Spinal motor neuron excitability in newborns following fetal distress: sub-clinical depression revealed by soleus H-reflex

Kumar, Subhankar; Dereddy, Narendra; Bd, Bhatia; Prakash, Udai

doi:10.1016/j.clinph.2005.06.007

Cited by 11 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Spinal cord injury after H–I may contribute to the clinical picture of hypoxic-ischemic encephalopathy (Rorke, 1982) since it is accompanied by hypotonia, weakness, and decreased motoneuron excitability (Kumar et al, 2005; Prakash et al, 2005; Volpe, 2008). Spinal cord injury is often problematic to detect clinically since spinal signs are often overshadowed by cerebral signs of injury such as altered mental status and seizures.…”

Section: Discussionmentioning

confidence: 99%

Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy

Drobyshevsky

Quinlan

2017

Experimental Neurology

View full text Add to dashboard Cite

While antenatal hypoxia-ischemia (H–I) is a well-established cause of brain injury, the effects of H–I on the spinal cord remain undefined. This study examined whether hypertonia in rabbits was accompanied by changes in spinal architecture. Rabbit dams underwent global fetal H–I at embryonic day 25 for 40 min. High resolution diffusion tensor imaging was performed on fixed neonatal CNS. Fractional anisotropy (FA) and regional volumetric measurements were compared between kits with and without hypertonia after H–I and sham controls using Tract Based Spatial Statistics. Hypertonic kits showed evidence of damage from hypoxia not only in the brain, but in spinal cord as well. Hypertonic kits showed reduced FA and thickness in corticospinal tracts, external capsule, fimbria, and in white and gray matter of both cervical and lumbar spinal cord. Dorsal white matter of the spinal cord was the exception, where there was thickening and increased FA in hypertonic kits. Direct damage to the spinal cord was demonstrated in a subset of dams imaged during H–I with a 3T magnetic resonance scanner, where apparent diffusion coefficient in fetal spinal cords acutely decreased during hypoxia. Hypertonic kits showed subsequent decreases in lumbar motoneuron counts and extensive TUNEL- and Fluoro-Jade C-positive labeling was present in the spinal cord 48 hours after H–I, demonstrating spinal neurodegeneration. We speculate that global H–I causes significant loss of both spinal white and gray matter in hypertonic newborns due to direct H–I injury to the spinal cord as well as due to upstream brain injury and consequent loss of descending projections.

show abstract

Section: Discussionmentioning

confidence: 99%

Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy

Drobyshevsky

Quinlan

2017

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…[11][12][13] The babies were comfortably placed in prone position on the lap of mothers with a small pillow underneath the lower limb; therefore, limbs remained extended. Investigations were done with the help of Biopac Student Lab Advanced System and GRASS stimulator (model S88).…”

Section: Methodsmentioning

confidence: 99%

“…The procedure has been standardized over the years in our laboratory. [11][12][13][14] The strength of stimulus for eliciting the H-reflex was submaximal, it preferentially activate the large Ia sensory fibers. Whereas it was supramaximal strength of stimulus for observing maximum (MRL).…”

Section: Methodsmentioning

confidence: 99%

H-reflex conduction velocity in babies from birth to 6 month of age

Debbarma¹,

Bhagat²,

Chowdhary³

et al. 2017

Natl J Physiol Pharm Pharmacol

Self Cite

View full text Add to dashboard Cite

Background:The neurological assessment of newborn babies is clinically difficult due to its subjectivity. H-reflex and H-reflex conduction velocity (HRCV) are especially useful in pediatric nerve conduction studies. It evaluates proximal segment of nerve which includes Ia sensory afferent and motor component of the peripheral nerve. Aims and Objectives: To assess the H-reflex latency (HRL) and HRCV in first 6 months of postnatal period and their correlation with other anthropometric variable such as weight, height, and head circumference. Materials and Methods: 26 full-term babies between the age group from birth to 6 months of age were the study participants. HRL and HRCV were recorded in the right lower limbs at posterior tibial nerve-soleus muscle in all the babies. Results: The values of HRCV had significantly increased at 3-6 months of age, and it was strongly correlated with HRL but weakly correlated with age of the babies. Conclusion: The proximal nerve conduction velocity i.e. HRCV was significantly increased from birth time to 3-6 months of age due to rapid myelination and maturation of nerve fibers. This rise in velocity has also maintained the HRL to a comparable level in all the babies even with the increment of height. The HRL and HRCV could be useful as a complementary method along with clinical examination to assess functional integrity of the spinal cord.

show abstract

“…Neonatal outcomes included large for gestational age (LGA, de ned as birthweight > 90th percentile for gestational age and sex), small for gestational age (SGA, de ned as birthweight < 10th percentile for gestational age and sex), macrosomia (de ned as birthweight ≥ 4000 g), neonatal asphyxia (de ned as cannot spontaneously initiated breathing and Apgar score = 1 to 7) within the rst minute after delivery. Fetal distress in utero was de ned by late-decelerations in fetal heart rate [26].…”

Section: Study Population and Data Sourcesmentioning

confidence: 99%

Maternal Low Fasting Plasm Glucose in the Second Trimester is Associated with Neonatal Asphyxia

Yuan

Yang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Neonatal asphyxia (NA) is associated with neonatal respiratory distress syndrome, cerebral palsy and neonatal death. Risk factors for NA have been identified as maternal hypertension, premature birth and anemia. While the effect of maternal fasting plasm glucose (FPG) in the second trimester of pregnancy on NA remains unclear. Method Retrospective data from 9661 singleton newborns and mothers were analyzed from January 2016 to July 2018 in Tongzhou district, Beijing. Multivariate logistic regression was used to investigate the risk factors of NA, adjusted for gestational hypertension, triglyceride in the second trimester of pregnancy, fetal distress in utero and preterm birth. Results Of the 9,661 newborns, 26 (2.7‰) were diagnosed with neonatal death (Apgar score 1min = 0) and 52 (5.4‰) with varying degrees of asphyxia (Apgar score 1min = 1 to 6). The asphyxia group showed lower FPG [asphyxia group vs non-asphyxia group, 4.5±0.4 vs 4.8±0.5 mmol/L, P<.01], higher triglyceride level (asphyxia group vs non-asphyxia group, 3.0±1.3 vs 2.5±1.9 mmol/L P<.01) in the second trimester, higher rates of gestational hypertension, fetal distress in utero, preterm birth than the non-asphyxia group (P<.05). Multivariate logistic regression revealed that lower FPG in the second trimester was an independent risk factor of NA [adjusted odds ratio (AOR) 0.26; 95% CI 0.08 to 0.80]. Conclusion Pregnant women with low fasting glucose in the second trimester of pregnancy are at increased risk of birth asphyxia in their offspring.

show abstract

Spinal motor neuron excitability in newborns following fetal distress: sub-clinical depression revealed by soleus H-reflex

Cited by 11 publications

References 19 publications

Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy

Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy

H-reflex conduction velocity in babies from birth to 6 month of age

Maternal Low Fasting Plasm Glucose in the Second Trimester is Associated with Neonatal Asphyxia

Contact Info

Product

Resources

About