.3, and 15.3+/-2.6 pg/mL) (p<0.001).
INTERPRETATION: Our study shows an over-expression of neurotrophic factors in the CSF of newborns with MMC. This neurotrophin up-regulation may stimulate axonal sprouting and synaptic reorganization of the damaged neural cells at the site of spinal cord lesion. The neurotrophic factor up-regulation may represent a particularly important biochemical markers of spinal cord damage and might be associated with the severity of spine injury in MMC patients.
PMID: 17881265
BACKGROUND: Neurotrophic factors play a crucial role in the stimulation of sprouting, synaptic plasticity and reorganization after spinal cord damage. The aim of this study was to investigate the expression of some neurotrophic factors [brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), and nerve growth factor (NGF)] in the cerebrospinal fluid (CSF) of newborns with myelomeningocele (MMC) and to determine their correlations with this malformation.
METHODS: To measure the expression of BDNF, GDNF, and NGF, we collected CSF samples of six newborns during the neurosurgical operation to correct the open MMC and of 10 matched controls. Endogenous neurotrophic factor levels were quantified using a two-site immuno-enzymatic assay. The statistical analysis was performed using the Mann-Whitney two-tailed two-sample test.
FINDINGS: In the CSF of patients analysis of neurotrophic factor expression showed a significant increase of BDNF, GDNF, and NGF compared to the mean level of the control group (445.8+/-82.3, 86.5+/-2.6, and 59.9+/-6.2 pg/mL, respectively, respect to 10.2+/-5.9, 19.9+/-11.3, and 15.3+/-2.6 pg/mL) (p<0.001).
INTERPRETATION: Our study shows an over-expression of neurotrophic factors in the CSF of newborns with MMC. This neurotrophin up-regulation may stimulate axonal sprouting and synaptic reorganization of the damaged neural cells at the site of spinal cord lesion. The neurotrophic factor up-regulation may represent a particularly important biochemical markers of spinal cord damage and might be associated with the severity of spine injury in MMC patients.
PMID: 17881265
GDNF Plasma Levels in Spina Bifida: Correlation with Severity of Spinal Damage and Motor Function
Chiaretti A, Rendeli C, Antonelli A, Barone G, Focarelli B, Tabacco F, Massimi L, Ausili E. GDNF Plasma Levels in Spina Bifida: Correlation with Severity of Spinal Damage and Motor Function. Journal of Neurotrauma. 2009 Jan 6.
Abstract Glial-derived neurotrophic factor (GDNF) is one of several powerful survival factors for spinal motoneurons that play a key role in sprouting, synaptic plasticity, and reorganization after spinal cord damage. The aim of this study was to investigate the expression of GDNF in plasma of children with spina bifida (SB) and to determine its correlation with both the severity of spinal cord damage and the motor function of these patients. To measure the GDNF expression, we collected plasma samples from 152 children with SB and in 149 matched controls. Endogenous GDNF levels were quantified using a two-site immuno-enzymatic assay. The statistical analysis was performed using the Mann-Whitney two-tailed two-sample test. In children with SB the mean levels of GDNF (131.2 +/- 69.6 pg/mL) were significantly higher (p < 0.001) with respect to the mean levels of the control group (102.7 +/- 6.8 pg/mL). Moreover, in open SB, the GDNF levels (139.2 +/- 81.1 pg/mL) were significantly higher (p < 0.05) with respect to closed SB (117.2 +/- 41.3 pg/mL). In terms of the motor function of patients, we found that in children with poorer motor function, the GDNF levels (134.5 +/- 67.4 pg/mL) were higher, but not statistically significant (p < 0.1), than in patients with better motor outcome (122.3 +/- 72.2 pg/mL). Our study demonstrates GDNF over-expression in children with SB. This upregulation is significantly associated with the severity of spinal cord damage in SB patients and appears to correlate with poor motor function of children, representing an important biochemical marker of the severity of spine injury.
PMID: 19125682
Abstract Glial-derived neurotrophic factor (GDNF) is one of several powerful survival factors for spinal motoneurons that play a key role in sprouting, synaptic plasticity, and reorganization after spinal cord damage. The aim of this study was to investigate the expression of GDNF in plasma of children with spina bifida (SB) and to determine its correlation with both the severity of spinal cord damage and the motor function of these patients. To measure the GDNF expression, we collected plasma samples from 152 children with SB and in 149 matched controls. Endogenous GDNF levels were quantified using a two-site immuno-enzymatic assay. The statistical analysis was performed using the Mann-Whitney two-tailed two-sample test. In children with SB the mean levels of GDNF (131.2 +/- 69.6 pg/mL) were significantly higher (p < 0.001) with respect to the mean levels of the control group (102.7 +/- 6.8 pg/mL). Moreover, in open SB, the GDNF levels (139.2 +/- 81.1 pg/mL) were significantly higher (p < 0.05) with respect to closed SB (117.2 +/- 41.3 pg/mL). In terms of the motor function of patients, we found that in children with poorer motor function, the GDNF levels (134.5 +/- 67.4 pg/mL) were higher, but not statistically significant (p < 0.1), than in patients with better motor outcome (122.3 +/- 72.2 pg/mL). Our study demonstrates GDNF over-expression in children with SB. This upregulation is significantly associated with the severity of spinal cord damage in SB patients and appears to correlate with poor motor function of children, representing an important biochemical marker of the severity of spine injury.
PMID: 19125682
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