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Traumatic spinal cord injury is a life-changing condition with a significant socio-economic impact on patients, their relatives, their caregivers, and even the community. Despite considerable medical advances, there is still a lack of options for the effective treatment of these patients. The major complexity and significant disabling potential of the pathophysiology that spinal cord trauma triggers are the main factors that have led to incremental scientific research on this topic, including trying to describe the molecular and cellular mechanisms that regulate spinal cord repair and regeneration. Scientists have identified various practical approaches to promote cell growth and survival, remyelination, and neuroplasticity in this part of the central nervous system. This review focuses on specific detailed aspects of the involvement of cations in the cell biology of such pathology and on the possibility of repairing damaged spinal cord tissue. In this context, the cellular biology of sodium, potassium, lithium, calcium, and magnesium is essential for understanding the related pathophysiology and also the possibilities to counteract the harmful effects of traumatic events. Lithium, sodium, potassium—monovalent cations—and calcium and magnesium—bivalent cations—can influence many protein–protein interactions, gene transcription, ion channel functions, cellular energy processes—phosphorylation, oxidation—inflammation, etc. For data systematization and synthesis, we used the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) methodology, trying to make, as far as possible, some order in seeing the “big forest” instead of “trees”. Although we would have expected a large number of articles to address the topic, we were still surprised to find only 51 unique articles after removing duplicates from the 207 articles initially identified. Our article integrates data on many biochemical processes influenced by cations at the molecular level to understand the real possibilities of therapeutic intervention—which must maintain a very narrow balance in cell ion concentrations. Multimolecular, multi-cellular: neuronal cells, glial cells, non-neuronal cells, but also multi-ionic interactions play an important role in the balance between neuro-degenerative pathophysiological processes and the development of effective neuroprotective strategies. This article emphasizes the need for studying cation dynamics as an important future direction.
Traumatic spinal cord injury is a life-changing condition with a significant socio-economic impact on patients, their relatives, their caregivers, and even the community. Despite considerable medical advances, there is still a lack of options for the effective treatment of these patients. The major complexity and significant disabling potential of the pathophysiology that spinal cord trauma triggers are the main factors that have led to incremental scientific research on this topic, including trying to describe the molecular and cellular mechanisms that regulate spinal cord repair and regeneration. Scientists have identified various practical approaches to promote cell growth and survival, remyelination, and neuroplasticity in this part of the central nervous system. This review focuses on specific detailed aspects of the involvement of cations in the cell biology of such pathology and on the possibility of repairing damaged spinal cord tissue. In this context, the cellular biology of sodium, potassium, lithium, calcium, and magnesium is essential for understanding the related pathophysiology and also the possibilities to counteract the harmful effects of traumatic events. Lithium, sodium, potassium—monovalent cations—and calcium and magnesium—bivalent cations—can influence many protein–protein interactions, gene transcription, ion channel functions, cellular energy processes—phosphorylation, oxidation—inflammation, etc. For data systematization and synthesis, we used the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) methodology, trying to make, as far as possible, some order in seeing the “big forest” instead of “trees”. Although we would have expected a large number of articles to address the topic, we were still surprised to find only 51 unique articles after removing duplicates from the 207 articles initially identified. Our article integrates data on many biochemical processes influenced by cations at the molecular level to understand the real possibilities of therapeutic intervention—which must maintain a very narrow balance in cell ion concentrations. Multimolecular, multi-cellular: neuronal cells, glial cells, non-neuronal cells, but also multi-ionic interactions play an important role in the balance between neuro-degenerative pathophysiological processes and the development of effective neuroprotective strategies. This article emphasizes the need for studying cation dynamics as an important future direction.
Objective. To establish the effect of neurogenic shock (NS) on the course of acute complicated injury of the cervical spine.Material and Methods. The retrospective study included 96 patients with acute complicated injury of the cervical spine. The criteria for the presence of NS were determined as mean blood pressure (BP) < 70 mm Hg, and heart rate (HR) < 60 per minute. Two groups were distinguished: Group 1 included 13 patients with NS, and Group 2 – 83 patients without NS. The main characteristics of patients and the course of spinal cord injury were analyzed from the moment of admission to the 30th day of follow-up.Results. There were no statistically significant differences between the groups in terms of gender, age, level of spinal injury, severity of spinal cord injury and comorbidity. Admission BP and HR in patients with NS were below the reference values and had statistically significant differences in comparison with similar indicators in patients of Group 2. On the first day of treatment in the intensive care unit (ICU), hemodynamic support was required for all patients of Group 1, and for 69 patients of Group 2 (83.1 %). The duration of hemodynamic support in Group 1 was 11 days [6; 15], and in Group 2 – 7 days [4; 14]; p = 0.231. Blood lactate and pH levels were consistent with reference values at all stages, with no intergroup differences. Differences in the severity of organ dysfunctions (SOFA scale) were registered only on the seventh day of treatment in the ICU (p = 0.010); there were no significant differences in the severity of the patients’ condition (APACHE II scale). The presence of NS was accompanied by a statistically significant increase in the complication rate. The duration of treatment in the ICU was 28 days [22; 57] in Group 1, 23.5 days [11; 37] in Group 2 (p = 0.055), and that in the hospital – 58 days [44; 70] in Group 1 versus 41.5 [24; 59.5] in Group 2 (p < 0.025). Positive dynamics in the neurological status was noted at discharge in 15.0 % of Group 1 patients and in 19.3 % of Group 2 patients.Conclusion. The prevalence of NS in isolated injury of the cervical spine was 13.5 %. The development of NS significantly increases the complication rate and duration of hospital stay, but does not exclude the possibility of regression of existing neurological disorders.
Introduction. Cerebral salt-wasting syndrome and diabetes insipidus are serious complications of craniocerebral injury and spinal cord injuries. Each of the syndromes in some cases causes a life-threatening condition. This determines the importance of timely diagnosis and emergency intensive care measures. In the literature, there are only single descriptions of combinations of these symptoms in one patient.Clinical case report. A victim with craniocerebral injury and cervical spinal cord injury underwent, according to emergency indications, emptying and drainage of a tense subgaleal hematoma of the fronto-parieto-occipital region, spinal cord decompression, and stabilization of the spine. Postoperative follow-up and intensive care: on the 1st day the rate of diuresis was 2.5 mL/kg/h, blood glucose level – 14.18 mmol/L, and sodium level – 148–158 mmol/L. The patient was diagnosed with diabetes insipidus, and a therapy with desmopressin at a dose of 0.6 mg/day, restoration of fluid volume with hypotonic solutions, and correction of hyperglycemia was started. On the 4th day blood sodium level was 133 mmol/L, and blood glucose level – 8.67 mmol/L. On the 5th day, hyponatremia of 126–115 mmol/L was noted with a diuresis rate of 4 mL/kg/h and glicemya level of 7.86 mmol/L. The development of cerebral salt-wasting syndrome was diagnosed, and the infusion of hydrocortisone 400 mg/day and of 10% NaCl solution was started. On the 6th day glucose level returned to normal. On the 9th day of follow-up, an increase in the volume of diuresis was again observed, and desmopressin therapy was continued. Stable normalization of water-electrolyte balance, urine output, and glucose levels were observed on the 16th day of follow-up.Conclusion. Monitoring of fluid balance and electrolyte composition of blood serum, and adequate replacement therapy were the conditions for successful treatment of a rare combination of diabetes insipidus and cerebral salt-wasting syndrome in patients with concomitant craniocerebral and spinal cord injuries.
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