18 research outputs found

    Recovery of Sensorimotor Function in Rats Following Acute Rapid Eye Movement Sleep Deprivation and Controlled Cortical Impact

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    Traumatic brain injury (TBI) resulting from bomb blasts and explosions is common among military personnel. The effects of Rapid Eye Movement (REM) sleep deprivation on the sensorimotor behavior and physiological mechanisms related to TBI are unknown. Thirty-two Long Evans rats were randomly assigned to REM sleep deprivation (RSD) with controlled cortical impact (CCI), social isolation (SI) with CCI, or normal housing (NH) with CCI or Sham. Two behavioral tasks [beam walk and bilateral tactile adhesive removal somatosensory (BTARS)] testing motor and sensory function were used to investigate recovery of function. Brain tissue was analyzed using Cresyl Violet stain (cell bodies), GFAP (astrocytes) and Fluoro Jade-B (dying cells) labeling. Results indicated that 24 hour RSD immediately prior to CCI impaired recovery of sensorimotor function when tested on the adhesive removal task. Recovery of sensorimotor function as a result of 24 hour RSD immediately prior to CCI was not significantly impaired when tested on the balance beam walk task. Results also indicated that sleep deprivation seemed to intensify inflammation, lesion size and neuron loss when compared to non sleep deprived animal

    Microstructural abnormalities in deep and superficial white matter in youths with mild traumatic brain injury

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    BACKGROUND: Diffusion Tensor Imaging (DTI) studies of traumatic brain injury (TBI) have focused on alterations in microstructural features of deep white matter fibers (DWM), though post-mortem studies have demonstrated that injured axons are often observed at the gray-white matter interface where superficial white matter fibers (SWM) mediate local connectivity. OBJECTIVES: To examine microstructural alterations in SWM and DWM in youths with a history of mild TBI and examine the relationship between white matter alterations and attention. METHODS: Using DTIDWM fractional anisotropy (FA) and SWM FA in youths with mild TBI (TBI, n=63) were compared to typically developing and psychopathology matched control groups (n=63 each). Following tract-based spatial statistics, SWM FA was assessed by applying a probabilistic tractography derived SWM mask, and DWM FA was captured with a white matter fiber tract mask. Voxel-wise z-score calculations were used to derive a count of voxels with abnormally high and low FA for each participant. Analyses examined DWM and SWM FA differences between TBI and control groups, the relationship between attention and DWM and SWM FA and the relative susceptibility of SWM compared to DWM FA to alterations associated with mild TBI. RESULTS: Case-based comparisons revealed more voxels with low FA and fewer voxels with high FA in SWM in youths with mild TBI compared to both control groups. Equivalent comparisons in DWM revealed a similar pattern of results, however, no group differences for low FA in DWM were found between mild TBI and the control group with matched psychopathology. Slower processing speed on the attention task was correlated with the number of voxels with low FA in SWM in youths with mild TBI. CONCLUSIONS: Within a sample of youths with a history of mild TBI, this study identified abnormalities in SWM microstructure associated with processing speed. The majority of DTI studies of TBI have focused on long-range DWM fiber tracts, often overlooking the SWM fiber type

    Recovery of Sensorimotor Function in Rats Following Acute Rapid Eye Movement Sleep Deprivation and Controlled Cortical Impact

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    Traumatic brain injury (TBI) resulting from bomb blasts and explosions is common among military personnel. The effects of Rapid Eye Movement (REM) sleep deprivation on the sensorimotor behavior and physiological mechanisms related to TBI are unknown. Thirty-two Long Evans rats were randomly assigned to REM sleep deprivation (RSD) with controlled cortical impact (CCI), social isolation (SI) with CCI, or normal housing (NH) with CCI or Sham. Two behavioral tasks [beam walk and bilateral tactile adhesive removal somatosensory (BTARS)] testing motor and sensory function were used to investigate recovery of function. Brain tissue was analyzed using Cresyl Violet stain (cell bodies), GFAP (astrocytes) and Fluoro Jade-B (dying cells) labeling. Results indicated that 24 hour RSD immediately prior to CCI impaired recovery of sensorimotor function when tested on the adhesive removal task. Recovery of sensorimotor function as a result of 24 hour RSD immediately prior to CCI was not significantly impaired when tested on the balance beam walk task. Results also indicated that sleep deprivation seemed to intensify inflammation, lesion size and neuron loss when compared to non sleep deprived animal

    Исследование нарушений функциональных связей между сетью пассивного режима работы мозга и структурами мозжечка у пациентов с легкой черепно-мозговой травмой в острой стадии по данным фМРТ состояния покоя

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    Mild traumatic brain injury (mTBI) is the most common neurological damage in children that's why it is extremely important to identify and analyze biomarkers that can help in predicting patient's treatment and recovery in period of mTBI. Aim of this study is to verify a hypothesis that functional connectivity disturbances between intact cerebellum and DMN nodes are included in symptomatic manifestation of mTBI.Methods. 28 MR negative patients with mTBI were studied in age from 12 to 17 years (mean age – 14.7 years). The control group consisted of 23 healthy children. All MRI studies wereperformed on a Philips AchievadStream 3.0 T scanner equipped with a 32-channelPhilips dStream head coil. A 4 min rsfMRI gradient-echo echo planar imaging (EPI)sequence was acquired (TR = 3000 ms, echo time (TE) = 30 ms, 80 dynamics withdynamic scan time = 3 s). fMRI data were processed using functional connectivitytoolbox CONN.Results. No statistically significant differences in correlation strengths between control group and group of patients were detected as a result of DMN analysis. Intergroup seed-basedcorrelation ROI analysis revealed statistically significant (p < 0.05) differencein links between DMN regions and vermis (cerebellum): positive link in control group and negative link in groupof patients.Conclusions. The revealed changes in DMN neuronal connection and cerebellar regions in acute stage of mTBI patients can be an initial step of damages leading to cognitive deficit which can be developed in future.Легкая черепно-мозговая травма (лЧМТ) является наиболее распространенным неврологическим повреждением у детей, поэтому чрезвычайно важно идентифицировать и проанализировать биомаркеры, которые могут помочь в процессах лечения и выздоровления пациента с лЧМТ.Цель исследования: подтвердить гипотезу о том, что нарушения функциональных связей между неповрежденным мозжечком и узлами сети DMN включены в симптоматическое проявление лЧМТ.Методы. Обследованы 28 МР-негативных пациентов с лЧМТв возрасте от 12 до 17 лет (средний возраст 14,7 года). Контрольная группа состояла из 23 здоровых детей. Все МРТ-исследования проводились на сканере Philips Achieva dStream 3,0 Tл, оборудованном 32-канальной головной катушкой Philips dStream. Проведена фМРТ состояния покоя (EPI последовательность, TR = 3000 мс, время эха (TE) = 30 мс, 80 динамиков с динамическим временем сканирования 3 с). Данные фМРТ обработаны с использованием программного пакета CONN.Результаты. Не обнаружено статистически значимого различия в значениях коэффициентов функциональных связей между областями сети DMN в группах пациентов и контроля. Межгрупповой анализ выявил статистически значимое (р < 0,05) различие в нейронных связях между частями DMN и червем мозжечка (vermis, структурная часть мозжечка): положительная связь в контрольной группе и отрицательная связь в группе пациентов.Заключение. Выявленные изменения в нейрональных связях между областями DMN и мозжечка у пациентов с лЧМТ в остром периоде могут быть начальным этапом повреждений, приводящих к когнитивному дефициту, который может развиться в будущем

    Diabetes insipidus after traumatic brain injury

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    Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI

    Dealing with Danger in the CNS: The Response of the Immune System to Injury

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    Fighting pathogens and maintaining tissue homeostasis are prerequisites for survival. Both of these functions are upheld by the immune system, though the latter is often overlooked in the context of the CNS. The mere presence of immune cells in the CNS was long considered a hallmark of pathology, but this view has been recently challenged by studies demonstrating that immunological signaling can confer pivotal neuroprotective effects on the injured CNS. In this review, we describe the temporal sequence of immunological events that follow CNS injury. Beginning with immediate changes at the injury site, including death of neural cells and release of damage-associated molecular patterns (DAMPs), and progressing through innate and adaptive immune responses, we describe the cascade of inflammatory mediators and the implications of their post-injury effects. We conclude by proposing a revised interpretation of immune privilege in the brain, which takes beneficial neuro-immune communications into account

    Effects of voluntary physical exercise, citicoline, and combined treatment on object recognition memory, neurogenesis and neuroprotection after traumatic brain injury in rats

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    Final publication is available from Mary Ann Liebert, Inc., publishers. http://dx.doi.org/10.1089/neu.2014.3502The biochemical and cellular events that lead to secondary neural damage after traumatic brain injury (TBI) contribute to long-term disabilities, including memory deficits. There is a need to search for single and/or combined treatments aimed at reducing these TBI-related dysfunctions. The effects of citicoline and of voluntary physical exercise in a running wheel (3 weeks), alone or in combination, on TBI-related short-term (3 h) and long-term (24 h) object recognition memory (ORM) deficits, and on neurogenesis and neuroprotection were examined using a rodent model of TBI(controlled cortical impact injury). Citicoline improved memory deficits at the two times tested, while physical exercise only in the long-term test. Physical exercise had a clear neuroprotective effect as indicated by reduced interhemispheric differences in hippocampal formation and lateral ventricle volumes and in density of mature neurons in the hilus of the dentate gyrus and the perirhinal cortex. Physical exercise also increased cell proliferation and neurogenesis in the granular cell layer of the dentate gyrus. Some degree of neuroprotection of citicoline was suggested by reduced interhemispheric differences in the volume of the hippocampal formation. Contrary to what was expected, the effects of citicoline and physical exercise did not sum up.Furthermore, a negative interference between both treatments was found in several behavioral and histological variables. The promising profiles of both treatments as therapeutic tools in TBI when applied singly, underscore the need to carry out further works looking for other combined treatment regimens that increase the benefit of each treatment alone
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