Osmolality of CSF in inflammatory diseases of central nervous system

Dupanovic, Brankica; Andric, Bogdanka; Terzic, Dragica

doi:10.1016/j.ijid.2012.05.518

Cited by 2 publications

(2 citation statements)

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“…Importantly, the osmolality of biofluids is known to change during or due to various clinical pathologies. Altered osmolality of CSF and blood samples were previously found in different inflammatory diseases in the CNS as compared to a control group in one prospective human study [ 8 ]. In another prospective study of 179 patients with different neurological disorders, it was found that patient CSF osmolality was higher than serum osmolality regardless of the neurological condition, suggesting that an osmotic gradient in the CNS is a homeostatic condition [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

“…A change in osmolality from homeostatic equilibrium in the human body is often associated with various pathologies directly or indirectly including kidney disorders [ 4 ], semen quality [ 5 ], osmotic demyelination syndrome [ 6 ], and various ion imbalance disorders [ 7 ]. A prospective study of 160 patients revealed that the osmolality of blood and CSF were found to be altered in patients with identified inflammatory diseases of the CNS [ 8 , 9 ]. Notably, osmotic demyelination syndrome is a CNS disorder connected to osmotic imbalance generated due to elevated levels of sodium in the serum that leads to degeneration of myelin and oligodendrocytes, blood–brain/spinal cord-barrier breakdown, microglial activation, and astrocyte death [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

Pukale,

Adkins-Travis,

Aryal

et al. 2024

Fluids Barriers CNS

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Background Syringomyelia (SM) is characterized by the development of fluid-filled cavities, referred to as syrinxes, within the spinal cord tissue. The molecular etiology of SM post-spinal cord injury (SCI) is not well understood and only invasive surgical based treatments are available to treat SM clinically. This study builds upon our previous omics studies and in vitro cellular investigations to further understand local fluid osmoregulation in post-traumatic SM (PTSM) to highlight important pathways for future molecular interventions. Methods A rat PTSM model consisting of a laminectomy at the C7 to T1 level followed by a parenchymal injection of 2 μL quisqualic acid (QA) and an injection of 5 μL kaolin in the subarachnoid space was utilized 6 weeks after initial surgery, parenchymal fluid and cerebrospinal fluid (CSF) were collected, and the osmolality of fluids were analyzed. Immunohistochemistry (IHC), metabolomics analysis using LC–MS, and mass spectrometry-based imaging (MSI) were performed on injured and laminectomy-only control spinal cords. Results We demonstrated that the osmolality of the local parenchymal fluid encompassing syrinxes was higher compared to control spinal cords after laminectomy, indicating a local osmotic imbalance due to SM injury. Moreover, we also found that parenchymal fluid is more hypertonic than CSF, indicating establishment of a local osmotic gradient in the PTSM injured spinal cord (syrinx site) forcing fluid into the spinal cord parenchyma to form and/or expand syrinxes. IHC results demonstrated upregulation of betaine, ions, water channels/transporters, and enzymes (BGT1, AQP1, AQP4, CHDH) at the syrinx site as compared to caudal and rostral sites to the injury, implying extensive local osmoregulation activities at the syrinx site. Further, metabolomics analysis corroborated alterations in osmolality at the syrinx site by upregulation of small molecule osmolytes including betaine, carnitine, glycerophosphocholine, arginine, creatine, guanidinoacetate, and spermidine. Conclusions In summary, PTSM results in local osmotic disturbance that propagates at 6 weeks following initial injury. This coincides with and may contribute to syrinx formation/expansion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

Pukale,

Adkins-Travis,

Aryal

et al. 2024

Fluids Barriers CNS

View full text Add to dashboard Cite

show abstract

Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

Pukale

Adkins-Travis

Aryal

et al. 2023

Preprint

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Background The molecular etiology of syringomyelia (SM) post-spinal cord injury (SCI) is not well understood and only invasive surgical based treatments are available to treat SM. This study builds upon our previous omics studies and in vitro cellular investigations to further understand local fluid osmoregulation in post-traumatic SM (PTSM) to highlight important pathways for future molecular interventions. Methods A rat PTSM model consisting of a parenchymal injection of 2 µL quisqualic acid (QA) and an injection of 5 µL kaolin in the subarachnoid space, followed by laminectomy at the C7 to T1 level was utilized. 6 weeks prior to the initial surgery, parenchymal fluid and cerebrospinal fluid (CSF) were collected, and the osmolality analyzed. Immunohistochemistry (IHC), metabolomics analysis using LC/MS, and mass spectrometry-based imaging (MSI) were performed on injured and laminectomy only spinal cords. Results We demonstrated that the osmolality of the local parenchymal fluid encompassing syrinxes was higher compared to control spinal cords after laminectomy, indicating a local osmotic imbalance due to SM injury. Moreover, we also found that parenchymal fluid is more hypertonic than CSF, indicating establishment of a local osmotic gradient in the PTSM injured spinal cord (syrinx area) forcing fluid into the spinal cord parenchyma to form and/or expand syrinxes. IHC results demonstrated upregulation of betaine, ions, water channels/transporters, and enzymes (BGT1, KCC4, AQP1, AQP4, CHDH) at the injury site as compared to caudal and rostral sites to the injury, implying extensive local osmoregulation activities at the injury site. Further, metabolomics analysis corroborated alterations in osmolality at the injury site by upregulation of small molecule osmolytes including betaine, carnitine, glycerophosphocholine, arginine, creatine, guanidinoacetate, and spermidine. Conclusions In summary, PTSM results in local osmotic disturbance that propagates up to 6 weeks following initial injury. This coincides with and may contribute to syrinx formation/expansion.

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Osmolality of CSF in inflammatory diseases of central nervous system

Cited by 2 publications

References 0 publications

Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

Investigating post-traumatic syringomyelia and local fluid osmoregulation via a rat model

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