Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma, Hari Shanker

doi:10.2174/1381612053507837

Cited by 157 publications

(227 citation statements)

References 272 publications

(480 reference statements)

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“…128 In vivo disease models If in the previous examples the integrity of the BBB was maintained and the brain was considered as a "non-pathologic" brain, in the following examples, several researches have been reviewed concerning neuro-pathologies in which the BBB integrity and permeability is seriously compromised. 12,51,103,135 These pathologies could vary from neurodegenerative diseases (Parkinson, Alzheimer and Huntigton's) to epilepsy, infectious brain diseases, strokes and many others.…”

Section: Nanoparticles and Liposomesmentioning

confidence: 99%

Nanoparticle transport across the blood brain barrier

et al. 2016

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While the role of the blood-brain barrier (BBB) is increasingly recognized in the (development of treatments targeting neurodegenerative disorders, to date, few strategies exist that enable drug delivery of non-BBB crossing molecules directly to their site of action, the brain. However, the recent advent of Nanomedicines may provide a potent tool to implement CNS targeted delivery of active compounds. Approaches for BBB crossing are deeply investigated in relation to the pathology: among the main important diseases of the CNS, this review focuses on the application of nanomedicines to neurodegenerative disorders (Alzheimer, Parkinson and Huntington's Disease) and to other brain pathologies as epilepsy, infectious diseases, multiple sclerosis, lysosomal storage disorders, strokes.

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Section: Nanoparticles and Liposomesmentioning

confidence: 99%

Nanoparticle transport across the blood brain barrier

et al. 2016

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“…11 An investigation has been done to evaluate macromolecular transport structures that increased after the brain and spinal cord had been subjected to a variety of injuries. A theory was hypothesized that a unique endothelial cell system formed transendothelial cell channels defined as vesiculo-canalicular or vesiculo-tubular structures.…”

Section: Discussionmentioning

confidence: 99%

Imaging Diagnosis—postmyelographic Epidural Leakage Due to Increased Meningeal Permeability

Carstens

Kitshoff

2007

Vet Radiology Ultrasound

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The dog had acute pain in the hind quarters and a mild lameness in the right hind leg for 48 h. When examined, there was loss of conscious proprioception, paralysis, and hyperreflexia of both hind legs, with loss of superficial and retention of deep pain. The panniculus reflex was absent at approximately the tenth thoracic vertebra (T10). There was some ataxia present in the forelimbs, but forelimb reflexes were normal as was the presence of superficial and deep pain. There was urine dribbling and increased ease in expressing the urinary bladder. The neurological examination was consistent with a spinal cord lesion between T10 and L6. Laboratory FindingsAbnormal laboratory parameters were low red cell count at 5.21 x 10 12 /l (reference value of 5.5-8.5 21 x 10 12 /l), low hematocrit of 0.349 (reference value 0.37-0.55) and mildly elevated white cell count of 18.5 x 10 9 /l (reference value 6.0-15.0 x 10 9 /l). The absolute mature neutrophil count was slightly elevated at 14.99 x 10 9 /l (reference value 3.0-11.5 x 10 9 /l), as was the absolute monocyte count at 1.85 x 10 9 /l (reference value 0.15-1.35 x 10 9 /l). ImagingSurvey spinal radiographs were normal. A myelogram was performed by placing a 22G 75mm Terumo spinal needle into the subarachnoid space at L5/L6. Two milliliters of cerebrospinal fluid (CSF) was withdrawn, which was mildly blood contaminated. Nine milliliters of 300mgI/ml iohexol was then injected into the subarachnoid space. In multiple views there was interrupted epidural leakage extending from the dorsal aspect of the subarachnoid space at the level of mid T12 caudally to the dorsal aspect of mid lumbar vertebra 2 (L2) (Fig. 1). Although this leakage did not communicate with the myelogram puncture site at L5/L6, it was initially thought to be iatrogenic. On the dorsoventral views a patchy contrast opacity was seen over the spinal cord from mid T10 to mid T13, hampering the evaluation. No signs of spinal cord compressive lesions were seen. The next day the dog had no deep pain in the hind legs and there was progression of the forelimb ataxia. A followup cervical myelogram was performed to determine whether a compressive lesion cranial to T13 was

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“…Since spinal cord injury increases permeability of the blood-spinal cord barrier, 23,24 it is reasonable to consider whether p-glycoprotein inhibition is necessary to increase methylprednisolone concentrations in the injured spinal cord. However, Braughler and Hall demonstrated that methylprednisolone entry into injured spinal tissue was greater than in uninjured tissue only if methylprednisolone was administered within 1 h of injury.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporine-A-mediated inhibition of p-glycoprotein increases methylprednisolone entry into the central nervous system

Bernards

2005

Spinal Cord

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Study design: Prospective, randomized, pharmacokinetic study. Objective: To determine if cyclosporine-A-mediated inhibition of p-glycoprotein would increase methylprednisolone entry into the central nervous system thereby permitting a reduction in the systemic methylprednisolone dose. Setting: Department of Anesthesiology, University of Washington, Seattle, USA. Methods: Microdialysis probes were used to obtain cerebrospinal fluid and gluteal muscle extracellular fluid samples for measurement of methylprednisolone concentration in pigs. At time zero, a methylprednisolone bolus was given and an infusion started. At 210 min, after reaching a stable methylprednisolone concentration, a cyclosporine-A bolus was given (either 10 or 30 mg/kg) and microdialysis samples collected until 420 min. Plasma samples were collected at 10, 30 min and then every 30 min until the study's end. Results: Cyclosporine-A bolus produced a dose-dependant increase in methylprednisolone concentration in plasma, muscle and cerebrospinal fluid. Importantly, the magnitude of the increase in cerebrospinal fluid was significantly greater than the increase in plasma and muscle. Conclusions: The relatively greater increase in cerebrospinal fluid concentrations of methylprednisolone is consistent with increased penetration of the blood-brain barrier secondary to cyclosporine-mediated p-glycoprotein inhibition. Theoretically, increased methylprednisolone entry into the central nervous system should allow a reduction in the systemic methylprednisolone dose and a consequent decrease in glucocorticoid-mediated side effects.

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Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Cited by 157 publications

References 272 publications

Nanoparticle transport across the blood brain barrier

Nanoparticle transport across the blood brain barrier

Imaging Diagnosis—postmyelographic Epidural Leakage Due to Increased Meningeal Permeability

Cyclosporine-A-mediated inhibition of p-glycoprotein increases methylprednisolone entry into the central nervous system

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